Psychiatry

PSYCHOPATHOLOGY
Psychopathology studies disorders of psychic functions, that is, disorders of consciousness, perception,
attention, ideation, memory, intelligence, affectivity and will.
In psychiatry most of the physical examination is based on symptoms (reported by the patient) and not
signs (objectivable), except for a few things: for example, the assessment of the IQ for a person's
cognitive examination, is done by administering tests.
It is more and more fashionable thecultural framework of the patient, in light of the fact that we are now in
a multiethnic and globalized society. Acquiring objective data on his family, on his "race", on his "ethnicity",
on the cultural group, on his language during a psychic examination is a cornerstone of the physical
examination together with the physical elements of the patient. Think of the importance of cultural
syndromes, tutyou those situations due for example to war; adaptation disorders that constitute a chapter
of the DSM and the so-called post-traumatic stress disorder.
As in anatomy, it is important to virtually “dissect” mental functions. Obviously, for example, we speak of
attention disturbance, but this cannot affect memory, cognitive patrimony and other functions. Therefore
it is difficult for a psychic alteration to be present without affecting other psychic functions.

For a didactic question, the different psychic functions are divided. They are:
-
vigilance
-
the space-time orientation
-
communicative contact (language or extra-verbal contact)
-
attention
-
the sense-perceptions
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intelligence or cognitive assets, much more used
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the memory
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the ideation
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affectivity
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psychomotor skills

Much more easily, other authors tend to group these 10 functions into subgroups which are the so-called:
• Cognitive functions: attention, memory, intelligence or cognitive heritage, ideation, vigilance,
orientation.

• Affective functions: here enters the great cauldron of affectivity.

• Volitional functions: psychomotor or will.

It is important to understand the function of a certain psychic function because from these, that is
from their alteration, a series of disorders can arise that are in some way "transcategorial", belonging
to various syndromic pictures: for example, a state of anhedonia may concern a depressed person or a
schizophrenic; a state of apathy can occur in the course of dementia, schizophrenia, depression, etc.
Psychic functions are important in various spheres of life and in the implications that a disease can
give from a psychological point of view, so much so that today the distinction between organic and
functional disease has become thinner and the Cartesian dualism that he saw completely separate.

The mental examination is also important for legal issues: for example, people who want to have a
relative banned or cases of crimes in which the person is declared incapable of understanding and
willing and therefore acquitted (criminal vice, Art. 88 of the Code Criminal). Imputability is, by
definition, the ability to understand and understand. A person with "total vice of mind" is incapable,
while one
 a person with a “partial defect” has seriously diminished capacities and according to the Criminal
Code, even if it is imputable and punishable, his penalty must be reduced.
The doctor evaluates the ability to understand and want by trying to place the subject in a specific
syndromic class and trying to understand, on the basis of his knowledge, if that syndrome is a chronic
and progressive degenerative condition or is acute and related at the moment. We must then try to
understand if the condition of understanding and wanting was present at the time of the crime, for
example expressed by a condition of strong stress or by the use of psychoactive substances.

CONSCIOUSNESS
Consciousness is the state of awareness of oneself, of one's body and of the external environment, an
instantaneous integrative function of all brain activities that coordinates, finalizes and focuses them in
order to optimize adaptive behaviors. We can make a distinction between quantitative and qualitative
disturbances.
• Among the quantitative disturbances of consciousness we have:
• Hypnoid state: intermediate state between consciousness and loss of consciousness with
alterations in lucidity or alertness, numbness, drowsiness that is clouding or dulling (drowsiness)
which normally occurs in the phase of falling asleep with a state of semi-sleep or in the case of
chronic trauma or coma hyperglycemic due to alteration of glucose metabolism.
• Confusional state: in which the patient does not remember his name, where he is, he does not
recognize places and people, he does not remember where he lives, the date, if it is morning,
afternoon or evening, for which he presents temporal-spatial disorientation , often does not react
to stimuli and does not respond to questions, or has a disjointed, disorganized, incomprehensible
and incoherent language, behavior that is inappropriate to the context, up to coma in the most
severe cases.
• Among the qualitative disturbances of consciousness we have
• Twilight state: it consists of a narrowing of the field of conscience, ie the subject only retains
some events, ideas or affective themes with or without temporal-spatial disorientation, as
happens in temporal epilepsy or hysteria. Sometimes a short-lived twilight state manifests itself
in very intense stressful situations such as catastrophes, bereavement, danger to one's life.
• Oneyroid state: in which the patient is no longer able to control the external reality due to the
presence of hallucinations and delusional ideas experienced with intense emotional participation.
• State of delirium: arises abruptly with alteration of the state of consciousness, mental confusion,
temporal-spatial and personal disorientation, i.e. the patient does not remember the date, where
he is and why he is in that place, does not remember his name and personal data , associated
with short- and long-term memory deficits, i.e. deficits in the fixation and recall of memories,
attention deficit, formal alterations of thinking with loosening of associative links, up to delusions
of persecution, harm or reference, poorly systematized, inconsistent and unstable as they tend to
disintegrate. Often the patient presents alterations of perception with visual, auditory, tactile,
kinesthetic illusions, while hallucinations are rarer and occur only in very serious forms of
confusion, such as visual hallucinations. All this also causes mood changes with anxiety, fear,
irritability, agitation with inappropriate, dangerous, aggressive behaviors, escapes in a state of
mental confusion. Delirium has a fluctuating course with a transitory course, it regresses
completely, except in the case of delirium that develops in a picture of dementia or another pre-
existing cognitive disorder, or it favors the onset of some complications such as rhythm
alterations sleep-wakefulness with insomnia, catatonic stupor, psychomotor agitation.
• Furthermore we have the disturbances of the ego consciousness that is of the self-consciousness such as
• Depersonalization: it is the altered perception of oneself with a feeling of detachment from
one's body. It is an unpleasant experience that occurs in case of schizophrenia, use of alcohol and
drugs (hallucinogens), drugs (barbiturates), depressive disorders, panic attacks. Depersonalization
is divided into:
• Autopsychic depersonalization (extraneousness of one's thoughts to one's mind).
• Somatopsychic depersonalization (the patient perceives parts of his own body as being
detached or belonging to other people).

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 • Allopsychic depersonalization or derealization (altered perception of the surrounding
environment with a sense of strangeness, dream or unreality as if the patient were living in
a film).
• Transitivism the patient attributes his actions, perceptions and thoughts to other people
(schizophrenia).
• Apersonation it consists in the self-attribution of other people's actions, perceptions and thoughts.

SENSE-PERCEPTIONS
The sensoperceptions represent a complex system that allows the interaction between the individual and
the external environment, in fact, the sense organs continuously receive various stimuli from the external
environment that are filtered and organized constituting the sensations or sensory stimuli that are
transmitted to the brain areas. cortical and sub-cortical where they are re-elaborated, obtaining the
perception that allows the interaction between the subject and the external environment.

Perception: final result of a complex organizational and integrative activity of the excitations
coming from the stimulation of the peripheral sense organs in this process the sensations are
processed through functions of different nature (memory, affectivity, intelligence) and integrated
in such a way as to allow the knowledge of internal and external reality.

Sensation: any stimulus that reaches my sensory organs ("I go out the door and see a light in the
sky"), unlike a perception, there is the recognition of the sensory stimulus ("I go out the door, I see
a light in the sky and I recognize which is a flash "). The difference lies in recognition, a function
that involves the activation of a series of different cortical areas. Therefore, in perception, we
recognize that particular stimulus that reaches our sensory organs (sensation) thanks to the
associative areas of the brain. To be able to say that that is a flash, you must have had previous
experience of lightning, go and code that stimulus between the flashes until you say "that is a
lightning".
There may be disturbances in sense-perception, both of an organic nature (think of how many lesions of
the nerve pathways can alter sense-perception: spinal trauma that interrupts the pain and thermal
pathways) and of a functional nature. In this last case there are influences from affectivity and cognitive,
intellectual and memory functions.
Sensory-perception disorders are divided into disorders:
• Qualitative:
• Alterations in the perception of stimuli:
•Erythropsia: altered color perception of objects that suddenly appear
rare disorders often ace- colored red (although the sensory pathways are intact).
ciate to bipolarism
•Xanthopsia: objects appear colored in yellow (although the sensory pathways are inte-
hallucin poisoning gre).
genes (LSD), lesions of the
the ocular apparatus, injuries • Micropsy: altered perception of the size of objects that appear smaller
of the temporal region of their real size (although the sensory pathways are intact).
parieto-occipital, epiles-
both, post-alcoholic disorders • Macropsy: objects appear larger than their real size (despite the pathways
(delirium tremens) sensory are intact).
• Non-hallucinatory alterations in perception: unlike real hallucinations, they can be found both
in normal and pathological conditions including:
• Representation: the patient mentally relives an experience of the past in the absence of
the sensory stimuli that had evoked it but it can be favored by the presence of strong
emotions)
• Hallucinosis: hallucinatory perception of which the subject is able to recognize the
pathological nature by not accepting it as a real perception, generally it is related to organ
pathologies of the CNS such as lesions of the brain stem and temporomocipital lesions.
• Illusion: distorted perception of an existing object (for example a noise is perceived as a
sound of a bell, or I see a coat hanger and I think it is a madonna), which can be corrected
more or less quickly by switching to a correct perception of reality. They can be caused by
hallucinogens, delirium ...

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 • Pareidolia: tendency to find orderly structures and familiar shapes in disordered images
(seeing a face or an animal in a cloud).
• Pseudo-hallucinations: they concern their internal organs, they are perceived to be moving
or altered (eg patient who reports that his intestine is rotten or that the brain is moving in
the skull).
• Hallucinations: false perceptions or perceptions with a corporeal character of an object that is
not present, not criticized by the patient, that is, he perceives a non-existent object, but
according to him they are real perceptions or experiences, perfectly congruent.
• They are classified according to the sensory area involved in:
• Auditory hallucinations: they are the most frequent in psychiatry. Typical of
schizophrenia (or psychotic disorders related to schizophrenia, such as paranoia), in
which the patient hears whispered but understandable voices of unknown or known
subjects.Among the auditory hallucinations found what are defined as first-order
symptoms according to Schneider: comment sound of the acts, conversation of
voices, echo of thought, imperative hallucinations.
1. Sound commentary of the proceedings: the patient hears a voice, or several
voices, which comment on his behavior.

2. Talk of voices: the patient hears voices talking to each other and gets upset,
because it bothers. Often it does not interact with the voices, unlike what happens in
the hallucination reaction in which the patient speaks with the voices thus offering
the doctor an objective sign. Voices can be threatening and the patient becomes
distressed as a result. The person believes the rumors, acts accordingly, goes after
them.
3. Echo of thought: it is a very annoying condition in which the patient has an idea, a
thought and hears a repeated piece (a syllable of a word). The patient is able to
distinguish between his thoughts and the voice that takes him back.

4. Imperative hallucinations: the patient does exactly what the voice says to do: the
hallucination gives you an order and you execute it and unfortunately very often it is a
self or heteroaggressive order. They are dangerous because they are the ones
responsible in many cases of suicide or extended suicide (one kills oneself and even
one's own children to save oneself from some threat).
• Visual hallucinations: they are quite frequent in psychopathology: not as frequent
as auditory and not as infrequent as kinesthetic, tactile, etc.
They are divided into:
• Zooptics: objects that become animals are dispersed.
• Autoscopic: in which pieces of oneself are seen outside the body.
• Dysmegalopsic: alterations in which hallucinated objects are altered in their
size.
• They are usually the expression of post-alcoholic disorders or organic-
degenerative encephalopathies. They can occur in delirium tremens: the
subject undergoes a real confusional phase (different from delirium), with
alteration of consciousness and space-time disorientation and very often
terrifying or zooptic hallucinations are present. Delirium tremens occurs in
patients in a state of chronic alcoholic intoxication when, at some point, they
experience psychophysical stress (intense cold, severe fever) or abrupt
withdrawal of alcohol, which it ignites the state of delirium. It is a very
severe acute state of confusion, characterized by an alteration of the state of
consciousness (altered vigilance) and the person experiences space-time
disorientation, often terrifying hallucinations and various types of dispersions
such as micropsies, macropsies, etc. In addition, the patient presents tremor,
metabolic alterations and hydro-electrolyte balance. It has an extremely
variable prognosis: it can return completely, it can resolve completely, but
most of the time, if not taken in time, it can lead to death. In some cases it
explodes an underlying picture of dementia: after the acute phase, the
patient reveals the dementia that persists.
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 • Olfactory and gustatory hallucinations: characterized by the perception of
disgusting odors or tastes, they involve subjects suffering from schizophrenic
disorders in a delusional context, complex partial seizures in temporal epilepsy or in
tumors of the temporal lobe, which can begin in this way. Gustatory hallucinations
can cause poisoning delusions, that is, the mistaken belief that they can be
poisoned, especially by relatives and refuse food for this reason.
• Kinesthetic or somatic hallucinations: represented by sensations of heat or cold
(thermal hallucinations), sensations of wetness (water hallucinations), sensation of
being touched (tactile hallucinations), sensation of electric shock on the body
(haptic hallucinations), or the patient has a misperception of one's body, for
example a stone or glass body, longer or twisted limbs, or perceives hallucinatory
body movements. The dispersions can be affecting external organs such as the skin,
or internal organs, giving the patient the impression that, for example, something is
pushing on the intestine.
• Sexual hallucinations: tactile / kinesthetic hallucinations affecting one's sexual
organs (the person feels touched at the level of his sexual organs).
• Extracampal hallucinations: hallucinations outside one's sense-perceptive range
(eg a lady who reports hearing voices from the 8th floor and lives on the 4th floor).
• Negative forms: there is a sense organ that is stimulated, but I disperse it
negatively (I do not see, do not feel it), although the sense organs are intact.
• Hypnagogic / hypnopompic hallucinations: physiological hallucinations preceding
(falling asleep) and following (awakening) REM sleep. You feel touched, called, etc.
In the first case they are called hypnagogic, in the second hypnopompic.
• NB: in the disturbances of sense-perception, the patient has little "insight", is not aware of
what is happening, awareness of illness. In the long run, however, a patient understands
the problem thanks to new therapies and psychoeducation. Remember that, initially, they
go to the doctor for the distress that comes with the rumors, not the rumors themselves.
• They are classified according to the type of perceived hallucinatory in:
• Elementary: sensory stimuli very banal and simple and concern only one sensory
channel eg. the person hears a rustle or noise
• Complex: the dispersions are much more structured and complex: the rustle has
become a voice that says certain words and often it can even involve more than one
sensory channel. This is very common in adolescents who are becoming
schizophrenic and come to tell us that they hear rustling and very often go to the
otorino. Then, a few months pass and that rustle becomes a voice.

The distinction between elementary and complex hallucination is well noticeable in

the initial phase of schizophrenia, when the simple despair becomes more structured
(rustle> voice).
• They are classified according to the mode of onset into:
• Functional: hallucinatory perception that arises only when the sensory structure
concerned is active at that moment, therefore it is able to receive sensory stimuli.
• Reflected: hallucinatory perception in the context of a specific sense organ that
occurs when there is a stimulation of a different sensory sensory structure.
• Aetiopathogenesis:
We have tried to explain hallucination in many ways: functional magnetic resonance,
alteration of some potentials evoked in the learning of certain sensory stimuli.
Psychodynamists (those who believe in psychological hypotheses to explain mental
illnesses) have attributed to hallucinations exclusively the mental formulation of internal
drives. A true etiopathogenetic theory does not exist yet.
• Aetiopathogenetic hypotheses:
• Physiogenic theories: “antidromic” excitation or irritative phenomena of the
central and peripheral areas and pathways of sensoriality.

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 Psychodynamic hypotheses: centrifugal projection of intolerable and repressed or
desired and unattainable unconscious affective and impulse contents.

There are many pathological situations that cause alterations in sense-perceptions,

especially schizophrenia, hallucinations typical of schizophrenias are sound
commentary of the acts, conversation of voices, echo of thought, imperative
hallucinations. When you hear about psychotic disorders you must think above all of
delusions and hallucinations: these, in addition to schizophrenia, can also be present
in other conditions, even in the short term such as some acute emotional reactions
that can lead to alterations in sense-perceptions ( paraphrenias); confusional states,
above all in delirium tremens and in some acute psychotic attacks that involve acute
despair that resolves almost completely, with restitutio ad integrum. Furthermore,
Hallucinations may be present in bipolar disorder: a severely depressed person or a
person in a manic state may present with some hopelessness. Some dementias may
also present with hopelessness.
• Quantities:
• Hyperesthesia: can occur in cocaine or amphetamine intoxication, in which the flow of sense-
perceptions is increased.
• Hypoesthesia: slowing of the flow of sense-perceptions, eg. during a depression.

ATTENTION
Attention is a cognitive control function, a selective property of consciousness through which the subject
focuses on a particular internal or external stimulus, ignoring or inhibiting other stimuli that occur at the
same time, so we speak of selective, focused attention. or concentrated, which can be involuntary,
passive, spontaneous due to very intense and emotional stimuli or voluntary, active, in which the subject
voluntarily focuses on a stimulus to achieve a certain purpose. Attention is dispersed during the semi-sleep
phase, increased attention or hyperprosexia occurs in delusional and manic patients, decreased attention
or hypoposexia occurs in depressed patients.

MEMORY
Memory is the ability to fix, preserve and recall experiences and information acquired from the
environment, for which it is composed of three essential functions: that is
1. Fixation of mnemonic traces.
2. Storage.
3. Retention or storage of information and recalling of past memories.
A distinction is made between short-term memory and long-term memory, depending on the time elapsed
between fixing and recalling the memory. The memories that vanish first are those of recent acquisition,
while the memories that have more links with pre-existing ones are more fixed, retained and recalled.
We distinguish:
• Quantitative memory disorders:
• Hypermnesia: increase of the global memory capacity or limited to some particular sectors with
a strong memory for numbers, music. It can be permanent in intellectually gifted people or
transient from intense emotional states, manic syndrome.
• Hypomnesia: progressive weakening of memory skills (depressive syndrome).
• Amnesia: more or less severe memory deficit, with a distinction between short-term memory
disorders with fixation deficiency, that is, the ability to acquire new memories, and long-term
memory disorders with deficits in retaining and recalling acquired memories.
• Based on the pathogenic event, a distinction is made between:
• Organic amnesia (memory deficit from organic lesions from head trauma,
intoxication, vascular pathologies, dementia syndromes. Amnesia mainly concerns
the most recent events but if the brain damage is extensive it tends to become
widespread).

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• Psychogenic amnesia (transient and reversible memory deficit in the absence of

organic lesions.
• Amnesia mainly concerns events or memories of particular conflictual significance and
takes the name of selective amnesia or all events or memories relating to facts or people
and takes the name of systemic amnesia. In particular, we remember hysterical amnesia,
which concerns events of great emotional and affective impact, in which mechanisms for
the removal of conflicting memories come into play).
• Furthermore, a distinction is made between:
• Lacunar amnesia: memory deficit more or less limited to certain periods of time.
• Retrograde amnesia: pcs. does not remember the facts prior to the pathogenic
event.
• Anterograde amnesia: pcs. he does not remember the events that occurred after the
pathogenic event.
• Retro-antegrade amnesia: pcs. he does not remember the events that occurred
before and after the pathogenic event.
• Qualitative memory disorders:
• Allomnesia or illusions of memory: memories are deformed, incomplete, inadequate, distorted,
the past is recalled in a distorted way, some characters are accentuated, others are minimized or
reduced. Allomnesias are frequent in normal subjects and in patients suffering from mania,
melancholic depression, paranoid with delusional ideas.
• Pseudomnesia or hallucinations of memory: memories are the result of the subject's fantasy or
imagination (false memories) typical of the Korsakoff syndrome of alcoholics or dementia, or the
patient attributes the meaning of memory to a situation never experienced (false recognitions ,
déjà vu) frequent in normal conditions in very tired subjects with a great emotional state or in
patients with temporal lobe pathologies and schizophrenia.

IDEATION and THOUGHT

Ideation represents the highest level mental activity because it allows the individual to create abstract
concepts or ideas, that is the thought which, thanks to the faculty of abstraction, judgment and
reasoning, allows the evaluation of reality and solving problems based on to the knowledge acquired.
Thought disorders are divided into:
• Disorders of the thought form: they concern the organization of thought, i.e. alterations in grammar,
syntactic and semantics and are divided into:
• Quantitative Thought Form Disorders:
• Ideational acceleration (ideorrhea): ideas follow one another quickly one after the other
with a deficit of the association between ideas and communication up to logorrhea or the
flight of ideas as in manic and hypomanic episodes.
• Ideatory slowdown (bradypsychism or mental viscosity): ideas follow one another slowly
with poverty of communication, to the point of silence as in melancholy depression or
dementia.
• Narrowness of the ideational field: decrease compared to the normal subject in the
number of ideas, as in the case of mental insufficiency or dementia.
• Qualitative disorders of the thought form:
• Dissociation of thought: alteration of the association of individual ideas with thoughts
expressed in an incongruous, disconnected, strange, incoordinated, chaotic way,
incomprehensible speech, up to the so-called word salad in which the patient loses the
thread of the speech and the coherence of the sentence, such as in schizophrenia,
characterized by disorganized thinking with alterations of the form and execution of
thought with the phenomena of derailment (the patient expresses different ideas, passing
from one theme to another, without any associative connection between the ideas
themselves), tangentiality (the patient gives meaningless answers to questions),
inconsistency (the speech is incomprehensible), circumstantiality (the patient's speech is
inconclusive, dispersive,superficial) and illogical (the patient reaches a conclusion without
a deductive-logical procedure).
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• Concretism: inability to make abstractions or generalizations, difficulty in classifying

objects according to different criteria, use of symbols, interpreting proverbs.
• Perseveration: the patient repeats in a stereotyped way words, ideas, subjects (for
example, he gives the same answer to two different questions). It is different from
obsession in which repetitive thinking generates anxiety. Typical of dementias (vascular or
degenerative), in the elderly, who repeat the same things over and over (short-term
memory is skipped).
• Particularism: alteration of thinking with greater interest in secondary and irrelevant
topics than the main ones with the addition of unnecessary details, deficit of the ability to
synthesize, as in the case of mental insufficiency, epilepsy, dementia syndromes.
• Other disorders of the thought form:
• Autistic thinking: self-centered thinking, very concrete and isolated from socio-
environmental aspects. It is typical of schizophrenia, autism and some schizophrenic
syndromes, and borderline personality disorder.
• Obsession: typical of OCD and hypochondria. The idea is repetitive but egodistonic: the
subject does not want this idea, he knows that it is ugly and since he does not want it gives
anxiety. Even a phobia can become an obsession: in the obsession the thing that scares you
comes to mind even in the absence of the stimulus. In phobia, knowing that one is afraid in
the presence of the stimulus, the stimulus is avoided but in obsession the thought is
repeated also in other situations. To try to overcome the obsession, I carry out “exorcising”
behaviors, the so-called compulsions (eg I have an obsession with a dirty chair, I always go
to clean it).
• Disturbances in the content of thought:
• Prevailing ideation: the pc. uses as a priority certain types of ideas or thoughts that often form
in relation to particular affective states, divided into prevailing active ideas linked to ethical,
political, religious or scientific beliefs and passive prevailing ideas often linked to unpleasant
events such as an intervention surgical. The prevailing ideation does not indicate a
psychopathology in progress, even if in the depressive syndromes, states of anxiety and
personality disorders often the patient. presents prevailing ideas with unpleasant content with
phobic or obsessive aspects.
• Delirium: pathological, unreal, absurd thought of which the patient is strongly convinced and
from which he does not allow himself to be removed from either experience or criticism. A
delusional idea is characterized by certainty, incorrigibility and impossibility of the contents. The
person who has this idea believes in it, has no insight, is convinced of his idea, unlike what
happens with the obsessive idea in which the subject questions it ("maybe it's not mine" and has
anxiety).
• The delusional idea can be:
• Primary: when it arises primarily without any secondary concern regarding the
person's events or emotions that cannot be deduced from other psychic contents and
elements of the person.
• Secondary: when it derives from events that have occurred. It is difficult to
understand what is real or constructed. It derives from the patient's particular
emotional states.
• The typical forms of delirium occur in schizophrenia, mood disorders, abuse of
psychoactive substances and can be classified in relation to:
• Shape and structure: it can be elementary if it concerns a few ideas or
systematized if it concerns many ideas.
• Direction: it can be retrograde if it is directed to the past or centrifugal if it
encompasses all the surrounding environment.
• Course: episodic, chronic, recurrent, residual.
• Content.
• Based on the delusional themes, they are divided into:
• Persecutory delusions: more frequent, particularly in the case of schizophrenia
• Of reference (I am convinced that they are talking badly about me, or that
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Ricci, De Girolamo in memory of D'Altilia, Tucci, Di Turi (special thanks to Ricciardi & Potenza)
the news is talking about me).
• Of poisoning (false belief that they can be poisoned).

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Ricci, De Girolamo in memory of D'Altilia, Tucci, Di Turi (special thanks to Ricciardi & Potenza)

• Influencing or controlling (belief that someone can control our thoughts or

insert pieces of thought into our thoughts, typical of schizophrenia).
• Of persecution in a broad sense (conspiracies against himself).
• Expansive delusions:
• Of greatness and genealogical (it is believed to be an important person or
children of a noble person even if it is not true).
• Of reform (in which you believe you have invented ideas that they will have
followed or have invented a certain thing).
• Erotomanics (where you think you are particularly liked by the other sex "from
the way you looked at me I realized that you fell in love with me" and you
begin to persecute the other person).
• Delusion of body (somatic) transformation: some parts of oneself are believed to
have changed.
• Palignostic deliriumConviction of recognizing loved ones in strangers or that a loved
one has been mistaken for an impostor.
• Delusion of harm: conviction of being robbed (by family members, roommates or
healthcare personnel).
• Delusion of jealousy: conviction of being betrayed.
• Mystical delusion: one feels close to God or important divinities as far as some
inventions are concerned or one feels involved in strange doctrines, oriented or not,
they are delusions close to "divinities".
• Metempsychotic delirium: belief of living reincarnated in a person.
• Religious delusion: there are false beliefs of a religious nature.
• Pseudoscientific delusion: false or meaningless scientific theories are elaborated.
• Depressive delusions:
• Delusion of guilt or self-accusation (it is not the sense of guilt! it is a delusion
of conviction of guilt for one's own omissions or actions with a search for
punishment).
• Delusion of ruin: you think you are ruined or failed but this does not
correspond to the truth.
• Hypochondriac delirium: not to be confused with hypochondria minor or
neurotic, the subject resorts to medical consultations and is so convinced that
it is not possible to change his mind. In hypochondria minor or neurotic (closer
to anxiety disorders), on the other hand, there is the doubt of having
something: the subject is afraid of some disease while in delirium he is
convinced that he has it, so much so that he undergoes important tests or
even interventions.
• Delusion of denial or nihilistic: in which some parts of one's body or even oneself
are denied
• Delusion of theft: it is thought that one's ideas can be read from the outside.
• Delusion of insertion: it is thought that thoughts not recognized as one's own have
been inserted into one's mind.
• Delusion of influence: one thinks that one's ideas can be modified by external
forces.
• Delusion of diffusion of thought: one thinks that one's thoughts spread outside one's
mind and that others can listen to them.
• Delirium: formal modes of expression
• Delusional state of mind: experience of transformation of reality without however
this being configured in a precise delusional content -> delusional atmosphere and /
or mood constitutes the foundation or premise of the delusional idea, refers to the
external world and the internal world -> l delusional mood manifests itself as a
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complex and vague feeling of a very particular and indescribable tonality: it is made
up of strange, arcane, singular forebodings, it is a state of bewilderment,
uncertainty, it is an experience of the world as if it were acquiring a new,
indescribable, chaotic meaning , of imminent disaster, of imminent threat almost at
times of the end of the world, the subject feels like an instrument in the magical
hands of circumstances.
• Delusional perception: attribution of a completely abnormal and incomprehensible
meaning to a correct perception on a formal level -> the subject perceives exactly
the data of reality, but to these he attributes an abnormal, erroneous meaning,
which in any case tends to refer to himself . It has two characteristics: establishing a
relationship without reason and referring to oneself, that is, considering this
meaning as directed towards oneself and as if it were imposed by others.
• Delusional interpretation: attribution of an erroneous but probable and
understandable meaning to a correct perception on a formal level -> particular
experience of the subject who feels a sort of sudden inspiration, a kind of revelation
(such as being called to a task special, to a religious or political mission, or to be
endowed with special magical gifts or qualities, or to be persecuted or loved. The
following are distinguished: true or primitive delusional ideas (which cannot derive
from other experiences, neither emotional nor rational) and secondary or delirious
or pseudo-delusional or similar delusional ideas (which are justified or understood in
the light of a lived fact or a pre-existing state of mind).
• Delusional intuition: an idea that suddenly arose in the subject's mind without any
relationship with reality, is accepted as an indisputable truth.
• The delusional idea is an abnormal psychic elaboration that contaminates various psychic
functions because it disturbs the ideation, the judgment and the state of mind, perhaps the
perception, therefore for its understanding it is necessary to start from the psychic totality
of the individual. Delusional ideas are preceded by a delusional state of mind (which
evolves towards a delusion has generally a predisposition to develop a delusion) which
almost seems to constitute the matrix of the delusion itself. In this particular experience,
which involves the affective side of the personality, true feelings vibrate (the person
believes in his idea and goes after it even with his affective part) and ill-defined feelings of
apprehension, distrust, threat, anguish and of transformation of the world.

AFFECTIVITY
Affectivity includes emotions, feelings and mood. Emotions were affective states of abrupt onset, of short
duration, of rapid decline, accompanied by somatic phenomena, ie happiness, agitation, fear, anxiety or
panic attacks. The feelings or passions have been more lasting and stable affective states, divided into
somatic feelings that is well-being, malaise, satiety, fatigue, pain, and psychic feelings that is joy,
sadness, strength, mistrust, love and hate. The mood is the basic affective state of all mental activities
that conditions the quality and intensity of the experiences, the cognitive, volitional and behavioral
activity. In normal conditions a person can say that he is in a good mood or bad mood, cheerful or sad,
while in pathological conditions it is called depression, hypomania,
Main alterations in affectivity:
• Depression: decrease of the basic affective tone which can involve a possible and momentary
hypofunction of the other psychic abilities.
• Vital sadness: impairment of the somatic experience connected to the internal sensation of feeling
alive, vital, fresh.
• Anxiety: emotional state definable as a feeling of painful expectation of a threatening or dangerous
condition.
• Apathy: apparent or real decrease or disappearance of feelings and emotions with absence or reduction
of reactivity to environmental stimuli.
• Cenestopathies: subjective sensations (without organic cause) of bodily suffering.
• Hypochondria:
• Maior: delirium in which there is the belief that you are suffering from a serious disease or
malformation.
• Minor: set of prevailing disorders and ideas regarding one's own state of health (typical of
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neurotic personalities)

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• Dysphoria: increased tendency to moodiness, irritability and pessimism.

• Affective lability: extreme ease of basic mood changes due to low intensity stimuli.
• Phobia: defining symptom of phobic neurosis, peculiar morbid fear apparently unmotivated.
• Mania: mood exalted, euphoric, with megalomanic themes of varying intensity.
• Affective ambivalence: presence or coexistence of feelings of opposite polarity (hate-love, fear-desire).
• Affective inadequacy: emotional attitude that does not correspond to the decisive stimulus or situation.

WILL
Will indicates the reflected and conscious form of activity and the individual's ability to find the means to
achieve his goals. We distinguish:
• Quantitative Disorders of Will:
• Excess of will: involves motor restlessness, impulsivity, logorrhea, insomnia, up to psychomotor
agitation, as observed in manic states, anxiety and schizophrenia.
• Weakening (hypobulia) or complete loss (abulia) of primary or secondary will apathy or
numbness of affect is observed in normal subjects in conditions of fatigue or strong emotions, in
patients with depression and catatonic schizophrenia.
• Qualitative Disorders of Will:
• Impulses proper: they are complex acts that the patient performs without or against the
intervention of the will, such as pyromania and kleptomania.
• Forced ideas and representations (obsessions): these are thoughts that impose themselves on
the patient against his will, hindering the flow of ideas and often result in forced or compulsive
actions, such as numerical compulsions (counting objects, making calculations), behavioral
(washing hands continuously ), ambulatory (walking avoiding touching certain points).
• Mannerisms: clumsy attitudes or gestures, studied that are repeated in a stylized way,
accompanying the patient's mimicry and activity, typical of schizophrenia and autistic disorders.
• Stereotypies: the subject always repeats the same movements or the same syllables, even for
long periods of time, as happens in schizophrenia or normally like the swing of the chair.
• Suggestibility: tendency of the person to substitute his own will for that of another without
apparent awareness, to the point of becoming pathological, for example he mechanically and
quickly obeys orders, imitates the movements of the interlocutor.
• Tic: repeated irregular movements of muscle groups in functional relationship to each other.
• Stuttering: difficulty in verbal expression from tonic-clonic spastic contractions of the phono-
respiratory musculature.

INTELLIGENCE
Intelligence is the set of all mental activities that favor the adaptation of the subject to the tasks of life,
to elaborate certain strategies and solve problems thanks to the capacity of judgment, understanding,
reasoning, attention, fixation, ideation.
Types of intelligence:
• Abstract: critical ability to understand and elaborate concepts.
• Mechanics: ability to understand, handle, invent mechanisms.
• Social: ability to behave rationally and wisely in human relationships.
IQ:
• Ratio between mental age (sum value of scores obtained in the tests of intellectual efficiency passed by
the subject) and chronological age, multiplied by 100.
• normal values: 80-120.

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• mental deficiency: <70.

Mental deterioration:
• Acquired weakening and impairment of intellectual functions
• Physiological: linked to age -> if less than 10-20% of the values established according to the
Wechler-Bellevue reagent (scale used to evaluate intelligence in adults).
• Pathological: clinically evident through the clinical signs of dementia ->> 20% of the values
established according to the Wechler-Bellevue reagent.
States of mental insufficiency:
Alterations for organic causes of a developing intelligence (the organic lesion occurs when the brain
structures have not yet completed their normal anatomo-functional development).
• Oligophrenia: mental retardation congenital or acquired in early childhood, caused by an organic brain
disease.
• Frenasthenia: as oligophrenia.
• Mental weakness.
Dementia or dementia:
Deterioration of an already fully formed intelligence due to irreversible alterations of the competent
brain structures.
• Etiology
• toxic
• inflammatory
• traumatic
• vascular
• Typology
• senile dementia -> age> 60 years.
• presenile dementia -> age <60 years.

Psychomotor behavior disorders

Psychomotor behavior -> expression on a motor level (mimic, gestural) and of the relational life of the
individual's affective-drive world.
Main ailments:
• Psycho-motor excitement: confusional (pathological intoxication, delirium tremens), euphoric (mania,
toxic states), anxious (anxiety crisis), schizophrenic (impulses, stereotypies).
• Psychic or motor arrest.
• Catatonia: psychotic syndrome characterized by persisting in a bodily attitude assumed spontaneously
or by imposition.
• Cataplexy: disorder that causes a loss of muscle tone usually caused by strong emotions such as tears,
laughter, joy, etc. and from their memory or happens randomly during the day.
• Sitophobia: stubborn refusal of food.
• Automation in command.
• Negativism.
• Mannerisms: disturbance in behavior and in the way of expressing oneself, which become unnatural,
clumsy, artificial, caricatured; manifests itself spec. in the course of schizophrenia.
• Stereotypies.
• Paleokinesias: archaic gestures and movements repeated in the same way.
• Escape.
• Stuttering.

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CLASSIFICATIONS IN PSYCHIATRY
DSM-IV is the Diagnostic and Statistical Manual of Mental Disorders developed by the American Association
of Psychiatry. It represents the most widely used classification system for mental disorders at national and
international level, with classification, description of mental illnesses and diagnostic criteria useful for
planning therapy and making a prognostic judgment.
The DSM-IV was based on a multiaxial or multidimensional method that allows a global evaluation of the
patient with distinction between V axes:

Axis I - Clinical and other conditions of clinical attention: delirium, dementia, amnestic and other
cognitive disorders, mental disorders due to a general medical condition, substance-related
disorders, schizophrenia and other psychotic disorders, mood disorders , anxiety disorders,
somatoform disorders, dissociative disorders, sexual and identity disorders in general, eating
disorders, sleep disorders, impulse control disorders not elsewhere classified, adjustment
disorders;

Axis II - Personality Disorders and Mental Retardation: paranoid, schizoid, schizotypic, antisocial,
borderline, histrionic, narcissistic, avoidant, dependent, obsessive-compulsive personality
disorder, mental retardation;

Axis III: General Medical Conditions: infectious or parasitic diseases, neoplasms, endocrine,
nutritional and metabolic diseases, diseases of the nervous system, diseases of the eye and
adnexa, of the ear and mastoid process, of the circulatory system, respiratory system, digestive
system, musculoskeletal system, skin and subcutaneous tissue, genitourinary system, pregnancy,
childbirth and puerperium, congenital malformations and chromosomal abnormalities, injuries
from poisoning or other external agents, external causes of morbidity and mortality , factors
influencing the state of health and contact with health services;

Axis IV - Psychosocial and Environmental Problems: problems in groups, problems related to the
social environment, school, work, economic problems, problems of access to health services,
problems related to interaction with the legal / crime system, other problems;

Axis V - Global Evaluation of Functioning: useful for planning treatment and giving a prognostic
judgment, using the Scale for the Global Evaluation of Functioning to evaluate psychological,
social and occupational functioning, Global Evaluation of Relational Functioning, Scale of
Defensive Functioning .
Compared to the latest version of the Manual, the DSM-5 has made significant changes regarding the
structural organization, categories and diagnostic criteria.
The DSM-5 has changed the organization of the chapters to reflect a life-span approach.
The Manual begins with the disorders most diagnosed in the early stages of life (Neurodevelopmental
Disorders) and ends with those relevant to old age (Neurocognitive Disorders).
A considerable change concerns the abandonment of the multiaxial assessment system, to which we were
accustomed by the DSM-III, as it was judged as unnecessary in order to make a diagnosis of mental
disorder.
In order to increase diagnostic specificity, the NOS (Not Otherwise Specified) Disorder designation has
been replaced with two options: Other Specified Disorder and Unspecified Disorder, to allow the clinician
to specify whether or not the a disorder that does not fully correspond to the symptoms necessary to
enter the corresponding diagnostic category.
Before the publication of the manual there was a lot of anticipation regarding the introduction of
dimensional changes, especially in relation to personality disorders, in response to the critical issues posed
by the categorical diagnostic approach; however in its final version the DSM-5 brings innovations in a very
limited dimension compared to expectations.
Regarding personality disorders, categories and criteria remained unchanged from the DSM-IV, while a
proposed dimensional approach for personality disorders was published in the DSM-5, but in a separate
section (Section III) and indicated as an “Alternative model” for personality disorders. Section III of the
Manual also includes dimensional scales for assessing the severity of symptoms. Within the Manual, the
term dimensional is then used with different meanings from the original one and in this sense the DSM-5
presents as a novelty in a dimensional key the grouping of multiple disturbances into a broader category
(as was the case, for example, for autism spectrum disorders),

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internalizing and externalizing factors and the quantitative specifiers of symptom severity listed within
some disorders.

PSYCHIATRIC THERAPIES
Psychiatric Therapy is based on psychopharmacological therapy, psychotherapy and other methods.
- Psychopharmacological therapy includes antidepressants, mood stabilizers, anxiolytics-hypno-inducing
drugs and antipsychotics.
1. Antidepressants they are divided into tricyclics, selective serotonin reuptake inhibitors (SSRIs),
monoamine oxidase inhibitors (MAOIs), substituted benzamides, new generation antidepressants.
It is simplistic to consider depression as due to a drop in serotonin.
The serotonergic pathways originate in the NUCLEI of the RAFE and project everywhere in the CNS (limbic
system, pre-frontal / dorso-lateral / ventro-medial cortex, hypothalamus, etc.). There are seven
serotonin receptors of which 5HT1A is an important target of antidepressant drugs. It is a G protein
coupled receptor with inhibitory functions. 5HT2A is important for antipsychotic drugs. 5HT3 is the only
ionotropic receptor that allows the passage of Na +, Ca ++, K +. 5-HT3 is found at the level of the CTZ and
therefore mediates the emetic response to certain substances and in fact one of the adverse effects of
antidepressants at the beginning is precisely that of inducing nausea and sometimes vomiting in
particularly sensitive subjects because the increased availability of serotonin involves easier interaction
with downstream receptors, therefore also with 5-HT3. Abdominal cramps are also transient effects that
show us that the drug has arrived in adequate concentrations in the CNS.
5HT4 expressed more in the intestine. 5HT5-6-7 less important for the action of antidepressant drugs
except subtype 7 which is also a target of vortioxetine.
The receptors that interest us in addition to neurotransporters, those of serotonin and noradrenaline, are
the receptors:
- α2 (in particular): it is a presynaptic receptor and in addition to being an autoceptor it is a presynaptic
heteroreceptor. It is also found on serotonergic neurons and blocking it, we will see, with a particular
drug called mirtazapine, improves both noradrenergic and serotonergic transmission;
- α1 is mostly a target of side effects. In fact, the tricyclics, which target this receptor, cause
hypotension (undesirable effect);
- the down-regulation of β1, it is not known what the precise reason is, which follows the fact that the AD
drug reaches optimal levels in the plasma, causes an antidepressant effect.
The role of dopaminergic transmission, which consists of 4 pathways, is crucial in schizophrenia. Also in
this case we must not simplify with hypofunction and hyperfunction, although this is the mechanism that
explains the action of our drugs which in any case turn out to be effective.
The dopaminergic receptors we remember are the:
 D1 - like (D1, D3, D5) - exciters
 D2 - like (D2, D4) - inhibitors
D2 is crucial in the function of antipsychotics, but its stimulation by certain drugs especially at low doses
(I am thinking of aripiprazole which is a partial agonist or amisulpride) also mediates antidepressant
actions above all because at the beginning all psychotropic drugs act first at the presynaptic and then at
the postsynaptic level.
As for the dopaminergic pathway, the role of the dopamine transporter is important for antidepressant
drugs. Some of our drugs that block it have an important antidepressant action, especially improving the
motivational aspect of the patient's energy.
The increased availability of neurotransmitter in the synaptic wall is rapid: the NT increases immediately
but the antidepressant effect is observed after 4-6 weeks. NT clearly increases because all anti-
depressants, except MAOIs and NASSAs, block the serotonin transporter. Then there is also the
polymorphisms regarding this transporter to be considered, that is, there are subjects who have a
polymorphism of the SERT promoter for which they have low levels of this neurotransporter.
Paradoxically, this is the serotonergic paradox, those with little neurotransporter are more vulnerable,
less resilient, both to anxiety disorders, to stress and to depressive disorders. This is explained by the
morphology of the raphe nuclei (we will see later).

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Side effects are the first to appear, therapeutic effects within 6 weeks. Clearly, if they are not observed
within 6 weeks, we must first review the dosage of the drug, as well as consider polymorphisms of the
cytochromes, otherwise, excluding these too, we are faced with a condition of resistance.
The dorsal nucleus of the raphe, the main one, from which the projection neurons originate, actually has
a central portion (core) and two lateral portions in which serotonergic interneurons are also present. The
down-regulation of somatodendritic 5-HT1A which is present on projection serotonergic neurons occurs
precisely because it is decisive that the increase in serotonin occurs in the synaptic wall at the level of the
raphe nucleus, within this serotonin-serotonergic synapse.
The side effects are initially determined by the fact that the increased availability of serotonin causes this
to act as a ligand on all the receptors present in the same and therefore the HT2A present at the limbic
level can determine an increase in anxiety that is often observed at the beginning of the anti-depressive
treatment for this it is necessary to cover them with a benzodiazepine therapy, generally for a month or
so and then to taper off. Once the antidepressant drug has reached the optimal dosage (4-6 weeks) it
produces the effect and this dosage should be maintained, according to the guidelines, for 6 months,
preferably for 1 year in which the patient has no symptoms and then it passes to a gradual reduction. The
times vary according to the molecule we are considering. For example,
Stimulation of 5-HT2A receptors in the sleep centers of the brain stem can cause rapid muscle movements
(myoclonus) during the course of a night's rest; it can also cause sleep fragmentation with possible
nocturnal awakenings
Stimulation of the 5-HT2A receptors can inhibit the spinal reflexes of ejaculation, in fact it is common for
patients to complain of retrograde ejaculation. In the beginning also reduced libido; nausea and vomiting
are caused more than by the stimulation of 5-HT2A, of 5-HT3. Intestinal cramps, diarrhea are mediated by
the activation of 5-HT4.
Stimulation of 5-HT2A receptors in mesocortical pleasure centers can reduce local dopaminergic activity
and lead to apathy or reduced libido.

I. Tricyclic Antidepressants work

i. blocking the reuptake of neurotransmitter monoamines at the level of presynaptic
receptors, with a consequent increase in their concentration at the level of the
synaptic cleft causing a regulation of postsynaptic receptors at a lower level (down-
regulation), including Imipramine and Desipramine with mainly noradrenergic action
and Clomipramine with mainly serotonergic action.
ii. They have anti-histaminergic
action H1 iii. Antimuscarinic action
M1
iv. They act on sodium channels and can have effects that alter cardiac conduction
v. They have an anti 𝜶1 effect
Tricyclic antidepressants are used as first choice drugs in patients with severe,
melancholic depression, as second choice drugs in patients with mild to moderate
depression resistant to other therapies, panic attack, obsessive-compulsive disorder
(Clomipramine).
Side effects arise from the ability of tricyclic antidepressants to inhibit other receptors:
i) α1-adrenergic receptors (orthostatic hypotension, dizziness, reflex tachycardia)
ii) muscarinic receptors (dry mouth, constipation, urinary retention, memory changes,
sinus tachycardia)
iii)5-HT2 serotonergic receptors (ejaculation disorders, hypotension) iv) H1
histamine receptors (sedation, weight gain, hypotension)
v) H2 histamine receptors (confusional state, dysarthria).

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Tricyclic antidepressants are contraindicated in patients with narrow-angle glaucoma,

prostatic hypertrophy at risk of urinary retention, patients on MAOI therapy, they should
also be avoided or used with great caution in patients with severe heart disease with risk
of rhythm disturbances. or from cognitive disorders and epilepsy.
It is important that the (corrected) QT in men does not exceed 450 ms and in women 470
ms. the risk of QT lengthening is that of torsades de pointes which easily becomes
ventricular fibrillation. Unfortunately, tricyclics in particular, but also antipsychotics as
well as some antibiotics and antiarrhythmics carry this risk.
Absolute contraindications are acute myocardial infarction and decompensated heart
failure.

II. Selective Serotonin Reuptake Inhibitors (SSRIs) selectively act on the serotoninergic system by
inhibiting the reuptake of serotonin at the receptor level, including Citalopram, Paroxetine,
Sertraline, Fluvoxamine, Fluoxetine (Prozac).
SSRIs are used as first choice drugs in patients suffering from major depression, dysthymia,
panic attack, obsessive-compulsive disorder, eating disorders in particular high-dose
fluoxetine in patients with bulimia. They can also be used in patients with social phobia,
impulse disorders, some personality disorders, negative symptoms of schizophrenia in
association with antipsychotic therapy.
The most common side effects of SSRIs are dyspepsia and nausea which usually appear
transiently in the initial stages of therapy, rarely sexual disturbances such as delayed
ejaculation.
They are contraindicated in patients undergoing therapy with MAOIs to avoid serotoninergic
syndrome following an increase in serotonin as SSRIs prevent their reuptake, MAOIs prevent
their degradation, causing abdominal cramps, meteorism, diarrhea, tremors myoclonus, motor
incoordination, hyperreflexia, tachycardia, hypertension, manic symptoms, hyperthermia,
cardiovascular collapse and death.
(i)Fluoxetine is one of the first to be synthesized, the famous Prozac, inhibits SERT and
NET; it blocks the 5-HT2c receptor in particular, a receptor located on the GABA-ergic
interneurons at the bridge between the locus coeruleus and the ventral tegmental
area and then the downstream areas therefore blocking this inhibitory transmission
that is blocking this excitatory receptor on an inhibitory neuron disinhibits firing both
noradrenergic and dopaminergic with the consequent effects in terms of productivity,
motivation and mood.
(ii) Paroxetine at low dosages it inhibits SERT (up to 20 mg) but when we switch to 40-60
mg it also inhibits NET and therefore works a bit like a dual. Blockade of paroxetine
NO synthetase should be considered especially for men of sex because this causes
erectile dysfunction, since NO blockade impairs blood flow in the corpora cavernosa.
It is a side effect to consider: all antidepressants can initially cause this problem, but
for paroxetine it is particularly marked. Like fluoxetine it is a cytochrome 2D6
inhibitor.
(iii)Citalopram and escitalopramthey are the most selective. Citalopram is rarely used
because it lengthens the QT and has an antihistamine block. Escitalopram (Cipralex) is
used more.
(iv)Fluvoxamine,like paroxetine and sertraline, it is widely used in obsessive compulsive
disorders for which, however, the dosages to be reached are much higher than
depression and the maintenance time of the drug is longer. It inhibits CY-P1A2, as well
as olanzapine and clozapine, while cigarette smoke is an inducer. It also inhibits
CYP2C9 / 19.
(v)Sertraline, like fluvoxamine, acts on σ receptors, receptors still framed in an unclear
way but apparently these too would have a function in regulating monoaminergic
transmission and also apparently the interaction, it is not clear whether in terms of
agonism or antagonism, would have therapeutic effects on anxiety. At high dosages it
also inhibits the dopamine transporter.

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III.Monoamine oxidase inhibitors (MAOIs) they act by inhibiting monoamine oxidase, that is
mitochondrial enzymes located in the presynaptic cell, responsible for the catabolism of all
monoamines after their reuptake at the level of the synaptic cleft.
Currently they are little used due to toxicity problems, especially in the liver, and to the
dietary and pharmacological restrictions to which the subject must undergo during treatment,
as they interact with drugs with a sympathomimetic effect and with foods containing a high
concentration. tyramine, monoamine contained in fermented cheeses, red wine and some
legumes, as the inhibition of monoamine oxidase prevents tyramine catabolism causing severe
and even fatal hypertensive crises.
The most recent MAOIs, such as Toloxatone, determine a selective and reversible inhibition of
type A monoamine oxidase, involved in the pathogenesis of depression, are more tolerated
and prescribed without dietary and pharmacological restrictions when combined with
traditional MAOIs such as Tranylcypromine.
They are therefore second-rate drugs, but very effective in atypical depression and panic
disorder.
IV. The Substituted Benzamides are represented by Sulpiride, Levosulpiride and Amisulpride,
which act by blocking dopaminergic receptors, especially D2: at low doses they act on the
presynaptic receptors with greater dopaminergic activity, behavioral activation and
antidepressant action, while at high doses they act on the post receptors. -synaptic with lower
dopaminergic activity, that is with inhibiting, antipsychotic action, useful in case of psychotic
depression with delusions and kinesthetic hallucinations. Amisulpride is indicated in some
somatoform disorders obtaining good results and in a short time in gloxidinia or burning mouth
syndrome. Among the side effects we have the increase in prolactin at high doses.
V. Among the new generation antidepressants we have:
• specific and noradrenergic serotonergic antidepressants (NASSA) including Myrta-
zapine which acts by increasing noradrenergic and serotonergic transmission by
blocking the central presynaptic α-adrenergic receptors and blocking the 5HT2 and
5HT3 receptors;
• selective norepinephrine reuptake inhibitors (NARI) including Reboxetine which
inhibits the reuptake of noradrenaline at the receptor level. It exists theoretically,
it is very little used. It has a dropout rate comparable to that of SSRIs, but requires
very repeated doses because it has a very short half-life;
• selective serotonin and norepinephrine reuptake inhibitors (NSRIs): they have an
action similar to tricyclics but it is more effective and better tolerated because it
has no antihistamine and anticholinergic activity.
They are: venlafaxine (Efexor at a dose less than 75mg per day behaves like SSRIs),
duloxetine (Cymbalta), tramadol (Contramal) also has an anti-pain and opiate
action, Milnacipran.
Duals have a very pure action on serotonin at low doses, at medium doses they also
inhibit the norepinephrine transporter, at high doses even weakly the DAT (blockade
of the dopamine transporter) but, even at medium doses they interact with the
pathway dopaminergic. In fact, the NA transporter at the cortex level has a high
affinity for dopamine: the DAT at the cortical level is poorly expressed therefore the
reuptake of dopamine at the cortical level is mediated by the NET. Hence, blocking
the noradrenergic transporter also means improving dopaminergic transmission.
Side effects include serotonin syndrome, hyponatremia (due to inappropriate ADH
secretion), insomnia, headache, constipation, nausea, dry mouth, sexual
dysfunction, asthenia, sweating.
Among the indications we find fibromyalgia and neuropathic pain, depression, GAD,
social phobia, panic disorder and post-traumatic stress disorder.
• NDRI: the main one is bupropion which is a molecule that is best known for its
smoking cessation effect because we know that dopamine, therefore the connection
VTA-nucleus accumbens, in the reward and reinforcement mechanisms the effects of
pleasure and positive reinforcement. This is when the transmission

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dopaminergic in this circuit is phasic, massive enough to mediate the reinforcement.

(same mda as cocaine).
Bupropion gives a tonic inhibition of the dopamine transporter, for this reason it
does not determine a positive reinforcement and addiction, on the contrary, it is
very effective in defeat- ing. Bupropion is rarely used on its own, but mostly in
association with SSRIs and SNRIs because they have a complementary mechanism of
action, especially in the most difficult or resistant forms of depression. Its
mechanism of action involves the blocking of NET and DAT: remember that in the
prefrontal cortex, the NET also recaptures dopamine, therefore the action of
improving dopaminergic transmission with bupropion is quite evident.
• SARI: trazodone in addition to blocking the serotonin transporter (5-HT2A, 5-HT2C)
also blocks the H1 receptor of histamine and mild block of the α1 antagonism. It is
mainly used in combination with other antidepressant drugs both to improve the
adverse effects mediated by the blockade of H1 but above all to improve sexual
dysfunction thanks to the blockade of 5-HT2A. However, the risk of trazodone is to
cause priapism, sedation, dizziness, hypotension, syncope, bradycardia, nausea,
vomiting, edema, blurred vision, constipation, dry mouth. It is indicated in
depression when the insomnia component predominates and in anxiety disorders:
panic attack, post traumatic stress, and GAD.
• AGOMELATIN: We have said that depression is associated with a phase delay and
circadian rhythms, an increase in plasma cortisol, an alteration in body temperature
and above all it can be observed how the production of meltonin by the pineal gland
is inhibited. We know that melatonin is produced in the evening when there is a lack
of luminous information in the retina and optic chiasm. The melatonin produced
binds the MT1 and 2 receptors favoring the mechanisms that lead to falling asleep.
Agomelatine has a vicarious action on melatonin, it also blocks 5-HT2C receptors
with the effects seen above. It is currently rarely used for liver side effects. Neutral
on body weight, does not give symptoms of discontinuation,
• MULTIMODAL (vortioxetine and vilazodone): Only vortioxetine (Brintellix) is
marketed. By multimodal mechanism of action we mean a mechanism of inhibition
of the neurotransporter and of action on the other serotonin receptors, however all
this action has a therapeutic effect, not side effects as the tricyclics do.
In addition to inhibiting the serotonergic neurotransporter, vortioxetine is a full
agonist of the 5-HT1A receptor. Therefore, the increase of serotonin in the synaptic
wall with the blockade of SERT plus the action of full agonist on 5-HT1A causes its
down-regulation more rapidly so it is not necessary to wait 6 weeks, with
vortioxetine already in 2 -3 weeks we observe the first therapeutic effects.
1. Block reuptake of serotonin: antidepressant and anxiolytic activity.
2. 5HT1A agonism: reduces antidepressant latency time - presynaptic action;
amplification of the antidepressant-postsynaptic action; potential anxiolytic
effect.
3. 5HT3 antagonism: increases antidepressant efficacy; improves cognition; reduces
nausea.
Other effects are 5-HT1B partial agonism, 5-HT1D antagonism with unclear roles.
The role of 5-HT3, 5-HT7 is very important, as it mediates cognitive effects,
considered by the literature to be a need not met with anti depressants.
vi. Subjects receiving antidepressant treatment will generally continue to complain
or present impairments in cognitive performance in tests compared to healthy
control subjects. The 5-HT3 block is important because this receptor is expressed on
distinct interneurons in cortical highs and lows that regulate glutamatergic
transmission. Blocking the 5-HT3 receptor of high interneurons at the cortical level
causes glutamatergic transmission to be uninhibited and this correlates with an
improvement in the cognitive profile: we know that glutamatergic transmission on
MDA receptors mediates the processes of long term potentiation, which does not
happen. if the low interneurons are also blocked. This is done instead by ketamine,
which blocks the MDAs of both the high and low interneuron, blocking the in-

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low ternal neuron eliminates the synchronizing action of these inter-neurons on the
electrical activity of the brain. This is why ketamine, in the long run, in addition to
the psychotomimetic effect, has a deleterious effect on cognitive performance. The
5-HT7 block elicits cholinergic and monoaminergic transmission according to the
studies, the 5-HT3 block not only increases the release of glutamate but also of
acetylcholine and histamine.

2. Mood stabilizers they are indicated in the therapy or prevention of mood disorders, including lithium
salts, carbamazepine, valproic acid, lamotrigine, gabapentin, topiramate, oxcarbazepine.
I. Lithium is a monovalent cation, which belongs to the class of alkali metals, has a high electric
field, and enters the cells through the Na + channels. Therefore it is not a drug that has a
receptor action: its action is at the intracellular level in specific signal transduction pathways.
Lithium competes above all with cations such as Na + -K + -Ca2 + -Mg2 +. In particular, the
competition with Na + is important to take into consideration especially in those patients who
are undergoing antihypertensive therapy that involves the use of diuretics (and in particular
we will see that a class of these is not recommended in association with Li).
Lithium is an inhibitor of Inositol-1-phosphatase, therefore it acts on the cycle of
phosphoinositides that we know with the formation of inositol triphosphate (IP3) then activate
the calcium channels.
The Ca2 + in the mechanisms of neurotransmission (therefore of vesicular exocytosis of the
neurotransmitter) is fundamental, therefore lowering the levels of intracellular Ca2 + means
theoretically reducing the firing of monoaminergic neurons (serotonin / noradrenaline /
dopamine) [even if it has been seen in some studies that Li enhances serotonergic transmission
(hence the antidepressant action) at the hippocampal and cortical level]
It also inhibits Protein Kinase C (such as Carbamazepine)
Li also inhibits Glycogen Synthase Kinase 3 (GSK3), which phosphorylates and degrades
β-catenin.
The β-catenin, when present at physiological levels in the intracellular compartment,
activates the mechanisms of gene transcription and transduction that lead to greater
neurotrophism: that is, in the treatment with Lithium it has been seen that the levels of BDNF
(neurotrophins) increase, and this too correlates both with the likely antidepressant action
and with an efficacy almost in prophylactic terms on neurodegenerative diseases [in particular
on Alzheimer's positive effects of treatment with Li have been seen].
Increases the expression of Bcl-2 (like Valproate).
Among the lithium salts we have lithium carbonate used as a drug of first choice in the
prevention of mood disorders, long-term therapy of bipolar disorders (antimanic and
antisuicidal par excellence) and schizoaffective, treatment of recurrent major depression as
an alternative to long-term therapy with antidepressants, or it is combined with
antidepressants in the case of resistant forms to enhance their effect, and is used as a drug of
second choice in the therapy of manic episode as an alternative to neuroleptics.
Lithium is characterized by a lower response in mixed states or with dysphoria and in rapid
cycles, where Valproate acts better.
In the past it was also used as an antidepressant, a strategy that is now mainly used in
resistant depression as a potentiating agent.
It has a prophylactic action against manic episodes.
In some areas such as Austria, Texas, Japan, the waters seem richer in this cation and
apparently suicide rates are lower in these populations.
From a pharmacokinetic point of view, Lithium:
✴ is rapidly and completely absorbed in the gastrointestinal tract.

✴ has a half-life of 10-24h -> here we are talking about Lithium Carbonate
The extended release formulation of Lithium Sulphate ["Resilient"] has recently been
on the market, which has an advantage over Lithium Carbonate: the LC is generally
given 3 times a day at 8-14-20, but of these three the evening administration is the
most risky because it has been shown by several studies that the nocturnal peak of
the

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lithemia causes an accumulation of the cation inside the kidney and this would be at
the basis of interstitial nephritis - and then consequent renal failure - which many
patients undergo in chronic therapies, because you understand well that bipolar
disorder as a chronic disease tends to require a lifetime treatment (≠ treatment with
antidepressants which can be eliminated over time).

✴ is not metabolized: it passes only through the renal emunctory -> is filtered by the
gromerulus and reabsorbed at the level of the proximal tubule, where it is affected by the
concentration of Na +, in the sense that the greater the concentration of Na +, the greater
the excretion of lithium (and vice versa => that's why you have to pay attention to low-
sodium diets and treatment with diuretics)
95% is eliminated in the urine, 5% in the faeces, sweat, bile, saliva.
Dosage:
✴ “Resilient” -> tablets: it is initially given in a fractional manner morning and evening, then
it is administered only in the evening. Thus the patient has both an advantage from a
practical point of view (because I reduce the frequency of administration), and the
nocturnal peak that I told you is then at the basis of the accumulation in the renal
interstitium is avoided.
✴Lithium Carbonate (or Lithium Salts) -> 150-300 mg capsules. Acute: 900-1800 mg / day.
In the full-blown manic phase it can also be administered at a dosage that reaches up to
1800mg / day.
Maintenance: 600-1200 mg / day.

Latency of effect is likely to be shorter than antidepressants -> 1-3 weeks.

Plasma levels of lithium should be monitored and must remain between 0.5 and 1.4mEq / L
after the first week every 15 days for two months and then once a month.
Lithium is contraindicated in patients suffering from pathologies of the thyroid gland
(competes with iodine), kidneys and heart. Lithium poisoning occurs when plasma levels are
above 1.5-2 mEq / L with early symptoms i.e. polyuria, nausea, vomiting, diarrhea, tremors,
dizziness, dysarthria, subconfusion, and late symptoms i.e. oligo- anuria, ataxia,
hyperreflexia, mental confusion, convulsions, coma.
Before starting the therapy, the patient must be subjected to a series of checks, evaluating
renal, hepatic, cardiac, thyroid and neuronal function by means of a blood count with
leukocyte formula, uremia, creatininemia, total and fractionated bilirubin, transaminase,
phosphatase alkaline, thyroid hormones FT3, FT4 and TSH, urinalysis, ECG and
electroencephalogram (EEG), which must be repeated after 1 month of therapy and
subsequently every 6 months.
As for the side effects->
Frequent:
- polydipsia, polyuria
- fine tremor of the hands
- weight gain [I haven't seen one in two years]
- fatigue
- metallic taste in the mouth, nausea
- diarrheal stools
- edema
- poor concentration, memory problems
Occasional:
- vomiting, diarrhea
- induction or exacerbation of acne or psoriasis, folliculitis
- goiter, hypothyroidism

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- nephrogenic diabetes insipidus

- progressive reduction of renal glomerular function
- interstitial nephritis
Rare:
- hair loss, exophthalmos
- pseudotumor cerebri
- hypoglycemia, hyperthyroidism
- Raynaud's phenomenon
- Seizures

It has been seen that patients with bipolar disorder who took lithium had an almost double risk
of the fetus developing congenital malformations in particular affecting the cardiovascular
system and specifically a lower positioning of the tricuspid valve with consequent atrialization
of the right ventricle: Ebstein's anomaly. This clearly when the treatment is chronic: therefore
also in the first three months of pregnancy the balance between which are the risks of a lack
of treatment in a patient with bipolar disorder and which are the risks for the fetus. In mild
forms of Ebstein's disease, unborn patients are asymptomatic or may present with a systolic
murmur, exertional dyspnea, fatigue, or palpitations. In severe forms,
Recall that lithium carbonate is often associated with carbamazepine and / or sodium
valproate or valproic acid (anticonvulsants). He can go to find agranulocytosis caused by
clozapine.
II. The anticonvulsants. These drugs are generally used in epilepsy and bipolar disorder through
the following mechanisms:
a. They affect the ion conductance of the neuronal membrane (they reduce the
conductance to Na+ and Ca2+, increasing the conductance at K.+) [→ therefore the
duration of the hyperpolarization phase of the cell increases, so that there is no
sustained physical firing of the monoaminergic neurons].
b. They reduce excitatory neurotransmission (glutamic acid, acetylcholine, aspartate), in
particular the glutamate-mediated one (reducing its release). They therefore reduce
glutamate-induced excitotoxicity.
c. In compensation for the reduction of excitatory transmission, the inhibitory one
(GABA) will increase [both as an indirect compensation, and precisely on the basis of
the pharmacodynamic action of certain anticonvulsants] (by increasing the synthesis
of GABA, its release or inhibiting its degradation).

1. Carbamazepine is used as a drug of first choice in the mixed depressive-

manic episode, useful for its action of sedation and containment of
aggressive behaviors, or as a second choice drug in bipolar disorders resistant
or intolerant to lithium, and is a predictor response in the forms of dysphoric
mania and in rapid cyclers.
From a pharmacodynamic point of view:
✴Inhibits protein kinase C.
✴Inhibits the activity of adenylate cyclase
✴Reduces the activity of inositol monophosphatase
✴Increases GABAergic neurotransmission
✴ Blocks voltage-gated Na + channels
✴ Activate the channels of the K +
✴Inhibits the release of Glutamate

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✴Improves serotonergic transmission.

From a pharmacokinetic point of view:
✴The molecule is slowly absorbed in the gastrointestinal tract
✴It is quite bound to plasma proteins (70-80%)
✴It is a metabolic inducer of CYP3A4
✴It has an active metabolite in the form of epoxide, which has a half-life of
34h
✴ Half-life: 26-65h after single dose, 12-17h after repeated doses
70% urinary elimination
✴2 administrations per day with steady state in 2-4 days.
The dosage range is 400-1200 mg / day.
During administration, blood counts with leukocyte formula, platelets,
reticulocytes, sideremia, electrolytes, hepatic and renal function should be
evaluated every two weeks. Thyroid function, ECG, and pregnancy test must
be evaluated every six months as it can be associated with syndactyly (?).
Side effects are sedation, confusion, dizziness, nausea, vomiting, diarrhea,
blurred vision, SIADH, reduced contraceptive activity, blood dyscrasias,
benign leukopenia, aplastic anemia and agranulocytosis, Stevens-Johnson
syndrome, heart problems and rare psychosis.
Oxacarbazepine is a carbamazepine ketoderivative, with respect to which it
has fewer side effects as it does not form epoxide. It should not be co-
administered with Valproic Acid (which could potentiate its side effects).
2. Valproate sodium is used as an antimanic drug, antidepressant (not very
active and some studies have shown how it increases the risk of suicidal
ideation in the early stages), as a prophylaxis of bipolar disorder and a
predictor of response in rapid cycles, in mixed episodes and in dysphoria .
From a pharmacodynamic point of view, valproic acid:
✴Inhibits the glutamate transmission,
voltage-dependent Ca2 + channels.
✴Inhibits the phosphorylation of the Na + VD channel, making it practically
desensitized → and therefore this correlates with the reduction of
membrane depolarizations and with a stabilization of neuronal activity
→ which is also used for prophylactic purposes of those forms of
psychosis that occur after antipsychotic treatment at high doses ,
which leads to hypersensitization of the D2 receptors.
Valproate would interfere with these mechanisms which lead to the
up-regulation probably also through this reduction of the membrane
depolarization phases, thus stabilizing the membrane itself.
✴Increase the concentration of GABA.
✴Increases neurogenesis [inhibits GSK3β, interfering with β-catenin and
with those mechanisms that lead to neuronal neurotrophism.
✴Increases (like Lithium) the expression of Bcl-2 [which we know is an
anti-apoptotic gene → thus determining neuroprotection.
From a pharmacokinetic point of view:
✴ It has a half-life of 9-16h and is metabolized by 𝜷-oxidation by
mitochondria and microcrosomes
Has 75% plasma protein binding

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It is an inhibitor of cytochrome P450 3A4 which intervenes in the metabolism of many psychotropic drugs
but also of azole antifungals, macroclides, etc.
It is a metabolic inhibitor drug, therefore it intervenes in the catabolism of Carbamazepine and reduces
the metabolism of Lamotrigine.
It is eliminated 97% via the kidney, and the remainder via the faeces.
We generally use 300 - 500 mg prolonged-release tablets [given its rather
long half-life, it would be preferable to administer it twice a day. / ml in
both men and women]
The dosage is 15mg / kg day.
Platelet, hepatic and pancreatic evaluation, PT, PTT and aPTT are
important during treatment. These checks must be carried out monthly for
the first few months and then once or twice a year.
Weight monitoring is also important because weight gain is very common,
although there is no receptor bound by this drug that can explain it.
Side effects include sedation, dizziness, tremor, ataxia, abdominal pain,
nausea, vomiting, diarrhea, constipation, alopecia, polycystic ovary,
hyperandrogenism, insulin resistance, toxic hepatitis, teratogenesis.
In fact, the use of valproate is closely related to the manifestation of spina
bifida, a neonatal malformation or defect due to the incomplete closure of
one or more vertebrae, resulting in a malformation of the spinal cord.
Furthermore, exposure to valproate in pregnancy would cause a reduction in
intellectual abilities, speech, memory problems, and also a risk of
developing autism spectrum disorders about three times higher than normal.
This drug also correlates well with the correction of 'supersensitivity
psychosis' which is a complication of long-term antipsychotic treatment, in
which the patient develops new or re-emerging psychotic symptoms,
generally accompanied by dyskinesia, due to prolonged blocking of
dopaminergic receptors. . This process involves metabolic pathways such as
β-arrestin, and GSK-3. However, the latter is inhibited by valproate which
will therefore have a prophylactic action against this complication.
However, lower dosages of valproate are used, which in any case can be
substituted for this effect by lamotrigine and phenytoin.
The use of antiepileptics in addition to antipsychotic drugs (FGAs) in
patients with treatment-resistant schizophrenia and SP was evaluated in two
studies in 1990 (Chouinard et al., “Treatment of neuroleptic-induced
supersensitivity psychosis with antiepileptic drugs: report of a series of 43
cases "- Sultan, Chouinard, Beaundry," Antiepileptic drugs in the treatment
of neuroleptic-induced supersensitivity psychosis "); the antiepileptics used
were valproic acid, carbamazepine, phenytoin, with marked improvement in
symptoms as confirmed by the Clinical Global Impression (CGI) of
Improvement.
In the era of SGAs, antiepileptic drugs (valproic acid, lamotrigine, ga-
bapentin) are still administered early in the treatment of schizophrenia in
order to enhance the therapeutic effects of antipsychotics and prevent the
need for dose increases of the antipsychotic. SP and resistance to
treatment.
3. Lamotrigine, approved in the United States as a prophylaxis of bipolar disorder, is
used by us in the form of bipolar disorder type 2. It is less effective

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in the prophylaxis of the manic episode compared to Lithium, more valid in the
prevention of the depressive episode.
From a pharmacokinetic point of view, it has a long half-life (33h), has no active
metabolites and is excreted via the renal emunctorium.
Furthermore, it does not interact with lithium, but valproate increases plasma levels
of la-motrigine by inhibiting the cytochrome CYP3A4 which metabolizes it. On the
contrary, Carbamazepine works instead.
It is administered itself in the form of 25mg tablets, precisely because the titration
must be done at 25mg per week, up to a dosage range between 100 and 200mg. In
fact, a dramatic increase in plasma levels increases the risk of Stevens-Johnson
syndrome.
Side effects include severe skin rash, blood dyscrasias, benign skin rash, sedation,
blurred vision, headache, tremor, ataxia, nausea, vomiting, abdominal pain,
constipation.
4. Gabapentin is considered useful in the prevention of bipolar disorder and particularly
in the forms associated with disorder or social phobia. It is present in an immediate
release formulation. It has a very short half-life so it is given three times a day. Its
elimination takes place via the kidneys. Side effects include sedation, blurred vision,
dizziness, tremor, ataxia, dry mouth, vomiting, diarrhea, constipation, weight gain,
peripheral edema.
5. Topiramate has a prophylactic action in rapid-panic cycle disorder, reduces appetite
and is therefore often associated with antipsychotics that cause weight gain. It has a
half-life of 21h, renal elimination and is present in immediate release formulations.
Side effects include sedation, confusion, speech problems, dizziness, tremor, ataxia,
stagnation, blurred vision, paresthesia, nausea, weight loss, metabolic acidosis,
kidney stones.
III.Among the Other Mood Stabilizers, some calcium channel blockers (Vertraamil) and new
generation antipsychotics (Clozapine, Risperidone, Olanzapine) are considered.
3. Anxiolytic, hypno-inducing drugs are used to reduce anxiety and induce sleep without altering the
sleep-wake rhythm, compared to barbiturates used in the past, among which we have:
I. Benzodiazepines with anxiolytic, hypno-inducing, sedative, muscle relaxant and
anticonvulsant action, even if they are not the drugs of choice for anxiety disorders, while they
are indicated in case of anxious symptoms in patients suffering from depression or phobia,
'generalized anxiety in the absence of other concomitant disorders or panic attack therapy
(starting with benzodiazepines and continuing with SSRI antidepressants to avoid the
phenomena of tolerance and dependence on benzodiazepines in the case of long-term
therapy), schizophrenia or manic disorder (benzodiazepines are associated with antipsychotics
by increasing the sedative effect to control psychomotor agitation).
These molecules are nothing more than positive allosteric modulators of the GABA-A receptor,
that is, they facilitate the action of the natural ligand of that receptor and have their own
specific site of action.
GABA [γ-aminobutyric acid] is synthesized starting from glutamic acid (which comes from glial
cells → which among other things also participate in the re-uptake of this neurotransmitter) by
the enzyme glutamic acid decarboxylase [ GAD], then stored in the vesicles and then released.
The action of GABA ends through a mechanism of re-uptake and then intracellular metabolism
mediated by GABA transaminase [GABA-T] - present both in the presynaptic gabaergic neuron
and in the glial cell.
GABA acts at the postsynaptic level on three receptor types, of which two have been studied
(GABAA and GABAB) while the other (GABAC) is not yet well studied.
GABAA → rec. ionotropic
GABAb → rec. metabotropic associated with inhibitory G protein
GABAA is essentially a pentamer, each subunit of which is made up of four transmembrane regions.

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Of this pentamer it is good to consider which are the subunits that compose it, because on the
basis of these the function which is then mediated by the receptor is different. The subunits
include α (from 1 to 6), β (from 1 to 3), γ (from 1 to 3), δ, ε, π, θ and ρ → but those that
interest us are essentially α, β, γ and δ. The most common association is formed by 2 𝜶 + 2 𝜷 +
1𝜸.
A receptor presenting α1γ2 subunits is that receptor whose activation mediates the sedative
effect and GABAA receptors generally have a phasic inhibition action on the postsynaptic
neuron where they are located.
The anxiolytic action would be attributable to the presence, instead of the α1 subunit, of the
α2 and α3 subunits: in fact, compounds are being studied that should have a selective action
on this third type of receptor precisely to divide those molecules that are purely anxiolytic
from those which are sedative, because in any case BDZ have a sedative effect.
On the other hand, those that are present at an extrasynaptic level possess the δ subunit and
are activated by neurosteroids and by alcohol in particular. Instead, they mediate a slower
type of tonic inhibition. Alcohol has a drug addictive power because it has an opioidomimetic
action and because it inhibits with the inhibitory interneurons that modulate the mesolimbic
pathway (therefore the one that connects the ventral tegmental area or dopaminergic area
A10 with the accumulation nucleus): each when this path begins to have a phasic activity, the
substance that elicits this type of activity has addictive power.
BDZs have their own binding site located between α and γ subunits or between α and δ
subunits, which is different from the GABA binding site → for this reason they are defined
allosteric modulators: that is, they act on a site other than that where the natural ligand acts.
Barbiturates have an additional site of action which is within this channel and these do not
require the presence of GABA to act, but in themselves facilitate the opening of this channel (≠
BDZ which act only with GABA), thus causing a much more intense hyperpolarization, so much
so that in the past it was effectively used for suicidal purposes.
Benzodiazepines have the advantage of having their own antagonist, flumazenil. It is a drug
that is used only in a hospital setting (eg to reverve the sedative effect of BDZ when
administered for anesthetic purposes or when overdosed by the patient).
Benzodiazepines are classified according to their plasma half-life and this is important because
those with a long half-life are those that generally do not give addiction phenomena, while
those with a short half-life (which are mainly triazolobenzodiazepines) give a marked
dependence always for that action we mentioned earlier on the mesolimbic circuit.

Benzodiazepines with a short half-life are indicated in case of risks of accumulation from
advanced age, liver or kidney diseases or when an immediate but short-lasting effect is
required, for example for insomnia from falling asleep or anxiety that appears in some hours of
the day.

Medium or long half-life benzodiazepines are used to achieve more prolonged and stable
anxiolytic coverage or to ensure less disturbed sleep after falling asleep or to remedy early
awakening insomnia.
Benzodiazepines are manageable, mildly toxic drugs responsible for minor side effects,
including sedation, asthenia, ideomotor slowing and reduction of

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cognitive performance which generally occurs in the first days of therapy and progressively
tends to decrease, while if they persist, the posology must be changed.
In general, in the initial stages, the minimum daily dosage is divided into 2-3 administrations
over 24 hours, which must be progressively increased every 2-3 days until the minimum
effective dose is reached.
The duration of treatment should not exceed 6 months to avoid tolerance and dependence
phenomena, while in the case of prolonged use of high-dose benzodiazepines followed by an
abrupt interruption of the drug, withdrawal syndrome or benzodiazepine withdrawal secondary
to physical and psychological dependence. Physical dependence occurs abruptly a few days
after discontinuing the drug with anxiety, insomnia, irritability, headache, muscle aches,
paraesthesia, tremors, tachycardia. Psychological dependence manifests itself with anxiety as
the sense of security given by the relationship with the drug is lacking, and with a strong desire
for the substance (craving).
The absolute contraindication to benzodiazepines is myasthenia gravis.

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Z-Drugs have similar action to benzodiazepines: Zolpidem, Zaleplon, Zopiclone. They act on
GABA receptors with 𝜶1𝜸2 subunits with physical inhibiting action. They are born as purely
hypno-inducing drugs.
4. Antipsychotics are divided into classical or neuroleptic antipsychotics and new generation
antipsychotics.
To talk about antipsychotic drugs we must keep in mind the dopaminergic pathways and clearly, those
that are involved in a psychotic syndrome (especially schizophrenia, delusional disorder as well as
bipolar disorder with psychotic manifestations) are regarding the pathophysiology:
A. The mesolimbic pathway: ventral tegmental area> nucleus accumbens
B. The mesocortical pathway: ventral tegmental area> dorsolateral prefrontal cortex (hence
cognitive dimension) and ventromedial (affective dimension).
Our drugs will inevitably affect the nigro-striatal and tubular-infundibular pathways, in particular the
latter two are targets in terms of side effects especially of conventional or typical antipsychotics.
The dopamine receptors are:
—D1-like: D1, D3, D5 with excitatory function
—D2- like: D2, D4 with inhibitory function. D2 is also a presynaptic autoreceptor. This is important
because amisulpride, a drug used in dysthymia, at low doses would mainly block presynaptic D2 by
eliciting dopaminergic firing.

I. Classic or Neuroleptic Antipsychotics they are indicated to sedate the patient in case of
psychomotor agitation, aggressive and violent behaviors, manic or hypomanic episodes,
confusional states, positive psychotic symptoms (delusions, hallucinations). They have no
effect on negative symptoms. They bind D2 receptors with 50 times greater affinity to D1 and
D3 receptors.
The effect is directly proportional to the level of occupancy D2 which, however, is also
fundamental for the extrapyramidal side effects. In fact, after a certain percentage threshold,
that is, the blocking of more than 80% of the D2 receptors of the CNS causes extrapyramidal
symptoms: tremor, dystonia, in the long run tardive dyskinesia. Dystonia and tardive dyskinesia
are different things that require different treatments, in fact the dystonia is due to the massive
D2 block so there is a hypothetical dopaminergic hypofunction at the level of the nigro-striatal
pathway, dyskinesia, on the other hand, calls into question the concept of super-sensitization of
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D2s and therefore mainly causes abnormal movements

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evils at oral-oral levels, of the facial muscles. The first, the dystonias, are treated with
anticholinergic drugs as we know that acetylcholine has a modulatory action on the movement at
the level of the nuclei of the base. When there is an excessive D2 block and a relative cholinergic
hyperfunction, tremors appear, so this imbalance must not exist. While, for tardive dyskinesia
tetrabenazine is used which works a bit like reserpine and has the function of making the D2
receptors reoccupy by dopamine and thus restore normalcy, although in most cases when tardive
dyskinesia appears it is irreversible (usually after 2-6 months of treatment).
Newer antipsychotic drugs have a relatively high affinity for the 5HT2A receptor and lower for D2
receptors. This 5HT2A / D2 balance seems to underlie the anti-psychotic actions of the new
generation drugs.
These include:
a. Phenothiazines: among the aliphatic ones we remember
chlorpromazine and fluphenazine with depot administration. These
de-pot administrations allow for the intramuscular injection of the
molecule carried by a lipid system that allows a prolonged release, in
most cases monthly, for fluphenazine even 21 days, desperidone
depot should be administered every 15, just to guarantee that that it
is the patient's compliance because unfortunately psychotic patients,
by virtue of the absence of awareness of the disease, will always tend
not to want to take drugs);
b. Thioxanthenes: they are not used here;
c. Butyrophenones: haloperidol, high-potency antipsychotic for anto-
nomasia, greater potency of phenothiazines on block D2 which instead
associate with block D2 also other actions such as block M1 muscarine,
α1, anti-histaminergic, therefore phenothiazines have a more sedative
action than to butyrophenones such as haloperidol which is the
delirium lytic par excellence). Haloperidol blocks 93% of D2. It should
be used with caution in heart patients.
d. Diphenylbutylpiperidine: they are not used;
e. Dibenzazepine: loxapine is a drug that has come back into vogue
because now there is intranasal administration of the same that can
be given in acute and is very effective on acute psychomotor
agitation.
The main contraindications to neuroleptics were comatose, previous neuroleptic malignant
syndrome, pregnancy. They should be used with caution in the elderly, patients with tardive
dyskinesia, Parkinson's disease, major depression, pheochromocytoma, cardiovascular disease,
acute or chronic pulmonary disease, renal failure and prostatic hypertrophy.
II. The New Generation Antipsychotics they are the -pine compounds (clozaoine, olanzapine,
quietapine), the benzamides (amilsupride and tiapride) and the -done compounds (risperidone,
ziprasidone, paliperidone, lurasidone).
The pharmacodynamic aspect that distinguishes a typical drug from a typical one is 5-HT2A
blockade. in fact another of the typical antipsychotic acronyms is SDA (Serotonin-Dopmin-
Antagonist), ie antagonist of dopaminergic and serotonergic receptors. The interaction
between dopamine and serotonin and between the receptors of both sees the 5-HT2A receptor
as the protagonist, whose block is decisive both in terms of reducing the incidence of
extrapyramidal effects and improving the patient's cognitive-affective profile.

Extrapyramidal symptoms appear more with 'done' compounds.

• Clozapine acts like
a) dopaminergic antagonist especially of D4 receptors (in the
hippocampus and prefrontal cortex) and D1,
b) 5-HT2A serotonin antagonist, 5-HT2C and 5-HT7 blocker
c) has antiadrenergic activity,
d) antihistamine (H1 block drowsiness and weight gain),

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e) anticholinergic.
f) Antimuscarinic (M3 block in the pancreas causes insulin resistance)
It is used as a second-line drug in patients resistant to other antipsychotics or in
patients with tardive dyskinesia. It is the second choice drug in schizophrenia.
Among the main side effects we have agranulocytosis (leukopenia) with a high risk
of mortality, for which, before therapy and during treatment, the patient's blood
count must be monitored once a week for the first 3 months, then Once / month:
therapy should not be started if the leukocyte count is less than 3500 / mm3, while
it must be stopped if the leukocyte count falls below 3000 / mm3 or if the absolute
neutrophil count is <1500 / mm3. It also blocks the D3 receptor and studies have
shown that this block contributes to antipsychotic therapeutic actions.
Causing both weight gain and insulin resistance, it is involved in the pathogenesis of
the metabolic syndrome.
What is indicated by Stahl as receptor X (X, because it has not yet been identified),
is another receptor that appears to be involved in the pathogenesis of the metabolic
syndrome. It is a receptre that is apparently also affected by olanzapine which for
the same reasons as clozapine causes weight gain in most patients which sometimes,
in most patients, within a few years causes an increase of 25 kg: at that point it is
necessary to make a balance between how much it is necessary to cure the
psychosis without damaging the body of the subject.
• Risperidone is used as a drug of first choice in the therapy of schizophrenic disorders
as at low doses (3 mg / day) it acts as an antagonist of 5-HT2 (5-hydroxy-
sitriptamine, serotonin) with an activating action, effective against symptoms
negative and disorganized, while at high doses (6 mg / day) it acts as a
dopaminergic D2 antagonist with sedative action, effective against positive
symptoms. Among the side effects we have the increase in body weight and
prolactin.
(Compounds -done, compared to compounds -pine, have a more delirious-
lytic action. Compounds -pine act better on mood, so much so that
olanzapine and quietapine are precisely indicated in bipolar depression.)
• Olanzapine acts as an antagonist of 5-HT2, 3 and 6 serotonergic receptors, and of
D1, 2, 3 and 4 dopaminergic receptors, it also has high affinity for α1-adrenergic,
histamine H1 and muscarinic receptors. It is an excellent antipsychotic, with
efficacy comparable to that of neuroleptics on positive symptoms and superior to
them on negative symptoms. Therefore Olanzapine is considered a drug of first
choice in the treatment of schizophrenic disorders. Among the side effects we have
sedation which in some cases is considered a therapeutic effect, arterial
hypotension, weight gain.
• Quetiapine is a very interesting drug because it can have three types of use: 25 mg
which is the basic dosage gives a strong antihistamine action, in fact it is used in
elderly patients with dementia both to promote sleep and to determine an action of
containment of any agitation (low dosages in the elderly are good because they have
a slowed metabolism). If we go up in dose, up to 300 mg (we no longer consider the
elderly but the adult patient), quetiapine has an antidepressant action mediated
both by the block 5-HT2C, 5-HT2A, but above all the active metabolite of quetiapine
, norquetiapine is an inhibitor of the norepinephrine transporter: therefore in this
sense, it would have an anti-depressant action. At dosages up to 800-900 mg the
block on D2 prevails and therefore the antipsychotic action.
• Aripiprazole is considered atypical among the atypicals as it is a partial agonist on
D2 receptors, even at low doses it would have an antidepressant action (2.5-5 mg).
Among other things, aripiprazole and risperidone are also used in pediatric neuro-
psychiatry at low doses and are the only PAs used in children in case of psychomotor
agitation in autism or in some forms of intellectual disability.
It also has a partial antihistamine action and blocks 5-HT2A. Among its side
effects we have akathisia with agitation, restlessness, tendency to have
difficulty staying still.

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The tubero-infundibular pathway mediates hypothalamic-pituitary control: we know that

dopamine has an inhibiting action, controlling the secretion of prolactin while serotonin favors it.
This is why dopamine agonists, such as bromocryptin, are given when lactation is to be inhibited.
Classical antipsychotic drugs, by determining an incisive block of D2, are the drugs most burdened
by hyperprolactinemia. This in addition to gynecomastia in men and favoring the secretion of milk
in women, effects on libido, also has effects of cognitive impairment, therefore of deterioration
of cognitive performance. For example, among the atypical, risperidone that goes on D2
massively, is a drug burdened by this side effect. However,
Among the new antipsychotics of the latest release, Lurasidone which is part of the "done"
compounds as well as being particularly effective on the D2 receptor and on 5-HT2A has a blocking
action on the 5-HT7 receptor which would improve the cognitive symptomatological profile .
Another important aspect to always consider for atypical antipsychotics is the intensity of binding
with respect to the D2 receptor. In fact, while the conventional antipsychotic has a long-lasting
bond on the D2 receptor, the atypical ones and in particular I am referring to clozapine and
quetiapine have that aspect that goes under the name of fast-dissociation or kiss and run, that is,
they block the receptor and detach themselves rapidly, favoring the action of endogenous
dopamine. A massive block, in fact, of long duration of the D2 receptor would cause that
phenomenon of supersensitivity of the D2 receptor. This hypersensitivity of the D2 receptor in
addition to giving tardive dyskinesia is responsible for psychotic re-bound, that is, the system
responds to the incisive block with an increase in the D2 receptor expressed at the post-synaptic
level and this causes the psychotic symptoms to reappear sometimes even new, that is, never
experienced by the patient. The up-regulation mainly concerns the high affinity D2 receptors and
this mechanism calls into question the intracellular systems which then make the internalization
mechanisms no longer work well.

—The Electroconvulsive Therapy or Electro Shock (ECT) in Italy is out of use, while it is widely used in the
Anglo-Saxon countries. The electroshock is performed under general anesthesia with assisted mechanical
ventilation and administration of curare to obtain muscle relaxation and avoid muscle seizures: 1 or 2
electrodes are applied at a temporal level and an electrical stimulus of 100-300 V is given for about 0.5-
1.5 seconds causing a generalized cerebral convulsion. Before subjecting the patient to electroshock, the
physical and neurological conditions must be assessed and subjected to a cardiological and anesthetist
examination. Electroshock can be used in cases of severe depression resistant to antidepressants and at
high risk of suicide, manic disorder with severe arousal state at high risk of destructive behaviors and
refractory to psychopharmacological therapy, refractory or intolerant schizophrenia to neuroleptics with
previous neuroleptic malignant syndrome or agranulocytosis. Absolute contraindications to electroshock
are intracranial hypertension, recent MI, coronary insufficiency, aortic or cerebral aneurysm,
anticoagulant treatments, obstructive respiratory diseases, while relative contraindications are cardiac
arrhythmias and epilepsy. The main side effects of electroshock are of the cognitive type, ie short
confusion, memory disturbances. Absolute contraindications to electroshock are intracranial hypertension,
recent MI, coronary insufficiency, aortic or cerebral aneurysm, anticoagulant treatments, obstructive
respiratory diseases, while relative contraindications are cardiac arrhythmias and epilepsy. The main side
effects of electroshock are cognitive, ie short confusion, memory disturbances. Absolute contraindications
to electroshock are intracranial hypertension, recent MI, coronary insufficiency, aortic or cerebral
aneurysm, anticoagulant treatments, obstructive respiratory diseases, while relative contraindications are
cardiac arrhythmias and epilepsy. The main side effects of electroshock are cognitive, ie short confusion,
memory disturbances.
—Psychotherapy is based on a series of methods that use psychological tools for therapeutic purposes. The
psychotherapist has the task of restructuring the patient's personality, restoring psychosocial, work,
relational functioning, that is, to favor reintegration into society, modifying or correcting abnormal
behaviors, through various techniques that derive largely from Psychoanalysis. - nalysis founded by
Sigmund Freud who studies and treats the unconscious processes of the personality and the psychic
conflicts that occur between the 3 instances of the mind, namely Id, Ego and Superego.
In clinical practice it is important to create an excellent doctor-patient relationship, establishing rigid
rules from the initial stages, avoiding any interference during the analytical work, i.e. the analyst and the
patient must respect the times of the sessions and their duration, without moving or cancel appointments,
avoiding even the handshake at the beginning and end of the session, as well as social relations outside
the analysis.
Sessions are usually frequent, up to 3-5 times / week for 5-10 years.
During the psychoanalytic session, the analyst and the patient do not have to look at each other, that is,
the analyst stands behind the patient, since the patient must be concentrated on his own mind.
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The analyst uses the method of free associations to try to eliminate the resistances between the
individual's drives and defenses, bringing out the conflicts and unconscious thoughts, which are
unacceptable and responsible for psychic disorders, i.e. the patient must let words, images, flow into his
mind. memories, fantasies, dreams and

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he must report everything that comes to mind without the need to structure the speech or articulate it
logically.
The analyst tries to interpret what lies behind the patient's sentences or draws the patient's attention to
his own defenses. When the relationship between doctor and patient becomes more intense, a
relationship called transference is generated in which the patient experiences the therapist as a
significant figure from his own past, useful for bringing out conflicts and unconscious thoughts, with the
transfer of feelings and experiences from the patient to the doctor, originally turned towards the
significant characters of his own infantile world, for which the patient passes from admiration to
contempt up to frustration because the psychoanalyst does not encourage, does not console, does not
absolve the patient. The therapist can respond to this situation with the counter-transference by having
feelings for the patient.
Psychodynamic Psychotherapy has the task of investigating the emotional experiences of the subject,
understanding and resolving the experiences related to the disorder, starting from the assumption that the
human psyche is structured and changes continuously in a dynamic way, following the interaction between
drives and conflicts that derive from this and that are expressed above all on an unconscious level.
During the session the patient can be in a lying position with the therapist behind him, or there is a face-
to-face interview. In fact, compared to psychoanalysis, psychodynamic psychotherapy is based on the
conversation between psychotherapist and patient, in which the psychotherapist actively participates. 1-2
sessions / week are needed for 2-3 years.
Brief Psychodynamic Psychotherapy it is so-called because the analyst works on a limited field of
investigation, i.e. the patient talks with the analyst on a previously agreed topic, called focus, such as a
symptom (anxiety, phobia), an obsessive idea, a depressive state, a conflictual situation that worries or
causes the patient to suffer, a situation of mourning crisis, separation, loss of work, trying to mitigate or
eliminate a symptom and improve the patient's psychosocial functioning. During the interview the
therapist participates actively, speaking face to face with the patient; in some schools the therapist is
even aggressive, causes deep frustration in the patient and generates a relationship with high emotional
tension. The main technical tool of brief psychotherapy is clarification which makes the patient more
aware of his own conflicts and deep experiences, working on the pre-unconscious, that is, on what can be
made aware in a short time also on the cognitive level. In addition, brief psychotherapy is also based on
interventions of reassurance and encouragement.
The number of sessions is fixed, 10-12, 20-25 depending on the school, with 1 session / week. Brief
psychodynamic psychotherapy is indicated in anxiety disorders, dysthymia, bulimia and some somatoform
disorders, it is contraindicated in psychosis.
Cognitive-Behavioral Psychotherapy it is based on cognitive and behavioral techniques. Cognitive
Psychotherapy is based on the cognitivist theory or cognitivism founded by Ellis and Beck who established
that the primary psychopathological core of depression is represented by cognitive disorders, that is,
illogical, irrational thoughts, abnormal subjective prejudices, for which the depressed patient lives. and
sees reality considering above all the negative aspects with a pessimistic vision of the present and the
future, from which Beck's triad derives, that is negative thoughts and beliefs towards oneself, towards the
world and towards the future. Therefore, cognitive psychotherapy has the task of teaching the patient to
self-observe himself in a critical way through the reconstruction of his history, bringing out and removing
irrational beliefs, that is, irrational thoughts and beliefs,
It is indicated in patients suffering from depressive disorders and anxiety disorders, especially
agoraphobia, social phobias, obsessive-compulsive disorders.
1-2 sessions / week are needed for 1-2 years.
Cognitive-constructivist psychotherapy (Kelly) is based on the evaluation of the success or failure of the
individual in achieving their goals, but in this case the task of psychotherapy is not to eliminate the
symptoms but to understand the adaptive meaning of the symptoms, i.e. the patient must understand the
function of internal balance that the symptom carries out in order to try to replace it with a more
appropriate reaction such as to satisfy other personal needs as well.
Behavioral Psychotherapy it is based on deconditioning and conditioning techniques with the aim of
reducing or eliminating psychic symptoms and modifying or eliminating pathological behaviors by replacing
them with more functional behaviors. In fact, according to modern behaviorism, psychopathological
disorder is the result of an inadequate behavioral response following an incorrect learning, while psychosis
is the result of a lack of learning.
The deconditioning techniques are the most used in clinical practice, among which we have reciprocal
inhibition (an incompatible behavior is associated with the pathological one to extinguish it, for example
in patients suffering from generalized anxiety it is possible to resort to relaxation techniques , that is
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yoga, training

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autogenous, to induce muscle relaxation and inhibit anxious activation as anxiety is incompatible with a
condition of psychophysical relaxation), systematic desensitization (indicated for the therapy of phobias,
subjecting the patient to progressively more anxious stimuli to inhibit the phobic alarm response),
flooding-implosion (these are shock therapies indicated in patients suffering from phobic disorders,
subjecting them abruptly to intense, traumatic anxiety-inducing stimuli, without the possibility of escape
or avoidance, to desensitize them to stimulus itself or reduce anxiety in subsequent exposures), multiple
repetition (the patient must repeat the learned behavior continuously and intentionally until it is
extinguished, used in some forms of tics and obsessive-compulsive symptoms).
The conditioning techniques have the task of favoring the psychosocial integration of the patient through
psycho-pedagogical and rehabilitative interventions useful in patients suffering from mental disorders with
intellectual deficits, such as mental insufficiency and dementia, and in patients suffering from residual
schizophrenia with - behavioral rences. Conditioning uses positive or negative reinforcements, such as
rewards or disapproval, to foster a better and lasting learning process.
Relational Psychotherapy it is based on the principle that to understand a psychic disorder the individual
must be studied in the relationship with others, trying to correct the abnormal or pathological
relationships of the couple or family group on which the pathological behaviors depend.
The therapist welcomes the family in the room where the session will take place, while in an adjacent
room there is another therapist who observes the session through a mirrored glass, informing the family in
advance and has the task of supervising the activity of the first therapist who involved in the pathological
family system, he continually risks being overwhelmed and absorbed in abnormal functioning,
unconsciously adapting to it.
In the first phase the therapist evaluates the functioning of the system he has to treat and the abnormal
relationships, in the second phase he tries to modify the abnormal behavior with a more functional one, in
fact the therapist during the session is part of the system and actively intervenes by modulating its
functioning . Relational psychotherapy is indicated above all in patients with mental anorexia and in the
prevention of exacerbations of schizophrenic psychosis.

SCHIZOPHRENIA AND OTHER PSYCHOTIC DISORDERS

Schizophrenia indicates a group of serious mental disorders, of a psychotic nature, clinically
heterogeneous, but which have in common the basic psychopathological mechanism, i.e. the splitting of
mental processes, for which the psychic functions operate independently until the complete disintegration
of mental life and dissociation between thought, affectivity and will.
From an epidemiological point of view it has a ubiquitous distribution in the various geographical areas
and in the various social classes with a prevalence of 0.5-1.5% and an annual incidence of less than 0.09%.
Variability in the rate is reported between races / ethnicities, between countries, and by geographic
origin in immigrants and children of immigrants.
The psychotic manifestations of schizophrenia typically emerge between late adolescence and the mid-
fourth decade of life: pre-adolescent onset is rare. The peak age of onset of the first psychotic episode is
in the first half of the third decade in men and towards the end of the third decade in the female. Onset
may be sudden, but the majority of individuals experience slow and gradual development of a variety of
clinically significant signs and symptoms. Half of these individuals exhibit depressive symptoms.
Age of early onset has traditionally been viewed as a negative predictor. Males have worse premorbid
adjustment, worse school performance, more severe negative symptoms, and cognitive impairment.
Most individuals with schizophenia still require daily support and many maintain a state of chronic disease,
with exacerbations and remission of active symptoms, while others have a course of progressive
deterioration.
About 5-6% of individuals with schizophrenia die from suicide, 20% attempt suicide on one or more
occasions, many have significant suicidal ideation. Suicidal behavior is sometimes a response to
hallucinations that command harm to oneself or others.
Rates of comorbidity with substance-related disorders are high in schizophrenia. Over half of individuals
with schizophrenia have a tobacco use disorder and regularly smoke cigarettes. In schizophenia,
comorbidity with anxiety disorders is increasingly recognized. Rates of obsessive-compulsive disorder and
panic disorder are high in individuals with schizophrenia compared to the general population. Schizotypal
or paranoid personality disorder can sometimes precede the onset of schizophrenia.

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Life expectancy is shortened in individuals with schizophrenia due to associated medical conditions.
Weight gain, diabetes, metabolic syndrome, and cardiovascular and pulmonary disease are more common
in schizophrenia than in the general population.
L’Eziologia della schizofrenia non è ancora chiara, probabilmente è multifattoriale legata a fattori am-
bientali, sociali, mentre tra i Fattori di Rischio abbiamo:

hereditary factors (schizophrenia in 60% of cases occurs in predisposed subjects with a positive
family history affecting mainly first degree relatives with a variable risk of 4-8% in the case of a
brother of a schizophrenic, 50% if the subject has a monozygotic twin sibling schizophrenic, 30% in
the case of children with parents both schizophrenic; multiple genetic alterations have been
identified on chromosomes 6, 8, 11 and 22)

age (in most cases the disorder affects the age group 15-45 years, in particular towards 14-24
years in males and 25-35 years in females; after 45 years the risk is decreases progressively with
age),

seasonality of birth (the incidence is high in those born in the last period of the winter season)

stressors especially in pregnant women, such as husband's death, job loss, obstetric complications,
early maternal separation stress.
The pathogenetic hypotheses concern an altered neurodevelopment (neuronal migration, neuronal
selection, synaptogenesis and cerebral circulation are involved), neurodegeneration or the progressive
alteration of neurodevelopment. The most accredited theory concerns the alterations of synaptogenesis.
Normally immature neurons are characterized by the presence of hair-like dendritic branches (filopodia)
and an axonal cone that expand and extend in search of a partner with whom to establish synaptic
contacts. Once contact has been established, a biosynthetic process begins which transforms the filopodus
into a dendritic spine and induces changes in the area of the neuron with which it came into contact that
transform it into a synaptic area. Once the synapse is formed, if it is functionally efficient it survives. It is
divided into phases and it has been suggested that the rapid decrease in cortical synaptic density after the
onset of puberty is one of the most important events favoring the onset of schizophrenia.
It has also been observed that most of the genes believed to be involved in vulnerability to schizophrenia
are also involved in the regulation of synaptic function. In particular, some of these genes influence
receptor functionality (GRM3), others the signal transduction mechanisms (RGS4), others plasticity and
synaptogenesis. Synapses and glutamate transmission appear to be most affected. There is also evidence
of involvement of dopaminergic synapses.
From a clinical point of view, schizophrenia manifests itself with positive and negative symptoms,
disorganized symptoms and catatonic symptoms.
1. The Positive Symptoms they are due to an abnormal functioning of mental processes with distortion of
reality, including delusions and hallucinations.
1.1. The delusion it is a pathologically distorted judgment characterized by extraordinary conviction
and unparalleled subjective certainty; the fact of not being influenced by concrete experience
and by stringent refutations; the absurdity of the content. The term delirium derives from the
Latin 'de lira', that is 'going out of the rut': it therefore indicates a deviation from the way of
thinking or judging that is typical of every culture. Delusions can be classified according to the
following criteria:
1.1.1. The presence or absence of an alteration of the state of consciousness (lucid delirium and
confused delirium or delirium)
1.1.2.The presence of a greater or lesser internal structure (elementary delirium and
systematized delusion)
1.1.3.The presence or absence of absurdity of the content (bizarre and not bizarre delusion)
1.1.4. The formal mode of onset (primary and secondary delirium or deliroid)
1.1.5 The presence of one or more themes
1.1.6. The characteristics of the content
1.1.7. The congruence or not with the depressed or manic
mood. The pathognomonic delusions of schizophrenia are:
1. delusions of thought theft (the patient believes that other people can read his mind)

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2. delusions of influence (the patient believes that his thoughts are controlled by external
forces)
3. thought diffusion delusions (the patient believes his thoughts are spreading outside his mind
so that he or others can hear them)
4. thought insertion delusions (the patient believes that thoughts that he does not recognize
as his own have been inserted into his mind).
5. Delusions of thought transmission (the subject is convinced that someone can transmit ideas
at a distance in the subject's mind.
6. Furthermore, schizophrenia can manifest itself with nonspecific delusions such as delusions
of persecution (the patient feels persecuted, followed, spied on or believes he has the world
against)
7. referral delusions (patient believes news from newspapers, TV, or other events related to
him)
8. delusions of grandeur (the patient is convinced that he has supernatural, almost divine
powers)
9. mystical-religious delusions (the patient has false beliefs of a religious nature)
10. pseudoscientific delusions (the patient develops false or meaningless scientific theories)
11. genealogical delusions (the patient believes he is related to famous people)
12. erotomanic delusions (the patient believes that an important person is in love with him)
13. delusions of jealousy (the patient is convinced that he is being betrayed)
14. somatic delusions (the patient believes that his body is transformed, he gives off a bad smell)
15. delusions of harm (the patient believes he is being robbed by family members, roommates or
healthcare personnel if hospitalized).
16. Delusion of denial (the patient denies the existence of his own bodily reality and external
reality. It is also called nihilistic delirium and is present in Cotard's syndrome)
17. Polygnotic delirium (belief that you have already known or recognize completely strangers or
strangers as relatives or friends)
18. Delirium of infestation or dermatozoal delirium (belief that the skin or scalp is infested with
small insects or parasites that move, dig burrows, cause an annoying itch, etc.)

2. The hallucinations they are false perceptions or perceptions without an object, that is, the
patient perceives a non-existent object, not criticized or rather they are not recognized as
hallucinations but are experienced by the patient as normal perceptions, experiences of reality,
perfectly congruent. True hallucinations have also been defined as 'psychosensory hallucinations'
to distinguish them from pseudo-hallucinations which are also defined as 'psychic hallucinations'.
They have the following characteristics:
2.1. SENSORY - BODY: they are anchored to sensory qualities relevant to each sense and
therefore have a physical character similar to that of real perceptions
2.2. SPACIALITY: they have a precise location in space and therefore can appear external and
distant.

We have various types of hallucinations:

2.3. auditory hallucinations are the most frequent and typical of schizophrenia, the patient hears
whispered but understandable voices of unknown or known subjects, voices that give orders,
prohibitions or impose actions (imperative or compulsory hallucinations), voices that discuss
with each other on various topics or talk about the patient criticizing or praising his actions
(interview of voices), voices that repeat the contents of the patient's thought (echo of
thought), commenting voices that criticize, comment, approve or disapprove of the actions;
2.4. tactile somatic hallucinations, where the patient feels particular sensations on the body
surface such as the crawling of a snake, being caressed, touched or struck;

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2.5. kinesthetic-visceral hallucinations, in which the patient feels particular internal somatic
sensations such as animals biting organs, squeezing hands;
2.6. the hallucinations of the body scheme in which the patient perceives transformations in his
own body, asymmetries, displacements of parts;
2.7. olfactory hallucinations, gustatory and visual which are rarely observed in schizophrenia.
2. The Negative Symptoms they are due to a deficit of mental functions. They are common in the
prodromal and residual stages and can be severe. Individuals who have been socially active may
become withdrawn from previous habits. We have:
2.1. alogia (poverty of speech, i.e. of language and communication skills with a reduction in the flow
of ideas, short speech, poor in content and short answers to questions),
2.2. flattening of affectivity (emotional indifference to the surrounding environment and poor
emotional reactivity to stimuli, with fixed gaze and lack of expressiveness),
2.3. apathy and avolition (the patient is listless, spends a lot of time doing nothing or for aimless
activities, neglects personal hygiene),
2.4. anhedonia (inability to feel pleasure and joy in any situation with total indifference, lack of
feelings and emotions towards people, lack of interest in normal daily activities and hobbies, up
to social withdrawal, for which schizophrenia is characterized by a severe deficit in social,
occupational, emotional and sexual functioning).
2.5. abulia, i.e. a decrease in voluntary and spontaneous purposeful activities. The individual may
remain seated for long periods of time and show little interest in participating in work or social
actions.
3. Disorganized Symptoms they are represented by formal thought disorders, bizarre behavior and
affective incongruity with dissociation between thought and affectivity.
3.1. In formal thought disorders the patient presents disorganized thinking with alterations in the form
and execution of thought characterized by various phenomena such as:
3.1.1. derailment (the patient expresses different ideas, passing from one theme to another,
without any associative link between the ideas themselves),
3.1.2. tangentiality (the patient gives meaningless answers to questions),
3.1.3. inconsistency (the speech is incomprehensible),
3.1.4. circumstantiality (inconclusive, dispersive, superficial speech),
3.1.5. illogicality (the patient comes to a conclusion through an illogical deductive procedure).
3.2. Bizarre behaviors are incongruous attitudes, inadequate to the circumstances that can involve
physical appearance, clothing, social and sexual behavior, moreover, stereotypes that is the
patient always repeats the same movements or the same syllables in an afinalistic way and
mannerisms that is mimic attitudes - extravagant, inappropriate gestures that tend to repeat.
3.3. By affective incongruity we mean when the patient has inappropriate emotional reactions with
respect to his thoughts or the events of the surrounding environment, for example he becomes
aggressive after a manifestation of affection or bursts out laughing in a situation of pain or
sadness.
4. The Catatonic Symptoms are very serious, among which we have:
4.1. catalepsy (tendency of the patient to maintain the same position for long periods of time, even
uncomfortable; we speak of waxy flexibility of the muscles when it is possible to put a limb or
the patient's body in a position that is maintained for a long time due to hypertonia muscle),
4.2. passive negativism (the patient tends to remain rigidly immobile in the position chosen by him,
opposing external attempts to modify it, such as the sign of the psychic pillow when the patient
remains with his head raised from the bed as if it were resting on the pillow),
4.3. active negativism (the patient does exactly the opposite of what is required of him)
4.4. psychomotor arrest (state of inhibition and psychomotor passivity to the point of stupor in which
the patient is indifferent to what happens in the environment, lies motionless maintaining full
clarity of conscience and does not react to painful stimuli).

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Depersonalization, derealization, somatic worries can occur which can sometimes reach delusional
intensity. Anxiety and phobias are common.
Cognitive deficits in schizophrenia are common and are strongly linked to functional and occupational
impairments. These deficits may include decreases in declarative memory, working memory, language and
other executive functions, as well as slower processing speeds. Abnormalities in sensory processing and
inhibitory capacity were also found.
Some individuals with psychosis may lack 'insight' or awareness of their disorder (anosynosy). This lack
includes unawareness of the disorder and may be present throughout the course of the disease. This
symptom is the most common predictor of non-adherence to treatment, but also of higher relapse rates,
more mandatory treatments, worse psychosocial functioning, aggression, and worse disease course. .
Hostility and aggression can be associated with schizophrenia although spontaneous or random aggression
is uncommon. It is more common in males.

Diagnosis of schizophrenia is clinical, evaluating symptoms and signs, information obtained from relatives
and friends. According to the DSM-5, the following criteria must be respected for the diagnosis of
schizophrenia:
A. Two or more of the following symptoms, present for a significant portion of time during the
one-month period (or less if treated effectively). At least one of these symptoms must be 1.,
2. or 3.:
1. Delusions;
2. Hallucinations;
3. Disorganized speech (for example, derailment or inconsistency);
4. Grossly disorganized or catatonic behavior;
5. Negative Symptoms (decreased expression or emotions, or lack of confidence).
B. For a significant portion of time since the onset of the disorder, the level of functioning in one
or more of the main areas, such as work, interpersonal relationships, or self-care is markedly
below the level reached before onset (or when onset is in childhood or adolescence, the
inability to reach the expected level of interpersonal, school or work functioning occurs).
C. Continuing signs of the disorder persist for at least 6 months. This 6-month period must include
at least 1 month of symptoms meeting criterion A, and may include periods of prodromal or
residual symptoms. During these prodromal or residual periods, the signs of the disorder may
be evidenced only by negative symptoms or by two or more symptoms listed in criterion A in
attenuated form (eg extravagant beliefs, unusual perceptual experiences).
D. Schizoaffective disorder and depressive or bipolar disorder with psychotic features were
excluded because (1) there were no manic or major depressive episodes concurrent with the
active phase of symptoms, or mood during the active phase, they occurred for a minority of
the total duration of the active and residual periods of the disease.
E. The disorder is not attributable to the physiological effects of a substance or to another medical
condition.
F. If there is a history of autism spectrum disorder or childhood-onset communication disorder,
the additional diagnosis of schizophrenia is made only if pre-eminent hallucinations or
delusions are present for at least 1 month, in addition to the other required symptoms of
schizophrenia.
Specify if:

First episode, currently in acute episode;

First episode, currently in partial remission;

First episode, currently in complete remission;

Multiple episodes, currently in acute episode;

Multiple episodes, currently in partial remission;

Multiple episodes, currently in complete remission.

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The following course indicators should only be used after one year of duration of the disorder and if they
do not contradict the diagnostic course criteria. Also you have to specify if it is with Catatonia.
CT and MRI show anomalies of the superomedial temporal lobe associated with positive symptoms,
cortical and frontal ventricular anomalies associated with negative symptoms, moreover an alteration of
dopaminergic regulation by a notable reduction in the density of related postsynaptic D2 receptors was
highlighted. to positive symptoms.
Psychopharmacological Therapy has the task of controlling symptoms and avoiding relapses by
administering antipsychotic drugs divided into classical antipsychotics or neuroleptics and new generation
antipsychotics.
1. Classic or neuroleptic antipsychotics are drugs with dopamine-antagonist action, such as haloperdol,
fluphenazine, chlorpromazine, promazine, which have affinity for post-synaptic dopamine receptors
D2 and D4 present in the limbic system and in the cortex exerting action antipsychotic, controlling
positive symptoms (hallucinations, delusions), mental confusion and partly dissociative symptoms.
Since dopamine D2 receptors are also present in the neostriatum, the blocking of these receptors
causes the onset of extrapyramidal side effects such as:
1.1. acute dystonia (appearing within 3-4 days of neuroleptic administration or dose increase, with
spastic torticollis, oculogyric crisis, blepharospasm, laryngeal dystonia, limb dystonia; therapy is
based on the administration of intramuscular anticholinergics) ,
1.2. iatrogenic parkinsonism (onset a few weeks after starting therapy with tremors, muscle stiffness
and bradykinesia; the dose of the neuroleptic should be reduced and an anticholinergic such as
Biperidene should be administered),
1.3. akathisia (onset several weeks after initiation of therapy or after dose escalation, causing motor
restlessness with an inability to sit still and sit; it is necessary to reduce the dose of the
neuroleptic, administer β-blockers or benzodiazepines) ,
1.4. tardive dyskinesia (onset after long-term therapy, especially after the suspension or reduction of
the dosage of neuroleptics, manifesting itself with involuntary movements of the tongue or face,
fingers and limbs; there is no specific therapy).
Furthermore, neuroleptics are responsible for other side effects such as hyperprolactinaemia (with
gynecomastia, galactorrhea, amenorrhea and weight gain), antihistamine H1 action (sedation which
can be useful in schizophrenic and drowsiness), anticholinergic action (dry mouth, constipation,
increased intraocular pressure, urinary retention), antiadrenergic action (hypotension and reflex
tachycardia). The most fearful complication is neuroleptic malignant syndrome which onset acutely
within hours of neuroleptic administration with hyperthermia (T ° C above 39 ° C), muscle rigidity and
rhabdomyolysis with increased plasma creatine phosphokinase (CPK), up to mental confusion,
2. The new generation antipsychotics they are more selective for the receptors of the dopaminergic
system, also endowed with serotoninergic action, among which we have Clozapine, Risperidone and
Olanzapine, which compared to neuroleptics have several advantages:
2.1. they act faster and more effectively on positive and negative symptoms
2.2. they are more effective in forms of schizophrenia resistant to other therapies
2.3. they are more tolerated by the patient because they have a lower sedative effect and a low risk
of extrapyramidal and anticholinergic undesirable effects, although in the case of Clozapine
frequent haematological checks must be performed to assess the presence of granulocytopenia /
agranulocytosis.
Sometimes antipsychotics are combined with benzodiazepines to enhance the sedative action of
antipsychotics and induce sleep, or low-dose antidepressants (SSRIs) are used in cases of severe
schizophrenia with disabling negative symptoms or depression superimposed on schizophrenia,
avoiding to excessively disinhibit the patient or the aggravation of positive symptoms.
Social Rehabilitation Therapy and Psychotherapy they have the task of stimulating the recovery of the
patient's autonomy and self-sufficiency, favoring reintegration into the family or community, through
cognitive-behavioral techniques, group and systemic-relational therapies.
The DSM-4 distinguished 4 subtypes of schizophrenia heterogeneous by way of onset, clinical picture,
evolution and prognosis, ie disorganized, paranoid, residual and catatonic schizophrenia.

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1. Disorganized or Hebephrenic Schizophrenia begins at a young age (Hebe: goddess of youth) often in
subjects under the age of 20 with a positive family history of schizophrenia. From a clinical point of
view there is a premorbid phase with poor school or work performance, followed by schizophrenic
psychosis which generally has a sneaky onset dominated by disorganized symptoms. The course is
chronic with periodic exacerbations that progressively worsen the basic clinical picture with the onset
of positive symptoms in particular delusions of theft, diffusion or insertion of thought with
fragmentary ideas, poorly systematized with variable content, auditory hallucinations rarely congruent
with the delirium. Negative symptoms manifest themselves in phases of remission or intercritical
periods. Evolution is slow and progressive with affective and intellectual impoverishment of the
patient up to dementia, depression and risk of suicide in 10% of cases in the initial stages of the
disorder or in case of improvement after an exacerbation. The response to medical and socio-
rehabilitation therapy is rather limited with a poor prognosis.
2. Paranoid Schizophrenia begins between the ages of 20 and 35 in both sexes, generally in an acute,
abrupt manner, with a clinical picture dominated by positive symptoms, that is, persecutory
delusions, reference and grandeur, with well-structured, systematized ideas, more constant content
and rich in details, auditory, tactile and body schema allusions, congruent with delusions, often
associated with disorganized symptoms, rarely with negative symptoms. The course is chronic with
phases of exacerbation dominated by positive symptoms experienced with great emotional
participation, associated with psychomotor agitation and in the most serious cases with a state of
transient delirium.
3. Residual Schizophrenia generally begins in young male subjects, is characterized above all by negative
symptoms, with progressive affective and intellectual impoverishment of the patient and, due to poor
collaboration and communication difficulties with the patient, the prognosis is often unfavorable with
difficulty in achieves a good level of work and social functioning.
4. Catatonic Schizophrenia represents an evolutionary phase of schizophrenic disorder rather than a
subtype of it, characterized by severe psychotic manifestations with a prevalence of disorganized and
negative symptoms such as to require hospitalization, administering intramuscular neuroleptics with a
greater antipsychotic effect, associated with forms more resistant to tricyclic antidepressants with a
powerful disinhibiting effect. In severe and drug-resistant forms, electroshock (ECT) can be used.
In DSM-5, subtypes were eliminated due to their unsatisfactory reliability and validity. Furthermore, the
DSM-5 does not treat catatonia as an independent class but recognizes catatonia associated with another
mental disorder, catatonic disorder due to another medical condition and catatonia without specification.

Among other Psychotic Disorders we have schizophreniform disorder, schizoaffective disorder, delusional
disorder and brief psychotic disorder, which may be associated with schizophrenia or have characteristics
similar to schizophrenia or evolve towards schizophrenia.
1. Schizophreniform Disorder is characterized by the typical symptoms of schizophrenia but lasting less
than 6 months, which after 6 months evolves in 60% of cases towards real schizophrenia, in 20%
towards schizoaffective disorder, in 20% towards remission.
2. Schizoaffective Disorder is a mixed psychosis characterized by the coexistence or alternation between
schizophrenic symptoms, especially delusions and hallucinations, and affective disorders present for
most of the total duration of the disorder, especially depression and manic or hypomanic state, for
which therapy is based on the association between antipsychotics, mood stabilizers, ie lithium salts
plus Carbamazepine or Valproate and socio-rehabilitation therapy.
The diagnosis is made when there is an uninterrupted period during which a mood episode is present
in conjunction with criterion A of schizophrenia; delirium or hallucination for two weeks or more in
the absence of a mood episode during the duration of the illness; Symptoms that meet the criteria for
a mood episode are present for most of the total duration of the active and residual periods of the
disease; the disturbance is not attributable to the effects of a substance (criterion attributable to all
4)
3. Delusional Disorder is characterized by well-structured (even bizarre) delusions, rich in details and
lived with intense emotional participation, in particular delusions of grandeur, erotomanic, jealousy,
persecution, somatic, with mood and behavior of the patient consistent with the content of the
delirium, not associated with hallucinations and dissociations of thought. It is diagnosed by the
presence of one or more delusions lasting a month or more, but criterion A for schizophrenia is not
met. The

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functional involvement was not massive and if there were major manic or depressive episodes, these
were brief.
4. Brief Psychotic Disorder is a serious mental disorder that arises abruptly after a very stressful or
traumatic event such as bereavement, with sudden onset of delusions, hallucinations, meaningless
speech, inappropriate behavior, but resolves quickly within a few minutes or days, without results and
with complete psychic recovery of the patient. It is diagnosed by the presence of at least one of the
first four symptoms of schizophrenia (thus excluding negative symptoms) and at least one of the first
three must be present. The duration is at least one day but less than a month. Biaogna specify if
characterized by a marked stress factor, if it onset in post partum, if there is catatonia and the
current severity.

GLUTAMATERGIC HYPOTHESIS OF SCHIZOPHRENIA (it was in pharmacotherapy but it doesn't make sense
there)
It has been found that psychomimetic substances such as phencyclidine and ketamine can induce
worsening of symptoms in schizo-phrenic patients and psychotic symptoms in normal subjects.
Phencyclidine and ketamine share the NMDA blockade of glutamate. In addition, low plasma levels of CSF
glutamate were also found in patients, receptor binding studies on the brains of post-mortem patients
have highlighted an increase in NMDA receptors, the increase in NMDA receptors suggests that these
receptors have a a form of hypofunction that would justify a compensatory response from the system with
an up-regulation.
Atypical antipsychotics seem to antagonize the effects of ketamine and the other NMDA antagonists, so in
a sense they would improve, it is not yet known how, glutamatergic transmission.
In any case, in schizophrenia, in addition to the dopaminergic hypothesis of mesolimbic hyperactivity and
mesocortical hypoactivity, the problem would also involve a hypofunction of NMDA receptors. In this
sense, molecules are being studied that would improve the functioning of NMDA, therefore partial agonists
of the glycine site that we know facilitates the activation of NMDA or dyserine which is a full agonist on
the glycine receptor itself. given promising results even if they are not yet marketed on symptomatology
improvement; D-Cycloserine, a partial agonist at the glycine site, has been shown to improve negative
symptoms in schizophrenic patients both on its own and in combination with other antipsychotic drugs.
In a normal subject the NMDA receptor is present on the GABA-ergic interneuron and this discharges on
the other glutamate neuron (there are two glutamate neurons) modulating its action: this second
glutamate neuron does not stimulate too much the mesolimbic pathway, therefore mesolymbic
transmission is normal. If we have a hypofunctioning NMDA receptor on the GABA-ergic interneuron, the
second glutamatergic, says Stahl, goes to discharge massively, especially following stressful events
(biopsychosocial model to explain psychiatric disorders) and elicits a phasic firing of the second do
glutamate neuron with another phasic firing of the dopaminergic neuron, therefore positive symptoms:
delusions, hallucinations, etc.

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We can consider the same concept by considering the

ventral hippocampal cortex, only here we have to
consider more neurons: here in normality, the NMDA
works well so this second glutamatergic neuron of the
hippocampal cortex discharges moderately, it does not
inhibit this GABA-ergic neuron which in turn modulates
the second GABA-ergic therefore the VTA discharges in a
normal way at the level of the accumbens. In the absence
of this NMDA-mediated control, the second glutamatergic
will activate the GABA-ergic one, this GABA-ergic will
inhibit the second GABA-ergic of the pale nucleus so the
VTA is disinhibited and discharges in a phasic manner
causing the positive symptoms.
As for the negative symptoms, the concept is the same,
except that Stahl specifies that different populations of
glutamatergic neurons discharge on different populations
of dopaminergic neurons, so to consider the mesocortical
pathway instead we have to consider other areas of the
VTA, different than to those we have seen before and in
this case, the concept is always that of NMDA
hypofunction, only we will consider a dopaminergic
neuron which is instead generally inhibited by a GABA-
ergic interneuron at the level of the midbrain.

If the NMDA receptor on the GABA-ergic neuron fails, the second glutamatergic will excessively activate
the GABA-ergic interneuron so the mesocortical pathway is hypoactive. At the ventromedial level this
hypofunction will mediate the affective impoverishment and therefore the affective flattening, at the
level of the dorsolateral prefrontal cortex the cognitive deficits, in particular those of working memory,
selective attention deficit and then the motor disorganization and of speech.
From the genetic point of view, a much studied gene is COMT, an enzyme that metabolizes dopamine at
the level of the cortex, there are polymorphisms and in particular individuals who have met- met
polymorphism are more prone to have cognitive deficits than subjects val-val. clearly this would also be at
the basis of a greater therapeutic response to olanzapine, val-val individuals would respond better to
olanzapine and would have greater synaptic availability of dopamine at the mesocortical level.
As for the atypical antipsychotics, the 5-HT2A block and the 5-HT1A partial agonism would improve all
that profile we have seen before on the glutamatergic hypothesis of schizophrenia. In fact, the 5-HT2A
receptor is located at the somato-dendritic level of the second glutamate neuron. It is an excitatory
receptor associated with Gq protein and blocking it means going to remodel this dopaminergic activation.
Similarly, as far as cognitive-affective symptoms are concerned, the concept is the same: blocking 5-HT2A
on the second glutamate neuron would favor a more adequate meso-cortical firing. Therefore the 5-HT2A
block is decisive in the difference between the two types of antipsychotics.

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MOOD DISORDERS - BIPOLAR DISORDER AND RELATED DISORDERS

Mood Disorders are pathological, incongruous, inadequate affective reactions to events and situations that
can occur in an episodic, sporadic or transient manner and are the most commonly diagnosed conditions in
the psychiatric field.
Within the DSM-4, bipolar disorder was included in the chapter "Mood Disorders", including:
 Major Depressive Disorder
 Dysthymic Disorder
 Major Depressive Disorder Not Otherwise Specified
 Bipolar I Disorder
 Bipolar II Disorder
 Cyclothymic Disorder
 Bipolar Disorder Not Otherwise Specified
 Disorder Mood Due To General Medical Condition
 Substance-Induced Mood Disorder
 Mood Disorder Not Otherwise Specified
To introduce the chapter, the diagnostic criteria of the fundamental humoral episodes of the
aforementioned disorders:
 Major Depressive Episode
 Manic Episode
 Mixed Episode (disappears in DSM-5, replaced by the specifier with mixed characteristics to the 3 main
episodes)
 Hypomanic episode
In DSM-5, Bipolar Disorder and related disorders were separated from depressive disorders and placed
between the chapters on Spectrum Disorders of Schizophrenia and Other Psychotic Disorders and
Depressive Disorders, recognizing their position as a bridge between the two classes. diagnostic in terms
of symptoms, family history and genetics.
MANIACAL EPISODE
The Manic Episode manifests itself with a severe mood expansion with abrupt onset with euphoric
exaltation or dysphoric excitement, cognitive-perceptual, psychomotor and somato-vegetative disorders
more severe than the hypomanic episode. Sometimes the manic episode arises as the evolution of a
hypomanic episode with the appearance of various disorders during the transition phase. There may be
psychotic symptoms such as delirium with accelerated flow of ideas and loosening of associative links,
severe mental confusion, temporal-spatial disorientation, psychomotor agitation, severe impairment of
attention and memory, delusions congruent with mood manic that is delusions of greatness with a
pseudoscientific, mystical-religious, genealogical or erotomanic content, and incongruous delusions of
persecution and reference, fragmented and not very systematized. The patient rarely experiences
auditory hallucinations. In addition, there can be severe behavioral alterations of an explosive type
(excited-furious mania) with motor hyperactivity and excitement up to real fits of irrepressible fury and
pantoclastic behaviors (the patient has a tendency to break everything), marked aggression with serious
consequences, and severe impairment of psychosocial functioning such as to require hospitalization.
Generally, the manic episode lasts from a few weeks to a few months, followed by a recovery phase of the
psychic compensation. In addition, there can be severe behavioral alterations of an explosive type
(excited-furious mania) with motor hyperactivity and excitement up to real fits of irrepressible fury and
pantoclastic behaviors (the patient has a tendency to break everything), marked aggression with serious
consequences, and severe impairment of psychosocial functioning such as to require hospitalization.
DD -> unlike the depressed, the patient with manic episodes does not manifest this condition but for him
everything is normal and he is fine.
The criteria for the Manic Episode are:
A. A defined period of abnormally and persistently elevated, expanded or irritable mood and
abnormal increase in purposeful activity or energy, lasting at least a week and present for most of
the day most days (or of any duration if hospitalization is required).
B. During the period of mood alteration and increased energy or activity, three (or more) of the
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following symptoms (four if the mood is only irritable) are present at a significant level and
represent a noticeable change from at the usual level:
1. Hypertrophic self-esteem or grandiosity;
2. Decreased need for sleep
3. More talkative than usual or pushed to keep talking
4. Flight of ideas or subjective experience that thoughts follow one another quickly;
5. Distractibility, reported or observed;
6. Increased purposeful activity (social, work, school or sexual) or psychomotor agitation;
7. Excessive involvement in activities that have a high potential for harmful consequences
(e.g., uncontrolled shopping, improper sexual behavior, or reckless financial investments).
C. The mood alteration is severe enough to cause marked impairment in social or occupational
functioning or to require hospitalization to prevent harm to oneself or others, or psychotic
manifestations are present.
D. The episode is not attributable to the physiological effects of a substance (e.g., a substance of
abuse, a drug, or other treatment) or another medical condition.
NB: a complete manic episode that emerges during an antidepressant treatment, but which persists at a
complete syndromic level beyond the physiological effect of that treatment, represents sufficient
evidence of the presence of a manic episode, and, therefore, of a diagnosis of the disorder. bipolar I.
Therapy must be timely and adequate, requiring hospitalization or TSO in the event of extreme opposition
from the patient. Psychopharmacological therapy is based on neuroleptics useful for sedating the patient
and controlling psychotic symptoms, while lithium salts can be combined only after evaluating the efficacy
of the neuroleptics and after the patient has fully adhered to the therapy (compliance).
HYPOMANIACAL EPISODE
The Hypomanic Episode is a limited period of time (symptoms for at least 4 days) during which the mood is
constantly elevated with a marked change from the subject's typical mood. It is more nuanced than
manic, does not require hospitalization, and the patient does not manifest psychotic symptoms.
From the clinical point of view, the hypomanic episode has an abrupt onset with an increase in the tone of
the mood from which the other symptoms derive, that is, emotional-affective, cognitive-perceptive,
somato-vegetative and chrono-biological symptoms.
Symptoms of an emotional-affective type are a state of inexplicable euphoria and excessive joy, up to
irritation if one tries to limit the patient's pathological expansiveness and vitality. The hypomanic subject
feels intense and abnormal pleasure for any situation, presents a playful, playful and smiling attitude
(hilarity).
Symptoms of a cognitive-perceptive type are made up of difficulty concentrating, thought disorders with
an accelerated flow of ideas, that is, the patient's ideas follow one another rapidly with logorrhea often in
an incongruous and unproductive way. The contents of the thought are superficial, futile or joking. The
patient has a grandiose self-concept, high self-esteem and a poor capacity for criticism and judgment on
their limits which lead to inappropriate or dangerous behaviors, for example driving in an unpredictable
way, spending a lot of money, behaving aggressively. Sometimes the content of the thought presents
nuanced ideas of reference or persecution, for example the patient thinks he is looked at or hated by
everyone because he considers himself a special person, super-gifted, but without evolving towards
systematized and structured ideas of delirium. Furthermore, the patient presents psychomotor agitation
and exaltation of mimic-gestural expressiveness and in general the hypomanic patient is able to take care
of himself, maintain interpersonal relationships, study, work and lead a fairly congruous relationship life.
The somato-vegetative symptoms are hyperphagia, i.e. increased appetite and pleasure deriving from the
taste of eating with weight gain (but often motor hyperactivity and irregular feeding cause weight loss),
reduction of fatigue or the patient reports a sensation of considerable psychophysical energy and is able
to withstand even heavy work, alteration of the sleep-wake rhythm as the hypomanic sleeps for a few
hours but on awakening he feels very well and in full physical shape and begins his hyperactivity,
increased libido, that is, sexual desire and pleasure.
As regards the chrono-biological symptoms, the manic episode can recur with a seasonal rhythm.
The criteria for the Hypomanic Episode are:
A. A defined period of abnormally and persistently elevated, expanded or irritable mood and
abnormal and persistent increase in purposeful activity or energy, lasting at least 4 consecutive
days, and present for most of the day almost every day.

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B. During the period of mood alteration and increased energy or activity three (or more) of the
following symptoms (four if the mood is irritable only) were present, representing a noticeable
change from habitual behavior and manifest at a significant level:
1. Hypertrophic self-esteem or grandiosity;
2. Decreased need for sleep (e.g. feeling rested after only 3 hours of sleep)
3. More talkative than usual, or push to keep talking
4. Flight of ideas or subjective experience that thoughts follow one another quickly;
5. Distractibility, as reported or observed;
6. Increased purposeful activity (social, work, school, or sexual), or psychomotor agitation;
7. Excessive involvement in activities that have a high potential for harmful consequences
(uncontrolled shopping, improper sexual behavior or rash financial investments).
C. The episode is associated with a noticeable change in functioning, which is not characteristic of
the individual when asymptomatic.
D. The altered mood and change in functioning are observable by others.
E. The episode is not severe enough to cause marked impairment of function. social or work, or to
request hospitalization. If there are manifestations psychotic, the episode is, by definition, manic.
F. The episode is not attributable to the physiological effects of a substance (for example, a
substance of abuse, a drug, or other treatment) or another medical condition.
The hypomanic episode, in the absence of therapy, lasts from a few weeks to a maximum of 3 months.
The most frequent complication is the abuse of alcohol, while in 5-15% of cases the hypomanic episode
evolves towards the most frightening manic picture.
The diagnosis is clinical but clinical observation is often reached under the pressure of relatives or friends
because the patient feels good from a psycho-physical point of view and does not believe he is ill, in fact
it is difficult to obtain adherence to the therapy due to the reduced critical sense and judgment capacity,
up to resorting in extreme cases to the TSO compulsory health treatment.
The therapy of the hypomanic episode is mainly based on mood stabilizers, that is lithium carbonate,
which at medium-low doses favors the remission of symptoms within a few weeks. Waiting for lithium to
reach adequate concentrations and therefore manifest its effects, neuroleptic ampoules are administered
intramuscularly, ie Haloperidol, Chlorpromazine which are able to quickly calm the patient thanks to their
sedative activity, to contain the ideomotor hyperactivity, sleep-wake rhythm disturbances, improving the
clinical picture within a few days. Benzodiazepines are also useful in sedating the patient.
MIXED EPISODE
The Mixed Episode in DSM-5 no longer exists as such, it is a specifier of the 3 main episodes (manic,
hypomanic or depressive episode, with mixed characteristics). It is a serious mood disorder, characterized
by the coexistence of depressive and manic symptoms or by rapid fluctuations from depression to euphoria
or arises as the evolution of a major depressive or manic episode, such as to cause severe impairment of
psychosocial functioning of the patient with a high risk of suicide, requiring hospitalization or TSO, with
the administration of mood stabilizers (Carbamazepine), usually associated with long-lived
benzodiazepines (Diazepam) to increase the sedation of the patient, controlling aggressive behaviors.
Bipolar disorders are divided into bipolar disorder type I, type II and cyclothymic disorder.

TYPE I BIPOLAR DISORDER

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Type I Bipolar Disorder is a serious mood disorder with the appearance in the patient's life of both major
depressive episodes and manic or mixed episodes, alternating with periods of well-being.
From an epidemiological point of view, the prevalence in the general population is 0.4-1.6% with equal
distribution in the two sexes, often they are predisposed subjects with a positive family history with a
probability of developing the disorder equal to 24% in relatives of Grade I generally begins between the
ages of 15 and 40 (average age 30), although onset is early in those predisposed to or affected by a
personality disorder. Generally in women the first episode is depressive, while in men it is manic.The
course varies from individual to individual: sometimes the episodes are separated by a long latent or
asymptomatic phase of many months or years, while in the most serious cases the episodes follow one
another rapidly with short latency phases, so speaks of forms with rapid cycles. In some cases there is a
transition from manic episode to depression, in others the opposite is observed. Sometimes the clinical
picture is dominated by depression, other times by manic crises, more fearful.
Bipolar I Disorder is defined by 2 criteria:
A. The criteria for at least one manic episode were met.
B. The occurrence of the manic and major depressive episode (s) is not better explained by a
schizoaffective disorder, schizophrenia, schizophreniform disorder, delusional disorder or schizophrenia
spectrum disorder and other psychotic disorders with other specification or without specification.
Among the complications we have a high risk of suicide, aggressive behavior, alcohol abuse, severe
impairment of psychosocial functioning. Therapy in the event of a major depressive episode is based on
SSRI antidepressants, the administration of which must be interrupted when the clinical picture improves
to avoid the evolution towards a manic state, while in the case of a manic episode, recurrence is made. to
neuroleptics. The prophylaxis of recurrences by means of lithium carbonate is important, which allows to
improve the evolution of the disorder up to complete remission in 60-70% of cases, with therapy continued
for 5-10 years or for life. If lithium is ineffective, mood stabilizing action can be enhanced with
carbamazepine or sodium valproate.
TYPE II BIPOLAR DISORDER
Type II Bipolar Disorder is a mood disorder characterized by the appearance in the patient's life of both
major depressive episodes and hypo-mania episodes.
From an epidemiological point of view, the prevalence is 0.5% with a slightly higher frequency in females.
The family predisposition is marked, while the onset is between 30 and 50 years. From a clinical point of
view, type II bipolar disorder is less severe than type I due to the absence of psychotic symptoms during
the depressive episode and because the hypomanic episode is characterized by more attenuated symptoms
than the episode. manic.
Bipolar II Disorder is defined by the following criteria:
A. The criteria are met for at least one hypomanic episode and for at least one major depressive episode.
B. There has never been a manic episode.
C. The occurrence of the hypomanic episode (s) and major depressive episode (s) is not better explained
by a schizoaffective disorder, schizophrenia, schizophreniform disorder, delusional disorder or
schizophrenia spectrum disorder and other psychotic disorders with other specification or no
specification.
D. Symptoms of depression or unpredictability caused by frequent alternating between periods of
depression and hypomania cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning.

The course and therapy are identical to bipolar I disorder although the risk of complications is lower.

CYCLOTHYMIC DISORDER
Cyclothymic Disorder or Cyclothymia is characterized by a series of alternating hypomanic and depressive
episodes, with a slow and insidious onset, usually in adolescence or young adulthood, with a chronic-
fluctuating course, separated by a short an interval free from symptoms and with a more attenuated
clinical picture compared to bipolar I and II, even if among the complications we have severe psychosocial
impairment, or the evolution towards bipolar I or II in 15-50% of cases.
Cyclothymic disorder is defined by the following criteria:
A. For at least 2 years there have been numerous periods with hypomanic symptoms that do not meet the
criteria for a hypomanic episode and numerous periods with depressive symptoms that do not meet the
criteria for a major depressive episode.
B. During this 2-year period, hypomanic and depressive periods were present for at least half the time and
the individual was not symptom-free for more than 2 months.
C. The criteria for a major depressive episode, manic or hypomanic, were never met.
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D. The symptoms of Criterion A are not better explained by schizoaffective disorder, schizophrenia,
schizophreniform disorder, delusional disorder or schizophrenia spectrum disorder, and other psychotic
disorders with other or unspecified specifications.
E. Symptoms are not attributable to the physiological effects of a substance (eg, a substance of abuse, a
drug) or to another medical condition (eg, hyperthyroidism).
F. Symptoms cause clinically significant distress or impairment in social, occupational, or other important
areas of functioning.
The therapy is based on mood stabilizers.
BIPOLAR DISORDER AND SUBSTANCE / DRUG-RELATED / DRUG-RELATED DISORDERS
A. A significant and persistent mood alteration that dominates the clinical picture, characterized by
elevated, expanded, or irritable mood, with or without depressed mood, or marked reduction in
interest or pleasure in all, or nearly all, activities.
B. There is evidence from history, physical examination, or laboratory findings of 1) and 2):
1. Criterion A symptoms have developed during or immediately after substance intoxication or
withdrawal, or after exposure to a drug.
2. The substance / drug involved is capable of producing the symptoms reported in Criterion A.
C. The alteration is not best explained by a bipolar disorder or related disorders not induced by the
substance / drug. Such evidence of an independent bipolar or related disorder could include the
following evidence:
Symptoms precede the onset of substance / drug use; symptoms persist for a significant period of time
(eg, approximately 1 month) after acute withdrawal or severe intoxication has ceased; or there is other
evidence to suggest the existence of an independent bipolar disorder and related disorders not induced
by drugs / drugs (eg, a history of recurrent episodes not related to drugs / drugs).
D. The alteration does not occur exclusively in the course of a delirium.
E. The alteration causes clinically significant distress or impairment in social, occupational, or other
important areas of functioning.

BIPOLAR DISORDER (AND RELATED DISORDERS) DUE TO ANOTHER MEDICAL CONDITION

A. A significant and persistent period of abnormally high, expanded or irritable mood and an abnormal
increase in activity or energy that predominates in the clinical picture.
B. There is evidence from history, physical examination, or laboratory data that the alteration is the
direct pathophysiological consequence of another medical condition.
C. The alteration is not better explained by another mental disorder.
D. The alteration does not occur exclusively in the course of a delirium.
E. The alteration causes clinically significant distress or impairment in social, occupational, or other
important areas of functioning, or hospitalization is required in order to prevent damage to oneself or
the stars, or psychotic characterizations are present.

BIPOLAR DISORDER AND RELATED DISORDERS WITH OTHER SPECIFICATION

This category applies to manifestations in which symptoms characteristic of bipolar disorder and related
disorders, causing clinically significant distress or impairment in social, occupational, or other important
areas of functioning predominate but do not fully meet the criteria for any one. disorders of the
diagnostic class of bipolar disorder and related disorders. The bipolar disorder and other specification
related disorder category is used in situations where the clinician chooses to communicate the specific
reason why the manifestation does not meet the criteria for any specific bipolar and related disorders.
This is done by recording "bipolar and related disorders with other specification" followed by the specific
reason (eg, "
1. Hypomanic episodes of short duration (2-3 days) and major depressive episodes.
2. Hypomanic episodes with insufficient symptoms and major depressive episodes.
3. Hypomanic episode without previous depressive episode.
4. Short-term cyclothymia (less than 24 months).

SPECIFICATORS FOR BIPOLAR DISORDER AND RELATED DISORDERS

Anxiously: The presence of at least two of the following symptoms during most days of the current or
most recent episode of mania, hypomania or depression
1. Feeling agitated or tense.
2. Feeling unusually restless.
3. Difficulty concentrating due to worries.
4. Fear that something terrible might happen.
5. Feeling that the individual may lose control of himself / herself.
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Note: Distress due to anxiety has been observed as a prominent feature of both bipolar disorder and major
depressive disorder in both primary care and specialist mental health settings. High levels of anxiety have
been associated with an increased risk of suicide, a longer duration of the disease and a greater likelihood
of non-response to treatment. Consequently, it is clinically useful to accurately specify the presence and
severity levels of distress due to anxiety for treatment planning and treatment response monitoring.

With mixed characteristics: The mixed characteristics specifier can be applied to the current manic,
hypomanic, or depressive episode in bipolar I and bipolar II disorder:

Manic or hypomanic episode, with mixed characteristics:

A. The criteria for a manic or hypomanic episode are fully met and at least three of the following
symptoms are present during most days of the current or most recent episode of mania or hypomania:
1. Relevant dysphoria or depressed mood as reported by the individual (eg, feeling lonely, empty)
or by observation made by others (eg, the individual appears to be on the verge of tears).
2. Decreased interest or pleasure in all, or nearly all, activities (as indicated by subjective
consideration or observation made by others).
3. Psychomotor slowing almost every day (observable by others; not simply the subjective
impression of being slowed down).
4. Fatigue or lack of energy.
5. Feelings of self-deprecation or excessive or inappropriate guilt (not simply self-accusation or
feelings of guilt for being sick).
6. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a
specific plan or suicide attempt or a specific plan to commit suicide.
B. Mixed symptoms are observable by others and represent a change in the person's usual behavior.
C. For individuals whose symptoms fully meet the criteria for mania and depression simultaneously, the
diagnosis should be a manic episode, with mixed features, due to marked impairment and clinical
severity of complete mania.
D. Mixed symptoms are not attributable to the physiological effects of a substance (e.g., substance of
abuse, drug, other treatment).

Depressive episode, with mixed characteristics:

A. The criteria for a major depressive episode are fully met and at least three of the following manic /
hypomanic symptoms are present during most days of the current or most recent episode of depression:
1. Elevated, expanded mood.
2. Hypertrophic self-esteem or grandiosity.
3. More talkative than usual or pushed to keep talking.
4. Flight of ideas or subjective experience that thoughts succeed one another.
5. Increased energy or purposeful activity (social, work, school or sexual).
6. Excessive involvement in activities that have a high potential for harmful consequences (eg,
uncontrolled shopping, improper sexual behavior, or financial investments).
7. Decreased need for sleep (feeling rested by sleeping less than usual as opposed to insomnia).

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B. Mixed symptoms are observable by others and represent a change in the person's habitual behavior.
C. For individuals whose symptoms fully meet the criteria for an episode of both mania and depression
simultaneously, the diagnosis should be a manic episode, with mixed characteristics.
D. Mixed symptoms are not attributable to the physiological effects of a substance (e.g., a substance of
abuse, a drug, or other treatment).
While in disorders with RAPID CYCLES we have rapid fluctuations of depressive and manic phases. Instead
in the MIXED episode we have both episodes and symptoms at the same time and there is less oscillation
between the two phases.

With fast cycles: (can be applied to bipolar I or bipolar II disorder): Presence of at least four mood
episodes in the previous 12 months that meet the criteria for a manic, hypomanic, or depressive episode.
Note: Episodes are demarcated by either partial or complete remission of at least 2 months or a shift to an
episode of the opposite polarity (eg, major depressive episode to manic episode).
Note: The essential feature of rapid cycling bipolar disorder is the occurrence of four or more mood
episodes during the previous 12 months. These episodes can occur in any combination or order. Episodes
must meet the criteria of both duration and number of symptoms for a major depressive episode, manic or
hypomanic, and must be demarcated by a period of complete remission or a transition to an episode of
the opposite polarity, manic episodes and hypomanic are considered to be of the same pole. Except that
they occur more frequently, episodes that occur in the fast-cycling pattern are no different from those
with non-fast-cycling patterns.

With melancholic characteristics:

A. One of the following symptoms is present during the most severe period of the current episode:
1. Loss of pleasure for all, or which all, activities.
2. Loss of responsiveness to habitually pleasant stimuli (you don't feel better even temporarily,
when something good happens).
B. Three (or more) of the following:
1. A distinct quality of depressed mood characterized by profound dejection, despair, and / or
moodiness or so-called "empty mood".
2. Depression regularly worse in the morning.
3. Early awakening in the morning (i.e. at least 2 hours before usual awakening).
4. Marked psychomotor slowing or agitation.
5. Significant anorexia or weight loss.
6. Excessive or inappropriate feelings of guilt.

With atypical characteristics: This specifier can be applied when these characteristics predominate during
the majority of days of the current or most recent major depressive episode.
A. Mood responsiveness (i.e. mood improves in response to actual or potential positive events).
B. Two (or more) of the following features:
1. Significant weight gain or increased appetite.
2. Hypersomnia.
3. “Lead paralysis” (ie feeling of heaviness in the arms or legs).
4. An enduring pattern of sensitivity to interpersonal rejection (not limited to mood episodes),
resulting in significant social or occupational impairment.
C. The criteria for the type "with melancholic characteristics" or "with catatonia" during the same period
are not met.

With psychotic characteristics: Delusions and hallucinations occur at any time during the episode. If
psychotic features are present, specify whether they are congruent or not congruent with mood.
For example in bipolar manic disorder it is more frequent with delirium of grandeur; in depressive disorder
it is more frequent with delirium of guilt, that is, they are congruent with respect to mood.

With catatonia: This specifier can be applied to an episode of mania or depression if catatonic
characteristics are present during most of the episode.

With onset in the peripartum: This specifier can be applied to the current or, if the criteria for a mood
episode are not currently fully met, to the most recent episode of mania, hypomania or major depression
in bipolar I or bipolar II disorder, if the onset of mood symptoms occurs during pregnancy or in the 4 weeks
following delivery.

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With seasonal trend: This specifier applies to the lifetime pattern of mood episodes. The essential
feature is a regular seasonal pattern of at least one type of episode (i.e. mania, hypomania, depression).
Other types of episodes may not follow this pattern.
A. In bipolar I or bipolar II disorder, there was a regular temporal relationship between the onset of
manic, hypomanic, or major depressive episodes and a particular time of year (eg, autumn or winter).
B. Complete remissions (or a shift from major depression to mania or hypomania and vice versa) also
occur at a characteristic time of year (eg, depression disappears in spring).
C. Over the past 2 years, the individual's manic, hypomanic, or major depressive episodes demonstrated a
seasonal temporal relationship, as defined above, and there were no non-seasonal episodes of this
polarity during the 2-year period.
D. Seasonal manic, hypomania, or depression (as described above) substantially outnumber any
nonseasonal mania, hypomania, or depression that may have occurred lifetime in the individual.

TREATMENT OF BIPOLAR DISORDER

 LITHIUM + ATYPIC: Very often (especially in the more resistant forms) Atypical Antipsychotics are
associated with Lithium. Among the Atypicals for example - in those forms in which the depressive
component prevails - it has been seen that Lurasidone would act well on those forms in which social
withdrawal, apathy, apathy, cognitive deficit prevail in the symptomatological procession → Lurasidone
by blocking the 5-HT7 receptor would improve glutamate, cholinergic and histaminergic firing: pro-
cognitive action.
 VALPROATO + ATYPICAL1
 LITHIUM + VALPROATO (LI-VO): very common here
 LAMOTRIGINE + QUIETAPINE (LAMI-QUET): especially in depressive forms since the metabolite of
quietapine, norquietapine, inhibits the noradrenergic neurotransporter (NET).
 VALPROATO + LAMOTRIGINA (LA-VO)
 LAMOTRIGINA + LITHIUM + VALPROATO (LA-LI-VO)2
 LAMOTRIGINA + LITHIUM (LA-LI)
There are also divergent schools of thought regarding the treatment of the depressive phase of bipolar
disorder:
 BOSTON BIPOLAR BREW: any combination except antidepressants. Even the Sienese school strongly
discourages the use of antidepressants because this would facilitate a rapid change in the counterpolar
form.
 CALIFORNIA CAREFUL COCKTAIL
 TENNESSEE MOOD SHINE: in the latter two it has been seen that the antidepressant, if used for a short
period, is allowed because it facilitates a rapid recovery, but with adequate background stabilization
the counter-polar phase hardly manifests itself.

MOOD DISORDERS - DEPRESSIVE DISORDERS

The common feature of all depressive disorders is the presence of a sad, empty or irritable mood,
accompanied by somatic and cognitive changes that significantly affect the individual's ability to function.
The differences between them consist in the duration, in the temporal distribution or in the presumed
etiology. Major depressive disorder has a 12-month prevalence in the United States of around 7%, with
marked differences by age group: prevalence 3 times greater between 18 and 29 years than in the over
60s. It occurs at any age, with an incidence peak around 20 years, more frequent in women with 1.5 to 3
times higher rates, there is no gender difference for symptoms, course, response to treatment and
functional consequences. It has a very variable course, as some individuals do not reach

1 the most commonly used atypicals are aripripazole, paliperidone, lisperidone, quietapine, olanzapine, clozapine (in
resistant forms)
2 the lamotrigine and valproate combinations are very risky as valproate inhibits the metabolism of lamotrigine.

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they never, or rarely, go into remission, while others live many years with few or no symptoms. Chronicity
of symptoms increases the likelihood of underlying personality, anxiety, and substance use disorders, and
the presence of "mixed" and "psychotic" specifiers increases the risk of evolving into bipolar disorder and
schizophrenia, respectively. High mortality, mainly caused by suicide, in women the risk of suicide
attempts is greater, while an increased risk of suicide completion is associated with male sex, being single
or living alone, and having prevailing feelings of hopelessness. There is frequent comorbidity with
substance-related disorder, panic disorder, obsessive-compulsive disorder,
The following depressive disorders are listed in the DSM:
 Disruptive Mood Dysregulation Disorder
 Major Depressive Disorder (major depressive episode)
 Persistent Depressive Disorder (dysthymia)
 Premenstrual Dysphoric Disorder
 Substance / Drug Induced Depressive Disorder
 Depressive Disorder Due to Another Medical Condition
 Depressive Disorder with other specification
 Unspecified Depressive Disorder
MAJOR DEPRESSIVE EPISODE
The Major Depressive Episode is a limited period of time during which the mood is constantly severely
depressed, relative to the subject's typical mood. Often it is a sporadic episode followed by periods of
well-being or it arises as a complication of other psychopathological disorders, i.e. panic attacks,
obsessive-compulsive disorder, eating disorders, somatoform disorder.
From the clinical point of view, the onset of the major depressive episode can be subacute with slow and
progressive evolution or acute with abrupt onset. The patient presents a drop in mood, i.e. depressed
mood from which the typical clinical manifestations of depression arise, i.e. emotional-affective,
cognitive-perceptive, somato-vegetative and chrono-biological symptoms.
Symptoms of an emotional-affective type are depressed, sad, discouraged, dejected, depressed patient,
despairing and crying or withdrawing into himself and suffering with a sense of inner death, anhedonia,
i.e. inability to feel pleasure and joy in any situation, with total indifference, lack of feelings and
emotions towards the people with whom he lives, lack of interest in normal daily activities and hobbies,
to the point of causing an impairment of psychosocial functioning whose extent depends on the severity of
the depression, conditions general physical, age, cultural factors, character of the patient (in fact
sometimes the patient manages to lead a normal life, endures suffering, is able to work, to heal his
person, maintain contact with loved ones,other times there is a marked psychomotor slowdown, the
patient is completely inactive, spends the whole day in bed or in the armchair, in silence, without taking
care of personal hygiene, is disordered, dresses badly), anxiety with excessive worry and discomfort, often
associated with psychomotor agitation.
Symptoms of a cognitive-perceptual type are intellectual performance deficits with difficulty
concentrating, mental fatigue, short-term memory deficits with difficulty in fixing new memories, the
patient feels groggy, not very lucid, unable to read a newspaper, follow a speech and television programs
and ideation deficits with less fluid thoughts, congruent with the tone of the mood, difficulty making
decisions, low self-esteem, feelings of inadequacy, ideas of guilt, worries hypochondriac, economic and
thoughts of death ranging from fear of dying to the desire to die with a high risk of suicide. In the severe
forms the patient presents real delusions of guilt, economic ruin, hypochondriacs, rarely associated with
hallucinations.
Somato-vegetative symptoms are reduced appetite and eating pleasure with weight reduction, marked
asthenia with a feeling of tiredness or psychophysical exhaustion, altered sleep-wake rhythm with early
awakening in the morning or delayed insomnia after a short, very deep sleep or even insomnia from
delayed falling asleep or from multiple nocturnal awakenings for which the patient has the feeling of not
having rested, decreased libido, that is, of sexual desire and pleasure, somatic symptoms
(cardiocirculatory, that is, sense of chest and heart oppression, gastrointestinal that is dyspepsia and
constipation, urogenital ie dysuria).
We speak of chrono-biological symptoms because the depressive episode manifests itself with a recurrent
circadian oscillation, such as delayed insomnia, or with a certain seasonality.

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The course in a subject not subjected to adequate therapy foresees a variable duration from 6 months to 2
years, but generally there is remission with recovery of the psychic compensation. Complications include
death by suicide (15%), abuse of alcohol or other psychoactive substances to alleviate anxiety or to
achieve a state of euphoric compensation. In addition, there are clinical subtypes of major depression
based on the prevailing symptoms (the speficicator must always be associated):
 Melancholic depression: the prevailing symptoms are chrono-biological and psychomotor ones, that is
insomnia from early awakening, marked psychomotor slowdown, very severe and intense anhedonia with
fracture of the psychological continuum.
 Psychotic depression: characterized by a prevalence of very severe cognitive-perceptual symptoms,
with auditory, kinesthetic or somato-visceral delusions and hallucinations.
 Atypical depression: characterized by a prevalence of somato-vegetative symptoms but atypical with
respect to the norm, ie hypersomnia, hyperphagia with weight gain, psychomotor hyperactivity.
 Catatonic depression: characterized by a prevalence of psychomotor symptoms, ie psychomotor slowing
down to the state of catatonic stupor, possibly alternating with states of restlessness or psychomotor
agitation.
The diagnosis of major depression is clinical, the electroencephalogram (EEG) can highlight sleep
disturbances, while in recent years some studies are being carried out on neurotransmitters probably
involved in depression, namely noradrenaline, serotonin, acetylcholine, dopamine and GABA. .
The criteria for the Major Depressive Episode are:
A. Five (or more) of the following symptoms were simultaneously present during a 2 week period and
represent a change from previous functioning; at least one of the symptoms consists of points 1 or
2:
1. Depressed mood for most of the day, most days, as reported by the individual (feels sad,
empty, desperate) or as observed by others (eg appears whiny);
2. Marked decrease of interest or pleasure in all, or almost all, activities for most of the day,
almost every day (as reported by the subjective report or observation);
3. Significant weight loss, not due to diet, or weight gain (for example, a change of more
than 5% of body weight in one month) or decreased or increased appetite most days;
4. Insomnia or hypersomnia most days
5. Psychomotor agitation or slowing down most days (observable by others, not just
subjective feelings of being restless or slowed down)
6. Fatigue or lack of energy most days
7. Feelings of self-deprecation or excessive or inappropriate guilt (which can be delusional),
almost every day (not simply self-accusation or feelings of guilt about being sick);
8. Reduced ability to think or concentrate, or indecision, almost every day (as a subjective
impression or observed by others);
9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a
specific plan, or a suicide attempt, or a specific plan to commit suicide.
B. Symptoms cause clinically significant distress or impairment in social, occupational, or other
important areas of functioning.
C. The episode is not attributable to the physiological effects of a substance or to another general
medical condition.
Note: The AC criteria represent a major depressive episode
Note: Responses to significant losses (e.g. bereavement, financial ruin, loss from a natural
disaster, severe illness or disability) may include feelings of intense sadness, ruminations about
loss, insomnia, poor appetite, and weight loss denoted in the criterion. A, which may resemble a
depressive episode. While these symptoms may be understandable or considered appropriate to
loss, the presence of a major depressive episode in addition to the normal response to significant
loss should be considered with caution. This decision inevitably requires clinical judgment based
on individual history and cultural norms for the expression of pain in the context of loss.

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D. The occurrence of the major depressive episode is not better explained by a schizoaffective
disorder, schizophrenia, schizophreniform disorder, delusional disorder or other schizophrenia
spectrum disorder or psychotic disorder.
E. There has never been an episode of mania or hypomania.
Mour EDM
ning
Feelings of emptiness and loss. Persistent depressed mood, apathy and anhedonia.
Dysphoria that reduces over time, in waves More persistent depressed mood, unrelated to
associated with thoughts or memories of the specific thoughts or worries.
deceased.
Positive mood and emotions can accompany pain. Pervasive misery and suffering.

Ideic content focused on thoughts and memories of Self-critical and pessimistic ruminations.
the deceased.
Preserved self-esteem (if present self-denigrating Feelings of self-deprecation and self-loathing.
ideation it is a perceived deficiency in relation to
the deceased).
Thoughts of death focused on the deceased, on Thoughts of death and suicidal ideation due to
“reaching the deceased”. feelings of worthlessness, of being undeserving of
life or unable to cope with the pain of depression.
Treatment of the major depressive episode must be timely and appropriate. The
first choice drugs are:
 Selective serotonin reuptake inhibitor antidepressants (SSRIs) such as Fluoxetine (Prozac) or
Fluvoxamine.
 Selective norepinephrine reuptake inhibitors (Reboxetine).
 Serotonin and noradrenaline reuptake inhibitors (Venlafaxine).
 Specific and noradrenergic serotonergic inhibitors (Mirtazapine).
In the initial stages, the lowest doses are started, until the minimum effective dose tolerable by the
patient is reached within 3-10 days, followed by the acute phase of treatment with the administration of
the drug at full dose for 1- 2 months to favor the complete remission of symptoms, and the maintenance
phase by gradually reducing the doses over 6 months, until the drug is discontinued.
Benzodiazepines can be useful as a symptomatic treatment of anxiety and insomnia.
Neuroleptics are contraindicated in the depressed patient because they increase depressive symptoms,
ideomotor inhibition, asthenia and difficulty concentrating, while only in cases of major depression with
psychotic symptoms (delusions, hallucinations) resistant to high-dose antidepressants , low-dose
neuroleptics can be administered.
Psychotherapy is mainly based on cognitive-behavioral techniques considering that the depressed patient
lives and sees reality considering above all the negative aspects with a pessimistic vision of the present
and the future. Cognitive psychotherapy is useful for rebuilding the patient's cognitive system, removing
erroneous beliefs, irrational ideas, helping the patient in his way of seeing things and relating to events.
Psychodynamic psychotherapy has the task of investigating the patient's experiences and resolving
conflicts related to the disorder. In Anglo-Saxon countries, electroshock therapy is used in cases of very
severe major depression and not responsive to psychopharmacological therapy.

MAJOR DEPRESSIVE DISORDER

 The 12-month prevalence of major depressive disorder in the United States is 7% with marked
differences by age group. In individuals 18 to 29 years of age, the prevalence is 3 times in individuals
aged 60 or older.
 It can first occur at any age, but the likelihood of onset increases markedly with puberty. The peak of
incidence is around 20 years.
 Females have 1.5 to 3 times higher rates than males beginning in early adolescence.
 The course of major depressive disorder is quite variable, as some individuals never, or only rarely,
achieve remission, while others live many years with little or no symptoms between episodes.
 Suicidal risk increased during the major depressive episode (high mortality).
 In women, the risk of suicide is greater, while an increased risk of suicide completion is associated with
male sex, being single or living alone and having prevailing feelings of hopelessness.
 The functional impairment of the subject can be very mild or vary up to complete disability, to the point
that the depressed individual is unable to meet the basic needs for self-care, is dumb or catatonic.

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 The chronicity of depressive symptoms substantially increases the likelihood of underlying personality,
anxiety, and substance use disorders.
 Recent onset is an important indicator of the likelihood of short-term recovery. Characteristics
associated with lower cure rates beyond the duration of the current episode include psychotic
characteristics, prevailing anxiety, personality disorders, and symptom severity.
 Many bipolar disorders begin with one or more depressive episodes. This is more likely in individuals with
adolescent onset of the disease, in those with psychotic features, with a family history of bipolar
disorder. The "mixed features" specifier increases the risk of future manic or hypomanic diagnoses. DDM
with psychotic features can evolve into schizophrenia.
 Frequent comorbidity with substance-related disorder, panic disorder, obsessive-compulsive disorder,
eating disorder, and borderline personality disorder.

When recording the name of a diagnosis, the terms should be listed in the following order: major
depressive disorder, single or recurrent episode, severity / psychotic characteristics / remission specifiers,
followed by all of the following specifiers with no codes applicable to the current episode .
Specifiers:
- Anxiously
- With mixed characteristics
- With melancholic characteristics
- With atypical characteristics
- With psychotic features congruent to mood
- With psychotic characteristics not congruent with mood
- With peripartum onset

PERSISTENT DEPRESSIVE DISORDER (DISTIMIA)

Persistent depressive disorder is a union of dysthymic disorder and chronic major depressive episode with
a 10-month prevalence in the United States of approximately 0.5% for persistent depressive disorder and
1.5% for chronic major depressive disorder. Major depression may precede persistent depressive disorder,
and major depressive episodes may occur during its course. Individuals whose symptoms meet the criteria
for major depressive disorder for 2 years should receive the diagnosis of persistent depressive disorder as
well as the diagnosis of major depressive disorder (as specified). There is difficulty in diagnosis as
symptoms become part of the individual's daily experience and therefore may not be reported. Early and
insidious onset, chronic course by definition. Early onset (before age 21) is associated with a higher
likelihood of comorbidities with cluster B and C personality disorders and substance use disorders.
Predictors of a more negative long-term prognosis include higher levels of neuroticism, greater symptom
severity, more impaired overall functioning, and the presence of anxiety disorders or conduct disorders.
The diagnostic criteria are:
A. Depressed mood for most of the day, for several days, as indicated by the subjective account or
observation of others, for at least 2 years (in children and adolescents the mood can be irritable and
the duration must be at least 1 years).
B. Presence, in addition to depression, of 2 (or more) of the following:
1. Little appetite or overeating.
2. Insomnia or hypersomnia.
3. Low energy or fatigue.
4. Low self-esteem.
5. Poor concentration or difficulty making decisions.
6. Feeling hopeless.
C. During the 2-year period (1 in children and adolescents) of the disorder, the individual has never been
without symptoms of Criteria A and B for more than 2 months.
D. The Criteria for Major Depressive Disorder may be present continuously for 2 years.
E. There has never been a manic or hypomanic episode and the criteria for a cyclothymic disorder are not
met.
F. The disorder is not best explained by a schizoaffective disorder, schizophrenia, delusional disorder, or
other schizophrenic spectrum disorder or psychotic disorder.
G. Symptoms are not attributable to the psychological effects of a substance (eg drug abuse or drug use)
or other medical conditions (eg hypothyroidism).
H. Symptoms cause significant difficulty or impairment in social, occupational, or other important areas of
functioning.
As for the depressive episode a possible specifier must be indicated:
- Anxiously
- With mixed characteristics

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- With melancholic characteristics

- With atypical characteristics
- With psychotic features congruent to mood
- With psychotic characteristics not congruent with mood
- With peripartum onset

In addition, it is necessary to specify whether:

- He is in partial remission
- He is in total remission
Has early onset (before age 21) Late
onset (after age 21)
Specify if (for the most recent 2 years of persistent depressive disorder):
With pure dysthymic syndrome (all criteria for a major depressive episode have not been met in at least
2 previous years).
With persistent major depressive episode (all criteria for a major depressive episode were met during
the previous 2-year period).
With intermittent major depressive episodes, with ongoing episode (all criteria for a major depressive
episode are met at the moment, but there have been periods of at least 8 weeks in the previous 2 years
with symptoms below the threshold for a major depressive episode).
With intermittent major depressive episodes, no episode in progress (All criteria for a major depressive
episode are currently not met, but there has been one or more major depressive episodes in at least the
previous 2 years.
Specify if:
- Mild
- Moderate
- Severe

DISORDER BY DISREGULATION OF THE DISRUPTING MOOD

Declared to avoid the risk of overdiagnosis of bipolar disorder in children, a new diagnostic category of
Disruptive Mood Dysregulation Disorder has been included in this chapter, for individuals up to 18 years of
age with persistent irritability and frequent episodes of behavioral dysregulation. Disruptive mood
dysregulation disorder (DMDD) is a psychic disorder that we find in children and adolescents and is
characterized by a persistent angry or irritable mood. Also characteristic of the disorder is the frequency
of outbursts of anger that are disproportionate to the situation experienced. In addition, these
manifestations are significantly more severe than the reactions of peers. Disruptive mood dysregulation
disorder first appears in the DSM-5.
• Prevalence at 6 months-1 year between 2 and 5%
• More common in boys and school-age children
Low conversion rates from severe, non-episodic irritability to bipolar disorder
Increased risk of developing unipolar depressive disorder and / or anxiety disorders in adulthood
Functional consequences: low academic achievement due to low frustration tolerance; compromise of
family and social relational life, with difficulty in starting friendships; dangerous behavior, suicidal
ideation or TS, severe aggression and psychiatric hospitalizations
• DD with Bipolar Disorders
• DD with Oppositional Defiant Disorder
• DD with Intermittent Explosive Disorder

PREMESTRUAL DYSPHORIC DISORDER

Premenstrual dysphoric disorder has a 12-month prevalence between 1.8 and 5.8%, onset at any time after
menarche with symptoms that cease after menopause. The essential features of the disorder are the
expression of mood lability, irritability, dysphoria and anxiety symptoms that occur repeatedly during the
premenstrual phase of the cycle. Behavioral and physical symptoms may also be present. Delusions and
hallucinations have been described in the luteal phase of the cycle but are rare. Premenstrual phase at
risk for suicide. Frequently a major depressive episode precedes the onset of the disorder. A differential
diagnosis is made for premenstrual syndrome, dysmenorrhea, mood disorders, use of hormonal
treatments. Onset can occur at any time after menarche.
Symptoms must be associated with clinically significant distress and / or with an obvious marked
impairment in social or occupational functioning in the week preceding menstruation.
Diagnostic criteria:

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A. In most menstrual cycles, at least 5 symptoms must be present in the last week before menstruation
begins, then begins to increase within a few days after menstruation begins and becomes minimal or
absent in the week following menstruation.
B. One or more of the following symptoms:
1. Affective lability, suddenly feeling sad or fearful.
2. Marked irritability or anger or increased interpersonal conflict.
3. Marked depressed mood, feeling hopeless or self-critical thoughts.
4. Marked anxiety, tension and / or feelings of being agitated or nervous.
One or more of the following symptoms are added, to arrive at a total of 5 symptoms in combination with
the previous criteria of criterion B:
1. Reduction of interest in activities.
2. Less concentration.
3. Asthenia, fatigue, lethargy.
4. Marked changes in appetite.
5. Insomnia or hypersomnia.
6. Feeling of being overwhelmed or losing control.
7. Physical symptoms such as various pains.
C. Symptoms are associated with interference in work, school, relationships and social activities. The
alteration is not just an exacerbation of the symptoms of other disorders, such as a major depressive
disorder, a panic disorder, persistent depressive disorder (dysthymia) or a personality disorder (although it
may occur in conjunction with any of these disorders).
Criterion A should be confirmed by daily forward evaluations for at least two symptomatic cycles.
Symptoms are not attributable to the physiological effects of a substance (eg, a drug of abuse, a drug,
another treatment) or another medical condition (eg, hyperthyroidism).

DEPRESSIVE DISORDER INDUCED BY SUBSTANCES / DRUGS

Indicates the presence of criteria and symptoms of depressive disorder related to the use of a substance or
drug or drug withdrawal.
A. Persistent mood confusion, characterized by depressed mood or with anhedonia, that is, less interest in
everything.
B. Evidence from medical history and physical examinations:
1. Symptoms of criterion a develop during or shortly after ingestion of the substance.
2. The substance or drug is capable of producing the symptoms of criterion A.
C. The disorder is not best explained by a depressive disorder that is not substance / drug induced.
Symptoms precede the use of a substance; symptoms persist for a period after the cessation of acute
withdrawal or severe intoxication.
D. Disorders do not occur exclusively during the course of a delirium.
E. Disorders cause obvious stress, alterations in social, occupational, or other areas of activity.

Assess whether symptoms occur while taking the substance or during withdrawal.
In a sample of the representative adult US population, the lifetime prevalence of the disorder is 0.26%.
The disorder must have its onset while the individual is using the drug or during withdrawal. Onset occurs
within the first few weeks or within the first month of drug use. When the drug is stopped, depressive
symptoms usually go into remission within a few days or weeks. If this does not happen and symptoms
persist for more than 4 weeks beyond the expected withdrawal period for a particular substance / drug,
other causes of depressed mood symptoms should be considered.
Substances implicated in drug-induced depressive disorder include:
 Antiviral agents (efavirenz).
 Cardiovascular drugs (clonidine, guanethidine, methyldopa, reserpine).
 Derivatives of retinoic acid (isotretionin).
 Antidepressants.
 Anticonvulsants.
 Anti-migraine drugs (triptans).
 Antipsychotics.
 Hormonal agents (corticosteroids, oral contraceptives, gonadotropin-releasing hormone agonists,
tamoxifen).
 Smoking cessation drugs (varencycline).

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 Immunomodulating drugs (interferon).

Differential diagnosis with: Substance intoxication and withdrawal, Primary depressive disorder,
Depressive disorder due to other medical condition.

DEPRESSIVE DISORDER DUE TO ANOTHER MEDICAL CONDITION

Diagnostic criteria:
A. Persistent period of depression or marked decrease in interest in everything.
B. There must be anamnestic, physical and laboratory evidence that the disorders are pathophysiological
consequences of other clinical conditions.
C. The disorders are not more expressed by other mental disorders.
D. Disorders don't just occur during the cause of delirium.
E. Disorders cause clinical stress and social alterations.

Etiology (i.e. a causal relationship to another medical condition based on clinical evidence) is the key
variable in the depressive disorder in question.
There are clear associations between depression and stroke, Huntington's disease, multiple sclerosis,
Parkinson's disease and brain damage from trauma; the neuroendocrine conditions most frequently
associated with depression are Cushing's disease and hypothyroidism.

Differential diagnosis with: Depressive disorders not due to another medical condition, Drug-induced
depressive disorder, Adjustment disorders.

DISORDER DEPRESSIVE WITH OTHER SPECIFICATION

The definition of depressive disorder with other specification applies to manifestations in which symptoms
characteristic of a disorder, which cause clinically significant distress or impairment in functioning in the
social, occupational, or other important areas, predominate but do not fully satisfy the criteria for any of
the disorders of the diagnostic class of depressive disorders. It is used in situations where the clinician
chooses to communicate the specific reason why the manifestation does not meet the criteria for any
specific depressive disorder. This is done by recording depressive disorder with other specification
followed by the specific reason.

1. Brief recurrent depression: Concomitant presence of depressed mood and at least four other symptoms
of depression for 2-13 days at least once a month (not associated with the menstrual cycle) for at least
12 consecutive months in an individual whose manifestation has never satisfied the criteria for any
depressive or bipolar disorder and does not currently meet the active or residual criteria for any
psychotic disorder.
2. Short-lived depressive episode (4-13 days): Depressed mood and at least four of the eight symptoms of
a major depressive episode associated with clinically significant distress or impairment that persist for
more than 4 days but less than 14 days, in an individual whose manifestation never met the criteria for
any depressive or bipolar disorder currently does not meet the active or residual criteria for any
psychotic disorder and does not meet the criteria for brief recurrent depression.
Depressive episode with insufficient symptoms: Depressed mood and at least one of the other eight
symptoms of a depressive episode associated with clinically significant distress or impairment that persist
for at least 2 weeks in an individual whose manifestation never met the criteria for any depressive or
bipolar disorder, currently not meets the active or residual criteria for any psychotic disorder and does not
meet the criteria for mixed symptoms of anxiety and depressive disorder.

DEPRESSIVE DISORDER WITHOUT SPECIFICATION

The definition of an unspecified depressive disorder applies to manifestations in which symptoms
characteristic of a disorder, causing clinically significant distress or impaired functioning in the social,
occupational, or other important areas, predominate but do not fully satisfy the criteria for any of the
disorders of the diagnostic class of depressive disorders. It is used in situations where the clinician chooses
not to specify the reason why the criteria for a specific depressive disorder are not met and includes
manifestations in which there is insufficient information to make a more specific diagnosis (for example in
emergency room settings. ).

DEPRESSIVE DISORDER THERAPY

FOLLOW NICE guidelines (the most reliable)
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- First choice: SSRIs and sometimes antipsychotics are combined or mood stabilizers such as lithium can be
used.
- Melancholic depression: SSRIs.
- Psychotic depression: possibly add haloperidol.
- Depression with suicidal ideation: ECT.

Sometimes SSRIs and BENZODIAZEPINES are used because with SSRIs in the early stages, the patient can be
agitated until good levels of serotonin are reached, this is called the PARADOX EFFECT OF SSRIs.
Therefore, benzodiazepines are associated.

ANXIETY DISORDERS
Under normal conditions, each individual has physiological alarm systems represented by anxiety, fear and
phobia. Anxiety helps the individual to identify and prevent dangers or potentially dangerous situations, in
order to react with appropriate behavior. Anxiety becomes pathological when the alarm reaction is
exaggerated with respect to the external stimulus or when it occurs in the absence of a stimulus,
characterized by somatic neurovegetative, neuromuscular and psychic manifestations with behavioral
reaction which, depending on the intensity of the anxiety-inducing stimulus, it can be a defense, attack,
avoidance, flight reaction.
Fear is caused by a known object or situation that induces the same reaction but of different intensity in
the same general reference population. The individual knows what he is afraid of and why. Fear becomes
pathological when it is induced by particularly traumatizing events on the emotional level that the
individual is unable to control.
Phobia is an abnormal alarm reaction caused by a known object or situation that does not induce the same
reaction in the same general reference population. The individual knows what he is afraid of but is aware
that it is an exaggerated or unmotivated fear, an irrational emotional reaction that he cannot control and
that becomes pathological when the subject implements avoidance behaviors that progressively reinforce
the phobia to the point of causing severe impairment of the individual's psychosocial functioning.
Anxiety disorders include those disorders that share characteristics of fear and anxiety and associated
behavioral disorders. In DSM5, anxiety disorders are presented in order of age of onset:

Separation Anxiety Disorder;

Selective Mutism;

Specific Phobia;

Social Anxiety Disorder (Social Phobia);

Panic Disorder;

Agoraphobia;

Generalized Anxiety Disorder;

Substance / Drug Induced Anxiety Disorder;

Anxiety Disorder Due to Another Medical Condition

Anxiety Disorder with other specification;

Unspecified Anxiety Disorder.
Furthermore, the chapter on anxiety disorders no longer includes obsessive-compulsive disorder (moved to
a new chapter dedicated to it) or post-traumatic stress disorder and acute stress disorder (moved to the
new chapter. traumatic and stressful).
1. Separation Anxiety Disorder it can affect children when separated from home or from the main
attachment figures by manifesting social withdrawal, apathy, sadness or difficulty concentrating in
work or play. They can show anger and aggression towards those who force separation.
The prevalence at 12 months is 0.9-1.9% in adults, while in children the prevalence from 6 to 12
months is 4% and in adolescents at 12 months it is 1.6%. More frequent in girls, there is no prevalence
between the two sexes in children. It is the most common anxiety disorder in children under the age
of 12.

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It often develops after a stressful event (death of a relative or pet, illness, change of school,
relocation, immigration, catastrophe) and can be heritable (estimate of 73%; children show increased
sensitivity to stimulation with CO2).
Regarding the risk of suicide there is no specific association with separation anxiety disorder, but
increased risk has been observed in several anxiety disorders.
Differential diagnosis is made with generalized anxiety disorder (anxiety mainly concerns attachment
figures), panic disorder (there is no being paralyzed by an unexpected panic attack), agoraphobia
(they are not anxious at the idea of being trapped or helpless in situations where escape is
problematic), conduct disorder (avoidance of school and truancy are not common), social anxiety
disorder (fear of being negatively evaluated prevails over separation from reference figures ), post-
traumatic stress disorder (intrusions and avoidance of memories associated with the traumatic event),
illness anxiety disorder (specific illnesses that may worry them), grief (intense longing or longing for
the deceased, intense sadness and emotional pain,concern for the deceased and the circumstances of
death), depressive and bipolar disorder (poor motivation or interest in the outside world),
oppositional-defiant disorder, psychotic disorders (in separation anxiety there are a real stimulus, they
usually manifest themselves only in certain situations, they are canceled by the presence of the
attachment figure), personality disorders (dependent disorder: indiscriminate tendency to depend on
others; borderline disorder: fear of abandonment by loved ones, but also problems related to identity,
autonomy, interpersonal functioning and impulsiveness).psychotic disorders (in separation anxiety
there are desperations of a real stimulus, they usually occur only in certain situations, they are
canceled out by the presence of the attachment figure), personality disorders (dependent disorder:
indiscriminate tendency to depend from others; borderline disorder: fear of abandonment by loved
ones, but also problems related to identity, autonomy, interpersonal functioning and
impulsiveness).psychotic disorders (in separation anxiety there are desperations of a real stimulus,
they usually occur only in certain situations, they are canceled out by the presence of the attachment
figure), personality disorders (dependent disorder: indiscriminate tendency to depend from others;
borderline disorder: fear of abandonment by loved ones, but also problems related to identity,
autonomy, interpersonal functioning and impulsiveness)
In children it is often associated with generalized anxiety disorder or. a specific phobia, while in
adults it is associated with a specific phobia, DSTP, generalized panic and anxiety disorder and social
anxiety, agoraphobia, obsessive-compulsive disorder, and personality disorders.

The criteria for Separation Anxiety Disorder are:

A. Excessive and inappropriate fear or anxiety about the stage of development involving separation
from those to whom the individual is attached, as evidenced by three or more of the following
criteria:
1. Recurrent and excessive discomfort when separation from home or major attachment
figures is expected or experienced;
2. Persistent and excessive worry about the loss of attachment figures or the possibility of
something harmful happening to them, such as illness, injury, disaster or death;
3. Persistent and excessive concern that an unforeseen event leads to separation from the
main attachment figure (loss, being kidnapped, having an accident, becoming ill);
4. Persistent reluctance or refusal to leave the house to go to school, work or elsewhere out
of fear of separation;
5. Persistent and excessive fear of or reluctance to be alone or without major attachment
figures at home or in other settings;
6. Persistent reluctance or refusal to sleep outside the home or to go to sleep without being
around a major attachment figure;
7. Repeated nightmares involving the theme of separation;
8. Repeated complaints of physical symptoms (headache, stomach aches, nausea, vomiting)
when separation from major attachment figures occurs or is expected.
B. Fear, anxiety, or avoidance are persistent, lasting at least 4 weeks in children and adolescents and
typically 6 months or more in adults.
C. The disorder causes clinically significant distress or impairment in social, occupational, or other
important areas of functioning.

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D. The disorder is not best explained by another mental disorder, such as refusal to leave the house
due to excessive resistance to change in autism spectrum disorder, delusions or hallucinations
regarding separation in psychotic disorders, refusal to go out without a trusted partner in
agoraphobia, worries about illness or other harm that can happen to significant people in
generalized anxiety disorder, or worries about having an illness in sickness anxiety disorder.

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2. Selective mutism it is characterized by excessive shyness, fear of social embarrassment, social

isolation and withdrawal, compulsive traits, negativism, temper tantrums, or mildly opposing
behavior.
It is a rare disorder (0.03-1%), and does not appear to change due to gender or race / ethnicity.
More frequent in children with onset before 5 years of age, variable degree of persistence.
Negative affect (neuroticism) or behavioral inhibition may play a role, as can a parental history of
shyness, social isolation, and social anxiety.
Parental social inhibition can serve as a model for social reticence and selective mutism in children
(often overprotective or more controlling parents).
There are genetic and physiological factors in common with social anxiety disorder.
Differential diagnosis is made for communication disorders (speech, phonetic-phonological, fluency
with onset in childhood or stuttering, social or pragmatic communication disorders),
neurodevelopmental disorders, schizophrenia and other psychotic disorders, anxiety disorder social or
social phobia (may be associated).
It is often associated with social anxiety disorder, separation anxiety disorder and specific phobia.

The criteria for Selective Mutism are:

A. Constant inability to speak in specific social situations in which you are expected to speak (for
example at school) despite being able to speak in other situations.
B. The condition interferes with academic or work achievement or social communication.
C. The duration of the condition is at least 1 month (not limited to the first month of school).
D. The inability to speak is not attributable to a lack of knowledge of or the type of language
required by the social situation.
E. The disorder is not best explained by a communication disorder and does not manifest itself
exclusively in the course of autism spectrum disorder, schizophrenia, or another psychotic
disorder.

3. The specific phobia it has a 12-month prevalence of 7-9% (5% in children and 16% in adolescents aged
13 to 17), females are more affected than males with a 2: 1 ratio. There is more than 60% chance of
attempting suicide.
There is comorbidity with other anxiety disorders, depressive and bipolar disorder, substance-related
disorders, somatic symptom disorder, and personality disorders.
Risk factors are negative affect (neuroticism) or behavioral inhibition (they are also risk factors for
other anxiety disorders), Parental overprotectivity or physical and sexual separation and abuse tend to
predict other disorders as well anxiety, negative or traumatic encounters with the feared object or
situation sometimes precede the development of the specific phobia.
There may be a genetic susceptibility (individuals with blood phobia, injections, wounds show a
propensity for vaso-vagal syndrome).
A differential diagnosis is made of agoraphobia (two or more feared situations), social anxiety disorder
(in this case the fear of being negatively evaluated prevails), separation anxiety disorder (situations
feared for separation from the caregiver or figure attachment), panic disorder (there is no being
paralyzed by an unexpected panic attack), obsessive-compulsive disorder (as a result of an obsession,
for example fear of blood contamination or not driving for fear of causing injury to others), disorders
related to traumatic and stressful events, eating disorders (avoidant behavior or aspects related to it),
disorders of the schizophrenia spectrum and other psychotic disorders (fear and avoidance due to
delusional thinking).

The criteria for Specific Phobia (Specify if it is an animal phobia, natural environment, blood-
injections-wounds, situational, other) are:
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A. Marked fear or anxiety about a specific object or situation (in children, fear or anxiety can be
expressed as crying, outbursts of anger, immobilization or clinging).
B. The phobic object or situation almost always causes immediate fear or anxiety.
C. The phobic object or situation is actively avoided or endured with intense fear or anxiety.
D. The fear or anxiety is disproportionate to the real danger represented by the specific object or
situation and to the socio-cultural context.
E. The fear, anxiety, or avoidance is persistent, usually lasting 6 months or more.
F. Fear, anxiety, or avoidance cause clinically significant distress or impairment in the social,
occupational, or other important areas of functioning.
G. The disorder is not best explained by symptoms of another mental disorder, including fear,
anxiety, and avoidance of situations associated with panic-like symptoms or other disabling
symptoms (such as agoraphobia), objects or situations related to obsessions (as in obsessive-
compulsive disorder), memories of traumatic events (as in post-traumatic stress disorder),
separation from home or attachment figures (as in separation anxiety disorder) or from social
situations ( as in social anxiety disorder).

4. Social anxiety disorder (social phobia) has a 12-month prevalence of 7% in the United States and 2.3%
in Europe.
Prevalence rates tend to decline with age, with females being more affected than males. The average
age of onset is 13 years. Females more frequently have social fears, depressive disorder, bipolar
disorder, comorbid anxiety disorder; males more often have a tendency to fear dating, oppositional-
defiant or conduct disorder, alcohol and drug abuse.
There is more than 60% chance of attempting suicide.
There is comorbidity with other anxiety disorders, depressive and bipolar disorder, substance-related
disorders, somatic symptom disorder, and personality disorders.
Risk factors are behavioral inhibition and fear of negative evaluation, child maltreatment and
adversity.
Genetic influence is subject to genotype-environment interaction: children with strong behavioral
inhibition are more susceptible to environmental influences, such as receiving an education according
to a model of social anxiety.
In addition, the disorder is heritable: first-degree relatives have a 2 to 6 times greater chance and
predisposition to the disorder involves the interaction of disorder-specific (fear of negative evaluation)
and non-specific (neuroticism) genetic factors.
Taijin-Kyofhsho syndrome (in Japan or Korea) is characterized by social-evaluative concerns typical of
social anxiety disorder, associated with the fear that the individual may make other people
uncomfortable, often experienced with delusional intensity.
Immigrant status is associated with lower rates of social anxiety.
Differential diagnosis is made for non-pathological shyness, agoraphobia (it may be difficult to escape
or no help is available), panic disorder (there is no being paralyzed by an unexpected panic attack),
generalized anxiety disorder (excessive worries about the quality of social performance), separation
anxiety disorder (situations feared for separation from the caregiver or attachment figure), specific
phobias (fear of being embarrassed or humiliated), selective mutism (do not fear negative evaluation
in situations where speaking is not required), major depressive disorder (they do not feel worthy of
appreciation), body dysmorphic disorder (worries about what they perceive as one or more defects or
imperfections in their appearance physical),delusional disorder (focus on being rejected by others or
offending others), autism spectrum disorder, (avoidant) personality disorder, oppositional defiant
disorder.

The criteria for Social Anxiety Disorder (specify if linked only to performance) are:
A. Marked fear or anxiety about one or more social situations in which the individual is exposed to
possible scrutiny by others. Examples include social interactions (having a conversation, meeting
unfamiliar people), being observed (while eating or drinking) and performing a performance

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in front of others (make a speech). In children, anxiety must manifest itself with peers and not just
during interactions with adults.
B. The individual is afraid of showing symptoms of anxiety and that they will be negatively evaluated
(humiliation, embarrassment), lead to rejection or be offensive to others.
C. Social situations almost invariably cause fear or anxiety (in children, fear or anxiety can be
expressed as crying, outbursts of anger, immobilization, clinging, withdrawal, or failing to speak
during social interactions).
D. Social situations are avoided or endured with intense fear or anxiety.
E. The fear or anxiety is disproportionate to the real threat posed by the social situation and socio-
cultural context.
F. The fear, anxiety, or avoidance is persistent, usually lasting 6 months or more.
G. Fear, anxiety, or avoidance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
H. Fear, anxiety, or avoidance are not attributable to the physiological effects of a substance or
other medical condition.
I. Fear, anxiety, or avoidance are not best explained by the symptoms of another mental disorder,
such as Panic Disorder, Body Dysmorphic Disorder, or an Autism Spectrum Disorder.
J. If another medical condition is present (Parkinson's disease, obesity, burn disfigurement or injury),
the fear, anxiety or avoidance is clearly unrelated or excessive.

5. Panic Disorder it is an unexpected and recurring event.

The criteria for Panic Attack are:
A. Unexpected and recurring attacks.
A panic attack is the sudden onset of intense fear or discomfort that peaks within minutes, during
which four or more of the following symptoms occur:
1. Palpitations, heart palpitations, or tachycardia;
2. Sweating;
3. Fine or large tremors
4. Wheezing or a feeling of choking
5. Feeling of asphyxia;
6. Chest pain or discomfort
7. Nausea or abdominal discomfort;
8. Feeling dizzy, dizzy, light-headed or faint;
9. Chills or hot flashes
10. Paresthesia (numbness or tingling sensations);
11. Derealization (feeling of unreality) or depersonalization (being detached from oneself);
12. Fear of losing control or going crazy
13. Fear of dying.
B. At least one of the attacks has been followed by 1 month (or more) of one or both of the following
symptoms:
1. Persistent worries about other panic attacks or their consequences (losing control, having
a heart attack, going crazy);
2. Significant maladaptive change in behavior related to attacks (behaviors to avoid panic
attacks, for example, avoiding exercise or unfamiliar situations).

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C. The disturbance is not due to the physiological effects of a substance (drug, drug) or other
medical condition (hyperthyroidism, cardiorespiratory disorders).
D. The disorder is not better explained by another mental disorder (e.g. panic attacks do not occur
only in response to feared social situations, as in social anxiety disorder; in response to
circumscribed objects or phobic situations, as in specific phobia ; in response to obsessions, such
as in obsessive-compulsive disorder; in response to memories of traumatic events, such as in post-
traumatic stress disorder; in response to separation from attachment figures, such as in separation
anxiety disorder)

One type of unexpected panic attack is the nocturnal panic attack (present in 1 / 4- 1/3 of individuals
with panic attacks).
There are often constant and intermittent feelings of anxiety.
The prevalence at 12 months is 2-3%, females are more affected than males with a 2: 1 ratio.
Average age of onset of 20-24 years.
Usual chronic course with symptomatic fluctuations.
It has the highest rate of suicide attempts and anticonservative ideation.
Risk factors are negative affectivity (neuroticism), that is the predisposition to experience negative
emotions and the sensitivity to anxiety, that is the predisposition to believe that the symptoms of
anxiety are harmful.
you. A history of fearful spells (paucisymptomatic attacks that do not meet the criteria for a panic
attack) can be a risk factor.
Experiences of sexual and physical abuse in childhood, cigarette smoking and stressful events can also
be risk factors.
Several genes can confer a vulnerability (role of the amygdala and related structures); increased risk
among the children of parents with anxiety, depressive and bipolar disorders; breathing problems such
as asthma are associated.
Agents with various mechanisms of action (sodium lactate, caffeine, isoproterenol, yohimbine, carbon
dioxide and cholecystokinin) cause more panic attacks than controls. For a certain percentage of
individuals, the attacks are related to medullary chemoceptors that are hypersensitive to carbon
dioxide, which cause hypocapnia and other respiratory changes.
Differential diagnosis is made for anxiety disorder with other specification or without specification
(only unexpected paucisymptomatic panic attacks), anxiety disorder due to another medical condition
(hyperthyroidism, hyperparathyroidism, pheochromocytoma, vestibular dysfunction, seizure disorders
and cardiopulmonary conditions such as arrhythmias, supraventricular tachycardias, asthma, COPD),
drug / drug induced anxiety disorder (cocaine, amphetamines, caffeine, cannabis, alcohol withdrawal
and barbiturates).
Panic attack therapy consists of pharmacotherapy with antidepressants such as SSRIs (Cita- lopram,
Escitalopram) and tricyclics (Clomipramine, Trazodone), benzodiazepines (Alprazolam) and beta-
blockers.
In addition, support psychotherapy is used to cope with phobic situations and cognitive-behavioral
psychotherapy with cognitive restructuring of the unpleasant sensations that accompany the crises and
gradual exposure to symptoms and panicogenic situations (techniques of imagery, relaxation,
behavior) .

6. Agoraphobia it is a disorder that can make homebound individuals unable to go out and dependent on
others for services or assistance to provide even basic needs, characterized by demoralization and
depressive symptoms, alcohol abuse and sedative drugs.
It has an annual prevalence of 1.7% in adolescents and adults, females are twice as affected as men.
Onset occurs before the age of 35 (average age 17) with a persistent and chronic course.
Risk factors are negative affectivity (neuroticism), sensitivity to anxiety, negative childhood
experiences (separation, death of a parent), stressful events, reduced family warmth and increased
overprotectivity. Heritability is 61%, it has the strongest and most specific association with the genetic
factor that constitutes the predisposition to phobias.

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Differential diagnosis is made for specific phobia of the situational type (it is limited to one of the
situations), separation anxiety disorder (parents or other attachment figures), social anxiety disorder
(fear of being negatively evaluated), panic, acute and post-traumatic stress disorder, major
depressive disorder (apathy, loss of energy, low self-esteem, anhedonia), other medical conditions (in
Parkinson's, Multiple Sclerosis, Crohn's).

The criteria for Agoraphobia are:

A. Marked fear or anxiety in two or more of the following situations:
1. Use of public transport (cars, buses, trains, ships, airplanes);
2. Being in open spaces (parking lots, markets, bridges);
3. Being indoors (shops, theaters, cinemas);
4. Stand in line or in the crowd;
5. Being away from home alone.
B. The individual fears or avoids these situations at the thought that it may be difficult to escape or
that help may not be available in case of panic-like symptoms or other disabling or embarrassing
symptoms (fear of the elderly of falling; fear of incontinence).
C. Agoraphobic situations almost always cause fear or anxiety.
D. Agoraphobic situations are actively avoided, involve the presence of a carer, or are endured with
intense fear or anxiety.
E. The fear or anxiety is disproportionate to the real danger and socio-cultural context.
F. The fear, anxiety, or avoidance is persistent, usually lasting 6 months or more.
G. Fear, anxiety, or avoidance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
H. If another medical condition is present (intestinal inflammation, Parkinson's disease) the fear,
anxiety or avoidance is clearly excessive.
I. Fear, anxiety or avoidance are not best explained by the symptoms of another mental disorder,
for example the symptoms are not limited to Situational Specific Phobia; do not involve only social
situations (Social Anxiety Disorder) and are not exclusively related to obsessions (Obsessive
Compulsive Disorder), disturbances in the perception of physical appearance (Body Dysmorphism
Disorder), memories of traumatic events (Post Disorder -traumatic Stress) or fear of separation
(Separation Anxiety Disorder).
Agoraphobia is diagnosed regardless of the presence of panic disorder. If the onset of symptoms meets the
criteria for panic disorder and agoraphobia, both diagnoses must be made.

7. Generalized anxiety disorder is characterized by tremors, contractures, jolts, aches, muscle pains,
somatic symptoms (sweating, nausea, diarrhea), symptoms of vegetative hyperactivation (increased
heart rate, dyspnoea, dizziness), conditions associated with stress (syndrome of irritable bowel,
headaches).
The 12-month prevalence is 0.9% among adolescents and 2.9% among adults and the lifetime risk of
morbidity is 9%. The prevalence of diagnosis occurs in middle age and decreases over the years.
Females are twice as affected as males, with an average age of onset 30 years.
Risk factors are behavioral inhibition, negative affect (neuroticism), avoidance of harm, childhood
adversities and parental overprotectiveness.
It is genetic in one third of cases.
Differential diagnosis is made for anxiety disorder due to another medical condition
(pheochromocytoma, hyperthyroidism), drug / drug induced anxiety disorder, social anxiety disorder
(concerned whether or not they are being evaluated ), obsessive-compulsive disorder (inappropriate
ideas that take the form of intrusive and unwanted thoughts, impulses or images), post-traumatic
stress disorder, and adjustment disorders (anxiety within three months of its onset and does not
persist for more than six months after the disappearance of the factor), depressive, bipolar and
psychotic disorders.

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The criteria for Generalized Anxiety Disorder are:

A. Excessive anxiety and worry, occurring on most days for at least 6 months, related to a series of
events or activities (work or school performance).
B. The individual has difficulty controlling worry.
C. Anxiety and worry are associated with three or more (in infants only one is required) of the
following six symptoms, with at least a few symptoms present for most days in the past six
months:
1. Restlessness, or feeling tense, with nerves on the edge of the skin;
2. Easy Fatigue;
3. Difficulty concentrating or memory lapses
4. Irritability;
5. Voltage muscular;
6. Sleep disturbances (difficulty falling or staying asleep or restless or unsatisfactory sleep).
D. The anxiety, worry, or physical symptoms cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning.
E. The condition is not attributable to the physiological effects of one substance (drug, drug) or
another medical condition (hyperthyroidism).
F. The disorder is not better explained by another mental disorder (anxiety or fear of having panic
attacks in panic disorder, negative evaluation in social anxiety disorder or social phobia,
contamination or other obsessions in obsessive-compulsive disorder, separation from attachment
figures in separation anxiety disorder, memories of traumatic events in post-traumatic stress
disorder, weight gain in anorexia nervosa, physical complaints in somatic symptom disorder,
perceived defects in physical appearance in body dysmorphic disorder, having severe illness in
sickness anxiety disorder, or delusional belief content in schizophrenia or delusional disorder)
Generalized anxiety disorder tends easily to become chronic and / or to evolve towards a panic disorder.
If taken care of properly, it improves within a few months.
The treatment is based on supportive psychotherapy to reduce stress and increase the subject's ability to
adapt, on analytical psychotherapy and on cognitive-behavioral psychotherapy to correct cognitive
distortions and aberrant behaviors. Regarding pharmacotherapy, the efficacy of benzodiazepines has been
proven (35% of patients show marked improvement, 40% moderate improvement, 25% unresponsive).
Predictors of positive response are acute onset of symptoms, marked somatic anxiety, presence of
precipitating stress, absence of depression and interpersonal problems, absence of previous therapies.
It is necessary to use the lowest possible dosages, slow titration, continuation of treatment for 4-8 weeks;
clinical re-evaluation; gradual withdrawal (20-30% of the dose per week).
The chronic use of benzodiazepines is necessary only in a limited number of cases, many patients do not
stop the benzodiazepine for dependence and not for therapeutic necessity (it is recommended not to
exceed 4-6 weeks of treatment).
Buspirone is especially effective in the presence of high levels of psychic anxiety and / or concomitant
depressive symptoms, it is not effective as an immediate anxiolytic due to its latency in therapeutic
action, it requires continued administration (3-4 weeks at a dose of 30- 60 mg / day). Symptoms of anxiety
recede slowly, maximum effect in the fourth week. Partially stimulating effects, with sleep disturbances.
Tricyclics and SSRIs (in antidepressant doses) and Venlafaxine (in lower doses) have an efficacy equal to
ben-zodiazepines with action mainly on psychic symptoms, they have a latency period of about a week.
Beta blockers are useful for peripheral somatic symptoms.

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8. Substance / Drug Induced Anxiety Disorder it should be placed in the differential diagnosis with
substance intoxication and withdrawal (when symptoms predominate the clinical picture), anxiety
disorder, delirium, anxiety disorder due to another medical condition.
The substances that can cause it are alcohol, caffeine, cannabis, phencyclidine, other hallucinogens,
inhalants, opiates, sedatives, hypnotics or anxiolytics, amphetamine, cocaine.
the criteria (specify whether with onset during intoxication, during withdrawal or after the use of a
drug and substance) are:
A. In the clinical picture, panic or anxiety attacks predominate.
B. Both elements are evident from the history, physical examination, or laboratory data:
1. The symptoms referred to in criterion A appeared during or immediately after intoxication
or withdrawal from substances or after taking a drug;
2. The substance or drug involved is capable of producing the symptoms of criterion A.
C. The condition is not best explained by a non-substance / drug-induced anxiety disorder. Evidence
of an independent anxiety disorder could be as follows:
1. Symptoms precede the onset of substance / drug use;
2. They persist for a considerable period of time (1 month);
3. There is other evidence to suggest the existence of an independent disorder.
D. The condition does not manifest itself exclusively during a delirium.
E. The condition causes clinically significant distress or impairment in social, occupational, or other
areas of functioning

9. Anxiety disorder due to another medical condition it can be caused by endocrine disorders
(hyperthyroidism, pheochromocytoma, hypoglycemia, adrenocortical hypercorticism), cardiovascular
disorders (congestive heart failure, pulmonary embolism, arrhythmia, atrial fibrillation), respiratory
diseases (COPD, asthma, pneumonia), metabolic alterations (deficiency vitamin B12, porphyria),
neurological diseases (neoplasms, vestibular dysfunctions, encephalitis, convulsive disorders).
Differential diagnosis is made for delirium, combined symptom manifestation, substance / drug
induced anxiety disorder, anxiety disorder, illness anxiety disorder, adaptation disorder, associated
feature of another mental disorder, anxiety with other specification or without specification.

The criteria for Anxiety Disorder Due to Another Medical Condition are:
A. In the clinical picture, panic or anxiety attacks predominate.
B. It is evident from the history, physical examination, or laboratory data that the disorder is the
direct pathophysiological consequence of another medical condition.
C. The condition is not better explained by another mental disorder.
D. The condition does not occur exclusively during a delirium.
E. The condition causes clinically significant distress or impairment in social, occupational, or other
important areas of functioning.

10. In anxiety disorders with other specification include:

10.1. the paucisymptomatic attacks
10.2.generalized anxiety that doesn't occur most days
10.3. the Khyal cap (wind attacks: Cambodian cultural syndrome with dizziness, tinnitus and neck
pain)
10.4. l'Ataque de nervios (attack of nerves: Latin American cultural syndrome with uncontrollable
shaking, screaming or crying, aggressive or suicidal behavior and depersonalization or
derealization).

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The category of anxiety disorder without specifications applies to manifestations in which symptoms
are characteristic of an anxiety disorder, causing clinically significant distress or impairment in social,
occupational, or other important areas of functioning predominate, but do not fully meet the criteria
for any of the disorders of the diagnostic class of anxiety disorders.
The clinician chooses not to specify the reason why the criteria for a specific disorder are not met.

OBSESSIVE-COMPULSIVE DISORDER AND RELATED DISORDERS

With DSM-5, obsessive-compulsive disorder leaves the chapter of anxiety disorders to gain a new dedicated
chapter and an autonomous nosographic entity along with other related disorders such as:

Obsessive Compulsive Disorder (OCD);

Body dysmorphic disorder;

Accumulation disorder;

Trichotillomania (hair pulling disorder);

Excoriation disorder (skin picking);

Obsessive Compulsive Disorder and Substance / Drug-Induced Related Disorders;

Obsessive Compulsive Disorder and Related Disorder Due to Another Medical Condition

Obsessive Compulsive Disorder and Other Specification Related Disorders;

Obsessive-compulsive disorder and related disorders without specification.
Obsessive-compulsive and related disorders that have a cognitive component have insight as a basis for
specifiers that it can be good or sufficient, poor, absent / delusional beliefs. For individuals whose OCD
symptoms and related disorders justify the specifier "with absent insight / delusional beliefs", these
symptoms should not be diagnosed as a psychotic disorder.
The inclusion of a chapter related to obsessive-compulsive disorder and related disorders within the DSM-5
reflects the growing evidence of the close interconnection between these disorders in terms of a range of
diagnostic validators (symptom analogies, high comorbidity between disorders, course of the disease,
family history, genetic aspects, environmental risk factors, neural substrates, biomarkers, temperament,
cognitive and emotional abnormalities, response to treatment) and the clinical usefulness of grouping
these disorders within the same chapter; clinicians are encouraged to examine all of these conditions in
individuals with one and to be aware of the overlaps between them. At the same time,
The criteria for Obsessive Compulsive Disorder are:
A. Presence of obsessions, compulsions or both:

Obsessions are defined by:
1. Recurrent and persistent thoughts, impulses or images, experienced at some time during
the disturbance as intrusive (see below) and unwanted and which in most individuals cause
marked anxiety or discomfort.
2. The subject attempts to ignore or suppress 3 such thoughts, impulses or images, or to
neutralize them4 with other thoughts or actions (i.e. putting in place a compulsion).

Compulsions are defined by:
1. Repetitive behaviors (e.g., washing hands, tidying up, checking) or mental actions (e.g.
praying, counting, repeating words mentally) that the subject

3 for example. avoiding triggers or repressing thoughts

4 for example. enacting a compulsion

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feels obligated5 to implement in response to an obsession or according to rules 6 which must

be strictly applied;
2. Behaviors or mental actions are aimed at preventing or reducing anxiety or discomfort or
preventing some feared events or situations; however, these behaviors or mental actions
are not realistically connected with what they are designed to neutralize or prevent, or are
clearly excessive.
B. Obsessions or compulsions are time consuming (for example, more than 1 hour per day) or cause
clinically significant distress or impairment in social, occupational, or other important areas of
functioning.
C. Obsessive-compulsive symptoms are not attributable to the physiological effects of a substance (e.g. a
drug, a drug) or to another medical condition.
D. as in disruptive behavior, impulse control and conduct disorders; ruminations related to guilt, as in
major depressive disorder; intrusive thoughts or delusional worries, such as in schizophrenia spectrum
disorders and other psychotic disorders; or repetitive behavior patterns, as in autism spectrum
disorders).
CRITERION A
Intrusiveness of obsessions
By intrusiveness we mean 3 different aspects of obsessive thoughts:
1. They can appear in the patient's mind in a way that is completely disconnected from the context and his
mental state. For example, the doubt that you have touched something contaminating that appears
while you are alone at home watching TV. However, a careful analysis usually finds that the thought is
the consequence of an automatic control activity (e.g. to be able to allow yourself to feel comfortable,
you have to check that everything is in order and that you were not neglecting any dangerous contact,
perhaps undervalued and neglected).
2. Experience from pc. in contrast to his values (eg in the mind of a very religious person can intrude a
blasphemous thought like a porchiddio; in a person who defines himself rational thoughts can intrude
without sense).
3. Incongrue with the vision that one has of reality (eg superstitious thoughts that something bad can
happen if you do not implement the compulsion, in a person who does not consider the functioning of
reality regulated by magical causal links).

The characteristics of an obsession are:

1. P.persistence or frequent recurrence in the mind of the individual (the obsession assumes excessive
relevance with respect to the remaining conscious ideational life).
2. Egodistonia (mental content annoys because it is intrusive and inappropriate).
3. The capacity of the individual however recognizes that obsession is the product of one's own mind (an
element that underlines the presence of a critical attitude).
4. Incoercibility (obsession cannot be effectively neutralized).
Egodystonia and critical attitude are important for the differential diagnosis with delirium. The latter, in
fact, does not have an egodistonic content and the patient does not criticize it, on the contrary he has the
absolute conviction of the validity of his thought content which cannot be destroyed with any argument or
contrary proof (egosynthony). The obsessive patient, on the other hand, is aware that obsessions are a
product of his own mind and are not imposed from the outside (unlike, for example, the

5 The pc. he recognizes that they depend on his will, but he feels obliged to carry them out (compellere means to oblige)

6The thought that something is wrong leads to repeating rituals until it is perceived that it is "right". In compulsions, the
unexceptionability of the action often counts more than the actual outcome.

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schizophrenic patient who may think that thoughts are the result of an insertion from the outside) even if
he tries to push them away and suppress them.
The peculiar characteristics that define a compulsion are:
1. Intentionality (the subject performs the compulsions with awareness, unlike the tic in which
conscious processing is lacking).
2. Purpose (the compulsion has a specific purpose or meaning conferred on it by the patient himself and
which, at least initially, tends to reduce and / or neutralize his anxiety or to prevent a feared event
or discomfort).
3. Repeatability (the subject repeats consecutively or in a short period of time a certain behavior, often
the repetitiveness is also expressed with a characteristic ritualization of the behavior).
Most individuals with obsessive-compulsive disorder have both obsessions and compulsions, but there are
cases where only obsessions are reported. The existence of “pure compulsive” disorders, on the other
hand, is questionable since compulsions are considered a form of the subject's response to obsessions; at
least initially the obsessive idea should therefore be present, although it is understood the possibility, in
the evolution of the disorder, that the compulsion may later be perpetrated autonomously.
The specific content of obsessions and compulsions varies between individuals. However, certain themes,
or dimensions, are common.

Themes or dimensions Obsession Compulsions

s
Cleaning Obsessions of contamination Compulsions of cleaning (washing)

Compulsions of repetition, order

Order and symmetry Symmetry obsessions and counting
Aggressive, sexual and religious
Forbidden or taboo Related compulsions
obsessions
thoughts
Relative compulsions to check
Fears of harm to oneself or (checking the gas tap; checking
Damage others that you have closed the front
door ...)

Other themes can be of superstitious origin (negative events that can happen if certain rules are not
followed), somatic (fear for parts of the body or for one's appearance), aggressive (impulses or thoughts of
hurting people even if they do not want it), homosexual (homoerotic impulses in heterosexual subjects),
relational (doubts about the partner or about the feelings towards him), religious and moral (thoughts or
images with blasphemous content), sexual and pedophilic (thoughts, images and sexual impulses towards
unbecoming people such as relatives and children).
These themes occur in different cultures. Importantly, individuals have symptoms that belong to more
than one dimension, are relatively constant over time in adults with the disorder, and may be associated
with different neural substrates. Some individuals also have difficulty throwing objects away and
accumulating them as a result of typical obsessions and compulsions, such as the fear of harming others.
WHAT AFFECTS THE CONTENT
The frequency and content of intrusions are influenced by mental states. The thoughts that intrude into
the minds of obsessive patients reflect their fears (eg, those who are afraid of harming others frequently
have obsessive thoughts of an aggressive type).
EMOTIONAL ANSWERS ASSOCIATED WITH DOC
Individuals with OCD experience a variety of emotional responses to situations that trigger obsessions and
compulsions. For example, many individuals experience marked anxiety, which can include recurrent
panic attacks. Others report strong feelings of disgust (fear of contagion is often associated with the
feeling of disgust). While engaging in compulsions, some individuals report a distressing sense of
incompleteness or uneasiness until things seem, give the impression that they are or sound “right”.
It is common in individuals with the disorder to avoid people, places and things that trigger obsessions and
compulsions. For example, individuals with contamination concerns can avoid situations

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public (restaurants, public restrooms) to reduce exposure to feared contaminants; individuals with
intrusive thoughts about causing harm can avoid social interactions.
CRITERION B
It makes it possible to distinguish OCD from occasional intrusive thoughts or repetitive behaviors, which
are common in the general population. Obsessive symptoms are an exasperated version of worry and
action that can be found in many people who do not deserve the diagnosis of OCD. There is a continuum
between obsessive-compulsive disorder and normality, ie there are no qualitative but only quantitative
differences.
Intrusive thoughts are qualitatively normal: (normally we can have the doubt of not having closed the car
or having left the gas on when leaving the house, so much so that we can go back to check). The
difference with people not suffering from obsessive-compulsive disorder is only in the severity of the
doubt, in its frequency, in the size of the measures, and, above all, in the fact that obsessive patients
evaluate obsessions very negatively, while the general population tends to not give them importance and
therefore to accept them more easily. Usually people don't give much weight to these kinds of thoughts,
they don't care and move on to something else.
Subclinical forms they are very common and are often seen during certain stages of normal development.
The frequency and severity of obsessions and compulsions varies among individuals with OCD.

OTHER CHARACTERISTICS OF DOC

Specify if:
 With good or enough insight: (most patients) the individual recognizes that OCD beliefs are definitely
or probably not true, or that they may or may not be true.
 With little insight: Individual thinks OCD beliefs are likely to be true.
 With absent insight / delusional beliefs: (4% of patients) the individual is absolutely sure that the
beliefs of the DCO are true.
• They are not aware of illness or can attribute meaning and utility to compulsive behaviors
1. Subjects in developmental age.
2. Subjects with schizotypal personality.
3. Subjects with so-called 'magical' primitive ways of thinking.

Many individuals with obsessive-compulsive disorder have dysfunctional beliefs. These thoughts can include:
1. Tendency to overestimate the threat.
2. Exaggerated sense of responsibility, perfectionism.
3. Intolerance to uncertainty.
4. Attaching too much importance to thoughts (for example, believing that having a forbidden thought is
as bad as doing it) and the need to control them.
It must be specified whether obsessive-compulsive disorder is related to tics (the individual has a current
or past history of tic disorder). Up to 30% of individuals with obsessive-compulsive disorder have lifelong
tic disorder. This is more common in boys with pediatric onset of the disorder. These individuals may
differ from those without a history of tic disorders in terms of OCD symptoms, comorbidities, family
course, and pattern of transmission.
DEVELOPMENT AND COURSE
The annual prevalence in the United States is 1.2%, with a similar international prevalence (1.1-1.8%).
Females show a slightly higher rate than males in adulthood, although males develop the disorder more
frequently in childhood. In the United States, the average age of onset is 19.5 years, and in 25% of cases,
onset occurs by age 14. Onset after age 35 is unusual, but it occurs. Males have an earlier age of onset
than females: nearly 25% of males have an onset before age 10. Symptom onset is usually gradual,
however acute onset has also been reported. If the obsessive-compulsive disorder is not treated, the
course is usually chronic,

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often with fluctuations of symptoms. Some individuals show an episodic course, and a minority has a
course that tends to get worse. Without treatment, remission rates in adults are low (20% for individuals
reevaluated 40 years later). Onset in childhood or adolescence may involve the presence of obsessive-
compulsive disorder throughout life. However, 40% of individuals with onset of the disorder in childhood or
adolescence may have remission in early adulthood. The course is often complicated by the co-presence of
other disorders.
RISK FACTORS AND PROGNOSIS
 Temperamental factors: Greater internalizing symptoms, higher negative emotionality, and behavioral
inhibition in childhood are possible temperamental risk factors.
 Environmental factors: Childhood physical and sexual abuse and other stressful or traumatic events
have been associated with an increased risk of developing obsessive-compulsive disorder. Some children
may develop a sudden onset of obsessive-compulsive symptoms, which has been associated with
different environmental factors, including various infectious agents and a post-infectious autoimmune
syndrome.
 Genetic and physiological factors: The incidence rate among first-degree relatives of adults with
obsessive-compulsive disorder is approximately two times higher than in first-degree relatives of those
who do not have the disorder; however, among first-degree relatives of individuals with onset of the
disorder in childhood or adolescence, the rate increases 10-fold. Family transmission is partly due to
genetic factors (eg a concordance rate of 0.57 for monozygotic twins versus 0.22 for dizygotic twins).
Dysfunctions affecting the orbito-frontal cortex, the anterior cingulate cortex and the striatum (cortico-
striatum-thalamus-cortical circuit - CSTC, originating and ending in the dorsolateral prefrontal cortex -
DLPFC) were more involved.

More precisely, the impulse involves a neuronal circuit centered at the level of the ventral striatum,
connected to the thalamus, ventral prefrontal cortex and anterior cingulate cortex.
Compulsivity in dorsal striatum, thalamus and orbitofrontal cortex. The impulses can become compulsions
due to neuroplastic changes involving the dorsal system and causing the migration of impulses from the
ventral to the dorsal circuits.

Obsessive Compulsive Disorder occurs all over the world. There is substantial similarity between cultures
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in gender distribution, age of onset and comorbidity of the disorder. Also, all over the world there

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it is a similar symptom structure involving cleansing, symmetry, accumulation, thoughts, taboos, or fear of
harm. However, there are local variations in symptom expression, and cultural factors can shape the
content of obsessions and compulsions.
Males have an earlier age of onset than females and are more likely to have comorbid tic disorder.
Differences in the pattern of symptom dimensions have been reported, whereby, for example, females are
more likely to develop symptoms in the cleanliness dimension and males are more likely to develop
symptoms in the dimensions of forbidden thoughts and symmetry. In the peripartum period, onset or
exacerbation of obsessive-compulsive disorder has been reported, as well as symptoms that may interfere
with the mother-infant relationship (e.g., obsessions of aggression leading to child avoidance).
Suicidal thoughts they occur at some time in about half of individuals with obsessive-compulsive disorder.
Suicide attempts are also reported in more than a quarter of individuals with this disorder; the presence
of comorbidities with major depressive disorder increases the risk.
OCD is associated with reduced quality of life, as well as with high levels of social and occupational
impairment. Impairment occurs in many different life areas and is associated with the severity of
symptoms. Impairment can be caused by the time taken by obsessions and by the implementation of
compulsions. Avoiding situations that can trigger obsessions or compulsions can also severely limit
functioning. Furthermore, specific symptoms can create specific obstacles. For example, obsessions about
harm can make relationships with family and friends perceive as dangerous; the result may be the
avoidance of these relationships. Obsessions related to symmetry can derail the timely completion of
school or work projects because the project never feels right, potentially leading to school failure or job
loss. Health consequences can also occur. For example, individuals with contamination concerns may
avoid doctor's offices or hospitals or develop dermatological problems (skin lesions due to excessive
washing). Sometimes the symptoms of the disorder interfere with its own treatment (for example, when
drugs are considered contaminated). Furthermore,
The patient generally fights against impulse and intrusive thinking to varying degrees: this conflict is
indicated by the term of resistance, which can be high in the workplace and minimal in the home, it can
fluctuate from day to day and during different episodes, until they disappear in the course of the disease
when the disorder takes on a chronic worsening course.
DIFFERENTIAL DIAGNOSIS
Differential diagnosis must be made for:
 Anxiety Disorders. Recurring thoughts, avoidance behaviors, and repetitive requests for reassurance can
also occur in anxiety disorders. However, the recurring thoughts that are present in generalized anxiety
disorder (e.g., worries) usually involve real-life aspects, while OCD obsessions usually do not involve
real-life aspects and may include - re instead bizarre, irrational or apparently magical contents;
furthermore, compulsions are often present and usually associated with obsessions. Similar to
individuals with OCD, individuals with a specific phobia may have a fear reaction in response to specific
objects or situations; however, in specific phobia the feared object is usually much more circumscribed,
and no rituals are present.
 Major depressive disorder. OCD can be distinguished from the rumination of major depressive disorder,
in which thoughts are usually congruent with mood and are not necessarily experienced as intrusive or
distressing (egosynthonic ruminations); moreover, ruminations are not associated with compulsions, as
happens in the typical manifestation of DOC. Prevalent ideation focused on past events; episodic course;
late onset.
 Other obsessive-compulsive disorders and related disorders. In body dysmorphic disorder, obsessions
and compulsions are limited to concerns about physical appearance, and in trichotillomania (hair pulling
disorder) the compulsive behavior is limited to hair pulling in the absence of obsessions. The symptoms
of storage disorder focus exclusively on the persistent difficulty in throwing away or separating from
one's possessions, marked discomfort associated with throwing away objects and their excessive
accumulation. However, if an individual has typical OCD obsessions (eg, concerns about incompleteness
or harm), and these obsessions lead to compulsive hoarding behaviors (eg,

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Food disorders. OCD can be distinguished from anorexia nervosa in that OCD obsessions and compulsions
are not limited to concerns about weight and food.
Tics (in tic disorder) and stereotyped movements. A tic is a sudden, rapid, recurring, non-rhythmic
movement or vocalization (e.g., blinking, clearing the throat). A stereotyped movement is repetitive, non-
functional, apparently guided motor behavior (eg, head banging, rocking, biting). Stereotypical tics and
movements are typically less complex than compulsions and are not aimed at neutralizing an obsession.
However, the distinction between complex tics and compulsions can be difficult. While compulsions are
usually preceded by obsessions, tics are often preceded by premonitory sensory impulses. Some individuals
have symptoms of both OCD and a tic disorder, in which case both diagnoses may be warranted.
Psychotic disorders. Some individuals with OCD have poor insight or even delusional beliefs typical of
OCD. However, they have obsessions and compulsions (which distinguishes their condition from delusional
disorder) and have no other characteristics of schizophrenia or schizoaffective disorder (eg, desperate
phenomena and formal thought disorders rarely occur in OCD). It may also be necessary to dd between
compulsions and stereotyped behaviors.
Other compulsive-like behaviorsCertain behaviors are sometimes described as "compulsive," including
sexual behavior (in the case of paraphilias), pathological gambling, and substance use (eg, alcohol use
disorder). However, these behaviors differ from OCD compulsions in that the individual usually derives
pleasure from the activity and may wish to resist it only because of its deleterious consequences.
Personality DOC. Although obsessive-compulsive personality disorder and OCD have similar names, the
clinical manifestations of these disorders are quite different. Obsessive-Compulsive Personality Disorder is
not characterized by intrusive thoughts, images or impulses, or by repetitive behaviors enacted in
response to these intrusions; instead, it involves an enduring and pervasive inactive pattern of excessive
perfectionism and rigid control. Furthermore, in obsessive-compulsive personality disorder there is ego-
syntony of the 'trait'. If an individual has symptoms of both OCD and OCD, both diagnoses can be made.

COMORBIDITY
Individuals with OCD often have other psychopathologies. Many adults with the disorder have a lifetime
diagnosis of an anxiety disorder (76%; eg, panic disorder, social anxiety disorder, generalized anxiety
disorder, specific phobia) or a depressive or bipolar disorder (63% a depressive or bipolar disorder, with
major depressive disorder being the most common [41%]). Onset of OCD is usually later than most anxiety
disorders (except separation anxiety disorder) and PTSD, but often precedes that of depressive disorders.
Comorbidity with obsessive-compulsive personality disorder is also common in individuals with OCD (eg,
ranging from 23% to 32%).
Up to 30% of individuals with OCD also have lifelong tic disorder. Comorbidity with tic disorder is more
common in boys with childhood OCD onset. These individuals tend to differ from those without a history of
tic disorders in the issues of their OCD symptomology, comorbidity, course, and family transmission
patterns. A triad of OCD, tic disorder, and attention deficit / hyperactivity disorder may also be observed
in children.
Disorders that occur more frequently in individuals with OCD than in individuals without the disorder
include several obsessive-compulsive and related disorders such as body dysmorphic disorder,
trichotillomania (hair pulling disorder) and excoriation disorder. (skin teasing). Finally, an association has
been reported between OCD and some disorders characterized by impulsivity, such as oppositional defiant
disorder.
OCD is also much more common in individuals with certain other disorders than would be expected based
on its prevalence in the general population; when one of these other disorders is diagnosed, the individual
should also be examined for the presence of OCD. For example, in individuals with schizophrenia or
schizoaffective disorder, the prevalence of OCD is about 12%. Rates of OCD are also high in bipolar
disorder, eating disorders, such as anorexia nervosa and bulimia nervosa, and Tourette's disorder.

THERAPY
The therapeutic approach is based on the use of drugs with anti-obsessional function and on cognitive-
behavioral psychotherapy: both are considered first choice therapeutic interventions.
Pharmacological therapy is based on antidepressants such as SSRIs (Fluoxetine, Fluvoxamine, Paroxetine,
Sertraline) and tricyclics (Clomipramine, although the latter has greater side effects and greater toxicity
in case of overdose).
In case of resistance to SSRI treatment at appropriate dosages and times, a switch to another SSRI or to
Clomipramine is tried. If this is not enough, an antipsychotic is added (off-label),

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chosen on a case-by-case basis according to the side effect profile; however all with uncertain clinical
benefit; among the 2nd generation antipsychotics: Risperidone. Prescribing 2 or more antidepressants at
the same time is not recommended as a strategy to enhance the therapeutic effect on obsessive-
compulsive symptoms.
Resistant OCD is defined as a disorder that does not present symptomatology improvement (reduction of
the Y-BOCS score by 35%) after two trials with high-dose SSRIs at adequate times.
Refractory OCD is defined as a disorder that does not present an improvement in symptoms (reduction of
the Y-BOCS score by 35% or 25%, depending on the authors) after two attempts with SSRIs at appropriate
doses and times plus strengthening and some alternative strategies.

Behavioral therapy is based on the technique of stopping thought or exposure to stimuli that cause
obsession and / or compulsion (gradual exposure (floating) or prevention of response (coping strategies)).

BODY DYSMORPHISM DISORDER

The criteria for Body Dysmorphic Disorder are:
A. Concern about one or more perceived defects or imperfections in physical appearance, which are
not observable or appear mildly to others.
B. At some point during the course of the disorder, the individual has engaged in repetitive behaviors
(for example, looking in the mirror, caring excessively about one's appearance, picking at the skin,
seeking reassurance) or mental actions (for example, comparing the physical appearance with that
of others) in response to concerns related to appearance.
C. The worry causes clinically significant distress or impairment in social, occupational, or other
important areas of functioning.
D. Appearance concern is no better justified by concerns about body fat or weight in an individual
whose symptoms meet the diagnostic criteria for an eating disorder.
CRITERION A
Individuals with body dysmorphic disorder (formerly known as dysmorphophobia) are concerned about one
or more perceived defects or imperfections in their physical appearance, which they believe to be ugly,
unattractive, abnormal, or misshapen. Concerns range from appearing "unattractive" or "not fair" to
appearing "horrible" or "like a monster".
Concerns can be focused on one or many areas of the body, most commonly:
1. Skin (e.g. perceiving acne, scars, wrinkles, wrinkles, paleness)
2. Hair (eg "thinning" of the hair)
3. Hair (e.g. excessive body or facial hair)
4. Nose (e.g. size or shape)
In fact, any part of the body can be an object of concern. Some individuals are concerned about a
perceived asymmetry of some areas.
The concerns are:
- Intrusive, unwanted.
- They consume time (they occur on average 3-8 hours a day).
- It is usually difficult to resist or control
them. CRITERION B
Excessive repetitive behaviors or mental actions (e.g. comparing) are performed in response to concerns.
The individual feels compelled to engage in these behaviors that are not pleasant and can increase anxiety
and dysphoria and these behaviors are time consuming and difficult to resist or control.
The most common behaviors are:
1. Compare your own appearance with that of others.
2. Check repeatedly in the mirror or on other reflective surfaces for perceived defects, or examine them
directly.
3. Excessive self-care (e.g., combing, shaving, shaving, shaving, or pulling hair).
4. Camouflage (e.g., repeatedly applying makeup or covering unwanted areas with things like a hat,
clothes, makeup, or hair).
5. Seek reassurance about what perceived imperfections look like.
6. Touch unwanted areas to check them.

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7. Excessive exercise or weight lifting. Search for

aesthetic treatments.
Some individuals tan excessively (eg, to darken "pale" skin or reduce perceived acne), change clothes
several times (eg, to disguise perceived blemishes), or shop as - pulsive (for example, of beauty products).
Compulsive skin teasing to improve perceived skin defects is common and can cause skin lesions,
infections, or ruptures of blood vessels.
CRITERION C and D
The worry must cause clinically significant distress or impairment in social, occupational, or other
important areas of functioning (Criterion C); usually both are present.
Body dysmorphic disorder must be distinguished from an eating disorder (Criterion D).

SPECIFY IF
With muscle dysmorphia: The individual is concerned that his body constitution is too small or
insufficiently muscular.
- It occurs almost exclusively in males.
- It consists of a concern about the idea that one's body is too small or insufficiently lean or muscular.
Individuals with this form of the disorder actually have a normal body or are also very muscular.
- They may also be concerned about other areas of the body, such as the skin or hair.
- Most (but not all) diet, exercise and / or lift weights excessively, sometimes causing bodily harm. Some
use androgenic-anabolic steroids and other potentially dangerous substances to try to make their bodies
bigger and more muscular.

BODY DYSMORPHISM BY PROXY

Proxy body dysmorphic disorder is a form of body dysmorphic disorder in which individuals are concerned
about perceived defects in another person's appearance.

INDICATE DEGREE OF INSIGHT:

- With good or enough insight: The individual recognizes that the beliefs of body dysmorphic disorder are
definitely or probably not true, or that they may or may not be true.
- With little insight: The individual thinks that the beliefs of body dysmorphic disorder are probably true.
- With absent insight / delusional beliefs: The individual is absolutely sure that the beliefs of the body
dysmorphic disorder are true.
Belief insight in body dysmorphic disorder can range from good to absent / delusional (i.e. delusional
beliefs consisting of the full belief that one's view of one's appearance is correct and undistorted). On
average, insight is poor.
Currently, one third or more of individuals have delusional beliefs related to body dysmorphic disorder.
Individuals with delusional body dysmorphic disorder tend to have greater morbidity in some areas (e.g.,
suicidal tendency), but this appears justified by their tendency to have more severe body dysmorphic
disorder symptoms.

CHARACTERISTICS ASSOCIATED TO SUPPORT DIAGNOSIS

 Many individuals with body dysmorphic disorder have ideas or delusions of reference, believing that
other people particularly notice or mock them because of their appearance. Body dysmorphic disorder is
associated with high levels of anxiety, social anxiety, social avoidance, depressed mood, neuroticism
and perfectionism, as well as low extraversion and low self-esteem.
 Many individuals are ashamed of their looks and their excessive focus on physical appearance, and are
reluctant to disclose their concerns to others.
Most individuals undergo cosmetic treatment to try to improve perceived defects. The most common are
dermatological treatment and surgery, but any type of intervention (eg, dental, electrolysis) may be
required. Occasionally, individuals may operate on their own. Body dysmorphic disorder appears to
respond poorly to such treatments and sometimes worsens. Some individuals take legal action or have
aggressive behaviors towards the doctor due to dissatisfaction related to the aesthetic result.
 Body dysmorphic disorder has been associated with executive dysfunction and visual processing
abnormalities, with a propensity to analyze and code details rather than holistic or general configuration
aspects of the visual stimulus. Individuals with this disorder tend to have a propensity for negative and
threatening interpretations of facial expressions and ambiguous scenarios.

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PREVALENCE
The prevalence point among US adults is 2.4% (2.5% in females and 2.2% in males). Outside the United
States (for example in Germany) the current prevalence is about 1.7-1.8%, with a similar gender
distribution to that in the United States.
The current prevalence is 9-15% among dermatological patients, 7-8% among US cosmetic surgery patients,
3-6% among international cosmetic surgery patients (most of the studies), 8 % among orthodontic patients
and 10% among patients undergoing oral or maxillofacial surgery. The median age of onset of the disorder
is 16-17 years, the median age of onset is 15 years, and the most common age of onset is 12-13 years. In
two thirds of individuals the onset of the disorder occurs before the age of 18. Subclinical symptoms of
body dysmorphic disorder begin, on average, at age 12 or 13. Subclinical worries usually develop gradually
to full disturbance, although some individuals may have a sudden onset of body dysmorphic disorder. Body
dysmorphic disorder usually appears to have a chronic course, although there is a likelihood of
improvement when evidence-based treatment is received. The clinical features of the disorder appear
largely similar in children / adolescents and adults. Body dysmorphic disorder also occurs in elderly
individuals, but little is known about the disorder in this age group. Individuals who have an onset of the
disorder before age 18 are more likely to attempt suicide, have higher comorbidities, and have a gradual
(rather than acute) onset of the disorder than individuals with onset of body dysmorphic disorder in
adulthood. . although there is a likelihood of improvement when evidence-based treatment is received.
The clinical features of the disorder appear largely similar in children / adolescents and adults. Body
dysmorphic disorder also occurs in elderly individuals, but little is known about the disorder in this age
group. Individuals who have an onset of the disorder before age 18 are more likely to attempt suicide,
have higher comorbidities, and have a gradual (rather than acute) onset of the disorder than individuals
with onset of body dysmorphic disorder in adulthood. . although there is a likelihood of improvement
when evidence-based treatment is received. The clinical features of the disorder appear largely similar in
children / adolescents and adults. Body dysmorphic disorder also occurs in elderly individuals, but little is
known about the disorder in this age group. Individuals who have an onset of the disorder before age 18
are more likely to attempt suicide, have higher comorbidities, and have a gradual (rather than acute)
onset of the disorder than individuals with onset of body dysmorphic disorder in adulthood. . but little is
known about the disorder in this age group. Individuals who have an onset of the disorder before age 18
are more likely to attempt suicide, have higher comorbidities, and have a gradual (rather than acute)
onset of the disorder than individuals with onset of body dysmorphic disorder in adulthood. . but little is
known about the disorder in this age group. Individuals who have an onset of the disorder before age 18
are more likely to attempt suicide, have higher comorbidities, and have a gradual (rather than acute)
onset of the disorder than individuals with onset of body dysmorphic disorder in adulthood. .

RISK FACTORS AND PROGNOSIS

- Environmental factors. Body dysmorphic disorder has been associated with high rates of neglect and
abuse in childhood.
- Genetic and physiological factors. The prevalence of body dysmorphic disorder is high in first-degree
relatives of individuals with obsessive-compulsive disorder.

DIAGNOSTIC ASPECTS RELATED TO THE CULTURE OF BELONGING

Body dysmorphic disorder has been reported internationally. It appears that the disorder may have more
similarities than differences between races and cultures, but that cultural values and peculiarities may
influence the content of symptoms to some extent.
The taijin kyofusho, included in the traditional Japanese diagnostic system, has a subtype similar to the
body dysmorphic disorder: shubo-kyofu ("the phobia of a deformed body").

WAIT GENDER-RELATED DIAGNOSTICS

Females and males appear to have more similarities than differences in most clinical features: for
example, unwanted areas of the body, types of repetitive behaviors, symptom severity, suicidal
tendencies, comorbidities, disease course, and treatment. aesthetic for body dysmorphic disorder.
However, males are more likely to have genital-related concerns, and females are more likely to have a
comorbid eating disorder. Muscle dysmorphism occurs almost exclusively in men.

RISK OF SUICIDE
Rates of suicidal ideation and suicide attempts are high in both adults and children / adolescents with
body dysmorphic disorder. Furthermore, the risk of suicide appears to be high in adolescents. A
substantial percentage of individuals attribute suicidal ideation or suicide attempts primarily to concerns
about physical appearance. Individuals with body dysmorphic disorder have many risk factors for
committing suicide, such as high rates of suicidal ideation and suicide attempts, demographics associated
with suicide, and high rates of comorbidity with major depressive disorder.
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FUNCTIONAL CONSEQUENCES OF BODY DYSMORPHISM DISORDER

Almost all individuals with body dysmorphic disorder experience impaired psychosocial functioning due to
their concerns about physical appearance (social activities, relationships, intimacy). Impairment can range
from moderate (avoidance of some social situations) to very severe and disabling (being completely
housebound, sometimes even for years). On average, psychosocial functioning and quality of life are very
poor. More severe symptoms of body dysmorphic disorder are associated with poorer functioning and
poorer quality of life. A high percentage of adults and adolescents were admitted to a psychiatric
hospital. Most individuals experience impaired functioning in the workplace,

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school or work, do not work). About 20% of young people with body dysmorphic disorder drop out of school
primarily because of body dysmorphic disorder symptoms.

DIFFERENTIAL DIAGNOSIS
1. Normal concerns about appearance and obvious physical defects. Body dysmorphic disorder differs
from normal appearance concerns in that it is characterized by excessive appearance preoccupations
and repetitive behaviors that are time consuming, are usually difficult to resist or control, and cause
clinically significant distress. or impaired functioning. Physical defects that are clearly evident (i.e. not
mild) are not diagnosed as body dysmorphic disorder. However, skin teasing as a symptom of body
dysmorphic disorder can cause significant skin lesions and scarring; in these cases, body dysmorphic
disorder should be diagnosed.
2. Food disorders. In an individual with an eating disorder, concerns about being fat are considered a
symptom of the eating disorder rather than the body dysmorphic disorder. However, weight concerns
may occur in body dysmorphic disorder. Eating disorders and body dysmorphic disorder may be
comorbid, in which case both should be diagnosed.
3. Other obsessive-compulsive and related disorders. The worries and repetitive behaviors of body
dysmorphic disorder differ from the obsessions and compulsions of OCD in that the former is focused
only on physical appearance. These disorders have other differences, such as lower insight into body
dysmorphic disorder. When skin teasing is designed to improve perceived skin defects, it is diagnosed as
body dysmorphic disorder, rather than excoriation disorder (skin teasing). When hair removal (by
peeling, pulling, or other ways of removal) is designed to improve perceived defects in the appearance
of facial or body hair, body dysmorphic disorder is diagnosed, rather than trichotillomania (tearing
disorder). of hairs).
4. Illness Anxiety Disorder. Individuals with body dysmorphic disorder are not worried about having or
contracting disease and do not have particularly high levels of somatization.
5. Anxiety Disorders. Social anxiety and avoidance are common in body dysmorphic disorder. However,
unlike social anxiety disorder (social phobia), agoraphobia, and avoidant personality disorder, body
dysmorphic disorder includes preeminent appearance-related preoccupation, which can be delusional,
and behaviors repetitive, and social anxiety and avoidance are due to concerns about perceived defects
in physical appearance and the belief or fear that others may regard these individuals as ugly,
ridiculous, or reject them because of their characteristics. physical ristics. Unlike generalized anxiety
disorder, in body dysmorphic disorder, anxiety and worry focus on perceived defects in appearance.
6. Major depressive disorder. The preeminent concern about the appearance and excessive repetitive
behaviors of body dysmorphic disorder differentiate it from major depressive disorder. However, major
depressive disorder and depressive symptoms are common in individuals with body dysmorphic disorder,
often appearing as secondary to the distress and impairment that body dysmorphic disorder causes.
Body dysmorphic disorder should be diagnosed in depressed individuals if the diagnostic criteria for body
dysmorphic disorder are met.
7. Psychotic disorders. Many individuals with body dysmorphic disorder have delusional beliefs related to
appearance (i.e. a full belief that their view of perceived delights is correct), which is diagnosed as
body dysmorphic disorder with absent insight / delusional beliefs, and not as a delusional disorder.
Reference ideas or delusions related to appearance are common in body dysmorphic disorder; however,
unlike schizophrenia or schizoaffective disorder, body dysmorphic disorder involves prominent concerns
about appearance and associated repetitive behaviors, while disorganized behavior and other psychotic
symptoms are absent (except for beliefs regarding the appearance, which can be delusional).
8. Other ailments and symptoms. Body dysphoric disorder should not be diagnosed if the concern is
limited to malaise or a desire to get rid of one's primary and / or secondary sexual characteristics in an
individual with gender dysphoria, or if the concern is focused on the belief that he a disgusting or
unbearable odor as in olfactory reference syndrome (which is not part of the DSM-5 disorders). Body
integrity identity disorder (apoteinnophilia) (which is not part of the DSM-5 disorders) involves the
desire to have a limb amputated in order to correct the discrepancy between a person's sense of body
identity and its current anatomy. However, the concern is not focused on the appearance of the limb,
as it would be in body dysmorphic disorder. The Koro, a culture-related disorder that usually occurs in
Asian Southeast, is the fear that the penis (in females the labia minora, nipples or breasts) is shrinking
or retracting and disappears within the abdomen, accompanied often from the belief that this will
result in death. Koro differs from body dysmorphic disorder in several

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ways, including a focus on death rather than concern for perceived ugliness. Dysmorphic worry (which is
not a part of DSM-5 disorders) is a much larger construct than body dysmorphic disorder and does not
equate to it. It involves symptoms that reflect excessive concern about minor defects or imaginary
imperfections in appearance.

COMORBILITY
1. Major depressive disorder is the disorder that is most frequently found in comorbidities, with an onset
usually subsequent to that of body dysmorphic disorder.
2. Social anxiety disorder (social phobia).
3. DOC.
4. Substance-related disorders they are frequently comorbid.

DISORDER BY ACCUMULATION (HOARDING DISORDER)

The criteria for Accumulation Disorder are:
A. Persistent difficulty in throwing away or separating from one's possessions, regardless of the real
value.
B. This difficulty is due to a perceived need to store items and the discomfort associated with
throwing them away.
C. The difficulty of throwing away one's possessions produces an accumulation that congestes and
clutters the living spaces and substantially compromises their intended use. If the living spaces are
clear, it is only thanks to the intervention of third parties (for example family members, cleaners,
authorities).
D. Accumulation causes clinically significant distress or impairment in social, occupational, or other
important areas of functioning (including maintaining a safe environment for oneself and others).
E. The accumulation is not attributable to another medical condition (e.g. head injury,
cerebrovascular disorder, Prader-Willi syndrome).
F. The accumulation is not better justified by symptoms of another mental disorder (for example,
obsessions in obsessive-compulsive disorder, reduced energy in major depressive disorder,
delusions in schizophrenia or other psychotic disorders, cognitive deficits in major neurocognitive
disorder , narrow interests in autism spectrum disorder).
About 80-90% of individuals with accumulation disorder show excessive acquisition. The most frequent
form of acquisition is over-buying, followed by the acquisition of free items (flyers, items thrown by
others). Theft is less common.
Some individuals may deny excessive acquisition when first examined, however this may emerge later in
the course of treatment. Individuals with accumulation disorder usually feel discomfort when they cannot
or are prevented from acquiring objects. Other common features of hoarding disorder include indecision,
perfectionism, avoidance, procastination, difficulty planning and organizing activities, distractibility.
Some individuals with accumulation disorder live in unsanitary conditions which may be a logical
consequence of severely cluttered spaces and / or which are associated with planning and organization
difficulties.
EPIDEMIOLOGY
There are no nationally representative studies of the prevalence of accumulation disorder. Population
surveys estimate that the prevalence point of clinically significant accumulation in the United States and
Europe is around 2-6%.
Accumulation disorder affects both males and females, but some epidemiological studies have reported a
significantly higher prevalence among males. This is in contrast to clinical specimens, which are mostly
female. Symptoms of accumulation appear to be nearly three times more prevalent in older individuals
(55-94 years of age) than in younger adults (34-44 years of age). Accumulation appears to begin early in
life and extends into the later stages.
The main features of hoarding disorder (i.e. difficulty throwing items away, excessive amount of clutter)
are generally comparable between males and females, but females tend to exhibit more over-acquisition
behaviors, particularly over-buying, than males.
COURSE

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Symptoms of accumulation can emerge around the age of 11-15, begin to interfere with daily functioning
in the mid-second decade, and cause significant impairment around the mid-third decade. Individuals who
take part in clinical research trials are usually in the sixth decade. Therefore, the severity of the
accumulation increases with each decade of life. Once symptoms begin, the course of the accumulation is
often chronic, with few individuals reporting a course with symptom fluctuations.
Pathological accumulation in children appears to be easily distinguishable from adaptive and
developmental behaviors of conservation and collecting. Since children and adolescents usually do not
control their own living environment and disposal behaviors, the possible intervention of third parties
should be considered at the time of diagnosis (for example parents who keep usable spaces, thus reducing
interference ).
Indecision is a key feature of individuals with storage disorder and their first degree relatives.
Individuals with storage disorder often retrospectively report stressful and traumatic life events that
precede the onset of the disorder or cause it to exacerbate.
Hoarding behavior is hereditary, and about 50% of hoarding individuals report having hoarding relatives.
Twin studies indicate that approximately 50% of the variability in accumulation behavior is attributable to
additive genetic factors.
While most of the research has been done in industrialized countries and western urban communities,
available data from non-western and developing countries suggest that accumulation is a universal
phenomenon with consistent clinical features.
Clutter impairs basic activities, such as moving around the house, cooking, cleaning, taking care of
personal hygiene and even sleeping. Quality of life is often considerably compromised. In severe cases,
buildup can put individuals at serious risk of fire, falling (especially the elderly), poor sanitation, and
other health risks. Hoarding disorder is associated with occupational impairment, poor physical health,
and high utilization of social services. Family relationships are often of great tension. Conflict with
neighbors and local authorities is common (a substantial percentage of individuals with severe hoarding
disorder have been involved in legal eviction proceedings and some have a history of eviction).
DIFFERENTIAL DIAGNODES
Differential diagnoses need to be made for other medical conditions, neurodevelopmental disorders,
schizophrenia spectrum disorders and other psychotic disorders, major depressive episode, neurocognitive
disorders, and obsessive-compulsive disorder.

TRICHOTILLOMANIA
The criteria for Trichotillomania are:
A. Recurring hair or hair pulling, leading to hair loss
A. Repeated attempts to reduce or stop hair or hair pulling.
B. Hair pulling clinically significant distress or impairment in social, occupational, or other important
areas of functioning.
C. Hair pulling or hair loss is not attributable to another medical condition (e.g. a dermatological
condition).
D. Hair pulling or hair pulling is not better justified by symptoms of another mental disorder (for
example, attempts to improve a perceived defect or imperfection in body dysmorphic disorder).
hair pulling can be accompanied by a range of behaviors or rituals involving them:
 Individuals may search for a particular type of hair to pluck (for example, hair with a specific texture or
color).
 They may attempt to pull out the hair in a specific way (for example so that the root comes out intact).

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 They can examine the hair visually, or manipulate it by touch or orally after it has been plucked (for
example, twist the hair or hair between the fingers, insert the strand between the teeth, die the hair or
hair until it breaks or swallows) .
Hair pulling can also be preceded or accompanied by various emotional states; it can be triggered by
feelings of anxiety or boredom, it can be preceded by an increased sense of tension (either immediately
before plucking the hair or when trying to resist the urge to pluck), or it can lead to gratification ,
pleasure or a sense of relief when the hair or fur is pulled out.
Hair pulling or hair pulling usually does not occur in the presence of other people, except close family
members.
Some individuals have an urge to pluck hair or hair from other people, and sometimes they may seek the
opportunity to do it on the sly. Some individuals may deny their hair pulling or hair pulling to others.
In the general population, the estimated annual prevalence for trichotillomania in adults and adolescents
is 1-2%. The disorder is more common in females than males, with a ratio of about 10: 1. This estimate
likely reflects the true male / female ratio of the condition, although it may reflect different treatment
seeking based on gender or cultural attitudes regarding appearance (e.g. acceptance of normal hair loss or
hair in the men).
Among children with trichotillomania, boys and girls are more equally represented. Hair pulling or hair
pulling may be observed in young children, but this behavior usually resolves during the early stages of
development.
Most of the time the onset of hair pulling or hair pulling in trichotillomania coincides with or follows
puberty.
Tear zones can vary over time.
Symptoms may eventually worsen in females experiencing hormonal changes (eg menstruation,
perimenopause). Usually the course of trichotillomania is chronic, with symptomatological fluctuations if
the disorder is not treated. For some individuals, the disorder can come and go for weeks, months, or
years. A minority of individuals go into remission without subsequent relapse within a few years of onset.
There is evidence of a genetic vulnerability to trichotillo- mania.
The disorder is more common in individuals with obsessive-compulsive disorder and their first-degree
relatives than in the general population.
Trichotillomania is associated with distress as well as with social and occupational impairment. There may
be irreversible damage affecting the growth and quality of the hair. Rare medical consequences of tri-
cotillomania include purpura in the fingers, musculoskeletal damage (for example, carpal tunnel
syndrome, pain in the back, shoulders, and neck), blepharitis, and dental injuries (for example, worn or
broken teeth due to hair biting. or hairs).
Ingestion of hair or dander (ringworm) can lead to trichobezoars, resulting in anemia, abdominal pain,
hematemesis, nausea and vomiting, bowel obstruction and even perforation. Differential diagnosis should
be made for normal hair or hair removal or manipulation, other obsessive-compulsive and related
disorders, neurodevelopmental disorders, psychotic disorder, other medical condition, and substance-
related disorders.

EXCORATION DISORDER
The criteria for Excoriation Disorder are:
A. Recurrent skin picking causing skin lesions.
B. Repeated attempts to reduce or stop skin teasing.
C. Skin teasing causes clinically significant distress or impairment in social, occupational, or other
important areas of functioning.
D. Skin teasing is not attributable to the physiological effects of a substance (e.g. cocaine) or
another medical condition (e.g. scabies).
E. Skin teasing is not better justified by symptoms of another mental disorder (for example, tactile
delusions or hallucinations in a psychotic disorder, attempts to improve perceived defects or
imperfections in appearance in body dysmorphic disorder, stereotypies in stereotypical movement
disorder or self-injurious intention in non-suicidal self-harm).

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In the general population, the prevalence of excoriation disorder in adults is 1.4% or slightly more. Three-
quarters or more of individuals with the disorder are female. This probably reflects the true male /
female ratio of the condition, although it may reflect different treatment seeking based on gender or
cultural attitudes regarding appearance.
Although individuals with excoriation disorder may experience the disorder at various ages, skin tightening
occurs more often during adolescence, frequently coinciding with or following the onset of puberty. The
disorder often begins with a dermatological condition, such as acne.
Tease areas can vary over time. The course is usually chronic, with periods of symptomatic fluctuations if
the disorder is not treated. For some individuals, the disorder can show up and go away for weeks,
months, or years.
Excoriation disorder is more common in individuals with obsessive-compulsive disorder and their first-
degree relatives than in the general population.
Excoriation disorder is associated with discomfort, as well as with social and occupational impairment.
Many individuals report avoiding social or entertainment events, as well as going out in public. Most
individuals with the disorder also report having occupational interference caused by teasing, on at least a
weekly or daily basis. A significant percentage of students with excoriation disorder report missing school
days, having difficulty managing responsibilities at school, or having difficulty studying due to skin picking.
Most individuals with the disorder spend at least 1 hour a day teasing, thinking about teasing, and resisting
the urge to tease.
Medical complications of skin teasing include tissue damage, scarring, and infections, and can be life
threatening. Synovitis of the wrists has rarely been reported due to chronic infusion. It frequently requires
antibiotic treatment for infections and may require surgery on some occasions.
Differential diagnoses should be made for psychotic disorder, other obsessive-compulsive or related
disorders, neurodevelopmental disorders, somatic symptoms and associated disorders, other medical
disorders or conditions, and substance / drug-induced disorders.

DISORDERS RELATED TO TRAUMATIC AND STRESSING EVENTS

In the DSM-4 only disorders diagnosed for the first time during infancy and childhood or adolescence,
anxiety and adaptation disorders, related to this area.
The DSM-5, compared to previous versions of the Manual, includes this chapter which includes:

Reactive Attachment Disorder;

Uninhibited Social Engagement Disorder;

Post-traumatic stress disorder;

Acute Stress Disorder;

Disorders of adaptation;

Disorder related to traumatic and stressful events with other specification;

Disorder related to traumatic and stressful events without specification.
The placement in the DSM-5 chapter reflects the close relationship between these diagnoses and the
disorders treated in the adjacent chapters: anxiety disorders, dissociative disorders, obsessive-compulsive
disorder.
A common feature of these disorders is exposure to a traumatic or stressful event, explicitly listed as a
diagnostic criterion. Furthermore, there is a variability in the expression of clinical suffering (symptoms
based on anxiety or fear, anhedonic symptoms, dysphoric symptoms, externalized anger and aggression
symptoms, dissociative symptoms).
By stressful events we mean those events that occurred in the life of an individual objectively
identifiable, delimitable and limited in time that modify the person's life situation in a variable and
substantial way, requiring a significant effort to adapt to their situation. . Therefore, a stressful event
involves a certain effort of readjustment, of readjustment. Of course, the difficulty is establishing the
threshold, '' which can be considered normal, which pathological ''?

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By traumatic event, on the other hand, we mean an event that involves a threat to life, a serious threat to
psychophysical integrity, accompanied by feelings of intense fear and a sense of helplessness. So a
traumatic event is something a little more important.
These disorders have been called differently over the years: for example in 1892 there was talk of post-
traumatic neurosis, in 1918 Simmel introduced the 'war neurosis'. With DSM II we start talking about
transient situational disturbances, giving some importance to the situations that could cause these
transient disturbances. Later with the DSM III of 1980 the concept of post traumatic disorder began to be
introduced and in the same manual of the same year the concept of adaptation disorder was introduced.
One is related to everyday stressful situations, the others connected to more traumatic events.
The Vietnam War and the Korean War are said to have greatly influenced the expression of PTSD. And then
a series of successive evolutions up to the ICD10 of 1993 and the DSM IV of 1994 which take up the concept
of post-traumatic stress and post-traumatic disorder, as you can already see in the ICD9 of 78 the concept
of 'acute self-reaction' is introduced. which becomes acute stress disorder 'in the new literature; so we see
that it has had a very, very long history. In the DSM they all go together to make up that great chapter of
trauma and stress disorder.
Biological changes of clinical significance in PTSD:
 Low cortisol levels and urinary hyposecretion of corticosteroids
 Hypersuppression of the response to dexamethasone
 Chronic thyroid hyperfunction with high total T3, free T3, high T3 / T4 ratio
 Orthosympathetic neurovegetative hyperreactivity to stimuli
 High HR
 Peripheral catecholaminergic hyperactivation
 Α-2-adrenergic receptor downregulation
 Altered neurobiology of sleep
 EEG activation parameters
 Provable reduction in hippocampal volume visible through imaging

I. Reactive attachment disorder is an internalizing disorder with depressive symptoms and withdrawn
behavior. It appears for the first time in DSM 5 as in DSM IV-TR it is considered a single disorder
called “reactive attachment disorder of infancy or early childhood” which had two subtypes:
inhibited and uninhibited. These disorders mainly concern childhood neuropsychiatry and the
criteria appear before the age of 5.
The criteria for Reactive Attachment Disorder are:
A. A constant pattern of inhibited, emotionally withdrawn behavior towards adult caregivers,
manifested by the presence of both of the following criteria:
1. The child seldom or minimally seeks comfort when he is experiencing discomfort;
2. The child rarely or minimally responds to comfort when experiencing discomfort.
B. Persistent social and emotional difficulties characterized by at least two of the following criteria:
1. Minimum social and emotional responsiveness to others;
2. Reduced positive emotions;
3. Episodes of unjustified irritability, sadness or fear, which are evident even during non-
dangerous interactions with adult caregivers.
C. The child experienced an extreme pattern of insufficient care as evidenced by at least one of the
following criteria:
1. Social neglect or deprivation in the form of a persistent lack of satisfaction with the basic
emotional needs for comfort, stimulation and affection on the part of adult caregivers;
2. Repeated changes of primary caregivers, which limit the possibility of developing stable
attachments (eg frequent changes of custody);

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3. Breeding in unusual contexts, which severely limit the possibility of developing selective
attachments (for example, institutions with a high number of children per caregiver).
D. The care described in criterion C is assumed to be responsible for the disturbed behavior
described in criterion A (for example the difficulties described in criterion A started as a result of
the lack of adequate care described in criterion C).
E. The criteria for autism spectrum disorders are not met.
F. Difficulties manifest themselves before the age of 5.
G. The child has a developmental age of at least 9 months.

II. The criteria for Disinhibited Social Engagement Disorder are:

A. A behavior pattern in which the child actively approaches and interacts with unknown adults and
has at least two of the following criteria:
1. Reduced or absent reticence in approaching and interacting with unknown adults;
2. Overly familiar verbal or physical behavior (which is not in accordance with the social
boundaries established by the reference culture and appropriate to age);
3. Decreased or absent remote control of the caregiver after he has ventured far, even in
unfamiliar contexts;
4. Willingness to go away with an unknown adult with little or no hesitation.
B. The behaviors described in Criterion A are not limited to impulsivity (as in attention deficit /
hyperactivity disorder), but include uninhibited social behavior.
C. The child experienced an extreme pattern of insufficient care as evidenced by at least one of the
following criteria:
1. Social neglect or deprivation in the form of a persistent lack of satisfaction with the basic
emotional needs for comfort, stimulation and affection on the part of adult caregivers;
2. Repeated primary caregiver changes, which limit the ability to develop stable attachments
(eg, frequent changes of custody);
3. Breeding in unusual contexts, which severely limit the possibility of developing selective
attachments (for example, institutions with a high number of children per caregiver).
D. The care described in criterion C is assumed to be responsible for the disturbed behavior
described in criterion A (for example the difficulties described in criterion A started as a result of
the lack of adequate care described in criterion C).
E. The child has a developmental age of at least 9 months.
John Bowlby and his followers invented a kind of '' strange situation '' in which a child (18 months)
introduced into a room, sees his caregiver away for about 3 minutes and his reaction is recorded, most of
it some children adopt this behavior: they cry and despair because they lose sight of their caregiver, in
front of a stranger, even if in a well-arranged room because it is full of toys and so on. when the
attachment figure returns (approximately 3, 6 minutes later) the child usually finds a way to calm down in
the caregiver himself. There are at least 3 other situations and many others have been described in which
the child behaves incongruously and on the basis of these other attachment situations have been
described to become a criterion of DSM 5.
Both Reactive Attachment Disorder and Uninhibited Social Engagement Disorder have a common etiology
which is social neglect or lack of adequate care in childhood.
III.The criteria for PTSD referring to adults, adolescents and children over 6 years of age (specifying if
there are symptoms of depersonalization or derealization and if there is delayed expression) are:

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7
A. Exposure to actual or threatened death, serious injury, or sexual assault in one (or more) of the
following ways:
1. Direct experience of the traumatic event;
2. Attending directly to a traumatic event that happened to others;
3. Learn about a traumatic event that happened to a family member or close friend. In the
event of an actual death or threatened death of a family member or friend, the event
must have been violent or accidental;
4. Experiencing repeated or extreme exposure to harsh details of the trauma event (eg first
responders collecting human remains, police officers repeatedly exposed to details of
child abuse. This criterion does not apply to exposure. through electronic media,
television, film, or images, unless the exposure is related to the work performed).
B. Presence of one (or more) of the following intrusive symptoms associated with the traumatic
event, which begin after the traumatic event:
1. Recurring, involuntary and intrusive unpleasant memories of the traumatic event (in
children over the age of six a repetitive game may occur in which themes or aspects
concerning the traumatic event are expressed);
2. Recurrent unpleasant dreams in which the content and / or emotions of the dream are
linked to the traumatic event (frightening dreams may be present in children without
recognizable content);
3. Dissociative reactions (e.g. flashbacks) in which the subject feels or acts as if the
traumatic event is recurring, such reactions can occur along a continuum, in which the
extreme expression is the complete loss of awareness of the environment. surrounding
yourself (in children, specific re-actualization of trauma can occur in play);
4. Intense or prolonged psychological distress upon exposure to internal or external triggers
that symbolize or resemble some aspect of the traumatic event;
5. Marked physiological reactions to internal or external triggers that symbolize or resemble
some aspect of the traumatic event.
C. Persistent avoidance of stimuli associated with the traumatic event, initiated after the traumatic
event as evidenced by one or both of the following criteria:
1. Avoidance or attempts to avoid unpleasant memories, thoughts or feelings relating to or
closely associated with the traumatic event;
2. Avoidance or attempts to avoid external factors (people, places, conversations, activities,
objects, situations) that arouse unpleasant memories, thoughts or feelings related to or
closely associated with the traumatic event.
D. Negative changes in thoughts and emotions associated with the traumatic event, initiated or
worsened after the traumatic event as evidenced by two (or more) of the following criteria:
1. Inability to remember some important aspect of the traumatic event (typically due to
dissociative amnesia and not to other factors such as head trauma, alcohol or drugs);
2. Persistent and exaggerated negative beliefs or expectations about oneself, others or the
world (for example "I am bad", "nobody can be trusted", "the world is absolutely
dangerous", "my entire nervous system it is permanently ruined ");
3. Persistent distorted thoughts related to the cause or consequences of the traumatic event
that lead the individual to blame himself or others;
4. Persistent negative emotional state (fear, horror, anger, guilt or shame);
5. Marked reduction of interest or participation in significant activities;

7
changes to criterion A from DSM IV:
• The criterion is more explicit in reference to the events that qualify traumatic experiences
• The subjective emotional reactions to the traumatic event such as intense fear, feelings of helplessness, horror, are no longer part of
criterion A.

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6. Feelings of detachment or estrangement from others;

7. Persistent inability to experience positive emotions (inability to experience happiness,
satisfaction, or feelings of love).
E. Marked changes in arousal and reactivity associated with the traumatic event (s) that began or
worsened after the traumatic event as evidenced by two (or more) of the following:
1. Irritable behavior and outbursts of anger (with little or no provocation) typically expressed
in the form of verbal or physical aggression towards people or objects;
2. Reckless or self-destructive behavior
3. Hypervigilance;
4. Exaggerated alarm responses;
5. Problems with concentration
6. Difficulty with sleeping (for example, difficulty falling or staying asleep or unrefreshing
sleep)
F. The duration of the alteration (criteria B, C, D, and E) is greater than 1 month. If it lasts less than
a month it is referred to as 'Acute Stress Reaction'.
G. The alteration causes clinically significant distress or impairment in social, occupational, or other
important areas of functioning.
H. The alteration is not attributable to the physiological effects of a substance or to another medical
condition.
The clinical manifestation of PTSD is variable.
• In some individuals fearful reliving of emotional or behavioral symptoms may be predominant.
• In others, anhedonic or dysphoric moods and negative thoughts can create greater suffering.
• Still others show a prominence of arousal and reactive-externalizing symptoms.
• While in others, dissociative symptoms predominate.
• Finally, some individuals show combinations of these symptom patterns.
SPECIFICATORS
A. 8With dissociative symptoms: The individual's symptoms meet the criteria for a post-
traumatic stress disorder and, furthermore, in response to the stressful event, the individual
experiences persistent or recurrent symptoms of one of the following two criteria:
• Depersonalization: Persistent or recurrent experiences of feeling detached from,
and as if one were an outside observer of, one's own mental processes or body
(e.g., feeling of being in a dream; feeling of unreality of oneself or one's body or
the slow passage of time)
• Derealization: persistent or recurrent experiences of unreality of the surrounding
environment (for example, the world around the individual is experienced by him as
unreal, dreamlike, distant or distorted)
B. With delayed expression: if the diagnostic criteria are not fully satisfied within 6 months of
the event (although the onset and expression of some symptoms may be immediate).

IV. The criteria for PTSD in children under 6 (specifying whether there are symptoms of
depersonalization or derealization and if there is delayed expression) are:
A. In children under 6 years of age, exposure to actual or threatened death, serious injury, or sexual
assault in one (or more) of the following ways:
1. Direct experience of the traumatic event;

8
to insert this attic the dissociative symptoms must not be attributable to the effphysiological effects of a substance.

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2. Directly witnessing a traumatic event that happened to others, particularly primary

caregivers (witnessing does not include events witnessed through electronic media,
television, film, or images);
3. Learn about a traumatic event that happened to a family member or caregiver.
B. Presence of one (or more) of the following intrusive symptoms associated with the traumatic
event, which begin after the traumatic event:
1. Recurring, involuntary and intrusive unpleasant memories of the traumatic event
(spontaneous and intrusive memories do not necessarily appear as unpleasant and can be
expressed as a reenacting game);
2. Recurrent unpleasant dreams in which the content and / or emotions of the dream are
linked to the traumatic event (it may not be possible to ascertain that the terrifying
content is linked to the traumatic event);
3. Dissociative reactions (e.g. flashbacks) in which the child feels or acts as if the traumatic
event is recurring. (Such reactions can occur along a continuum, where the extreme
expression is the complete loss of awareness of the surrounding environment). Trauma
specific re-actualization can occur in play;
4. Intense or prolonged psychological distress upon exposure to internal or external triggers
that symbolize or resemble some aspect of the traumatic event;
5. Marked physiological reactions in response to factors reminiscent of the traumatic event.
C. One (or more) of the following symptoms, which represent persistent avoidance of the stimuli
associated with the traumatic event or negative changes in thoughts and emotions associated with
the traumatic event, must be present, started or worsened after the traumatic event:

Persistent avoidance of stimuli:
1.Avoidance or attempts to avoid physical activities, places or factors that arouse
memory of the traumatic event;
2.Avoidance or attempts to avoid interpersonal people, conversations or situations
that arouse memories of the traumatic event.

Negative changes in cognition:
3.Substantial increase in the frequency of negative emotional states (fear, guilt,
sadness, shame, confusion);
4.Markedly diminished interest in or participation in significant activities, including
limiting play;
5.Socially withdrawn behavior;
6.Persistent reduction in the expression of positive emotions.
D. Alterations of arousal and reactivity associated with the traumatic event, initiated or worsened
after the traumatic event as evidenced by two (or more) of the following criteria:
1. Irritable behavior and outbursts of anger (with little or no provocation) typically expressed
in the form of verbal or physical aggression towards people or objects (including extreme
temper tantrums);
2. Hypervigilance;
3. Exaggerated alarm responses;
4. Problems with concentration
5. Difficulty with sleeping (for example, difficulty falling or staying asleep or unrefreshing
sleep).
E. The duration of the alteration is more than 1 month.
F. The alteration causes clinically significant distress or impairment in relationships with parents,
siblings, peers, or other caregivers, or in school behavior.
G. The alteration is not attributable to the physiological effects of a substance or to another medical
condition.

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Post-traumatic stress disorder (PTSD) is often associated with:

 developmental regression (such as language loss in young children),
 auditory pseudo-hallucinations (such as having the sensory experience of hearing one's thoughts speak in
one or more different voices),
 paranoid ideation,
 difficulty in regulating emotions
 difficulty in maintaining stability in interpersonal relationships.
The annual prevalence in the USA is 3.5% while in Europe it is 0.5-1%.
Groups at risk they are veterans, police officers, firefighters, emergency medical personnel.
Subthreshold manifestations are more common in old age than in PTSD (Physical decline, deterioration of
cognitive functions and social isolation may exacerbate symptoms). It can occur at any age, from the first
year of life.
Symptoms typically arise in the first 3 months after trauma, although there may be a delay of months or
even years before criteria for a diagnosis are met. Symptoms and their predominance may vary over time.
The duration of symptoms also varies, with full recovery within 3 months occurring in about half of adults,
while some individuals continue to show symptoms for more than 12 months and sometimes for more than
50 years.
The risk factors are divided into pre-traumatic, peri-traumatic and post-traumatic factors.
1. Among the pre-traumatic factors are:
• emotional problems of childhood before age 6
• previous mental disorders (Panic, Depression)
• low socioeconomic status
• low level of education
• exposure to previous trauma (especially during childhood)
• adversity in childhood
• cultural characteristics (fatalistic coping or self-accusation)
• lower intelligence
• racial / ethnic minority status
• history of psychiatric disorders in the family.
2. Among the peri-traumatic factors are:
• severity of the trauma
• perceived threat to life
• personal injury
• interpersonal violence.
3. Among the post-traumatic factors are:
• negative ratings
• inappropriate coping strategies
• development of acute stress disorder
• subsequent exposure to repeated factors that elicit traumatizing memories
• subsequent adverse life events
• losses of a financial or other nature related to the trauma.
There is a lifetime prevalence and a longer duration of the disorder in females than in males (at least in
part due to greater likelihood of exposure to traumatic events such as rape and other forms of
interpersonal violence).
PTSD is associated with suicidal ideation and suicide attempts.
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Differential diagnoses should be made for adjustment disorders, other post-trauma disorders and
conditions, acute stress disorder, anxiety disorders and obsessive-compulsive disorder, major depressive
disorder, personality disorders, dissociative disorders, conversion (functional neurological symptoms
disorder), psychotic disorders and trauma brain damage.
Therapy can be psychotherapeutic or pharmacological. The first-line drugs are SSRIs (Citalopram,
Fluoxetina, Fluvoxamina, Paroxetina, Sertraline). In addition, MAOs (Phenelzine, Moclobemide), tricyclics
(Imipramine, Amitriptyline, Desipramine), anticonvulsants (Carbamazepine, Valproate), antiadrenergics
(Clonidine, Propanolol) and benzodiazepines (Alprazepolam) can be used.

V. The criteria for Acute Stress Disorder are:

A. Exposure to actual or threatened death, serious injury, or sexual assault in one (or more) of the
following ways:
1. Direct experience of the traumatic event;
2. Attending directly to a traumatic event that happened to others;
3. Learn about a traumatic event that happened to a family member or close friend. In the
event of an actual death or threatened death of a family member or friend, the event
must have been violent or accidental;
4. Experiencing repeated or extreme exposure to harsh details of the trauma event (eg first
responders collecting human remains, police officers repeatedly exposed to details of
child abuse. This criterion does not apply to exposure. through electronic media,
television, film, or images, unless the exposure is related to the work performed).
B. Presence of nine (or more) of the following symptoms from each of the five categories relating to
intrusion, negative mood, dissociation, avoidance, and arousal that began or worsened after the
traumatic event:


Intrusion symptoms:
1.Recurring, involuntary and intrusive unpleasant memories of the traumatic event
(in children a repetitive game may occur in which themes or aspects concerning
the traumatic event are expressed);
2.Recurring unpleasant dreams in which the content and / or emotions of the dream
are linked to the traumatic event (frightening dreams may be present in children
without recognizable content);
3.Dissociative reactions (for example, flashbacks) in which the subject feels or acts
as if the traumatic event is recurring, such reactions can occur along a continuum,
in which the extreme expression is the complete loss of awareness of the
surrounding environment. (in children, specific re-actualization of trauma can
occur in play);
4.Intense or prolonged psychological distress or marked physiological reactions in
response to internal or external triggers that symbolize or resemble some aspect
of the traumatic event.

Negative mood:
5.Persistent inability to experience positive emotions (for example, inability to
experience happiness, satisfaction, or feelings of love).

Dissociative symptoms:
6.Altered sense of reality of one's environment or oneself (e.g. seeing oneself from
another perspective, being in a confused state, slowing down of time);
7.Inability to remember some important aspect of the traumatic event (typically
due to dissociative amnesia and not to other factors such as head injury, alcohol
or drugs).

Symptoms of avoidance:

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8.Attempts to avoid unpleasant memories, thoughts or feelings relating to or closely

associated with the traumatic event;
9.Attempts to avoid external factors (people, places, conversations, activities,
objects, situations) that arouse unpleasant memories, thoughts or feelings relating
to or closely associated with the traumatic event.

Symptoms of arousal:
10.Difficulty with sleeping (for example, difficulty falling or staying asleep or
unrefreshing sleep);
11.Irritable behavior and outbursts of anger (with little or no provocation) typically
expressed in the form of verbal or physical aggression towards people or objects;
12.Hypervigilance;
13.Problems with concentration
14.Exaggerated alarm responses.
C. The duration of the alteration (symptoms of criterion B) ranges from 3 days to 1 month after
exposure to the trauma (typically symptoms begin immediately after the trauma, but persistence
is required for at least 3 days and up to 1 month to meet the criteria of the disorder).
D. The alteration causes clinically significant distress or impairment in social, occupational, or other
important areas of functioning.
E. The alteration is not attributable to the physiological effects of a substance or another medical
condition and is not best explained by a brief psychotic disorder.
Acute stress disorder is associated with catastrophic or extremely negative thoughts about the role in the
traumatic event, the response to the traumatic experience, and the possibility of future harm. There is a
catastrophic interpretation of symptoms (flashbacks or emotional numbness cause decreased mental
capacity) and panic attacks may occur during the 1st month, chaotic or impulsive behavior and post-
concussive symptoms (headache, dizziness, sensitivity to light or noise, irritability, difficulty
concentrating) equally common in populations of individuals with and without brain damage.
The prevalence is 20% lower for traumatic events without interpersonal aggression, and 20-50% for
interpersonal traumatic events.
Risk factors are previous mental disorder, high levels of negative affect (neuroticism), greater perceived
severity of the traumatic event, avoidant coping style, history of previous trauma, female sex, high pre-
trauma reactivity.
Differential diagnoses should be made for adaptation disorders, panic disorder, dissociative disorder, post-
traumatic stress disorder, obsessive-compulsive disorder, and traumatic brain damage.
VI. The criteria for Adjustment Disorder are:
A. The development of emotional or behavioral symptoms in response to one or more identifiable
stressful events that occurs within 3 months of the onset of the stressful event.
B. These symptoms or behaviors are clinically significant, as evidenced by one or both of the
following criteria:
1. Marked suffering that is disproportionate to the severity or intensity of the stressful event,
taking into account the external context and cultural factors that can influence the
severity and manifestation of symptoms;
2. Significant impairment in social, occupational, or other important areas of functioning.
C. The stress-related disorder does not meet the criteria for another mental disorder and is not just
an aggravation of a pre-existing mental disorder.
D. Symptoms do not correspond to normal bereavement.
E. Once the stressful event or its consequences are over, the symptoms do not persist for more than
another 6 months.
It must be specified whether the disorder is acute (lasting less than 6 months) or chronic (6 months or
more) and whether the disorder is with depressed mood, anxiety, mixed (depressed mood and anxiety),
behavioral alteration or mixed with alterations of emotionality and conduct.

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Stressful events can be single, multiple, recurring and common.

It is a fairly common disorder (50% of consultation psychiatric interventions) and the risk factors relate to
disadvantaged living conditions.
Differential diagnosis should be made with post-traumatic stress disorder, acute stress disorder,
personality disorders, psychological factors affecting other medical conditions, and normal reactions to
stress.
VII. Disorder related to traumatic or stressful events with other specification -> This category applies to
manifestations in which symptoms characteristic of a disorder related to traumatic and stressful
events, which cause clinically significant distress or impairment of functioning in social, occupational,
or other important areas, predominate but do not satisfy fully the criteria for any of the disorders of
the diagnostic class of disorders related to traumatic and stressful events. The category “Disorder
Related to Traumatic and Stressful Events with Other Specification” is used in situations in which the
clinician chooses to communicate the specific reason why the manifestation does not meet the
criteria for any specific disorder related to traumatic and stressful events.
Examples of manifestations that can be specified using the term "with other specification"
include the following:
I. Adaptation-like disorders with delayed onset of symptoms occurring more
than 3 months after the stressful event.
II. Adaptation-like disorders with prolonged duration to more than 6 months
without the prolonged duration of the stressful event.
III. Ataque de nervios
IV. Other cultural syndromes +
V. Complicated persistent bereavement disorder: This disorder is characterized
by severe and persistent grief and bereavement reactions.
A. The individual has experienced the death of someone with whom he
had a close relationship.
B. Since death, at least one of the following symptoms has been present
for more days than it has been and at a clinically significant severity
level, and has persisted in adults for at least 12 months and in
children for at least 6 months after bereavement:
• A persistent longing / longing for the deceased person. In young
children, desire can be expressed in play and behavior, including
through behaviors that reflect being separated from, and even
reunited with, a caregiver or other attachment figure.
• Intense sadness and emotional pain following death.
• Concern for the deceased.
• Concern about the circumstances of death. In children, this
concern for the deceased can be expressed through play content
and behavior and can extend to concern about the possible death
of other close people.
C. Since death, at least six of the following symptoms have been present
for more days than they have not been present and at a clinically
significant severity level, and have persisted in adults for at least 12
months and in children for some minus 6 months after bereavement:
• Marked difficulty in accepting death. In children this
difficulty depends on the ability to understand the
meaning and definitive of death.
• Feeling disbelief or emotional numbness about the loss.

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• Difficulty in abandoning oneself to positive memories

concerning the deceased.
• Bitterness or anger in connection with the loss.
• Negative self-assessment in relation to the deceased or
death
• Excessive avoidance of memories of the loss.
• Desire to die to be close to the deceased.
• From the moment of death, difficulty in regaining trust in
others
• From the moment of death, feeling of being alone or
detached from others.
• Feeling that life is empty or meaningless without the
deceased, or the thought of "not making it" without the
deceased.
• Confusion about one's role in life, or diminished sense of
identity (eg, feeling that a part of oneself died along with
the deceased).
• From the moment of loss, difficulty or reluctance to
pursue one's interests or make plans for the future (e.g.,
friendship, activity).
D. The disorder causes clinically significant distress or impairment in
social, occupational, or other important areas of functioning.
E. The bereavement response is disproportionate or inconsistent with
religious or age-appropriate cultural norms.
Specify if:
With traumatic mourning—> bereavement due to murder or suicide with
persistent burdensome thoughts about the traumatic nature of death (often in
response to memories of the loss), including the last moments of the
deceased, the degree of suffering of the injuries, or the intentional or
intentional nature of the death.
Hallucinations or somatic complaints may occur.
It occurs mainly in females at any age. It takes at least a year to make a
diagnosis.

EATING OR EATING BEHAVIOR DISORDERS

Eating Disorders are anorexia and bulimia nervosa.
Anorexia Nervosa it is a serious disturbance in eating behavior of a psychogenic nature secondary to an
altered perception of one's own body image that the patient tries to correct or modify through weight loss
with a considerable reduction in body weight.
The prevalence in the general population is 1%, generally affecting adolescent female subjects in the 14-
18 years age group with M / F ratio = 1/9.
Clinically, anorexia generally has a subtle and insidious onset, rarely acute after a stressful event, such as
bereavement or being away from home, and is characterized by 4 pathognomonic symptoms:
1. Restriction of energy intake relative to need, which induces a significant low weight related to age, sex,
developmental evolution and physical health. Significant low weight is understood to be less than the
normal minimum or, for children and adolescents, less than the expected minimum.
2. Intense fear of gaining weight or gaining weight, or persistent behavior that interferes with weight gain,
despite a significantly low weight.

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3. Anomaly in the way the weight and shape of one's body is perceived; inappropriate influence of body
weight and body shape on self-esteem, or persistent loss of ability to assess the severity of current
weight loss.
It can be classified into:
 Mild: BMI≥ 17
 Moderate: BMI 16-16.99
 Severe: BMI 15-15.99
 Extreme: BMI <15
Amenorrhea is also included in the DMS-4, understood as the lack of at least three consecutive menstrual
cycles, and criterion 2 has been expanded and no longer means the mere fear of gaining weight.
Regarding the altered body image, the patient has a delusional perception of her own body with the
conviction of being fat, not criticizable, instead she does not present an altered judgment for the body
image of other people even if they are fatter .
As for weight loss, the patient tries to modify or change her body image by reducing her weight, until she
reaches a body weight lower than 85% of the normal one.
In DSM-4, according to the type of eating behavior assumed by the patient to achieve this goal, a
distinction is made between a restricted subtype and a subtype with binge eating and elimination
behaviors:
A. In the restricted subtype, food restriction can be global or partial, refusing to eat some specific foods,
generally meat and carbohydrates, following a vegetarian diet, sometimes arguing that the basis of this
diet is a religious purpose or ecologist but only to disguise his need to lose weight.
B. The subtype with binges and elimination behaviors is characterized by bulimic and obsessive-
compulsive behaviors and symptoms, i.e. the patient tries to comply with strict low-calorie diets but
fails and gives in to the urge to eat, consuming in a short time a large quantity of food with binge,
followed by the ritual of eliminating food through self-induced vomiting, abuse of laxatives or
diuretics, to promote the consumption of calories and reduce body weight.
There is also the intense fear of gaining weight, that is, a phobic attitude when the scale signals an
increase in body weight or for fear that this will happen, despite the patient being underweight.
There is also primary amenorrhea for at least 3 months, psychogenic from central hypothalamic
dysfunction which can be aggravated by abnormal eating behavior, weight reduction and possible increase
in physical activity with stress.
Among the associated manifestations and complications of anorexia nervosa are hyperactivity, depression
and social withdrawal. In the initial stages of the disorder the patient appears active and full of energy,
she sleeps little without feeling tired, dedicating herself to intense sporting activity to further reduce
body weight. Initially the mood is good, the patient feels good, she is sure of herself and of her choices,
she does not intend to cure herself as she considers herself absolutely in good health. In the advanced
stages the patient is no longer able to cope with the previous rhythms, so she is no longer hyperactive,
with a real picture of major depression or dysthymia. The patient progressively tends to isolate herself, to
avoid social, interpersonal, affective-sexual relationships to the point of assuming infantile and
inadequate behaviors.
Dietary restriction and elimination behaviors can cause hyponutrition, alterations in the hydroelectrolytic
and acid-base balance with deficiencies in proteins, carbohydrates, lipids, vitamins, mineral salts,
dehydration, arterial hypotension, bradycardia, dry skin brittle nails, hair loss, peripheral edema,
hypothermia, leukopenia, anemia, thrombocytopenia.
The course of anorexia nervosa is variable: sometimes the patient presents a single episode which resolves
completely within a few months without relapses, or alternating between clinical remission and relapse
occurs in 30% of patients. in cases there is chronicization with anorexia of mild-medium severity, in 10% of
cases the patient goes to death.
The therapy of anorexia requires the collaboration between psychotherapist, internist, dietician,
endocrinologist and gynecologist, in the most serious cases the patient must be hospitalized to restore the
nutritional state and the hydroelectrolytic balance. Psychotherapy represents the main treatment option
for the anorexic patient, even if the patient often refuses to seek treatment:

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gnitive-behavioral individual or family we try to eliminate irrational thoughts, restore the relationship
with food, eliminate the anomalous behaviors present in the family that underlie the disorder.
Psychopharmacological therapy is based on the administration of high dose Fluoxetine (60-80 mg / day)
useful for the control of binge eating in forms of anorexia with bulimic symptoms.

Bulimia Nervosa is a serious eating disorder of a psychogenic nature, more frequent in female subjects
with an M / F ratio = 1/9, usually begins around 18 years of age but often arrives at the doctor's
observation late or in many cases they are undiagnosed or confused for forms of obesity.
In DMS-5 we talk about bulimia when there are:
A. Recurring binges-> a binge is characterized by both of the following.
1. Eating, over a limited period of time (for example, over two hours), an amount of food that is
indisputably greater than what most people would eat in the same period of time under similar
circumstances.
2. Sense of lack of control over the act of eating during the episode (for example, feeling like you
can't stop eating or can't control what or how much you are eating)
B. Recurrent compensatory behaviors aimed at preventing weight gain, such as self-induced vomiting,
abuse-misuse of laxatives, diuretics, or other drugs; fasting or excessive exercise.
C. Compulsive binges and improper use of means of compensation occur on average at least once a week
for three months.
D. Self-assessment is inappropriately influenced by body shape and weight.
E. The disorder is not found only in the course of episodes of anorexia nervosa-
Severity is based on the number of inappropriate compensatory episodes per week:
 Mild: 1-3
 Moderate: 4-7
 Severe: 8-13
 Extreme: 14 or more.
Compared to DSM-IV, in the fifth for criterion C there is a reduction in the average minimum frequency
required of binges and inappropriate compensatory behaviors from two to once a week for three months,
and the two purgative and non-purgative types disappear. The non-purgative type was defined as the
person who uses fasting or excessive exercise as a reward, but is not in the habit of inducing vomiting or
using laxatives or diuretics.
Bulimia is similar to obsessive-compulsive disorder because the patient does a continuous mental work to
try to control and neutralize the urge to eat, but without success, for which there is a binge with a feeling
of discomfort, embarrassment and guilt, to which follows the conduct of elimination as an attempt to
compensate.
Vomiting can cause various complications, ie hypokalaemia, increased plasma amylases, dehydration,
colonic melanosis, dental erosions, salivary gland swelling, esophageal rupture.
Bulimia is often associated with other behavioral disorders or impulse control disorders, particularly
kleptomania, abuse of coffee, drugs, alcohol and other psychotropic substances, or is complicated by
depression, possibly due to the demoralization of the patient who cannot control the eating disorder.
The therapy of bulimia nervosa is mainly based on the administration of high doses of Fluoxetine (60-80
mg / day), cognitive-behavioral and psychodynamic psychotherapy. It is always necessary to stay in food
re-education centers.

We speak of Binge-eating Disorder when there are the following parameters:

A. Recurring binge eating episodes (see above)
B. Episodes of compulsive binging are associated with at least three of the following characters

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• Eating much faster than normal

• Eating until you have a painful feeling of overflow
• Eating large amounts of food while not feeling hungry
• Eating alone because of the embarrassment of the quantities of food ingested
• Feeling self-loathing, depression, or intense guilt after overeating.
C. Compulsive binges cause suffering and discomfort
D. Compulsive binges occur on average at least once a week for at least six months
E. Inappropriate compensatory behaviors are not used and the disorder is not only found in the course of
anorexia or bulimia nervosa.
As with bulimia, the minimum frequency of bingeing required for diagnosis has changed from at least
twice a week for six months to once a week for the past six months compared to DSM-IV.
It is often associated with alexitemia, the inability to communicate one's emotions
Psychotherapy and diet therapy for weight control give good results.

DSM-5 also refers to avoidant / restrictive food disorder. It is characterized by:

A. An abnormality in food and nutrition (e.g. lack of interest in food or food; avoidance based on the
sensory characteristics of food) that manifests itself through a persistent inability to take an adequate
nutritional and / or associated energy intake with one or more of the following
• Significant weight loss or inability in children to achieve growth-related weight
• Significant nutritional deficiency
• Dependence on internal nutrition or oral nutritional supplements
• Marked interference with psychosocial functioning.
B. The disorder is not related to a lack of food or associated with cultural practices
C. The disorder does not occur exclusively in the course of anorexia or bulimia nervosa and there is no
evidence of abnormality in the way in which the weight and shape of one's body is perceived
D. The abnormality is no longer attributable to a medical condition or other mental disorder. If the eating
disorder occurs in the course of another disorder, its importance outweighs basic and requires cynical
attention.
Infancy and early childhood nutrition disorder has been renamed and the criteria have been significantly
expanded because it was rarely used in DSM-IV and little information is available on children with this
disorder. In addition, many individuals significantly limit their food intake by experiencing physiological
and psychosocial problems without meeting the criteria for any disorder. Thus avoidant / restrictive
disorder was born to be a category capable of capturing this range of presentations.
Among these is Reverse Anorexia, that is the eminently masculine self-perception of frailty, characterized
by altered eating behavior, abuse of supplements, high-protein diets and compulsive physical exercise;
Orthorexia, that is the obsession with healthy food, focusing not on quantity but on quality.

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Other typical ailments are:

1. Atypical anorexia nervosa: All criteria are met, except that despite significant weight loss, weight
remains within or above the normal range
2. Bulimia nervosa (low frequency or limited duration)
3. Binge-eating (low frequency or limited duration)
4. Purgative Disorder: recurrent purgative behavior to change weight and shape of the body in the
absence of binge-eating.
5. Night Eating Syndrome: recurrent episodes of nocturnal feeding that occur after waking up or with
excessive consumption of food after the evening meal. there is awareness of having eaten. Night eating
is not justified by external influences such as changes in the sleep / wake cycle or by specific social
norms.
6. Pica:
• Persistent ingestion of non-food substances for a period of at least one month
• The ingestion of non-food substances is inappropriate with respect to the level of development
• Ingestion behavior is not part of a culturally sanctioned practice
• If the ingestion behavior occurs exclusively during the course of another mental disorder or
medical condition, it is sufficiently severe to warrant clinical attention on its own.
7. Rumination Disorder:
• Repeated regurgitation of food for a period of at least one month
• The behavior is not due to a gastrointestinal condition associated with another general
medical condition
• The behavior does not manifest itself exclusively during the course of anorexia and bulimia
nervosa
• If symptoms occur exclusively during the course of mental retardation or pervasive
developmental disorder, they are severe enough to warrant clinical attention.

In general, we can say that the risk of developing food intake disorders in first degree relatives has
increased by 10 times, and that studies carried out on twins have shown that this is due to genetic factors.
The risk is increased if there are premature babies, particularly if the baby was small for the gestational
age.
It also increases among those who had a lot of appetite as children, were suckers of shit and were fooled
because they were suckers. Childhood adversities such as psychological or sexual abuse, obsessive-
compulsive traits, such as perfectionism are also important.
Functional brain imaging studies of females with AN particularly when viewing rewarding stimuli, largely
report aberrant, often reduced activation in 'bottom-up' mesolimbic regions associated with somatic
states (eg appetite) such as in the striatum, hippocampus, amygdala, hypothalamus and cerebellum . This
is often in conjunction with increased activation in 'topdown' prefrontal cortical (PFC) regions, lin- ked to
cognitive evaluation, attention and executive functioning (eg working memory, goal-orientation, self-
reference, evaluation of salience) such as the dorsolateral prefrontal cortex (DLPFC, strongly implicated
in both appetite suppression and working memory function), medial prefrontal cortex (mPFC), orbito-
frontal cortex (OFC), and anterior cingulate cortex (ACC).

Thus, the excessive ruminations about weight, shape and eating in those who pathologically restrain their
appetite is reminiscent of classic, yet excessive, working memory function (modulated by genetic poly-
morphisms in COMT and BDNF).

The ability to restrain appetite in those with anorexia might be associated with excessive top-down acti-
vation (mainly DLPFC, wm) to varying degrees, combined with varying levels of desire to restrain an over
or underactive appetitive system. It is currently unclear whether increased DLPFC working memory-
related activation reflects a deficiency in working memory and a need to work harder.

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Conversely, in those who exhibit binge eating behavior (eg BN, BED), previous research summarises a
neural pattern to rewarding stimuli that is somewhat reversed, with a reduced or sporadic response in PFC
regions, combined with hyperactivation in mesolimbic areas.

A commonality between all ED subtypes is seemingly dysregulated neural activation in response to food
stimuli in the parietal cortex, and the insular cortex in the temporal lobe, regions associated with somato-
sensory perception and internoceptive awareness

It is proposed that an excessive activation at one or other extremes (eg restraint versus binge eating sy-
stems) in those with ED causes an imbalanced convergence on somatosensory brain regions, associated
with dysfunctional processing of the body state (linked to body image distortions) .

Emotional experiences that derive from somatosensory states can be positively or negatively arousing (eg
pleasant feelings during appetite satisfaction versus unpleasant anxiety and anger) and are linked to
areas of the 'temporoparietal junction' that are involved in creating a sense of self-control over one's ac-
tions. It has long been established that people with ED have problems identifying and expressing their
emotions, a core symptom known as alexithymia,

PERSONALITY DISORDERS
— Personality indicates a structured way of thinking, feelings and behaviors that characterizes the type of
adaptation and lifestyle of a person. It arises from a functional integration between temperament and
character. It constitutes the integrated organization of all the cognitive, affective, volitional and physical
functions of the individual.
— Personality traits represent sufficiently constant ways of perceiving, relating and thinking towards the
environment and oneself, which manifest themselves in a broad spectrum of social and personal contexts.
Only when such traits are rigid and non-adaptive and cause significant impairment in social and
occupational functioning, or subjective suffering, do they constitute personality disorders.
— The temperament is the biological or heredoconstitutional part of the personality present from birth
before the acquisition of the experiences of daily life, which expresses the fundamental and characteristic
affective disposition of each person, with a distinction between:
 depressive or dysthymic temperament, typical of the basically sad subject who tends to isolate himself,
to withdraw into himself, who has little confidence in himself, is dissatisfied and pessimistic,
 hyperthymic temperament, typical of the enterprising subject, very active, tireless, extroverted and
tending to sociability,
 cyclothymic temperament, in this case the individual's underlying affective tone fluctuates from a
nuanced depressive condition to a hyperthymic one, regardless of external events,
 irritable or dysphoric temperament, irascible subject, reacts with anger or aggression to any difficulty.
It refers to those aspects of the psychological organization that are most influenced by biological and
constitutional factors present from birth, but influenced by early and repeated psychosocial experiences:
level of Arousal (emotionality), person's reactivity to stimuli, psychobiological characteristics basic
emotional processes (pleasure and pain, regulation systems, anger and aggression, anxiety and fear,
sadness and psychic pain, sexuality, higher cortical functions and self-awareness)
— Character develops progressively on the basis of the experiences that the subject lives, learns and
acquires or internalizes. It is the most stable part of the personality, it reaches its complete development
in adulthood but it is not entirely unchangeable as it is influenced by new positive or negative experiences
that occur in the life of the individual. It constitutes the set of relational modes of an individual arranged
according to a perspective that gives each individual his or her originality. The psychoanalytic school has
understood the notion of character as a formation of compromise, that is, a peculiar solution of
psychological conflict.

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Personality Disorders are pathological personalities characterized by 3 levels of deviance:

 statistical deviance, in which the personality of the individual is abnormal with emotional reactions,
feelings, behaviors, ways of perceiving oneself, others and events that differ statistically from those
typical observable in the general population, associated with deficits in interpersonal functioning and
impulse control;
 functional deviance, in which the individual is unable to have an adequate working, relational and
social functioning or in which he can fully express his own intellectual potential;
 clinical deviance, when the statistical and functional deviance of the personality causes suffering or
discomfort to the individual or to others.
EPIDEMIOLOGY
They have a prevalence between 5 and 15%, manifesting themselves especially in adulthood and in a
socially maladjusted environment.
Imbalances in adolescents are generally transient and are characterized by a polymorphism that makes
them resemble various morbid pictures:
 extravagance, uncertainty, inconsistency, discontent and recrimination towards authority, uncritical
gregarism, mimesis in derived models and cultural stereotypes, delay in affective development and
scotomization of sexual activity, difficulty in building deep and authentic relationships, asociality
can be considered a mandatory step in development
They can be related to mechanisms put in place to overcome the adolescent identity crisis:
 control of libidinal drives and avoidance of connected anxieties better
structuring of the feeling of self
identification in new models
initiatives that allow a positive experience of oneself
pushed towards new relationships
autonomous psychology
the maturation delay in some of these stages or their incomplete elaboration leads to a delay in the
emancipatory processes that can evolve towards stable alterations of the personality.
We also remember that stable alterations of the personological structure are found in various forms of
mental illness even before it has manifested itself and represent a negative prognostic factor. They can
also be a symptom and consequence of another pathology.
ETHIOPATHOGENESIS
 cultural factors: characteristics of parent-child interaction at various levels of response
 maturational factors: some temperamental factors identified in childhood can be associated with
disorders in adulthood: eg. children with fearful temperament may develop avoidant personality
disorder, mild neurological signs in children are associated with borderline or antisocial personality
disorder
 biological factors: increased sex hormones, low platelet MAO activity, high endorphin levels,
borderline / antisocial EEG slowdowns

DSM V maintains in section II the same categorical approach to personality disorders as DSM IV while also
maintaining the subdivision by clusters A, B, C. However, it provides a new diagnostic approach model in
section III that tries to fill the gaps and uncertainties emerged from the use, for diagnostic purposes, of
the categories.
A. Cluster A includes paranoid, schizoid, and schizotypal personality disorder, that is, extravagant and
eccentric personalities.
• In paranoid disorder (30%) the patient sees the world against himself, presents negative
feelings and thoughts about other people that are perceived as aggressive, not friendly with
consequent attitudes of distrust, suspiciousness, hostility. This disorder increases the risk of
schizophrenia and delusional disorder.

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• With schizoid disorder we refer to introverted subjects, prone to withdrawal, solitary, little
interested or intolerant to emotional reactions and sexual relations.
• Schizotypic disorder is characterized by the coexistence of paranoid and schizoid personality
disorder, at high risk of developing schizophrenic psychosis.
B. Cluster B includes antisocial, borderline, histrionic and narcissistic personality disorder.
• With antisocial disorder we refer to criminals by tendency, aggressive, violent who do not
feel any sense of guilt for their actions.
• In borderline disorder, subjects are dominated by exaggerated and opposite feelings of
idealization or devaluation, excessive emotional reactions, disproportionate, difficulty in
controlling impulsivity and aggression with mood instability, behavior and interpersonal
relationships, high risk of suicide, depression, bulimia, substance abuse or addiction.
• In histrionic disorder, subjects are egocentric, showy, emotionally unstable with seductive
attitudes, who see life as a stage, lack naturalness because their behavior varies according to
the people in front of them, behaving as actors.
• In narcissistic disorder, subjects feel superior to others, they see themselves as very
beautiful, clever, intelligent, they organize their life in search of excessive admiration and
esteem to confirm their way of being, for which people exist only for their own gratification.
C. Cluster C includes avoidant, dependent, and obsessive-compulsive personality disorder.
• Avoidant disorder refers to very shy people who avoid interpersonal contact for fear of
frustration, due to their feelings of inadequacy and self-deprecation. It is often associated with
depressive or anxiety disorders, particularly panic disorder and social phobia.
• In dependent disorder, subjects are insecure and have low self-confidence and establish
pathological relationships of dependence on others, entrusting their responsibilities to others with
excessive suffering in the event of separation or loss. It predisposes to depressive and anxiety
disorders.
• In obsessive-compulsive disorder, subjects try to control events in an exaggerated way through
an exaggerated superstitiousness and the relationship with other people through rigidity,
inflexibility, avarice and perfectionism, for which they are not obsessive-compulsive symptoms,
but of subjects predisposed to mood disorders and anxiety disorders.
In section II there are some first general criteria.
The diagnosis of personality disorder requires an assessment of the individual's long-term pattern of
functioning, and the particular personality characteristics must be evident from early adulthood.
The personality traits that define these disorders must also be distinguished from characteristics that
emerge in response to specific situational stressful events or more transient mental states.
The assessment can also be complicated by the fact that the defining characteristics of a personality
disorder may not be considered problematic by the individual.
A. A habitual pattern of inner experience and behavior that deviates markedly from the expectations of
the individual's culture. This pattern manifests itself in two (or more) of the following areas
• Cognitiveness (ie ways of perceiving and interpreting oneself, others and events);
• Affectivity (i.e., the variety, intensity, lability, and adequacy of the emotional response);
• Interpersonal functioning;
• Pulse control
B. The habitual pattern is inflexible and pervasive in a variety of personal and social situations
C. The habitual pattern results in clinically significant distress and impairment of social, occupational,
and other important areas of functioning
D. The model is stable and long-lasting and onset can be traced back to at least adolescence or early
adulthood
E. The habitual pattern is no longer justified as a manifestation or consequence of another mental
disorder

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F. The habitual pattern is not related to the direct physiological effects of a substance or a general
medical condition.
ALTERNATIVE MODEL
However, an “Alternative DSM-5 Model for Personality Disorders” is included in section III of the DSM,
Proposals for New Models and Assessment Tools. It was in fact the classification system for PD that the
American Psychiatric Association intended to adopt tout court. But such were the criticisms and pressures
of the scientific community that at the last moment it was kept only as a hypothesis that needs further
study.
In this model, the diagnosis of a Personality Disorder is formulated essentially taking into consideration
these criteria:
Criterion A - Significant impairments of self (identity or self-directionality) and interpersonal
functioning (empathy or intimacy).
Criterion B - One or more domains of the pathological personality trait or facets / aspects of the
stretch.
Criterion C and D - Impairment in personality functioning and expression of the trait
personality of the individual are relatively stable over time and constant between situations.
Criterion E and F Impaired personality functioning and expression of the individual's personality
trait are not due to the direct physiological effects of a substance (for example, drug abuse, use of any
particular drug) or a medical condition general (for example, severe head trauma, particular effects of
metabolic pathologies, etc.).
Criterion G Impairment in personality functioning and the expression of the individual's personality
trait are not better understood as normative for the individual developmental stage or socio-cultural
environment.
CRITERION A
The alteration in self and interpersonal functioning represent the psychopathological core of personality
disorders and, in this alternative diagnostic model, they are considered on a continuum between normality
and pathology, depending on the level of adaptation and pervasiveness of the picture.
Specifically, the functioning of the Self includes two elements:
1. Identity, understood as the experience of a single self, with clear limits with respect to the external
world, capable of regulating one's own emotional experiences, stable in self-esteem and capable of
self-evaluation;
2. Self-directionality, understood as the ability to consistently pursue significant existential objectives
both in the short and long term, use of constructive and pro-social internal standards of behavior, self-
reflexive ability.
Interpersonal functioning it includes instead:
1. Empathy which refers to the ability to understand and evaluate the experience and motivations of
others, tolerate different perspectives, understand the effects of one's own behavior;
2. Intimacy, by which we mean the ability to maintain a deep and lasting relationship with others, the
desire and the ability to maintain closeness and a behavior based on mutual respect.
The scale of the level of functioning of the personality identifies, on the basis of these elements, five
levels of impairment of functioning, ranging from level 0, indicative of adaptive functioning, to level 4,
indicative of markedly altered functioning.
The alteration in personality functioning is considered predictive of the presence of a personality disorder:
the more severe the impairment in functioning, the more likely it will be the coexistence of more
personality disorders or a more severe personality disorder .
A moderate level of impairment (level 2) is required to make the diagnosis of sonality.
CRITERION B
Once the presence of a personality disorder has been established on the basis of impaired functioning
personal and interpersonal, on the basis of the elements previously considered (identity, self- nality,
intimacy, empathy), the definition of the type of disorder is based on what is established by the criterion
B, which defines pathological personality traits.

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These are essentially organized around five domains characterized on the basis of opposite polarities but
which create a continuum between them:
 Negative affect vs Emotional stability -> frequent and intense unpleasant emotional experiences
associated with behavioral correlates
 Detachment vs Extroversion -> avoidance of social situations
 Antagonism vs Availability-> assumption of hostile attitudes and behaviors responsible for symmetry of
interpersonal conflicts
 Disinhibition vs Conscientiousness -> needs immediate satisfaction of a need regardless of experience or
consequences
 Psychoticism vs Clarity -> rigid, bizarre, eccentric behavior, cognitive distortions of both processes and
contents
Within these five trait domains, 25 sub-dimensions (facets) can in turn be identified: from the
combination of the various dimensional aspects it is possible to formulate the diagnosis of a specific
personality disorder.
Each personality disorder is defined in this sense by the impairment of the functioning of the personality
(criterion A), which manifests itself with specific characteristics relating to the four main areas of
functioning and which represents the psychopathological core of the disorder, and acquires characteristics
depending on the presence or absence of some specific pathological traits (criterion B), as reported
below:

Typical characteristics of antisocial personality disorder they are an inability to comply with legal
and ethical behavior, a self-centered, insensitive lack of concern for others, accompanied by
falsehood, irresponsibility, manipulation and / or a tendency to take risks;

Typical characteristics of avoidant personality disorder they are the avoidance of social situations
and the inhibition in interpersonal relationships linked to feelings of ineptitude and inadequacy,
anxious concern for the possibility of being negatively evaluated and rejected, fear of appearing
ridiculous or feeling embarrassed;

Typical characteristics of borderline personality disorder they are instability in the image of the
self, personal goals, interpersonal and affective relationships, accompanied by impulsiveness, a
tendency to take risks and / or hostility;

Typical Features of Narcissistic Personality Disorder they are unstable and fragile self-esteem,
with attempts to regulate it by seeking attention and approval, or a manifestation or hidden
grandiosity;

Typical characteristics of obsessive-compulsive personality disorder they are the difficulty in
establishing and maintaining close relationships, associated with rigid perfectionism, lack of
flexibility and reduced capacity for emotional expression;

Typical characteristics of schizotypal personality disorder à are impairments in the ability to
establish social and affective relationships, eccentricities in cognition, perception and behavior,
which are associated with a distorted self-image and inconsistent personal goals, and are
accompanied by suspiciousness and reduced ability of emotional expression.
In section III, no diagnostic criteria are proposed for paranoid, schizoid, dependent and histrionic disorder.
These disorders as well as all those otherwise classified as "otherwise specified" or "unspecified" are part
of the DP-TS category (trait-specific personality disorders). This last category allows the clinician to make
a diagnosis without necessarily having to refer to a specific category and at the same time maintaining
diagnostic accuracy.
In this alternative model, with the distinction between criterion A and criterion B, the distinction between
two symptomatological levels is somehow proposed, albeit in a still incomplete way: the first would
identify the cardinal symptoms, which represent the psychopathological core of the disorder itself; the
second the characterizing elements.
Within each criterion, however, the choice between a list of interchangeable symptoms and considered to
be equal is maintained, and the diagnosis is made based on the presence of a certain minimum number of
symptoms, without any of them having a specific weight. compared to the other.

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DD
 If personality changes emerge and persist after the individual has been exposed to extreme stress, a
diagnosis of PTSD should be considered.
 If a person has a substance-related disorder, it is important not to make a diagnosis of personality
disorder based solely on behaviors that are consequences of drug intoxication.
 If lasting personality changes arise as a result of the physiological effects of a general medical condition,
a diagnosis of personality change due to a general medical condition should be considered.
 Personality disorders must be distinguished from personality traits that do not reach the threshold for a
personality disorder. Personality traits are diagnosed as a personality disorder only when they are
inflexible and non-adaptive, persistent, and cause significant social impairment or subjective suffering
THERAPY
Medical therapy allows you to control some symptoms. Psychodynamic, cognitive-behavioral and
relational psychotherapy is useful for modulating or modifying the character of the individual.

DISORDER PARANOID
Paranoid Personality Disorder is the result of a collection of behaviors, tendencies or personality
characteristics that are predominantly found in individuals who are then classified as suffering from
Paranoid Disorder.
Diagnostic criteria:
A. There is talk of "distrust and suspicion" towards others and four or more of the following characteristics:
• unrealistic suspicions of being exploited or harmed
• unjustified doubts about the loyalty of friends
• fear of confiding in others
• misunderstanding of the words of others, such as simple reproaches or other, towards more
threatening meanings
• prevalence of resentment towards others
• unjustified feeling of being attacked or harmed, and a tendency to react
• unjustified fear of being betrayed by a spouse
B. It must not occur during episodes of schizophrenia, bipolar disorder or depressive disorder with
psychotic manifestations, or other psychotic disorders or due to another medical condition
Description:
 rigid personality structure with inability to compromise, tendency to distrust others, rumination
 appearance of ideas in the subject that illuminate him as revelations, such as jealousies, desires for
revenge, hypochondria, suspiciousness
 continuous elaboration of these ideas and closure to the external world continuously misunderstood
 systematization of these ideas in a logical and coherent way, extended to different social areas.
 From state 3 onwards the patient has only personality paranoid, otherwise he is suffering from
personality disorder of the paranoid type (?)
it is more common among family members with schizophrenia
Course:
Chronic, the onset can be traced in childhood with lonely children, with social anxiety, lack of
relationship, behavior and particular ideation, often victims of bullying.
Risk factors:

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 genetic: schizophrenia, delusional disorder

 cultural: minority groups
Comorbidity:
Schizotypic, avoidant, schizoid, narcissistic, borderline, schizophrenia, depression, delusional disorder
Differential diagnosis:
 suspiciousness-> in the schizotypic there are cognitive-perceptual distortions, in the borderline it is not
the predominant aspect
 distrust-> the avoidant is afraid
 impulsiveness-> the antisocial for material usefulness, in the borderline for abandonment
 if this disorder is present in an individual who develops an episode depressive persecutory
delusions may be possible
 it is possible that paranoid disorder is more associated with delusional disorders than with schizophrenia

SCHIZOID DISORDER
Diagnostic criteria:
A. A pervasive pattern of detachment from social relationships and a narrow range of emotional
expressions or modalities in interpersonal situations. This characteristic appears in early adulthood, and
manifests itself in different ways and contexts (sometimes even only in some areas of the patient's life)
where at least four of the following symptoms appear in a prolonged and stable way:
1. The person does not feel desire or pleasure in having close relationships with other people,
including family.
2. It almost always prefers solitary activities or activities that involve completely superficial
relationships.
3. He has little or no interest in real sexual relationships and experiences.
4. He takes no real pleasure in any or almost no activity.
5. Lacks close friendships or confidants other than first degree relatives.
6. Appears emotionally indifferent to criticism or praise.
7. Demonstrates emotional "coldness", detachment or emotional flattening.
B. When these symptoms are not due: to neurological causes; they are not associated with schizophrenia,
nor with a psychotic mood disorder (see also Mood Disorders); they must concern an adult patient having
to exclude a developmental age disorder. In addition, the diagnosis of autism and Asperger's syndrome
must be ruled out. Less severe forms of autism can easily be confused with schizoid disorder in the
absence of information on the patient's medical history.
Description:
In the studies of Bleuer, Hoch and Meyer it emerged that this symptomatology can be noticed both before
the onset of schizophrenia and in the phases of remission or in some family members of patients suffering
from this syndrome.
Course:
Chronic: the onset can be traced in childhood with lonely children, with social anxiety, lack of relationship,
behavior and particular ideation, often victims of bullying
Risk factors:
 genetic: schizophrenia, schizotypic
 cultural: rural communities after relocation
Comorbidity: Schizotypic, avoidant, paranoid disorder, schizophrenia, depression
Differential diagnosis:
 posting-> in the schizotypic there are cognitive-perceptual distortions, in autism a worse functioning

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SCHIZOTYPIC DISORDER
Diagnostic criteria:
A - A pervasive pattern of social and interpersonal communication deficits, which implies a state of
discomfort of the subject in close interpersonal relationships, and a reduced capacity in them. The
subject's difficulty also concerns cognitive (or perceptual) distortions and eccentricity of behaviors. This
picture begins to present itself in early adulthood (otherwise it is another pathology). It occurs in multiple
contexts and is characterized by at least five of the following symptoms:
1. ideas of reference: belief that coincidences and random external events have a particular and
unusual meaning specific to themselves (recurring ideas that are not fixed ideas)
2. unusual beliefs or style of "magical thinking" (possible comorbidity with obsessive-compulsive
disorder), such as to influence behavior and not relevant to the norms and beliefs of the
cultural substrate (eg superstition, clairvoyance, telepathy, sixth sense, in adolescents- scenti
bizarre fantasies).
3. unusual perceptual experiences;
4. expressive style with obscure verbal content (vague, circumstantial or "tangential",
metaphorical, too elaborate or stereotyped)
5. suspiciousness or paranoid ideation
6. reduced affectivity, rigid and restrained or inappropriate to the contexts
7. strange, eccentric behavior or appearance
8. absence of close friends or confidants other than first degree relatives
9. excessive social anxiety, which does not diminish by becoming familiar with the person and,
unlike the avoidant disorder, tends to be associated with fears of paranoid structure and not
with negative judgments tive on itself
B - Symptoms do not appear concurrently with schizophrenia, nor with a psychotic-type mood disorder,
nor with other psychotic disorders or developmental disorders.
Unusual perceptual experiences can be, for example, illusions, auditory or visual, such as believing you
are seeing people - a pervasive form of normal pareidolia - in the shadows, in wallpaper designs, in smoke;
believe you "feel" the presence of absent people; or in moments of emotional distress, they can sometimes
suffer from transient psychotic episodes (with delirium, paranoia, dissociation, de-realization,
depersonalization, splitting, rarely true hallucinations, when they often occur they are auditory
hallucinations), short and with relatively low frequency (acute psychotic episode, brief psychotic
disorder).
Although there is sometimes egosyntonicity as a personality disorder, for the majority of the course the
patient with schizotypy maintains awareness, and becomes aware of the disturbances (presence of
residual insight), an awareness that is often compromised (except for periods of lucidity) in schizophrenia
and delusional disorder. Schizotypic patients, as in other personality disorders, function "on the border"
between neurosis and psychosis (so-called borderline organization of personality). If the criteria occur at a
young age before the onset of schizophrenia, the term "pre-morbid" is added to the disorder.
Course: like the others
Risk factors:
 neurodevelopment -> speech disorders or worse functioning due to autism
DD:
 distrust-> Narcissist avoids relationships for fear that his imperfections will be discovered, avoidant is
afraid
 psychoticism-> borderline has psychotic manifestations of a dissociative type in response to stress,
they establish intimate relationships which are then punctually destroyed
ANTISOCIAL DISORDER
Diagnostic criteria:
A. The subject shows non-observance and violation of the rights of others from the age of 15, which
manifests itself with at least 3 of the following elements:
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• inability to comply with social norms regarding legal behavior, with repetition of conduct
susceptible to arrest
• dishonesty: the subject lies, uses false names, scams others
• impulsiveness or inability to plan
• irritability and aggression
• non-observance of one's own safety and that of others
• irresponsibility: inability to meet financial obligations or to sustain a business activity
continuously
• lack of remorse
B. the individual is at least 18
years old
C. presence of a conduct disorder with onset prior to the age of 15
D. antisocial behavior does not manifest itself exclusively during a manic episode or during the course of
schizophrenia
Description:
 frequent comorbidity with substance and alcohol abuse
 greater concordance between homozygous criminal twins than dizygotes
 male first-degree relatives of people with somatization disorder show increased risk for both the
disorder itself and antisocial personality disorder
 it is hypothesized that the two disorders are alternative expressions of the same genetic predisposition,
with greater expression as somatization in women and antisocial personality in men
 the biological basis would consist in a hypofunction of the serotonergic systems responsible for
controlling the behaviors that cause negative consequences for the individual
Specify if:
 low levels of anxiety (negative affect)
 social withdrawal (posting)
 seeking attention (antagonism)
Prevalence:
 children with ADHD?
 it increases in people who abuse substances
Risk factors:
 genetic and environmental -> somatoform disorder, substance use
 cultural-> low socio-cultural background
Comorbidity: Histrionic, narcissistic, borderline, abuse, depression, anxiety, gambling
Differential diagnosis:
 borderline -> emotional, angry at abandonment, no antisocial conduct
 histrionic
 narcissist-> no antisocial conduct

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BORDERLINE DISORDER
Diagnostic criteria:
Borderline Personality Disorder is an affective, cognitive and behavioral area disorder. The essential
characteristics of this disorder are a pervasive modality of instability of interpersonal relationships, self-
image and mood, and a marked impulsiveness; these characteristics appear in early adulthood and are
identifiable, according to the DSM IV-TR, in the presence of five (or more) of the following elements:
desperate efforts to avoid real or imagined abandonment;
1. a picture of unstable and intense interpersonal relationships, characterized by alternating between
extremes of hyper-idealization and devaluation;
2. alteration of identity: self-image and self-perception markedly and persistently unstable;
3. impulsiveness in at least two areas that are potentially harmful to the subject (such as overspending /
gambling, promiscuous sexuality, substance abuse / alcohol use, reckless driving, overeating, etc.);
4. recurring threats, gestures, suicidal behavior, or self-mutilating behavior;
5. affective instability due to a marked reactivity of mood (eg episodic intense dysphoria or irritability and
anxiety, which usually last a few hours and, only more rarely, more than a few days);
6. chronic feelings of emptiness;
7. unmotivated and intense anger or difficulty in controlling anger (eg frequent fits of anger or constant
anger, recurrent physical fights etc.);
8. paranoid ideation or severe transient, stress-related dissociative symptoms.
[Criteria according to ICD-10:
Emotionally unstable personality disorder is described as an individual personality disorder characterized
by a certain propensity for impulsive actions regardless of the consequences, with the following
characteristics:
 unpredictable and capricious mood
 tendency to outbursts of emotion and inability to control explosive behavior
 grievances and conflicts with others, especially when impulsive actions are repressed and criticized.]
It is divided into two types:
1. an impulsive type, characterized by emotional instability and lack of control
2. a true borderline type, with self-perception breaking between inner goals and aspirations, chronic
feeling of emptiness, strained and unstable interpersonal relationships and a tendency to self-
destructive behavior, including suicidal gestures

Description:

the term refers to disorders that can be placed on the margin between neurosis and psychosis

frequent comorbidity with affective disorders, anxiety, substance abuse, nutrition

familiarity with borderline disorders

high familiarity for affective disorders
Prevalence:
 10% of outpatients
Course:
 Chronic -> symptoms lessen with advancing age
Risk factors:
 genetic -> antisocial, bipolar disorder, depression, substance use
 cultural -> transient and paraphysiological in adolescence
Comorbidity:
 with all other personality disorders
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 may co-occur with depression and bipolar disorder, DCA, abuse
Differential diagnosis:
 manipulation-> istrionic: less aggressive and self-destructive in intimate relationships

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 abandonment fears-> employee: becomes more requesting or sacrifices further to maintain the
relationship
 impulsiveness-> antisocial: for useful material
Therapy:
 low-dose antipsychotics
 mood stabilizers
 psychotherapy

ISTRIONIC DISORDER
Diagnostic criteria:
The DSM-IV-TR classification places this among the disorders of the group called ("cluster") B, that is,
personality with a "dramatic-unpredictable" trait. It appears within early adulthood. To be diagnosed as a
disorder it must manifest itself in a variety of contexts with the presence of at least five of the following
symptoms:
1. the person is uncomfortable in situations where he is not the center of attention
2. interaction with others is often characterized by sexually seductive or provocative behavior
3. manifests a rapidly changing and superficial expression of emotions
4. he constantly uses his physical appearance to draw attention to himself
5. the style of speech is excessively impressionistic and lacking in detail
6. shows self-dramatization, theatricality, and exaggerated expression of emotions
7. he is suggestible, for example he is easily influenced by others and by circumstances
8. consider relationships more intimate than they really are.
In theory, histrionic disorder was considered akin to hysteria. There is also a certain link between this and
narcissistic personality disorder, of which it is considered a subtype, by some authors.
Contrary to the hysteria codified in the classical sense, in which passivity and sexual disinterest can exist,
there is an excessively interactive, eccentric, overexcited behavior. The subject with histrionic
personality will show security, an apparent ability to express feelings, in an almost "theatrical" way,
tending to the position of leader and the manipulation of others. He can be uninhibited and sexually
promiscuous (like "Don Giovanni").
Risk factors:
 kind -> more frequent in women
 cultural-> some populations are more histrionic than others

Comorbidity:
 Borderline, narcissistic, antisocial, addict, somatoform disorder, major depression, conversion
disorder
Differential diagnosis:
 handling -> borderline more angry and destructive in intimate relationships
 seeking attention -> narcissist shows to be strong and powerful
 impulsiveness -> antisocial for material usefulness

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NARCIST DISORDER
Diagnostic criteria:
Diagnosis according to the DSM IV criterion requires that at least five of the following symptoms be
present in such a way as to form a pervasive pattern, that is, a pattern that tends to remain constant in
different situations and relationships:grandiose sense of self or an exaggerated sense of one's own
importance;
1. is occupied with fantasies of unlimited success, power, effect on others, beauty, or ideal love;
2. believes he is "special" and unique, and can only be understood by special people; o is excessively
concerned with seeking closeness / being associated with people of very high status (in some sphere);
3. desires or demands an admiration in excess of normal, or its real value;
4. he has a strong sense of his own rights and faculties, he is unrealistically convinced that other
individuals / situations must meet his expectations immediately;
5. he takes advantage of others to achieve his own goals, and feels no remorse;
6. lacks empathy: does not notice (does not recognize) or does not give importance to the feelings of
others, does not want to identify with their desires;
7. often feels envy and is generally convinced that others feel envious of him / her;
8. affective modality of a predatory type (unbalanced balance of power, with little personal commitment,
desires to receive more than what he gives, that others are emotionally involved more than he / she is)
and arrogant and presumptuous behavior.

There are also subtypes:

1. overt narcissism it is characterized by a high level of self-esteem and a low tolerance to criticism,
without anxiety, with emotional detachment.
2. Covert narcissism it is distinguished instead by high sensitivity to criticism, rumination and low self-
esteem, with anxiety and avoidance of relationships (it can be confused with avoidant personality
disorder).
Subjected to criticism, individuals with narcissism can generally react with anger, disdain, or insolence.
This can sometimes lead to a form of social withdrawal that can hide the sense of grandeur. Interpersonal
relationships are typically short-lived and scarce due to the narcissist's inability to perceive the emotions
of those in front of him and thereby offend the sensitivity of others. This pattern of behavior can also lead
to high results, thanks to insensitivity to criticism and security, but intolerance to criticism and the
constant need to feel admired can lead to failure. This may be associated with the development of
depressed mood, social withdrawal and persistent depressive disorder dysthymia, or major depressive
disorder.
Narcissistic personality disorder is also associated with forms of eating disorders such as anorexia nervosa
or substance use disorders (usually cocaine). Histrionic personality disorder, borderline, antisocial, and
paranoid disorder may also be associated with this disorder.
In diagnosing comorbidities, particular attention should be paid to a potential substance use disorder,
which can develop in association, and to a diagnosis of manic or hypomanic: these episodes can present
peaks of grandiosity and self-overestimation similar to those present in a narcissistic type disorder
Prevalence:
 1.5% in the population,> M
Course:
 chronic, it can be physiological or paraphysiological in adolescence
Comorbidity:
 Borderline, histrionic, antisocial, paranoid, dysthymia, major depression, DCA, abuse
Differential diagnosis:
 Handling-> antisocial: useful material
 Obsessivity-> OCD-P coercive perfectionism
 Seeking attention -> in the histrionic every means to be at the center of the scene, in the borderline
unstable image, self-directed aggression
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 social withdrawal -> distrust in the paranoid, in the schizotypical inability to relate

AVOIDING DISORDER
Diagnostic criteria:
A pervasive pattern of social inhibition, feelings of inadequacy and hypersensitivity to negative judgment,
which begins in early adulthood and is present in a variety of contexts, as indicated by four (or more) of
the following:
1. Avoid work activities that involve meaningful interpersonal contact for fear of being criticized,
disapproved or rejected.
2. He is reluctant to connect with people unless he is certain he likes him.
3. He shows limitations in intimate relationships for fear of being humiliated or ridiculed.
4. He worries about being criticized or rejected in social situations.
5. He is inhibited in new interpersonal situations due to feelings of inadequacy.
6. He sees himself as socially inept, personally unattractive or inferior to others.
7. He is unusually reluctant to take personal risks or to engage in any new business, as this can prove
embarrassing.
The avoidant personality was distinguished from the schizoid personality on the basis of the ability to
experience emotional involvement and being disturbed by the inability to relate adequately to others
social isolation active in the avoidant, passive in the schizoid
Course:
 Chronic-> it begins in childhood with children alone, ashamed, with intense fear in the presence of
strangers. At this age, it can be defined as almost physiological if excessive or limiting. Its expression in
later stages of development is pathological. It appears mainly in females.
Comorbidity:
 Borderline, dependent and cluster A, major depression, social anxiety, anxiety, agoraphobia
Differential diagnosis:
 Social withdrawal-> paranoid: distrustful

DEPENDENT DISORDER
Diagnostic criteria:
According to the DSM-IV and 5 the patient can be described as follows:
1. The person has difficulty making daily decisions without requiring an inordinate amount of advice and
reassurance.
2. He needs others to take responsibility for most areas of his life.
3. Has difficulty expressing disagreement with others for fear of losing support or approval
4. Has difficulty starting projects or doing things on their own (due to a lack of confidence in their own
judgment or abilities rather than a lack of motivation or energy).
5. He can go to anything to get care and support from others, even to the point of offering himself up for
unpleasant tasks.
6. He feels uncomfortable and helpless when it is only from exaggerated fears of being unable to provide
for himself.
7. When a close relationship ends, he urgently seeks another relationship as a source of care and support.
8. He is unrealistic worried about being left to fend for himself.
Course:
 chronic but in children and adolescents it could be physiological

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Comorbidity:
 Borderline, dependent and cluster A, major depression, anxiety, adaptation disorder
Differential diagnosis:
 abandonment fears-> borderline: reacts angrily to abandonment
 social withdrawal -> avoidant: more withdrawn and more socially inhibited

OCPD (OBSESSIVE-COMPULSIVE PERSONALITY DISORDER)

The official classification of the DSM-IV-TR predicts the presence of at least four of the following symptoms:
1. Excessive preoccupation with lists, details and organization at the expense of the overall goal
2. Perfectionism that interferes with the success of a job in a short time
3. Excessive dedication to work (not justified by economic needs) with a consequent reduction in the time
devoted to recreational activities
4. Inability to throw away old or useless objects, even when they have no emotional value
5. Inflexibility on ethical and / or moral positions (not justified by political or religious affiliation)
6. Reluctance to delegate tasks or work in a team
7. Overly thrifty lifestyle both towards oneself and towards others
8. Stiffness and stubbornness

Diagnosis according to the ICD-10 criterion : the classification of the ICD-10 (in which the disorder is
called in English Anankastic personality disorder, "Anancastic personality disorder") provides for the
presence of at least four of the following symptoms:
1. Excess of indecision and prudence
2. Concern about details, rules, lists, order and organization to the detriment of the general purpose of
the activity
3. Perfectionism that interferes with the success of a job
4. Excessive scrupulousness and responsibility
5. Dedication to work and productivity with consequent devaluation of recreational activities and
interpersonal relationships
6. Excessive pedantry and adherence to social conventions
7. Stiffness and obstinacy
8. Necessity of constant control and the requirement that others act exactly according to the dispositions
of the subject
Differential diagnosis:
 perfectionism -> the narcissist: he is already perfect
 absence of empathy -> narcissist: antisocial
 absolute adherence to the rules -> schizotypic: cognitive and perceptual distortions
Comorbidity:
 Narcissist, Paranoid, Borderline, major depression, social anxiety, phobia, OCD, DCA, BP, GAD,
dyspopophobia (serial accumulation)
Therapy:
 pharmacological therapies for short periods and limited to the most critical phases: antipsychotics with
sedative activity
 with regard to cluster B disorders with a greater impulsive component, mood stabilizing therapies for
longer times

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 in the context of personality disorders, the central role is offered by psychotherapy (mainly cognitive or
cognitive-behavioral)

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PSYCHIATRIC LEGISLATION, HISTORY OF PSYCHIATRY,

COMPULSORY HEALTH TREATMENTS (TSO)
The 1904 law is based on several aspects:
1. Orientation towards the protection of society against the deviant
2. Subordination of hospitalization in a psychiatric hospital to a provision of the judicial authority, at the
request of relatives, guardians or 'anyone else in the interest of the sick and society'
3. The inmate was immediately deprived of civil rights and the court appointed a guardian
4. The patient admitted definitively was registered in the criminal record
5. The supervision of the asylums was entrusted to the prefects and the Ministry of the Interior
This law therefore led to the internment of unwanted individuals, making their resignation impossible, and
to the increase of internment in asylums (with an increase in costs and a progressive increase in nosocos
and the number of beds).
The mini reform of 1968 had some innovative aspects:
1. Possibility of voluntary hospitalization in a psychiatric hospital (at the request of the patient and
abolition of the obligation to record in the criminal record)
2. More clearly sanitary definition of mental hospitals
3. Possibility of establishing Mental Health Centers for the purpose of following discharged patients.

Psychiatric legislation has undergone a fundamental change thanks to Law No. 180 of May 13, 1978 on
"Voluntary and Compulsory Health Checks and Treatments" in the field of psychiatric assistance and to Law
No. 833 of December 23, 1978 with the Institution of the Service National Healthcare which concerns the
entire reform of public health, definitively abolishing the previous laws on asylums and on the insane
(crazy).
1. Psychiatric assistance must be structured locally, carrying out the activities of diagnosis, therapy or
prevention of mental disorders in the social context where the patient lives.
2. Closure of psychiatric hospitals or asylums, often dilapidated and inadequate, establishing that public
hospitals must be equipped with psychiatric wards with a maximum number of 15 beds or 1 bed per
10,000 inhabitants for the treatment of acute mental disorders , operating in close liaison with the local
structures. The maximum number of beds is intended precisely as an overrun in asylums. Therefore, the
Diagnosis and Care Services (SPDC) were born.
Hospitalization of the mentally ill can be voluntary or compulsory by resorting to the TSO Compulsory
Health Treatment which is requested by a doctor in the case of patients with mental disorders who need
urgent therapy, patients who refuse treatment or when there are no conditions and circumstances that
allow other timely and suitable therapeutic measures to be adopted. A second doctor ascertains the
patient's condition and, if he agrees with the observations of his colleague, validates the provision of the
TSO which is finally ordered by the mayor who represents the highest local health authority, within 48
hours. In addition, everything must be notified to the Tutelary Judge who, "having taken the information
and arranged any investigations", will validate the provision or not.
The treatment must be activated only after having sought, with every possible initiative, the patient's
consent, and must be proposed and validated only after having actually visited the patient (crime of false
ideology and kidnapping.
There must be three conditions:
1. The existence of psychic alterations such as to require urgent therapeutic interventions
2. The non-acceptance by the patient of the treatments
3. The non-existence of conditions and circumstances that allow timely and suitable extra-
hospital health measures to be adopted.
The competence of taking and accompanying to the place of treatment, health operation, is of the
medical and nursing staff, even in the face of the need for coercion. The Municipal Police will only
intervene in the presence of a serious crime or disturbance of public order.

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The TSO usually takes place at the psychiatric ward competent for the territory and lasts 7 days during
which the treatment can be suspended if the conditions that determined it are lacking and the patient
eventually continues hospitalization under voluntary conditions or at the end of the 7 days can be
extended if the clinical conditions that determined it exist.
In accordance with Article 32 of the Constitution, the TSO must not violate respect for the human
person and his fundamental rights:
• The right to communicate with whomever it deems appropriate
The right to vote (which previously affected the possibility of hiring in the Public Administration)
The recognized faculties relating to the choice of doctor and place of treatment.
The TSO is not only required in the field of psychiatry but also in patients with infectious diseases and
venereal diseases to prevent the spread of infections, and in the event of an accident in the
workplace to avoid problems with insurance. It is not a matter of public security or judicial authority
and the concept of forced hospitalization in conditions of danger for oneself, for others or a public
scandal has been abolished, which was ordered by the magistrate upon reporting by a citizen, a
relative or a medical certificate, and who after an observation period of 1 month maximum, could be
permanently interned by the director of the asylum for judicial proceedings, for which the patient lost
the ability to act in a legal sense and was registered in the criminal record.

DEPARTMENT OF MENTAL HEALTH AND ITS SUBDIVISIONS,

ORGANIZATION OF PSYCHIATRIC CARE
1. The Department of Mental Health (DSM) is the coordinating center of all psychiatric assistance in the
area, that is, it deals with the organization, management and production of services aimed at
promoting mental health, prevention, diagnosis, treatment and rehabilitation of psychiatric patients,
which is organized in each local health company (ASL) as required by the Mental Health Protection
Objective Project (1994-96) for the adaptation of psychiatric assistance to law 833 of 1978. The DSM
consists of 1 or 2 modular units with a catchment area not exceeding 150,000 inhabitants. Each module
includes various territorial structures.
2. The Mental Health Center (CSM) it is the territorial psychiatric clinic that is the operational
headquarters responsible for the organization and coordination of all the activities of the departmental
module, ie assistance, including at home, prevention, care, rehabilitation and social reintegration.
3. The Psychiatric Diagnosis and Treatment Service (SPDC) it is the hospital psychiatric ward where
patients suffering from acute crises are admitted for short periods of time (voluntary hospitalization or
in TSO).
4. The Semi-residential Structures they include the day center dedicated to long-term therapeutic and
rehabilitation programs to facilitate patient resocialization and the Day Hospital with short-medium
term therapeutic and rehabilitation programs in the case of patients who do not need hospitalization.
5. The Residential Structures are therapeutic communities for medium-long periods of rehabilitation
treatment with individual and group activities, both work and socio-cultural, related to psycho-
pharmacological and psychotherapeutic treatments, among which we have the housing or home-family
communities that host few patients without a sufficient degree of autonomy, with the aim of promoting
autonomy and reintegrating the patient into the family and social context.

PRIMARY, SECONDARY AND TERTIARY PREVENTION IN

PSYCHIATRY
 Primary Prevention has the task of eliminating the risk factors that can favor the onset of mental
disorders, but this is not easy because:
• the factors are many
• present in primary institutions that is family, school and work
• not easily isolable or modifiable, considering that it is difficult to plan interventions for the
psychophysical well-being of citizens.
Therefore primary prevention is still entirely theoretical, difficult to apply on a practical level.
 Secondary Prevention is based on:
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• early diagnosis
• early and adequate therapy of mental disorders
• identification of subjects at psychopathological risk with the aim of reducing the prevalence of
psychic disorders, ie all cases found in a given population, and reducing the average duration of
psychic disorders. The identification of subjects at psychopathological risk, more exposed to
stressful agents, is based on the consideration of age groups (childhood, adolescence, old age),
social conditions such as poor, homeless, social marginalized, problems relating to dominant
culture that is ethnic minorities, religious, which are often more vulnerable to risk factors.
Secondary prevention often takes place in outpatient clinics and in general and specialized
medicine wards, both for psychopathological disorders pre-existing at hospitalization or
consultation, and for those that may arise as a result of a somatic disease and received therapies.
 Tertiary Prevention has the task of preventing exacerbations and relapses of mental disorders,
reducing the patient's degree of suffering, disability and social marginalization, due to chronic mental
disorders and promoting the recognition, development and use of residual functional capacities,
therefore an attempt is made to recover psychosocial functioning, the degree of autonomy or self-
sufficiency of the patient, interpersonal relationships.
Typically these are chronic young-adult patients, i.e. psychotic patients, borderline personalities, drug
addicts, alcoholics, homeless, social outcasts, who have never been hospitalized or have been
hospitalized for short periods of time in the acute phase, or subjects who refuse long-term treatment
or to be hospitalized or who have poor compliance with medical therapy, with progressive existential
degradation, isolation and social marginalization with a high risk of suicide, drug abuse, alcohol,
aggressive and violent behavior. These subjects are candidates for Psychiatric Rehabilitation, i.e. a
series of interventions to alleviate impairments, handicaps or disabilities and improve the quality of
their life as far as possible, favoring the patient's psychosocial recovery,

INFORMED CONSENT IN PSYCHIATRY

The Informed Consent is regulated by the code of medical deontology, legal and ethical rules, based on
the principle of self-determination and the will of the patient with respect to that of the doctor,
remembering that the dignity, life and health of the patient must be safeguarded, avoiding diagnostic
measures. - co-therapeutics that can permanently reduce the patient's physical integrity.
The doctor, taking into account the socio-cultural level of the patient, the ability to understand and
possible interference during the interview due to the pathology or drugs taken (psychotropic drugs), must
provide the patient with all the information on his illness, diagnostic investigations and to which he will be
subjected and the therapeutic procedures envisaged for the treatment of his pathology, indicating the
advantages, possibilities of recovery, possible consequences, complications or side effects due to the
diagnostic-therapeutic procedures.
The doctor must use clear, understandable but scientifically correct language and must answer all the
questions that are asked exhaustively, giving the patient the possibility to choose, otherwise the informed
consent loses its validity, making the intervention illegitimate diagnostic-therapeutic.
The doctor must not undertake any diagnostic-therapeutic activity without acquiring informed consent to
avoid problems from a medico-legal point of view, to compensate for any damage caused to the patient's
health or to have to answer for the crime of voluntary injury or manslaughter in the event of the patient's
death, except in cases where the doctor acts in a state of necessity:
 In the event of an epidemic, the WHO or the NHS may establish that the population must be subjected
to checks, vaccines and other treatments to avoid the spread of the infectious disease in the population.
 When the patient's health conditions are critical, the patient is unconscious and is unable to provide
consent (presumed consent) so the consent or dissent expressed by the patient's relatives or guardians
cannot be considered valid and there are no medical problems. legal (cause of justification,
exonerating, discriminating).
To be considered valid, consent must be:
 Personal: expressed directly by the patient, with the exception of minors and disabled or forbidden
subjects

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 Ricci, De Girolamo in memory of D'Altilia, Tucci, Di Turi (special thanks to Ricciardi & Potenza)

 Free and spontaneouso: reflects the ability to express one's will consciously and freely, with an
unconditional or constrained choice
 Informed: the patient must understand his illness, the significance of the usefulness of the treatments,
but also the undesirable effects
 Current: the consent concerns the proposed intervention and has no continuous value
 Manifest: it is not implicitly acquired with the consent of dissent or with tacit availability.

In psychiatry, the situation is more complex because often they are patients suffering from disorders that
prevent them from correctly receiving information on their clinical picture or that interfere with decision-
making functions, questioning the validity of the consent or dissent expressed by the patient.
In case of hospitalization or voluntary psychiatric consultation by the psychiatric patient, it is necessary to
inform in a correct and understandable way about the psychopharmacological therapeutic possibilities,
indicating the benefits, side effects and interactions that can be determined by other drugs or
psychoactive substances, especially alcohol and drugs.
Informed consent to psychotherapeutic treatment is important with correct information on the therapist's
psychological reference model, methods of implementation, duration, costs, possible and achievable
objectives.
In case of compulsory hospitalization in TSO these requisites are temporarily canceled but initiatives
aimed at ensuring the consent and participation of the patient are necessary.
The situation becomes more complex in the event of a disqualification or disqualification order.
 The interdiction order it is intended for patients with habitual mental illness such as to make them
unable to provide for their own interests, including those of a patrimonial nature and civil life.
 The provision of incapacitation it is intended for patients with habitual but less serious mental illness,
such as not to justify the total deprivation of the ability to act, or in the case of patients addicted to
alcoholic beverages or drugs that expose themselves and the family to serious economic prejudices .
Furthermore, it is possible to proceed with the interdiction or incapacitation in case of blindness or deaf-
mutism present from birth or childhood or when, due to lack of suitable education, the subject has had a
partial psychic development, for which he is unable to provide for his own interests.
In the event of a disqualification or incapacitation provision, the subject loses the ability to act and the
legal capacity, so that a guardian is appointed who becomes the legal representative of the subject in all
acts of extraordinary administration (property, personal), even if the interdicted person has the right to
information, which is useful for his or her participation in the treatment.

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