BIPOLAR DISORDERS

TOPIC OUTLINE
➢Introduction
➢History
➢Epidemiology
➢Neurobiology
➢Clinical Presentation
➢Diagnostic Classifications
➢Differential Diagnosis
➢Investigations
➢References

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INTRODUCTION
➢Mood disorders encompass a large group of psychiatric disorders in
which pathological moods and related vegetative and psychomotor
disturbances dominate the clinical picture.
➢considered as syndromes.
• Sustained over a period of weeks to months
• Represent a marked departure from a person’s habitual functioning
• Tend to recur, often in periodic or cyclical fashion.

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 Continued…
➢Disabling mood disorders afflict 5 to 8, milder but still clinically significant
mood disorders would raise lifetime rates to 17 percent

➢Bipolar disorders (previously called manic-depressive psychosis)consist of at

least one hypomanic, manic, or mixed episode.

➢Cyclothymia -a biphasic alternating pattern of numerous brief periods of

hypomania and numerous brief periods of depression

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HISTORY

➢Mania and melancholia are two of the earliest described human

diseases
➢State of raving madness with exalted mood was noted by the ancient
Greeks
➢Hippocrates (460–337 BC)was the first to systematically describe
melancholia and mania.
➢The idea of possible relationship between mania and melancholia
was first alluded by Soranus.

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➢The origin of "mania" is unclear, because of its roots in the mythological area
➢In the classical area four meanings of "mania" were described:
1. A reaction to an event in the meaning of rage or anger or excitation (like Homer
in his Ilias who described "Aias maenomenos", this means "Ajax in rage").
2. A biologically defined disease (Hippocrates, Aretaeus of Cappadocia and
others).
3. A divine state (Socrates, Plato).
4. A kind of temperament, especially in its mild form (Hippocrates).

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ARETAEUS OF
CAPPADOCIA: THE FIRST
DESCRIBER OF BIPOLAR
DISORDERS
➢lived in Alexandria in the 1st century
AD
➢is the most prominent representative
of the "Eclectics“
➢Mental disorders are biological in cause
➢was the first who definitively described
mania and melancholia as two different
images of one single disease

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➢His concept also included the idea of predisposing traits, suggesting
individuals who developed mania were characteristically labile,
irritable, angry or happy.
➢Emotional disorders as magnifications or exaggerations of existing
character trait.
➢He also observed mania and depression could occur simultaneously in
the same person.

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MODERN ERA
➢The first English text entirely
devoted to affective illness was
Robert Burton’s Anatomy of
Melancholy, published in 1621.

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Jean-Philippe Esquirol(1772-1840)
➢The first psychiatrist in modern times
to suggest that a primary disturbance
of mood might underlie many forms
of depression and related paranoid
psychoses.
➢He coined the term lypemania (from
the Greek, “sorrowful insanity”)

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Wilhelm Griesinger
➢Described (1845) the change from
melancholia to mania
➢He believed that the disease is "a
circle of both types with regular
changes".
➢Griesinger also described "seasonal
affective disorders“

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Jean-Pierre Falret
➢In 1851 ,"folie circulaire“;
characterized by a continuous
cycle of depression, mania and
free intervals of varying length.
➢In 1854 the concept of "folie á
double forme“ was presented by
Jules Baillarger.

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➢In 1863 Karl Kahlbaum introduced
both terms into German psychiatry in
his important book: The Grouping
and Classification of Mental
Disorders.
➢He supported falret’s concept.
➢He introduced Cyclothymia.

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EMIL KRAEPELIN (1856 to 1926)
➢ "father of modern psychiatry“
➢Established manic-depressive illness
as a nosological entity, His rationale
was based on;
1. the various forms had a common
heredity
2. frequent transitions from one to the
other occurred
3. recurrent course with illness-free
intervals
4. the superimposed episodes were
commonly opposite to the patient’s
habitual temperament
5. both depressive and manic features
could occur during the same episode
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➢Wernicke, Kleist and Karl Leonhard opposed emil kreapelin’s concept.
• Single episodes of mania or melancholia including recurrent
depression or recurrent mania without changing into one another
are something different from manic-depressive insanity
• Kleist differentiated between unipolar ("einpolig") and bipolar
("zweipolig") affective disorders
• Leonhard,who classified the "phasic psychoses" into "pure phasic
psychoses" (such as "pure melancholia", "pure mania", etc.) and
"polymorphous phasic disorders" ("vielgestaltige phasische
Psychosen").

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THE "REBIRTH" OF BIPOLAR DISORDER
• occurred in 1966 with two important publications
1. Genetic and peristatic factors have a synergic impact on the aetiology of
endogenous depression.
2. Gender plays an important role in the aetiology of endogenous depression.
There is a relationship between female gender and endogenous depression,
but bipolar disorders are equally represented in males and females.
3. Manic-depressive illness is nosologically not homogeneous. Unipolar
depression differs significantly from bipolar disorders in many characteristics
such as genetics, gender, course and premorbid personality.
4. Late-onset depression (Kraepelin's "Involutionsmelancholie") seems to belong
to unipolar depression and has only a weak relationship to bipolar disorders

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HYPOMANIA
➢was described, conceptualized and named by Erich Mendel in 1881 in
his book Die Manie to characterize a type of hyperthymic personality
➢C. G. Jung, in an early publication (1903), recorded in detail a number
of cases of manic mood changes (manische Verstimmung), patients
characterized by a stable submanic complex of symptoms,

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BIPOLAR SPECTRUM
➢Klerman (1981) distinguished six subtypes of bipolar disorders: mania,
hypomania, hypomania or mania precipitated by drugs,, depression with a family
history of bipolar disorder and mania without depression
➢In 1976 Dunner and co-workers distinguished bipolar II from bipolar I disease
➢New concept by Akiskal includes bipolar III (pseudo-unipolar disorders, defined as
recurrent depressions without spontaneous hypomania but often cyclothymic
personality with hyperthymic temperament and/or bipolar family history)
➢Bipolar0.25, Bipolar0.5,Bipolar 1, Bipolar1.5, Bipolar2,
Bipolar2.5,Bipolar3, Bipolar3.5, Bipolar4, Bipolar 5, Bipolar6.

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EPIDEMIOLOGY
➢The annual incidence of bipolar illness is considered generally to be less than 1
percent.
➢WMH Surveys, the cross-national lifetime prevalence of BPS disorders was 2.4
percent.
• Bipolar 1 ....... 0.6
• Bipolar 2 ...... 0.4
• Sub threshold bipolar........ 1.4

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Sex

➢Bipolar I disorder has an equal prevalence among men and women.

➢Manic episodes are more common in men, and depressive episodes
are more common in women.
➢Women, they are more likely than men to present a mixed picture
➢Women also have a higher rate of being rapid cyclers, defined as
having four or more manic episodes in a 1 -year period.

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 Age

➢Age of onset for bipolar I disorder ranges from childhood (as early as age 5 or 6
years) to 50 years or even older in rare cases, with a mean age of 30 years.
➢Bipolar men appear to have 4 to 5 years earlier onset than bipolar women
➢Slight tendency for higher age of onset in bipolar II disorder patients
➢Incidence of the depressive phase of bipolar disorder after childbirth is
relatively high.

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Race and Ethnicity
➢Rates of mood disorders are lower in blacks and Hispanic than
in whites.
Marital Status
➢Bipolar I disorder is more common in divorced and single persons
than among married persons.
Seasonal Factors
➢Spring and fall are the peak times for depression, just as
summer is for mania.
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Socioeconomic and Cultural Factors

➢Mood disorders can easily lead to unemployment, divorce, or low

income
➢Bipolar II disorder patients tend to belong to higher social
classes
➢Bipolar I disorder is more common in persons who did not graduate
from college

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Comorbidity

➢Alcohol abuse or dependence , panic disorder, obsessive-compulsive

disorder (OCD), and social anxiety disorder.
➢Men more frequently present with substance use disorders, women
more frequently present with comorbid anxiety and eating disorders.
➢Untreated mood disorders are high risk for suicide. it is “state-
dependent” and severity-dependent.

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Psychosocial Factors
Social Stressors
➢well recognized as risk factors
➢chronic stressors (e.g.unemployment, difficult marriage) play a
more important role than specific, acute stressors.
Social Support
➢frequency of the interactions is more important than the
amount.
Geographic Trends
➢weak, trend for lower prevalence of depression and higher rate
of mania in regions located closer to the Equator
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Personality and Temperament
➢Persons with certain personality disorders-OCD, histrionic, and
borderline may be at greater risk for depression
➢Bipolar I disorder (defined by manic attacks) not uncommonly arises
from the substrate of a depressive temperament.
➢Bipolar II disorder (characterized predominantly by depressive
attacks) arises more often from a hyperthymic or cyclothymic
baseline

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 NEUROBIOLOGY

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➢The neurobiological basis of bipolar disorders and the complex
interactions of environmental and inherited factors that create
vulnerability to abnormal moods remain essentially unknown.
➢The established approaches of neurochemistry and pharmacology
that gave rise to the present generation of antidepressant and mood-
stabilising drugs have highlighted the importance of
neurotransmitters and cell signalling pathways.

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Neurotransmitters
➢Of the biogenic amines, norepinephrine and serotonin were the two
primary neurotransmitters most implicated in the pathophysiology of
mood disorders.
➢Its now known that other neurotransmitters, including dopamine,
acetylcholine, histamine, GABA and glutamate also contribute to the
pathophysiology of these disorders.

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 Norepinephrine

➢Studies suggest that lower norepinephrine concentrations are present in

unipolar depression and higher concentration in bipolar patients.
➢Low levels of norepinephrine have been associated with cognitive
dysfunction,dysphoria, fatigue and apathy.
➢Gene studies reported associations between bipolar disorder and aspects
of noradrenergic neurotransmission or metabolism including links with
COMT.
➢Studies of lithium and other mood stabilizers suggest complex associations
with noradrenergic activity

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Serotonin:
➢Mood disorders are associated with a functional decrease in
serotonin neurotransmission. Depletion of serotonin may precipitate
depression.
➢A number of genetic studies observed abnormalities in serotonin
transporter genes in bipolar disorder.
➢Alterations in serotonin system are related to suicidal behavior.
➢ Some patients with suicidal impulses have CSF concentrations of
serotonin metabolites & low concentrations of serotonin uptake
sites on platelets.

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Dopamine:
➢Dopamine abnormalities in bipolar disorder have been relatively
understudied.
➢Excess dopaminergic neurotransmission occurring in mania, as
evidenced by the consistent finding that D2-receptor dopamine
agonists (antipsychotics) are nearly universally effective anti manic
treatments.
➢Dopamine agonists such as amphetamine or L-dopa may produce
manic-like syndromes

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• Other Neurotransmitter Disturbances
➢Acetylcholine (ACh) is found in neurons that are distributed
diffusely throughout the cerebral cortex
➢Cholinergic neurons have reciprocal or interactive relationships
with all three monoamine systems
➢Cholinergic agonists produce lethargy, anergia, & psychomotor
retardation in healthy subjects, can exacerbate symptoms in
depression, can reduce symptoms in mania, & Induce changes in
hypothalamic–pituitary adrenal(HPA) activity and sleep that mimic
those associated with severe depression
➢Increase in sensitivity to cholinergic agonists ---depression

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Glutamate and GABA
➢MRS studies have relatively consistently observed increases in
glutamate in bipolar mood states.
➢Gene studies identified a few associations with genes related to
GABA or glutamate activity.
➢The role of these two important neurotransmitters in the expression
of bipolar disorder remains unclear, and, as with monoamines,
abnormalities observed may simply reflect secondary findings from
primary lesions elsewhere.

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Second Messengers and Intracellular
Cascades.

➢Observations suggest that the neuropathology of bipolar disorder lies

below simple receptor activity to cell signalling and epigenetic
control.
➢The binding of a neurotransmitter & a postsynaptic receptor triggers
a cascade of membrane-bound & intracellular processes mediated by
second messenger systems
➢Receptors on cell membranes interact with the intracellular
environment via guanine nucleotide-binding proteins (G proteins)

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➢The G proteins, in turn, connect to various intracellular enzymes (e.g.,
adenylate cyclase, phospholipase C, and phosphodiesterase) that
regulate utilization of energy and formation of second messengers,
such as cyclic nucleotide (e.g.,cyclic adenosine monophosphate
[cAMP] and cyclic guanosine monophosphate [cGMP]), as well as
phosphatidylinositols (e.g., inositol triphosphate and diacylglycerol)
and calcium-calmodulin.
➢Second messengers regulate the function of neuronal membrane ion
channels
➢Mood stabilizing drugs act on G-protein and other second
messengers.

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Neuroanatomical Consideration
➢Both the symptoms of mood disorders and biological research
findings suggest the hypothesis that mood disorders involve the
pathology of the brain.
➢Anatomically, Bipolar disorders are more associated with changes in
the amygdala, temporal cortex, cerebellum, third ventricle, structures
near the third ventricle, and the prefrontal cortex,

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➢Modern affective neuroscience focuses on the importance of four
brain regions in the regulation of normal emotions:

❑Prefrontal cortex (PFC)

❑Anterior cingulate
❑Hippocampus
❑Amygdala

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➢Prefrontal Cortex : left side is involved in goal directed appetitive behaviors
whereas the right side is involved in inhibition of appetitive pursuits and avoidance
of behaviors “behaviors related to reward & punishment”

➢Anterior Cingulate :point of integration of attention and emotional input

“control of emotional arousal ”.

➢Hippocampus: involved in various forms of learning & memory including fear

conditioning / emotional & contextual learning .

➢Amygdala: process stimuli of emotional significance & coordination/ organization

of cortical
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Alteration In Hormonal Regulation

➢Severe early stress can result in long lasting alteration in

neuroendocrine and behavioral responses.
➢Chronic stress decreases the activity of gene coding for the
neurokinin brain-derived neurotrophic growth factor (BDNF) and also
neurogenesis.
➢There is elevated HPA activity in depression and adrenocortical
hyperactivity in case of mania.

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Sleep and Circadian Rhythm
➢In bipolar disorder, mania is typically accompanied by disturbed sleep and, in
particular, a decreased need for sleep.
➢Studies suggest that mania and hypomania may be triggered by sleep deprivation
in bipolar individuals.
➢Some have hypothesized that it is the sleep disturbance resulting from stress,
rather than stress directly, that triggers affective episodes in bipolar disorder.

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Structural and Functional Brain Imaging
• MRI of patients with bipolar disorder reveals an inordinate number of
hyper intense regions.

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➢MRI findings in Bipolar patients

❑White matter hyper intensities

❑Reduction of gray matter volume
❑Decreased frontal cortical area volume
❑Increased ventricular size.

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Glucose Metabolism
➢Increased glucose metabolism has been observed in several limbic
regions, particularly among patients with relatively severe recurrent
depression and a family history of mood disorder.

➢A 1997 investigation using PET suggests increased glucose

metabolism in the sub genual prefrontal cortex of manic patients
compared with normal controls and patients with bipolar and
unipolar depression.

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Genetic Factors
➢Numerous family, adoption, and twin studies have long documented
the heritability of mood disorders.
➢Recently, however, the primary focus of genetic studies has been to
identify specific susceptibility genes using molecular genetic methods.
➢In summary, family and twin data collectively suggest that genes
explain approximately 75 percent of the etiology of bipolar disorder
and 37 percent of major depression.

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Family Studies
➢Family data indicate that if one parent has a mood disorder, a child
will have a risk of between 10 and 25% for mood disorder.
➢If both parents are affected, this risk roughly doubles.
➢The risk is greater if the affected family members are first-degree
relatives rather than more distant relatives.
➢Compared to a rate of 1% in the general population, family studies
indicate a sevenfold higher morbid risk to first-degree relatives of
bipolar probands, suggesting a strong familial risk.

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Adoption Studies
➢These provide an alternative approach to separating genetic and
environmental factors in familial transmission.
➢The most common experimental design is one in which probands are
identified who have a mood disorder and were adopted at birth.
➢The rates of psychiatric illness are then determined in both the
biological and adoptive parents.
➢Although only a limited number of such studies have been reported
due to the difficulty in obtaining subjects, these results of such
studies are supportive of the role of genetics and are generally
consistent with the twin data.
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Twin Studies
➢These provide the most powerful approach to separating genetic
from environmental factors, or "nature" from "nurture."
➢Twin studies generally find a two to fourfold increase in concordance
rate for mood disorder in MZ twins compared to DZ twins, providing
the most compelling data for the role of genetic factors in mood
disorders.
➢Considering unipolar and bipolar disorders together, these studies
find a concordance rate for mood disorder in the monozygotic (MZ)
twins of 70 to 90 % compared with the same-sex dizygotic (DZ) twins
of 16 to 35 %.

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Linkage Studies
➢DNA markers are segments of DNA of known chromosomal location,
which are highly variable among individuals.
➢They are used to track the segregation of specific chromosomal
regions within families affected with a disorder.

➢When a marker is identified with disease in families, the disease is

said to be genetically linked.

➢Chromosomes 18q and 22q are the two regions with strongest
evidence for linkage to bipolar disorder.

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Psychosocial Factors
Life Events and Environmental Stress.
➢Stressful life events more often precede first, rather than subsequent,
episodes of mood disorders for both patients with MDD and bipolar I
disorder.

➢The stress accompanying the first episode results in long-lasting changes in

the brain’s biology.

➢These long-lasting changes may alter the functional states of various

neurotransmitter and intraneuronal signaling systems, changes that may
even include the loss of neurons and an excessive reduction in synaptic
contacts.

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➢Personality Factors: No evidence indicates that any particular
personality disorder is associated with later development of bipolar I
disorder; however, Pts. with dysthymic disorder & cyclothymic disorder are
at risk of later developing MDD or bipolar I dr.

➢Psychodynamic Factors in Mania

❑Most theories of mania view manic episodes as a defense against

underlying depression.

❑Abraham believed that the manic episodes may reflect an inability to

tolerate a developmental tragedy, such as the loss of a parent.
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 CLINICAL PRESENTATION

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➢Mood disorders are characterized by pervasive dysregulation of
mood and psychomotor activity and by related biorhythmic and
cognitive disturbances

➢Morbid mood states can be characterized by;

❑pathological mood,
❑endogenous reactivity,
❑recurrence and
❑Impairment
➢The two basic symptoms in mood disorders are depression and
mania.
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Mood Disturbances In Manic Epsiodes
➢MOOD ELEVATION: The mood in mania is classically one of elation,
euphoria, and jubilation, typically associated with laughing, punning
and gesturing.
➢LABILITY AND IRRITABILITY: The prevailing positive mood in mania is
not stable, patients can become extremely irritable and hostile
➢PSYCHOMOTOR ACCELERATION: is characterized by overabundant
energy and activity and rapid, pressured speech.
➢FLIGHT OF IDEAS: Thinking processes are accelerated; associations
are difficult to follow.

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➢IMPULSIVE BEHAVIOR: Manic patients are typically impulsive,
disinhibited, and meddlesome
• familiarity with total strangers and intrusive
• Heightened interest in every new activity
➢DELIRIOUS MANIA: extremely severe expression of mania (once
known as bell’s mania)frenzied physical activity that continues
unabated and leads to delirium and disorientation—a life threatening
medical emergency
➢WITH CATATONIC FEATURES: have prognostic and treatment
significance in mood disorders.
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Vegetative Disturbances In Mania
➢Hyposomnia. decreased need for sleep
• Some patients may actually go sleepless for several days. This
could lead to dangerous escalation of manic activity which might
continue despite physical exhaustion.
➢Inattention to Nutrition :weight loss may occur because of
increased activity and neglect of nutritional needs.
➢Hyper sexuality :may lead to sexual indiscretion

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Cognitive Distortions
➢Manic thinking is overly positive, optimistic, and expansive.
➢GRANDIOSITY inflated self-esteem and a grandiose sense of
confidence and achievements.
➢LACK OF INSIGHT, AND POOR JUDGMENT engage in harmful
activities and non adherence with medication regimens
during the manic phase.
➢DELUSION FORMATION. Grandiose delusions, delusions of
assistance, delusions of reference and persecution
➢Delusions occur in 75 percent of all manic patients.
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➢MOOD-INCONGRUENT PSYCHOSIS. can be understood to
arise from the powerful mental experiences of mania. Eg
first-rank schneiderian-type symptoms
➢HYPOMANIA VERSUS MANIA. preferably obtained from
significant others who have observed the patient
❑Duration of hypomanic experiences might be less important than
the fact that they recur

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Mood Disturbances in Depressive Episodes
➢ A depressed mood and loss of interest or pleasure are the key
symptoms in depression.
➢Generalized psychomotor retardation – most common
➢Decreased rate and volume of speech
➢Mood congruent delusions-
guilt,sinfulness,worthlessness,failure,poverty,persecution, terminal
somatic illnesses
➢Mood incongruent delusions-grandiose themes of exaggerated
power, knowledge and worth
➢Non delusional rumination about loss, guilt, suicide, death

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DIAGNOSTIC CLASSIFICATION
➢Bipolar I disorder,
➢Bipolar II disorder,
➢Cyclothymic disorder, and
➢Substance or medication induced bipolar and related disorder
➢Bipolar and related disorder due to another medical condition
➢Other specified bipolar and related disorder
➢Unspecified bipolar and related disorder

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Bipolar I Disorder
➢Typically begins in the teenage years, the 20’s, or the 30’s.
➢The first episode of bipolar I disorder may be manic, depressive or
mixed.
➢Three mode of onset
❑mild retarded depression or hypersomnia for few weeks or months
which then switches in to a manic episode.(common)
❑Severely psychotic manic episode with schizophreniform features
❑Several depressive episodes occur before the first manic episode.

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➢Manic episode has a rapid onset and may evolve over a few weeks,
➢Untreated manic episode lasts three months
➢After about five episodes ;the interepisode interval stabilizes at 6 to 9
months.
➢5 to 15 percent of those with bipolar disorder can be classified as
rapid cyclers.(four or more episodes per year).
➢Poorer prognosis than compared to those with MDD.

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Factors Affecting The Outcome Of Bipolar I
Disorder
GOOD PROGNOSIS POOR PROGNOSIS
Short duration of manic episodes Premorbid poor occupational status
Advanced age of onset Alcohol Dependence
Few suicidal thoughts Psychotic Features
Few coexisting psychiatric or medical problems Depressive Features
Interepisode Depressive Features
Male Gender

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Bipolar II Disorder
➢More prevalent than bipolar I disorder.
➢An average of 50 percent of persons with major depressive disorder have been
reported to conform to the bipolar II disorder pattern
➢Although the data are limited, a few studies indicate that bipolar II disorder is
associated with
❑With more marital disruption
❑With onset at an earlier age than bipolar I disorder.
➢Evidence also indicates that patients with bipolar II disorder are at greater risk of
❑Both attempting and completing suicide than patients with bipolar I disorder
and major depressive disorder.
➢ The course and prognosis indicate that the diagnosis is stable because there is a
high likelihood that patients will have the same diagnosis up to 5 years later.
➢ Is a chronic disease that warrants long-term treatment strategies.

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Cyclothymic Disorder
• begins insidiously before 21 years of age,
• frequent short cycles of subsyndromal depression and hypomania.
• Repeated romantic breakups or marital failures and Uneven
performance at school
• Characterized as dilettantes
• Polysubstance abuse occurs in as many as 50 percent of such persons

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Differential Diagnosis
➢Normal Bereavement
❑predominant affect is feelings of emptiness and loss,
❑The dysphoria in grief is likely to decrease an intensity over days to
weeks and occurs in waves
❑Accompanied by positive emotions and humor
❑Preoccupation with thoughts and memories of the deceased
❑Self-esteem is generally preserved
❑Marked psychomotor retardation is not observed

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Major Depressive Disorder Versus Bipolar
Disorder
❑Early age at onset ❑ High-density three-generation pedigrees
❑Psychotic depression before 25 years of ❑ Trait mood lability (cyclothymia)
age ❑Hyperthymic temperament
❑Postpartum depression, especially one ❑Hypomania associated with
with psychotic features antidepressants
❑Rapid onset and offset of depressive ❑Repeated (at least three times) loss of
episodes of short duration (less than 3 efficacy of antidepressants after initial
months) response
❑ Recurrent depression (more than five ) ❑Seasonality
❑ Depression with marked psychomotor ❑ Bipolar family history
retardation
❑ Atypical features (reverse vegetative ❑Depressive mixed state (with
signs) psychomotor excitement, irritable
hostility, racing thoughts, and sexual
arousal during major depression)

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 ➢Anxiety Disorders
❑early-morning awakening, psychomotor retardation, self-reproach,
hopelessness, and suicidal ideation are the strongest clinical markers of
depression
➢Personality Disorders
❑borderline, narcissistic, histrionic, and antisocial personality disorders need
special consideration.
➢Alcohol and Substance Use Disorders
❑mood disorder should be seriously considered as the primary diagnosis if
marked affective manifestations persist or escalate after detoxification
(e.g., 1 month).

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➢Schizophrenia
❑Young psychotic and disorganized bipolar patient
❑Rapid onset with noticeable change in behavior.
❑Detail should be given to longitudinal history
➢Schizoaffective Disorder
❑should be restricted to recurrent psychoses, with full affective and
schizophrenic symptoms occurring nearly simultaneously during each
episode.

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 Investigations
➢ Complete blood count ➢ Substance and alcohol screening
➢ Erythrocyte sedimentation rate ➢ Magnetic resonance imaging
➢ Fasting glucose ➢ Electrocardiography
➢ Electrolytes ➢ Pregnancy tests
➢ Thyroid hormone ➢ VDRL
➢ Creatinine and BUN ➢ PICT
➢ Liver and lipid panel

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 THANK YOU

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