QUICK REVIEW OF PSYCHIATRY

DR. NAGARAJU.SUVVARI
MD (Psych)
ASST. PROF. OF PSYCHIATRY
GOVT. HOSPITAL FOR MENTAL CARE
SANJEEVINI NEUROPSYCHIATRIC CARE
VISAKHAPATNAM
ANDHRA PRADESH

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SUBJECT MATTER:

QUICK Review of Psychiatry – In this book the topics broadly covered are Psychology,
Neurology in relation to Psychiatry (Anatomy, Physiology, Circuits & Pathways), Definitions
and Phenomenology, General Psychiatry, Psychiatry Case sheet and Neurology Case sheet.

The book has been written after an extensive study of most notably suggested books and
literature in the field of Psychiatry. It is tailored to meet the needs of any student related to
Psychiatry particularly the post graduates to go through the subject in no time before the
examination. For practitioners it would allow a quick recitation. The QUICK Review of
Psychiatry is a composite of Psychology, Psychopathology, Psychiatry, related Neurology and
Detailed Case sheet work up.

Starting with Psychology, which is, covered in around 20 pages deals with important
topics to be known to any exam going student.

In Neurology related to Psychiatry, the book covers Anatomy, Physiology, circuits and
pathways

Section of Definitions has the most common terminology used in the field of Psychiatry
and Psychopathology/Phenomenology.

Under Psychiatry, it covers,

Psychopharmacology including mechanism of action of all the drugs, indications,
dosage, adverse effects and contraindications.

Psychotropic drug dosage range in alphabetical order is mentioned under separate

heading.

Methods of treatment in psychiatry have briefing on ECT, DBS, Vagal Nerve Stimulation,
TCS, Psychosurgeries and Psychotherapies.

General Psychiatry includes rating scales used in various diagnosed conditions.

Forensic Psychiatry includes briefing on Indian Mental Health Act, Indian Lunacy Act
and NDPS Act.

Community psychiatry and Child Psychiatry are written under separate headings.

Appendices contain details of how to do a complete work up of a Psychiatry case and

Neurology case.

It is well versed that students opting Psychiatry as a post graduation course find the
subject rather difficult because the nomenclature and the definitions are almost new to them
as this is a branch which is not dealt extensively during their under graduation. When it comes
to the subject it has a great deal with Psychology, Neurology and Psychotherapies as well and a
student has to go through number of widely accepted text books to gain confidence in this area.
Revising all the books studied becomes a herculean task especially before the exams. Keeping
this in context I felt students in this area would need a very concise and short book that would
cover all the subjects and topics required within no time before examinations.

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I could hardly find any such book out in the market that would meet the requirement. There
are short handbooks available that deal with each subject separately, whereas this book is an
amalgam of all the required subjects under Psychiatry for a postgraduate.

I can assure that one cannot find a book of this type, which deals with all the required
subjects in Psychiatry. The Title itself is the essence of the book. QUICK Review of Psychiatry
for Postgraduates describes the need to revise fast before the examinations. I took a lot of pain
preparing this book and took care not to deviate from the classical definitions of all the
nomenclature.

All the briefings are done in either a few words or a maximum of one or two lines, in
bullets.

Mnemonics are provided for almost all-important sections, which makes it very easy for
a student to remember or recite.

Briefing was done on almost all the pioneers related to the field in the first few pages.

Almost all drugs used in Psychiatry are mentioned with minimum and maximum dosage
in alphabetical order in one page.

The Case sheet is done in detail covering almost all the questions which would be asked
by the interviewer under various headings. Diagnostic formulation is given in detail, which is
unusual in most of the books.

The book is definitely unique in all aspects!

I would like to thank all my teachers for enlightening the kind of knowledge that I persuaded to
write this book.
This book is dedicated to all the readers with the Quest for success.

My effort goes in vain if I do not mention my colleague, a close pal Dr. Venkata Kiran Vaddadi
who has always been encouraging and extending his help any time from start to the finish of
this book.
God Almighty…Sai Ram! Give me the strength in Pursuit of Knowledge!

First Edition -2010

Second Edition- 2016

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CONTENTS

TOPIC:- PAGE NOS

PSYCHOLOGY 05 - 45
PHYSIOLOGY 45 - 54
SUBSTANCE RELATED DISORDER 55 - 69
PSYCHOPHARMACOLOGY 70 - 114
PHYSICAL METHODS OF TREATMENT ` 114 - 117
PSYCHOTHERAPIES 117 – 118
GENERAL PSYCHIATRY
SCHIZOPHRENIA 118 - 133
MOOD DISORDERS 134 - 136
ANXIETY DISORDERS 136 -138
SOMATOFORM DISORDERS 139 - 141
NORMAL SEXUALITY & SEXUAL DISORDERS 142 - 144
SLEEP & SLEEP DISORDERS 145 -147
PERSONALITY DISORDERS 147 -149
PSYCHOSOMATIC MEDICINE 150 -159
PSYCHIATRIC RATING SCALES 159 -161
DELIRIUM 162 -163
DEMENTIA 163 -169
NEUROPSYCHIATRIC ASPECTS OF BRAIN TUMORS 169 -170
NEUROPSYCHIATRIC ASPECTS OF HEAD INJURY & INFECTIONS 170 -173
NEUROPSYCHIATRIC ASPECTS OF EPILEPSY 174 - 177
MOVEMENT DISORDERS 177 -178
HEADACHE 179
CHILD PSYCHIATRY 180 - 198
FORENSIC PSYCHIATRY 199 - 206
COMMUNITY PSYCHIATRY 207 - 210
PSYCHIATRIC CASE SHEET 211 - 232
THOUGHT & PERCEPTION DISORDERS 232 -243
DEFINITIONS 244 - 247
NEUROLOGY 248 - 266
NEUROLOGY CASE SHEET 267 – 281

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1) PSYCHIATRY; The medical speciality concerned with the study, diagnosis, treatment
and prevention of mental abnormalities and disorders.

2) PSYCHOLOGY; The science of human and animal behaviour which include the
application of this science to human problems.

3) Types of psychiatry ;
 CHILD PSYCHIATRY; -------- Underthe age of 12 years
 GERIATRIC PSYCHIATRY;----- Old age
 COMMUNITY PSYCHIATRY ;----- Community involvement
 FORENSIC PSYCHIATRY ; --------- Legal aspects
 CULTURAL PSYCHIATRY;------- Influence of cultural factors
 SOCIAL PSYCHIATRY;---------- Impact of social groups
 INDUSTRIAL PSYCHIATRY-------- Related to works and jobs
 DESCRIPTIVE PSYCHIATRY;------ Study of symptoms and phenomena
 DYNAMIC PSYCHIATRY;--------- Internal unconscious drives
 EXPERIMENTAL PSYCHIATRY;---- Research methods
 PASTORAL PSYCHIATRY; --------- Relation to religion

4) Schools of psychology
o Structuralism
o Gestalt psychology
o Functionalism
o Behaviourism
o Psycho analysis
o Modern psychology; biological, cognitive, developmental, humanistic, and
social.

5) Psyche; the soul

6) Mind; --------- The functional capacity of the brain
Cognition; --- Intellect
Conation; ---- Psychomotor action
Affect; ------ Emotional part
7) Sigmund Freud: father of psychiatry and psychology
8) Emil Kraepelin;
o Dementia precox
o Manic depressive psychosis
o Involutional Melancholia
o Personalities : Depressive, Manic, Irritable, Cyclothymic
o Paranoia
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9) Eugene Bleuler;
o Term- schizophrenia
o A s; ------ Autism, Ambivalence, Affect, Association

10) Carl G Jung;

o Collective unconscious
o Personal unconscious
o Complex
o Archetypes

11) Alfred Adler

o Theory of individual psychology
o Started child guidance clinic

12) Karen Horney

o Basic Anxiety
o Basic Hostility

13) Melanie Klein

o Paranoid Position
o Schizoid Position
o Depressive Position

14) Sandor Rado

o Adaptational psychodynamics

15) Eric Berne

o Transactional analysis
o Games
o Strokes
o Scripts

16) Herman Rorschach;

o projective tests of personality

17) Philippe pinel

Father of modern psychiatry

18) J.B Watson

o Father of Behaviourism

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19) Carl C Rogers
o Client oriented psychotherapy

20) Abraham Maslow

o Self-actualization theory; Basic needsSafety needsBelongings & Love
needs Esteem needsSelf-actualization

21) Aaron Beck

o Cognitive therapy
o Cognitive triad; -----Negative views of self, World, Future

22) Ivon Pavlov

o Classical conditioning learning theory (Nobel prize)

23) B.F.Skinner
o Operant conditioning learning theory

24) Albert Bandura

o Social learning theory

25) Joseph Wolpe;

o Systematic desensitization

26) Delay & Dinker;

o Chlorpromazine(CPZ- 1950)

27) William Cade;

o lithium

28) Ugo cerletti & Lucio Bini;

o Electro convulsive therapy

29) Oliver ;
o Camphor induced convulsions

30) Wagner Von Jauregg;

o Malaria treatment in general paresis of insane (nobel prize-psychiatrist)

31) Manfred sokel

o Insulin coma therapy

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32) Von Meduna ;
o Metrazole convulsive therapy

33)Friedman & Wilcox;

o Unilateral ECT

34)Martin seligman ;
o Learned helplessness

35)Otto Fenichel ;
o Counter phobic activity

36)Eric Kandel
o Habituation & sensitization (snail-Aplasia California)(Nobel prize-
psychiatrist)

37)Hans Berger :
o Electroencephalography

38)Elisabeth Kubler Ross ---------Stages of death (SABDA)

o Shock/Denial
o Anger
o Bargaining
o Depression
o Acceptance

39) John Bowlby;

o Attachment theory

40) George Engel;

o Bio psychosocial model

41) Jean Piaget ;-- cognitive developmental stages (Special Protection Control Force )
o Sensory motor stage -------------- (Birth-2years)
o Preoperational stage-------------- (2y -7y)
o Concrete operational stage ------ (7y-11y)
o Formal operational stage --------- (11y-end of adolescent)

42) Rapport ;- the spontaneous, conscious feeling of harmonious responsiveness that

promotes the development of constructive therapeutic alliance
Two types; - Communicative rapport & Emotional rapport

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43) Major Epidemiological studies in psychiatry
o Chicago study
o Midtown Manhattan study
o New Haven study
o Stirling county study
o National institute of mental health- Epidemiological Catchment Area study
(EACA study)

44)Franz Alexander : Association between specific personality traits and certain

psychosomatic disorders and he studied on
 Peptic ulcer
 Ulcerative colitis
 Essential hypertension
 Grave s disease
 Neurodermatitis
 Rheumatoid arthritis
 Bronchial asthma

45)DSM-IV ; contain 365 disorders and 17 sections

DSM-I------ 1952
DSM-II -----1968
DSM-III-----1980
DSM-IIIR ---1987
DSM-IV-----1994
DSM-IVTR -2000
DSM-V------2013

46)DSM-IV
Axis-I ;-----Clinical disorders
Axis-II------ Personality disorders & Mental retardation
Axis-III;----- Physical disorders or medical disorders associated mental disorders
Axis-IV; -----Psychosocial and Environmental factors contribute mental disorders
Axis-V: ---- Global Assessment of Functioning or children s Global Assessment scale
for children and teens under the age 18 years.

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 DEVELOPMENTAL THEORIES AND THE FIRST 3 YEARS OF LIFE

Sigmund Freud (1940) ---Psychoanalytic drive theory (psychosexual stages)

o Oral stage ---------(Birth -1year)

o Anal stage -------- (1y-3y)
o Phallic stage------ (3y-5y)----Oedipus complex(male), Electra complex (female)
o Latency stage ---- (5y-puberty)
o Genital stage------(adolescent& beyond)

Jean Piaget (1952) Cognitive development

o Sensory–motor intelligence ----------------(first 2 years)

o Modification of reflexes---------------------(birth–1 month)
o Primary circular reactions -----------------(1–4 months)
o Secondary circular reactions--------------(4–10 months)
o Coordination of secondary schemas ----(10–12 months)
o Tertiary circular reactions -----------------(12–18 months)
o Representational thinking -----------------(18–24 months)
o Preoperational intelligence ----------------(2–7 years)

Erik Erikson (1951) Psychoanalytic theory (psychosocial stages)

Stage associated virtue

o Trust Vs Mistrust------------- (Birth-18 months) ------------- Hope

o Autonomy Vs Shame-------- (18months-3years) --------- Will
o Initiative Vs Guilt ---------- (3y-5y)-------------------------------- Purpose
o Industry Vs inferiority ------ (5y-13y) ------------------------------- Competence
o Identity Vs Role confusion -- (13y-21y)----------------------- Fidelity
o Intimacy Vs isolation ----------- (21y-40y) ------------------------------- love
o Generativity Vs stagnation---- (40y-60y) ---------------------- Care
o Integrity Vs Despair------- (60y-death) ----------------------------- wisdom

Margaret Mahler (1975) Psychoanalytic theory(separation and individuation)

o Autistic phase -----------(birth–2 months)

o Symbiosis ------------- (2–4 or 5 months)
o Differentiation --------- (4 or 5–8 or 9 months)
o Practicing
 Early practicing (8 or 9–12 months)
 Practicing proper (12–18 months)
 Rapprochement (18–24 months)
 On the way to object constancy (24–36 months)

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John Bowlby (1969,1973, 1980) Attachment theory

o Phase of limited discrimination -----------------------(birth–2 months)

o Phase of limited preference ----------------------------(2–7 months)
o Phase of focused attachment and secure base -----(7–24 months)
o Phase of goal-corrected partnership----------------- (24–36 months)

Daniel Stern (1985) Psychoanalytic theory (sense of self-development)

o Sense of emergent self------------ (birth–2 months)

o Sense of core self -------------------(2–3 months)
o Sense of subjective self -----------(7–9 months)
o Sense of verbal self ----------------(18–20 months)

The patient – Doctor Relationship

 Rapport: - the spontaneous, conscious feeling of harmonious responsiveness that

promotes the development of a constructive therapeutic alliance.
 Rapport is conscious process, transference is unconscious process.

 Models of Interaction Between Doctor and Patient

o The paternalistic model / autocratic model.
o The informative model.
o The interpretive model
o The deliberative model

 Illness Behaviour:- Patients' reactions to the experience of being sick. The sick role
can include being excused from responsibilities and the expectation of wanting to
obtain help to get well.

 Biopsychosocial Model :- George Engel

o The biopsychosocial model is derived from general systems theory.
o The biological system emphasizes the anatomical, structural, and molecular
substrate of disease and its effects on the patient's biological functioning;
o The psychological system emphasizes the effects of psychodynamic factors,
motivation, and personality on the experience of illness and the reaction to it
o The social system emphasizes cultural, environmental, and familial influences
on the expression and the experience of illness.

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Normality: A state of physical, mental and social wellbeing not merely absence of
disease

 Functional Perspectives of Normality

 The four perspectives of normality as described by Daniel Offer and
Melvin Sabshin are
(1) normality as health,
(2) normality as utopia,
(3) normality as average,
(4) normality as process.

 Normality in Context
o Autonormal :- Person seen as normal by his or her own society
o Autopathological:- Person seen as abnormal by his or her own society
o Heteronormal :- Person seen as normal by members of another society
observing him or her
o Heteropathological:- Person seen as unusual or pathological by members of
another society observing him or her

 Epigenetic principle, which maintains that each stage is characterized by events or

crises that must be resolved satisfactorily for development to proceed smoothly.

 DEVELOPMENTAL PSYCHOLOGY The eight conventional stages of development are

as follows:
(1) The prenatal period (from conception to birth),
(2) Infancy (from birth to about 15 months),
(3) The toddler period (15 months to 2½ years),
(4) The preschool period (2½ to 6 years),
(5) The middle years (6 to 12 years),
(6) Adolescence (12 to 19 years),
(7) Adulthood (20 to 65), and
(8) Late adulthood (old age).

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 GENERAL PSYCHOLOGY
DEFINING PSYCHOLOGY:-
 Study of the soul ------- 16thcentury
 Study of the mind--------17thcentury
 Study of consciousness –18th century
 William James published principles of psychology in 1980
 Study of behaviour ------ 19th century
 William McDougall defined psychology as the science of behaviour. In
his book physiological psychology in .
 Psychology is the science which aims to give us better understanding
and control of the behaviour of the organism as a whole.
 J.B. Watson, is the father of behaviourisim.
 BEHAVIOUR:- Any manifestation of the life is activity (walking, swimming, thinking,
feeling…etc).
 BRANCHES OF PURE PSYCHOLOGY
 General psychology: - the fundamental rules, principles, and theories of
psychology in relation to the behaviour of normal adult.
 Abnormal psychology:- the behaviour of abnormal people in relation
to their environment.
 Social psychology:- Group behaviour and inter-relationship of people
among themselves.
 Experimental psychology:- scientific experiment of behaviour.
 Physiological psychology:- explains the biological and physiological
basis of behaviour.
 Parapsychology:- deals with the extra-sensory perception,
precognition, cases of claimed rebirth, telepathy, and allied
phenomena.
 Geopsychology:- explains the relationship of physical environment,
particularly weather, climate, soil, and landscape with behaviour.
 Developmental psychology:- explain the process and product of growth
and development in relation to the behaviour of an individual from
birth to old age.

 BRANCHES OF APPLIED PSYCHOLOGY.

 Educational psychology:- application of the psychological principles,
theories, and techniques to human behaviour in educational situations.
 Clinical psychology:- describes and explains the causes of mental
illness.
 Industrial psychology :- application of the psychological principles,
theories, and techniques to human behaviour in industrial situations.

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 SCHOOLS OF PSYCHOLOGY
 STRUCTURALISM:-
 Wilhelm Wundt started the world s first psychological
laboratory in Leipzig in 1879 with sole purpose of the systemic
study of the mind.
 He focused his attention on the analysis of the components of
consciousness.
 Consciousness or experience can be broken or analysed into
three basic elements: physical sensations, feelings, and images
such as memories and dreams.

 FUNCTIONALISM:-
 William James is one of the pioneers of the functional school of
psychology.
 He claimed that consciousness or experience cannot be broken
up into, and there is no way to separate ideas, thoughts,
sensations or perceptions.
 The consciousness or mental life, according to him, is a
continuous and flowing unity, a stream that carries the
organism in its adaptation to the environment.

 BEHAVIOURISM
 J.B. Watson is the father of behaviourism
 Consciousness cannot be proved by any scientific test,
therefore, we should concentrate only on the observable and
measurable behaviour.
 GESTALT PSYCHOLOGY
 The most prominent member in this school were Max
Wertheimer, Kurt Koffka, Wolfgang Kohler, and Kurt Lewin.
 Gestalt psychology used the term insight to describe this type
of human behavioural process as consisting of the following
three steps:
o Perception of the situation as a whole.
o Seeing and judging the relationships between various
factors involved in the situation.
o Taking an immediate decision and behaving accordingly.

 SCHOOL OF PSYCHOANALYSIS
 The most prominent member in this school were Sigmund
Freud, Alfred Adler (individual psychology), Carl jung
(analytical psychology)

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  Neo Freudians: Anna Freud, Karen Horney, Harry Stack
Sullivan, Erich Fromm, Erik Erikson, and (inz (artman …etc.

 HUMANIST PSYCHOLOGY
 Reflects the recent trends of humanism in psychology.
 Abraham Maslow, Carl Rogers, Gordon Alport…ect

 COGNITIVE PSYCHOLOGY
 Studies man s thinking, memory, language, development,
perception, imagery, and other mental processes in order to
peep into the higher human mental functions like insight,
creativity and problem solving.
 Jean Piaget is the most prominent cognitive psychologist.

 TRANSPERSONAL PSYCHOLOGY
 Deals with what we think and how we feel in our altered states
of awareness.

 PSYCHOANALYSIS- FREUD S SYSTEM OF PSYC(OLOGY

Structural theory of mind;
o Id
o Ego
o Superego
Topographical theory of mind;
o Conscious
o Preconscious
o Unconscious.
 Topographical theory of mind:
o If we were to compare the human mind to an ocean, pond, or river, then
the upper layer of the surface would represent the conscious mind, then
the bed would be identified with the subconscious, and the bottom would
form the unconscious.
o Conscious mind occupies the upper 1/10 of mind. The ideas, thoughts,
images that we are aware of, at any movement of our mental life.
o Sub-conscious mind stores all types of information just beneath the
surface of awareness as dormant and which can be easily brought to the
level of consciousness at a movement s notice whenever required.
o Unconscious mind is related to the vast part of mental life which is hidden
and is usually inaccessible to the conscious. It contains all the repressed
wishes, desires, feelings, drives, and motives, many of which relate to sex
and aggression.

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  Structural theory of mind:
o The Id represents the animal in men and is seated in the unconscious. It is
the source of mental energy and all instinctive energy of the individual.
o Id is quite selfish and unethical. It knows no reality, follows no rules and
considers only the satisfaction of its own needs and drives.
o Super ego represents the ethical and moral aspect of the psyche. It usually
develops in the child at the age of five years. It is idealistic in nature, and
perfection is its goal, rather than pleasure seeking or destruction.
o The Ego develops out of the Id and acts as an intermediary between three
sets of forces,
 The instinctive, irrational demands of the Id.
 Realties of the external world.
 The ethical and moral demands of the super ego.

 PSYCHODYNAMICS—BEHAVIOURAL PROCESS:

o LIFE AND DEATH INSTINCTS:

1. Freud believed in the role of instinct in driving human behaviour.
2. One s life instinct is engaged, the service of one s life and its main aims
are survival and propagation of the species. It is manifested through
sex and love.
3. Death instinct relates to the impulse for destruction. It is manifested
through acts of aggression, cruelty and even suicide.

o PSYCHOSEXUAL DEVELOPMENT
1. According to Freud, sex is life urge or fundamental motive in life. All
physical pleasures arising from any of the organ or any of the functions
are ultimately sexual in nature. these are following five stages;
 The oral stage (birth-2years):- Mouth represents the first sex
organ for providing pleasure to the child.

 The anal stage (2-3years): the child shifts from the mouth as the
erogenous zone to the organ of elimination, i.e. the anus or the
urethra. He derives pleasure by holding back or letting go of the
body s waste material through the anus or urethra.

 The phallic stage (4-6years): the child shifts from the

eliminating organs to genitals. At this stage children notes the
biological differences between sex and drive pleasure by playing
with and manipulating the genital organs. Electra complex in
girls and Oedipus complex in boys are seen in this stage.

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  The latency stage(6years-puberty): at this stage boys and girls
prefer to be in the company of their own sex and even neglect or
hate members of the opposite sex.

 The genital stage: at the time of puberty the boy and girl now
feels a strange feeling of strong sensation in the genitals and
attraction towards the members of opposite sex.

 DEFENSE MECHANISMS: At each phase of libidinal development, specific drive

components evoke characteristic ego defenses. The anal phase, for example, is
associated with reaction formation, as manifested by the development of shame and
disgust in relation to anal impulses and pleasures.

 George Valliant; Classification of defense mechanism;

 Neurotic
 Immature
 Mature
 Narcissistic.

NARCISSISTIC (DDP)
o D-Denial
o D-Distortion
o P-Projection

NEUROTIC (DIC, RED, RIS, RI)

o D-Displacement
o I-Inhibition
o C-Controlling
o R-Reaction formation
o E-Externalization
o D-Dissociation
o R-Repression
o I-Isolation
o S-Sexualisation
o R-Rationalization
o I-Intellectualization

IMMATURE (HP-RABISS)
o H-Hypochondriasis
o P-Passive aggressive behaviour
o R-Regression
o A-Acting out
o B-Blocking
o I-Introjection
o S-Schizoid fantasy
o S-Somatisation

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 MATURE (A3, S2, H)
o A-Altruism
o A-Anticipation
o A-Asceticism
o S-Sublimation
o S-Suppression
o H-Humour

 DEFENCE MECHANISMS VARIOUS DISORDERS

OCD
o Isolation
o Undoing
o Reaction formation
o Intellectualization
PHOBIA
o Displacement
o Projection
o Undoing
o Avoidance
PANIC DISORDER
o Reaction formation
o Somatization
o Externalization
P.T.S.D
o Denial
o Minimization
o Splitting
o Dissociation

 NARCISSISTIC DEFENSES (DDP)

o Denial: Avoiding the awareness of some painful aspect of reality by negating
sensory data.

o Distortion: Grossly reshaping external reality to suit inner needs and using
sustained feelings of delusional superiority or entitlement.

o Projection: Perceiving and reacting to unacceptable inner impulses and their

derivatives as though they were outside the self.

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 NEUROTIC DEFENSES (DIC, RED, RIS, RI)
o Displacement: Shifting an emotion or drive cathexis from one idea or object to
another that resembles the original in some aspect or quality.

o Inhibition: Consciously limiting or renouncing some ego functions.

o Controlling: Attempting to manage or regulate events or objects in the

environment to minimize anxiety and to resolve inner conflicts.

o Repression: Expelling or withholding from consciousness an idea or feeling.

Primary repression refers to the curbing of ideas and feelings before they have
attained consciousness: secondary repression excludes from awareness what
was once experienced at a conscious level.

o Externalization: Tending to perceive in the external world and in external

objects elements of one's own personality, including instinctual impulses,
conflicts, moods, attitudes, and styles of thinking.

o Dissociation: Temporarily but drastically modifying a person's character or

one's sense of personal identity to avoid emotional distress.

o Reaction formation: Transforming an unacceptable impulse into its opposite.

o Isolation: Splitting or separating an idea from the affect that accompanies it

but is repressed.

o Sexualisation: Endowing an object or function with sexual significance that it

did not previously have or possessed to a smaller degree to ward off anxieties
associated with prohibited impulses or their derivatives.

o Rationalization: Offering rational explanations in an attempt to justify

attitudes, beliefs, or behavior that may otherwise be unacceptable.

o Intellectualization: Excessively using intellectual processes to avoid affective

expression or experience.

 IMMATURE DEFENSES (HPRABISS)

o Hypochondriasis: Exaggerating or overemphasizing an illness for the purpose
of evasion and regression.

o Passive-aggressive behaviour: Expressing aggression towards others

indirectly through passivity, masochism, and turning against the self.

o Regression: Attempting to return to an earlier libidinal phase of functioning to

avoid the tension and conflict evoked at the present level of development.

o Acting out: Expressing an unconscious wish or impulse through action to

avoid being conscious of an accompanying affect.
o Blocking: Temporarily or transiently inhibiting thinking.

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 o Introjection: Internalizing the qualities of an object.

o Somatization: Converting psychic derivatives into bodily symptoms and

tending to react with somatic manifestations, rather than psychic
manifestations.

o Schizoid fantasy: Indulging in autistic retreat to resolve conflict and to obtain

gratification.

 MATURE DEFENSES (A3S2H)

o Altruism: Using constructive and instinctually gratifying service to others to
undergo a vicarious experience.

o Anticipation: Realistically anticipating or planning for future inner discomfort.

o Asceticism: Eliminating the pleasurable effects of experiences.

o Suppression: Consciously or semiconsciously postponing attention to a

conscious impulse or conflict.

o Sublimation: Achieving impulse gratification and the retention of goals but

altering a socially objectionable aim or object to a socially acceptable one.

o Humour: Using comedy to overtly express feelings and thoughts without

personal discomfort or immobilization and without producing an unpleasant
effect on others.

 PSYCHOANALYSIS AS A THERAPY
 Establishment of rapport
 Analysis: according to Freud, the behavioural problem or
mental illness is the result of repressed wishes and desires
dumped into the unconscious. The unconscious needs to be
explored by free association, dream analysis, and analysis of
daily psychopathology.
 Synthesis: after discovering the reasons or roots of the trouble,
attempts are made to restructure and restore the balance of the
psych.
 Breaking the rapport.

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 ADLER S SYSTEM OF )ND)V)DUAL PSYC(OLOGY
o Born in Vienna in 1870, Alfred Adler began his career as an ophthalmologist.
He joined Freud s school of psychoanalysis in .
o (is system is called individual psychology because it lays emphasis on the
individuality of human being in terms of unique characteristics at the time of
birth, the availability of an exclusive environment for growth and
development and adoption of specific style of life to achieve power and attain
perfection.

 JUNG S ANALYT)CAL PSYC(OLOGY

o According to Jung, one s mind consists of the following parts
1. Conscious mind: the upper layer of one s mind consists of memories,
thoughts, feelings that result from one s consciousness.
2. Personal unconscious: lies beneath the conscious layer, highly
individualistic and personal in nature. It contains all the repressed
desires, ideas, feelings, fears, guilt s, anxieties, dreams and fantasies
which might occur in the life time of an individual.
3. Collective unconscious: this is neither personal nor private but is
universal to all individuals. One s collective unconscious thus contain
the experiences of the whole race gathered over millions of ancestral
years specifically in the form of universal ideas or images called
Archetypes.
 Mother archetype, father archetype, hero archetype, and
persona are primary archetypes. Anima, animus, shadow, and
the self are secondary archetypes.
 Mother archetype: it is an eternal idea or image which is
inherited from generation to generation and is common and
universal to all cultures. The image of mother always appears to
be pious, warm, loving, protective, and nourishing.
 The father archetype: reflects strength, authority, and power.
 The hero archetype: the ideas which are quite universal and
identical like the images of god, birth and death, demon and
devil, saints and wise men and the existence some energy force
moving this world.
 Persona: this signifies the mask we wear to face society
introspective our real personality.
 Anima: this is associated with the female characteristics and
animus with image of maleness. So, every male has a female in
him and every female has a male in her.
 The shadow: it is resembles the concept of Freud s )d.

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 4. Jung s personality types:
o The introverted thinking type
o The extroverted thinking type
o The introverted feeling type
o The extroverted felling type
o The introverted sensational type
o The extroverted sensational type
o The introverted intuitive type
o The extroverted intuitive type

 ALFRED ADLER (1870-1937)

o Adler never accepted the primacy of the libido theory. Adler thought that
aggression was far more important, specifically in its manifestation as a strive
for power, which he believed to be a masculine trait. He introduced the term
masculine protest to describe the tendency to move from a passive, feminine
role to a masculine, active role. Adler's theories are collectively known as
individual psychology.
o Adler coined the term inferiority complex to refer to a sense of inadequacy
and weakness that is universal and inborn.
o Adler was one of the first developmental theorists to recognize the
importance of child's birth order in their families of origin. The firstborn child
reacts with anger to the birth of siblings and struggles against giving up the
powerful position of only child. The second-born child must constantly strive
to compete with the firstborn. Adler thought that a child's sibling position
results in lifelong influences on character and lifestyle.

 ERIC BERNE (1910-1970)

o Eric Berne developed his own school, known as transactional analysis. A
transaction is a stimulus presented by one person that evokes a
corresponding response in another. Berne defined psychological games as
stereotyped and predictable transactions that persons learn in childhood and
continue to play throughout their lives. Strokes, the basic motivating factors
of human behavior, consist of specific rewards, such as approval and love.
o All persons have three ego states that exist within them: the child, which
represents primitive elements that become fixed in early childhood; the adult,
which is the part of the personality capable of objective appraisals of reality;
and the parent, which is an introject of the values of a person's actual parents.

 DEVELOPMENTAL PSYCHOLOGY
 A few well- known theories are,
1. Freud s theory of psychosexual development.
2. Jean Piaget s theory of cognitive development.
3. Erikson s theory of psycho-social development.
4. Kohlberg s theory of moral development.

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 JEAN P)AGET S T(EORY: Swiss biologist and epistemologist.
o Epistemology : a branch of philosophy concerned with the nature of
knowledge.
o He defined intelligence as the ability to adjust, adapt, or deal efficiently with,
one s environment.
o The changes and developments in one s cognitive structure are brought about
by interaction with one s physical and social environment.
o According to him, there are two aspects of human mind cognitive structure
and cognitive functioning.
o Cognitive structure: the human baby is born with a few practical instincts and
reflexes such as sucking, looking, reaching, and grasping. These abilities are
called schemas.
o Cognitive functioning: The schemas decide how is the child going to respond
to the stimuli present in his physical or social environment.
o Assimilation refers to a kind of matching between the already existing
cognitive structures and the environmental needs as they arise.
o Accommodation as one tries to accommodate or adjust to new ways of
thinking and behaving in place of assimilating in the same old fashion.

Cognitive developmental stages (Special Protection Control Force)

o Sensory motor stage -------------- (Birth-2years)

o Preoperational stage-------------- (2y -7y)
o Concrete operational stage ------ (7y-11y)
o Formal operational stage --------- (11y-end of adolescent)

 Sensory motor stage :

o Sensory–motor intelligence (first 2 years)

 Modification of reflexes---------------------(birth–1 month)
 Primary circular reactions -----------------(1–4 months)
 Secondary circular reactions--------------(4–10 months)
 Coordination of secondary schemas ----(10–12 months)
 Tertiary circular reactions -----------------(12–18 months)
 Representational thinking -----------------(18–24 months)

o At birth the infant exhibits a limited number of uncoordinated reflexes such as

sucking, looking, reaching, and grasping.
o During next four months the uncoordinated reflexes are coordinated into
simple schemas providing the child with a general potential to perform certain
classes of behaviour.
o At age of 8 months the infant is able to recognise objects outside himself. He
begins to realise that the objects around him are separate from himself and
this is called object permanence.

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 Pre-operational stage: (2-7years)
o The child begins to replace direct action in the form of sensory or motor
exploration with symbols.
o The child seems to identify objects by their name and put them into certain
classes. Their mode of thinking and reasoning is quite illogical and sometimes
too imaginative.
o Approximately 4-7 years the child progresses to the formation of various
concepts at a more advanced level.
o His thinking is more egocentric.

 Concrete operational stage: (7-11years)

o The child learns to deal with concepts and ideas that exist only in the mental
terms.
o He begins to think in terms of a set of interrelated principles rather than single
bits of knowledge.
o His thinking become more logical and systematic.
o The child now develops the ability to both in terms of quantity and number of
objects.
 Formal operational stage(12-15 years)
o At this stage the child learns to deal with abstraction by logical thinking.
o He begins to construct relationships between concrete operations and
between symbols.

 ERIK ERIKSON (1951) PSYCHOSOCIAL STAGE

Stage associate virtue

 Trust Vs Mistrust (Birth-18 months) Hope

 Autonomy Vs Shame (18months-3years) Will
 Initiative Vs Guilt (3y-5y) Purpose
 Industry Vs inferiority (5y-13y) Competence
 Identity Vs Role confusion (13y-21y) Fidelity
 Intimacy Vs isolation (21y-40y) love
 Generativity Vs stagnation (40y-60y) Care
 Integrity Vs Despair (60y-death) Wisdom

1. Infant (Trust vs. Mistrust): needs maximum comfort with minimal uncertainty to
trust himself/herself, others, and environment.
2. Toddler (Autonomy vs. shame): works to master physical environment while
maintaining self-esteem.
3. Pre-schooler (Initiative vs. Guilt): begins to initiate, not imitate, activities; develops
conscience and sexual identity.

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4. School-age child (Industry vs. inferiority): tries to develop a sense of self-worth by
refining skills.
5. Adolescent (Identity vs. Role confusion): tries integrating many roles (child, sibling,
student, athlete, worker) into a self-image under role model and peer pressure.
6. Young adult(Intimacy vs. isolation): learns to make personal commitment to another
as a spouse, parent or partner.
7. Middle-age adult (Generativity vs. Stagnation): seeks satisfaction through
productivity in career, family, and civic interaction.
8. Older adult(Integrity vs. despair): reviews life accomplishment, deals with loss and
preparation for death.

 KO(LBERG S T(EORY OF MORAL DEVELOPMENT

o (e defined moral development as the development of an individual s sense of
justice. He identified three levels of moral development, each containing two
stages,
o Level –I: Pre-moral(age 4-10 years)
 Stage 1: the stage of obedience for avoiding punishment.
 Stage 2: the stage of conforming to obtain rewards or favours in return.
o Level-II: conventional morality (age 10-13 years)
 Stage 3: the stage of maintaining mutual relations and approval of
others.
 Stage 4: the stage of obedience for avoiding censure by higher
authority or social system.
o level III: (age 13 or adulthood or never)
 Stage 5: stage of conforming to the democratically accepted law and
morals of community welfare.
 Stage 6: stage of conforming to the universal ethical principles and the
call of one s conscience.

 COGNITION: The intellectual skills that allows you to perceive, acquire, understand,
and respond to information. This includes…..
o Ability to pay attention
o Remember
o Process information
o Solve problem
o Organize and reorganize information
o Communicate and act upon information
 Cognitive dysfunction:
o Primary: illness themselves that cause much of cognitive dysfunction.
o Secondary: Secondary to some other factors.

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 How does mental illness affect cognition: the mentally ill often experience problems
in the following aspects of cognition:
o Ability to pay attention.
o Ability to remember and recall information.
o Ability to process information quickly.
o Ability to respond information quickly.
o Ability to think critically, plan, organize, and solve problems.
o Ability to initiate speech.
 More common psychiatric disorders affects cognition:
o Schizophrenia
o BPAD
o GAD
o OCD
o PTSD
o ADHD
o Depression
o Panic disorder
o Delirium
o Dementia
o Degenerative disorder
 Aetiology of cognitive deficit:
o Genetic
o Epigenetic
o Developmental
o Environmental
 The above causes which leads to changes in,
o Cellular signalling.
o Gene transcription and mRNA transcription.
o DNA and epigenetic codes.
o Firing rate and pattern.
o Synaptic plasticity and neurogenesis.
o Neuromodulator release.
 EFFECT OF COGNITIVE DOMAINS
o Universal domains:
 Attention, working memory, executive functions.
 Procedural learning and memory.
 Speed of processing.
 Fear-extinction memory.
 Semantic memory.

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 o Higher domains
 Episodic memory.
 Social cognition.
 Verbal learning and memory.
 Language.

 CIRCUITS IN UNDERSTANDING COGNITIVE DOMAINS:

o Frontal lobe attention
o Basal ganglia working memory
o Thalamus executive memory

 Frontal lobe Basal ganglia

Dorsolateral prefrontal cortex dorsolateral caudate nucleus
Anterior cingulate gyrus Nucleus Accumbens
Orbitofrontal cortex ventromedial caudate nucleus

Globus pallidus
Substantia nigra

Thalamus
Ventral anterior nucleus
Medial dorsal nucleus

 Frontal lobe
o Prefrontal cortex (PFC) ------------- programming and planning.
o Anterior cingulate gyrus (ACC) ---- decision making.
o Orbitofrontal cortex (OFC) ------- response initiation.

Attention
Parietal lobe working memory
Intelligence

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 Hippocampal formation
o Hippocampus
o Entorhinal cortex
o Para hippocampus

Dentate gyrus (CA3 and CA1 pyramidal neurons)

Declarative memory and learning.

 Centro medial amygdala

Brainstem

Periaqueductal gyrus and facial motor nucleus

Conditioned fear memory

 Cerebellar modulation for cognition

Prefrontal cortex and parietal cortex

Thalamus pons

Basal ganglia cerebellum

 Social cognition and verbal learning

o Left hemisphere ---------- Verbal language
o Right hemisphere
 Prosody and abstract features of language
 Facial processing
 Theory of mind

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 Facial processing
o Facial perception --------- inferior occipital gyrus
o Facial recognition and matching ------- temporo-parietal junction
o Gaze tracing -------- superior temporal sulcus and temporo-parietal junction.
o Interpretation of facial emotions
 Amygdala
 Insula
 Prefrontal cortex
 Anterior cingulate gyrus
 Orbitofrontal cortex

MEMORY
It is a process which we encode, storage and retrieve of the information.
 Theories of memory
 Theory of general memory function
 Information-processing theory(Atkinson-Shiffrin theory)
 Level-processing theory

Theory of general memory function

o Encoding, Storage ,and Retrieval (ESR)

Information processing theory (Atkinson –Shiffrin theory)

o Information Sensory memoryShort term memorylong-term memory.

Levels of processing theory

o Perception Input analyserAnalysis of memoryElaboration of memory.

Chunk : the storage capacity of short-term memory can be increased by process

known as chunking. Most of us have learned to combine several items into a chunk.

WORKING MEMORY
An active space, in which information is retained, manipulated and held through
rehearsals.
It is just like a RAM in the computer
It contains; Central executive processor, Visual storage and Verbal storage

Sites of memory;
 Working memory-------- Lt Frontal cortex
 Declarative/ Explicit memory------Cingulate gyrus, and lateral temporal cortex
 Procedural /implicit memory------- Basal ganglia and cerebellum

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  Episodic memory--Ant. Thalamic nucleus, mammillary body, prefrontal cortex.
 Semantic memory: the meanings of the words of our language and the rules
for their use.
 Episodic memory: the long-term memories of specific things that happened to
us at a particular time and place. Eg when I was 18 years old, I joined the
M.B.B.S

Memory scales;
o PGI memory scale
o Wechsler memory scale
o Verbal-Adult intelligence scale

Tip of tongue phenomenon

The inability to recall information that is realizes one knows.

Papez circuit
o Thalamuscingulate gyrushippocampusamygdalahypothalamus
thalamuspre frontal cortex.

Amnesia
Inability to recall past information or inability to learn new information
Types;
 Psychogenic amnesia: May able to learn new information
 Organic amnesia: unable to learn new information
 Paramnesia: Distortion of recall and Distortion of recognition

Psychogenic amnesia;
o Dissociative/hysterical amnesia
o Katathymic amnesia/ motivational forgetting
o Anxiety amnesia
o Pseudo amnesia (depression)

Organic amnesia;

 Anterograde amnesia
Inability to learn new information after head injury/Inability to recall
the events after the head injury. More anterograde amnesia- WORST
PROGNOSIS

 Retrograde amnesia
Inability to recall the events prior to the head injury.More retro grade
amnesiaMORE BRAIN DAMAGE.

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  Blackouts Circumscribed anterograde memory loss seen in alcoholics
Paramnesias
 Distortions of recall
o Retrospective falsifications
o False memory
o Screen memory
o Confabulation
o Pseudologia fantastica
o Munchausen syndrome
o Vorbeireden/ Approximate answers
o Cryptamnesia
o Retrospective delusion

 Distortion of recognition ;
o Déjà vu feeling of familiarity in unfamiliar setting
o Deja entendu;
o Jamais vu ;  feeling of un familiarity in familiar setting
o Deja pense

LEARNING
Kimble: A relative permanent change in behaviour brought about by experience

Elements: change in behaviour, take place through practice, relatively permanent

Types of learning;-
o Classical conditioning,
o Operant conditioning,
o Social learning

CLASSICAL CONDITIONING;- proposed by Ivan petrovich Pavlov

Learning is thought to take place as result of contiguity of environment, it is also

called as respondent conditioning.

Classical Conditioning
o Classic (also called respondent) conditioning results from the repeated pairing of a
neutral (conditioned) stimulus with one that evokes a response (unconditioned
stimulus), such that the neutral stimulus eventually comes to evoke the response.

o The Russian physiologist and Nobel Prize winner Ivan Petrovich Pavlov (1849-1936)
observed in his work on gastric secretion that a dog salivated not only when food was
placed in its mouth but also at the sound of the footsteps of the person coming to feed
it, even though the dog could not see or smell the food.

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 o In a typical pavlovian experiment, a stimulus (S) that had no capacity to evoke a
particular response before training did so after consistent association with another
stimulus. For example, under normal circumstances, a dog does not salivate at the
sound of a bell, but when the bell sound is always followed by the presentation of
food, the dog ultimately pairs the bell and the food. Eventually, the bell sound alone
elicits salivation (CR).

o Because the food naturally produces salivation, it is referred to as an unconditioned

stimulus (UCS). Salivation, a response that is reliably elicited by food (UCS), is
referred to as an unconditioned response (UCR). The bell, which was originally
unable to evoke salivation but came to do so when paired with food, is referred to as
a conditioned stimulus (CS). Classic conditioning is most often applied to responses
mediated by the autonomic nervous system.

Extinction
o Extinction occurs when the conditioned stimulus is constantly repeated without the
unconditioned stimulus until the response evoked by the conditioned stimulus
gradually weakens and eventually disappears.

o In the previous example, extinction would occur if the bell (CS) is rung repeatedly
without the food (UCS) being given. Eventually, salivation (CR) does not occur when
the bell sounds, and extinction occurs.

o Extinction, however, does not completely destroy a conditioned response. If an

animal is rested after extinction, the conditioned response returns, although less
strong than originally, a phenomenon known as partial recovery.

o The American psychologist John B. Watson (1878-1958) used Pavlov's theory of

classic conditioning to explain certain aspects of human behavior. In 1920, Watson
described producing a phobia in an 11-month-old boy called Little Albert. At the
same time that the boy was shown a white rat that he initially did not fear, he was
exposed to a loud, frightening noise. After several such pairings, Albert became
fearful of the white rat, even when he heard no loud noise.

OPERANT CONDITIONING
o B. F. Skinner (1904-1990) developed a theory of learning and behavior known as
operant conditioning. Whereas in classic conditioning an animal is passive or
restrained and behavior is reinforced by the experimenter, in operant conditioning
the animal is active and behaves in a way that produces a reward; thus learning
occurs as a consequence of action. For example, a rat receives a reinforcing stimulus
(food) only when it correctly responds by pressing a lever.

o Operant conditioning is related to trial-and-error learning, as described by the

American psychologist Edward L. Thorndike.

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 o In trial-and-error learning, a person or animal attempts to solve a problem by trying
different actions until one proves successful. A freely moving organism behaves in a
way that is instrumental in producing a reward. For example, a cat in a Thorndike
puzzle box must learn to lift a latch to escape from the box. For this reason, operant
conditioning is sometimes called instrumental conditioning.

o Four kinds of operant conditioning are described. primary reward conditioning,

escape conditioning, avoidance conditioning, and secondary reward conditioning.

Respondent and Operant Behavior

o Skinner described two types of behavior: respondent behavior, which results from
known stimuli (e.g., the knee jerk reflex to patellar stimulation or the pupillary
constriction to light), and operant behavior, which is independent of a stimulus (e.g.,
the random movements of an infant or the aimless movements of a laboratory rat in a
cage).

Reinforcement Schedule (Programming)

o Reinforcers are described as primary when they are independent of previous
learning (e.g., the need for food or water) and secondary when they are based on
previously rewarded learning (e.g., giving money to a child with good grades). In
operant conditioning, the schedule of reward or reinforcement for a behavioral
pattern can vary in a process known as programming. The intervals between
reinforcements may be fixed (e.g., every third response is rewarded) or variable (e.g.,
sometimes the third response is rewarded; at other times, the sixth response is
rewarded).

o In operant conditioning, positive reinforcement is the process by which certain

consequences of a response increase the probability that the response will recur.
Food, water, praise, and money are positive reinforces.

o Experiments of positive reinforcement

 Thorndike s Experiment –Cat in a puzzle box

 Mazes
 Skinner s Experiments –Rats and Pigeons in an operant chamber

o Negative reinforcement is a process by which a response that leads to the removal of

an aversive event is increased. For example, an animal jumps off a grid to escape a
painful shock.

o Punishment is an aversive stimulus (e.g., a slap) that is presented specifically to

weaken or suppress an undesired response; punishment reduces the probability that
a response will recur.

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Negative reinforcement is related to two types of learning,
o Escape learning and avoidance learning. In escape learning, an animal learns a
response to get out of a place where it does not want to be (e.g., an animal jumps off
an electric grid whenever the grid is charged).

o Avoidance learning requires an additional response. The rat on the grid learns to
avoid a shock if it quickly pushes a lever when a light signal goes on.

Shaping Behaviour
o Shaping involves changing behavior in a deliberate and predetermined way. Shaping
is also called successive approximation.

Premack's Principle
o A concept developed by David Premack states that a behavior engaged in with high
frequency can be used to reinforce a low-frequency behavior. In one experiment,
Premack observed that children spent more time playing with a pinball machine than
eating candy when both were freely available.

 Reinforcement schedule
o Fixed ratio schedule
o Fixed interval schedule
o Variable ratio schedule
o Variable interval schedule

Social Learning Theory

o Social learning theory relies on role modelling, identification, and human
interactions. A person can learn by imitating the behavior of another person, but
personal factors are involved.

o Albert Bandura is a major proponent of the social learning school. According to

Bandura, behavior results from the interplay between cognitive and environmental
factors, a concept known as reciprocal determinism. Persons learn by observing
others, intentionally or accidentally; this process is described as modelling, or
learning through imitation.

Cognitive Learning
o Cognition is the process of obtaining, organizing, and using intellectual knowledge.

Cognitive Dissonance
o Cognitive dissonance means incongruity or disharmony among a person's beliefs,
knowledge, and behavior.

Neurophysiology of Learning
o One of the first theorists to explore the neurophysiological aspects of learning was
Clark L. Hull (1884-1952), who developed a drive reduction theory of learning. Hull
postulated that neurophysiological connections established in the central nervous
system reduce the level of a drive (e.g., obtaining food reduces hunger).

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 o An external stimulus stimulates an efferent system and elicits a motor impulse. The
critical connection is between the stimulus and the motor response, which is a
neurophysiological reaction that leads to what Hull called a habit. Habits are
strengthened when a response further reduces the drive associated with the aroused
need.

Habituation and Sensitization

o In the study of the snail Aplysia, Eric Kandel showed how simple forms of learning,
such as habituation and sensitization, can occur. Kandel studied a defensive reflex
involving the withdrawal of the snail's siphon when the animal is tactually
stimulated. If the snail is touched repeatedly, it is subject to habituation and learns
not to withdraw its siphon and gill. Habituation causes the organism to stop
responding reflexively as a result of the repeated stimulus.

LEARNING AND IMPRINTING

o )mprinting as a term was first used in by the Austrian ethologist Konard
Lorenz for describing the attachment behaviour of new-born birds to the first large
moving objects in their environment.
o In his initial experiments he demonstrated that ducklings and gooselings follow the
mother soon after hatching perhaps on account of the stimulation provided by her
movements and the noises she makes.
o Afterwards Lorenz used big objects like football in place of the mother to be followed
by new born ducklings and gooselings. He found that as soon as these birds were,
they began to follow the floating ball in the pond. Surprisingly, when the gooselings
were turned to their real mother later at a later stage.
o Imprinting thus represents a sense of strong connection or attachment that is made
between the new born organism ant the first object it may have initially responded
to.
o Imprinting thus represents an inborn perceptual process independent of any
training or experience.
o It is unquestionably a survival mechanism and whatever is the first object, it is
followed for safety, security, love and attachment.

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 INTELLIGENCE

The capacity to understand the world, think rationally and use of resources
effectively when faced with a challenge.

Theories of intelligence;
1) Factor theories
o G- Factor theory proposed by Spearman
o Multifactor theoryproposed by Thurstone
o Hierarchical theory

2) Process –oriented theories

o Piaget s theory
o Brunner s theory
o Information processing theory

Primary mental ability test; proposed by Thurstone (MN O P Q RS TU VW)

o MMemory
o NNumerical ability
o P-->perceptual ability
o RReasoning
o S Spatial ability
o V Verbal comprehension
o WWord fluency

 J.P. Guilford multi factor theory; (COP-456)

 4-Contents;
1) Figural.
2) Symbolic.
3) Semantics.
4) Behavioural.

 5-Operations;
1) Evaluation.
2) Convergent production.
3) Divergent production.
4) Memory.
5)Cognition

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  6-Products: -
1) Units
2) Classes
3) Relations
4) Systems
5) Transformation
6) Implications.

 Intelligence assessment :-
 Stanford –Binet intelligence scale.
 Intelligence coefficient (I.Q)= mental age/chronological age , proposed
by William stern.
 WECHSLER INTELLIGENCE TESTS :
 Wechsler adult intelligent scale (WAIS).
 WAIS – REVISED SCALE.
 Wechsler preschool and primary school scale of intelligence
 Wechsler intelligence scale for children.(WISC).
 WISC –REVISED SCALE.
 Wechsler adult performance intelligence scale
 WECHLERS ADULT INTELLIGENCE SCALE (WAIS)
It contains 6 verbal tests and 5 performance tests

Verbal tests(C-VAMSI) :
o C-Comprehension
o V-Vocabulary
o A-Arithmetic ability
o M-Memory span
o S-Similarities
o I-Information.

Performance tests (POP-BD)

o P-Picture arrangement
o O-Object assembly
o P-Picture completion
o B-Block design
o D-Digit symbol

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  WECHSLER ADULT PERFOMANCE INTELLIGENCE SCALE
It is Indian version of Wechsler test ,developed by Ramalinga swamy and it contains
hold and don t hold tests.

Hold tests don t hold tests

o Vocabulary test Digit span test
o Information test Similarity test
o Object assembly test Digit symbolisation test
o Picture completion test Block design test

It is used to assess deterioration coefficient=

Score of hold tests --score of don t hold test/score of don t hold test

 DEVELOPMENTAL SCREENING TESTS:

o Proposed by Bharath raj (1977)
o This test was based on developmental mile stones.
o It was useful between 3months- 15 years.

VINELAND – SOCIAL MATURITY SCALE:- Proposed by Malin

It assess 8 areas of life-
1) Eating skills
2) Dressing skills
3) Socialization skills
4) Occupational skills
5) Self-help skills
6) Communication skills
7) Locomotion skills
8) Self-direction skills

SEGUIN FORM BOARD

It is used to assess mental age, psychomotor coordination, visuo-spatial coordination.

STANDARD PROGRESSIVE MATRICE

o It is for normal people above 11 years age
o Colour progressive matrice for children (6y-11y)

BHATIA BATTERY; It contains 5 subscales

o Kohs block design test
o Alexander pass-along test
o Pattern drawing test
o Digit span test
o Picture construction test

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EMOTIONAL INTELLIGENCE:
 Abilities such as being able to motivate oneself and persist in the face of frustrations
 to control impulses and delay gratification
 to regulate one s mood and keep distress from swamping
 the ability to think
 to empathize and to hope.

Components of emotional intelligence

1.Self-awareness
2.Managing emotions
3.Motivating oneself
4.Recognizing emotions in others
5.Handling relationships

PERSONALITY
It is the dynamic organization with in the individual of those psychophysical systems
that determine its unique adjustment to his environment

 Personality disorder
An enduring pattern of inner experience and behaviour that deviate markedly from
expectations of the individual culture.

Classification of personality:
According to DSM-IV;---- cluster A , cluster B , and cluster C

Cluster A ; SSP ; ------characteristic behaviour is ODD and ALOOF

o S-Schizoid personality
o S-Schizotypal personality
o P-Paranoid personality

Cluster B (-BAN): characteristic behaviour is DRAMATIC, IMPULSIVE, and

ERRATIC
o H-Histrionic personality
o B-Borderline personality
o A-Antisocial personality
o N-Narcissistic personality

Cluster C OCD-A); characteristic behaviour is ANXIOUS AND FEARFUL

o O-Obsessive and Compulsive personality
o D-Dependent personality
o A-Avoidant personality

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  THEORIES OF PERSONALITY;

o Type and trait theories

o Dynamic theories
o Learning and behavioral theories
o Humanistic theories

TYPE AND TRAIT THEORIES

Type theories
o Eysenicks hierarchical theory
o Strike zone theory
Trait theories

ALPORT TRAITS
 Cardinal traits
 Central traits
 Secondary traits
HIPPOCRATIC TRAITS;
 Sanguine trait----- cheerful, vigorous, confident.
 Phlegmatic -------- calm and slow moving
 Melancholic ------ depressed and Morose
 Choleric ---------- hot tempered

INTROVERTS; shyness, social withdrawal, and tendency not to talk much

EXTROVERTS; tendency to go out, friendly and talkative.

DYNAMIC PERSONALITY THEORIES

o Freud psychoanalytic theory

 Structural theory of mind

 Topographical theory of mind
 Psycho sexual stages

o Jung s analytic theory

o Horney s psychoanalytic interpersonal theory
o Adler individual psychology

LEARNING AND BEHAVIORAL THEORIES

o Dollard Miller theory

o Skinners-radical behaviourism
o Bandura and Walters

40
HUMANISTIC THEORIES

o Rogers self-theory
o Maslow –self actualization

 MEASUREMENT OF PERSONALITY
o Pencil-paper tests
o Projective tests
o Behavioural test

 PENCIL-PAPER TESTS
 Minnesota Multiphasic Personality Inventory(MMPI);
It contain 566 statements (yes/no, true/false) and 10 clinical scales (HDHPMPPSHS)
o H- Hypochondriasis (Hs)
o D- Depression(D)
o H- hysteria (HY)
o P-Psychopathic deviate(pd)
o M-Masculinity &Feminity(Mf)
o P-Paranoia (pa)
o P-Psychasthenia(Pt)
o S-Schizophrenia(Sc)
o H-Hypomania(Ma)
o S-Social introversion

 Millon clinical multi axial inventory I & II

 16 personality factor test
 California personality inventory
 Eysencks personality questionnaire
 Jackson personality inventory

 PROJECTIVE PERSONALITY TESTS

o Rorschach test
o Thematic apperception test by Murray and Morgan
o Sentence completion test
o Holtzman ink blot test
o Draw a person test
o Make a picture test

RORSCHACH TEST
- Developed by Herman Rorschach in 1910
- Contains 10 ambiguous, symmetrical ink blot cards (I-X)
- Each has a specific meaning
- 5 cards achromatic(black & white), 5 cards chromatic (multicolour)
- Achromatic cards -I,IV,V,VI, & VII(black and white)

41
 - Chromatic cards II & III (black, white and red)& VIII, IX,X(multicolour)

Meaning of cards
I-Initial reaction to the world
IIThreatening nature
IIIInterpersonal relation
IVrelationship towards father
VReality card
VIAttitude towards sex
VII Attitude towards mother
VIIIReality card
IX Neurotic card
XSocial adaption

Scoring of Rorschach test;

o Response time
o Location
o Content
o Determinant

Response time
o < 5sec---Mania
o Long -- depression
o Variableschizophrenia

Location (Where it is seen)

 W - whole response
 DW confabulatory whole response
 D - Large usual response
 Dd -large unusual details
 d Small usual details
 dd small unusual details
 S white space response

Content (What is seen)

o (  living human being
o (d  Details of human figure
o A Animal
o Ad details of Animals
o At Anatomy(X-RAY, surgical specimens)
o Obs Objects
o N nature
o T topical(fire,blood,sex..ect)

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 Determinant;
Form; +/-
Movement;
 M  Human
 FM Animal
 Fm Inanimate

Colour;
o FC coloured object with form
o CF coloured object with indefinite form
o C colour only

Shading;
o FK shading with dimensions
o K shading as diffuse(smoke, clouds)
o FC surface shading(hair)
o C shading texture

 Apperception
Normal perception modified by emotion.

 MOTIVATION
It is a state of being that produces tendency towards action.

Theories of motivation
o Drive theory
o Incentive theory
o Opponent-process theory
o Optimum level theory

 TYPES OF CONFLICT
o Approach –Approach conflict
o Avoidance- avoidance conflict
o Approach –Avoidance conflict
o Multiple Approach-Avoidance conflict

43
 EMOTION
Is a psychological state arising due to feeling?
o Physiological changes in the body and face
o Cognitive interpretation of event
o Cultural influences that shape the experience and expression of feeling
THEORIES OF EMOTION
o Emotion and bodily states
 James-Lange theory
 Cannon-Bard theory
 Schachter-Singer theory
o Cognitive-Appraisal theory
o Theory of relationships among relations
o Theories of emotion and motivation.

 TESTS OF ORGANICITY
 Bender-Gestalt test
 Bender-Visual retention test
 Wechsler memory scale
 Luria-Nebraska Neuropsychological test battery
 PGI battery of brain dysfunction (5-sub scales)
o PGI memory scale
o Bhatia short battery
o Verbal-adult intelligence scale
o Nahor-Benson test
o Bender-Gestalt test
 NIMHANS test battery by C.R. Mukundan
 General arithmetic test battery

 ELEMENTS OF COGNITIVE THERAPY BY AARON BECK

 Cognitive triad; beliefs about one s self, World, and Future.

 Schemas; Ways of organizing and interpreting experiences.

 Cognitive distortions
o Arbitrary thinking; Drawing a specific conclusion without
sufficient evidence.

o Specific abstraction; Focus on single detail while ignoring other

more important aspects of the experience.

44
 o Over generalization; Forming conclusions based on too little and
too narrow experiences.

o Minimization and Magnification; under or over valuing the

significance of particular events.

o Personalization; tendency to self-reference external events

without out basis.

PHYSIOLOGY
 NEUROTRANSMITTERS (AMINES, AMINOACIDS,PEPTIDES)
Amines
 Serotonin (5HT)
 Dopamine (DA)
 Norepinephrine (NE)
 Epinephrine (E)
 Acetylcholine (Ach)
 Tyramine
 Octopamine
 Phenyl ethylamine
 Tryptomine
 Melatonin
 Histamine

Amino Acids
 Gamma-amino butyric acid (GABA)
 Glycine
 Glutamic acid (glutamate)
 Aspartic acid (aspartate)
 Gamma-hydroxy butyrate

PEPTIDE NEUROTRANSMITTERS

Hypothalamic-Releasing Hormones
o Corticotropin-releasing factor (CRH)
o Gonadotropin-releasing hormone (GnRH)
o Somatostatin
o Thyrotropin-releasing hormone (TRH)

45
Pituitary Peptides
o Corticotropin (ACTH)
o Growth hormone (GH)
o Lipotropin
o Alpha-melanocyte—stimulating hormone (alpha-MSH)
o Oxytocin
o Vasopressin
o Thyroid-stimulating hormone (TSH)
o Prolactin

Circulating Hormones
o Angiotensin
o Calcitonin
o Glucagon
o Insulin
o Leptin
o Atrial natriuretic factor
o Estrogens, Androgens
o Progestins
o Thyroid hormones

Gut Hormones
o Cholecystokinin (CCK)
o Gastrin
o Motilin
o Pancreatic polypeptide
o Secretin
o Vasoactive intestinal peptide (VIP)

Opioid Peptides
o Dynorphin
o Betaendorphin
o Metenkephalin
o Leuenkephalin
o Kyotorphin

Miscellaneous Peptides
o Bombesin
o Bradykinin
o Carnosine
o Neuropeptide Y
o Neurotensin Delta
o sleep factor
o Galanin
o Oxerin

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Gases Neurotransmitters
o Nitric oxide (NO)
o Carbon monoxide (CO)

Lipid Neurotransmitters
o Anandamide
o Neurokinins
o Tachykinins
o Substance P
o Neurokinin A
o Neurokinin B
MONO AMINE NEURONS IN THE BRAIN

 Dopamine mid brain ventral tegmental Area

 Serotoninpontine raphe nucleus
 Cholinergic nucleus basalis of meynert
 Nor-adrenergiclocus coeruleus of mid brain
 Histaminergic posterior hypothalamus
DOPAMINE
TYROSINEDopa  Dopamine ---Vinyl mandalic acid

MAO & COMT

D1 family-D1, D5--  cAMP

Dopamine receptors;
D2 family-D2, D3,D4- - cAMP

D1 D2 D3 D4 D5

Caudate Caudate N. Accumbens Frontal cortex hippocampus

Putamen Putamen Hippocampus Midbrain Hypothalamus

N. Accumbens N. accumbens

 DOPAMINE PATHWAYS
 MESOCORTICAL Ventral tegmental area to prefrontal cortex
 MESOLIMBIC ventral tegmental area to N. accumbens
 NIGROSTRIATAL Substantia nigra to Basal ganglia
 TUBEROINFUNDIBULARHypothalamus to Anterior pituitary

 Positive symptoms increased dopamine in mesolimbic pathway

 Negative symptomsdecreased dopamine in dorsolateral prefrontal cortex

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  Extra pyramidal symptomsdecreased dopamine in nigro striatal pathway

 Decrease dopamine in tuberoinfundibular pathway

 Increase prolactin
 Gynaecomastia
 Galactorrhoea
 Amenorrhea

SEROTONIN

TRYPTOPHAN5hydroxy tryptophan 5hydroxy tryptamine (serotonin) -- 5hydoxy

indole acetic acid.
COMT

Serotonin receptors (Four families)

5HT1 (ABDEF) -----  cAMP

5HT2 (ABC) ---------  IP3/DAG
5HT3------------------ Ligand gated
5HT4-7--------------- cAMP

 SEROTONIN PATHWAY

Prefrontal cortex amygdala striatum

Hypothalamus Thalamus

Cortex Rostral end of locus coerulous Hippocampus

LOCUS COERULOUS

Caudal end of locus coerulous

Medulla Brainstem Cerebellum

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  ADRENERGIC SYSTEM

TYROSINEDopadopamineNorepinephrineHMA
Adrenergic receptors
o Alpha (alpha 1& 2)
o Beta (beta 1,2,& 3)
o All are G-protein coupled

 ACETYLCHOLINE; (MEMORY,ATTENTION, AROUSAL )

ATP
+ CHOLINE
ACETATE--ACETYL CO-A-ACETYL CHOLINE---
+ Acetyl choline esterase ACETATE
CO A

CHOLINERGIC RECEPTORS
Nicotinic
o Nm- muscle, myoneural junction
o Nn- brain, autonomic ganglia
Muscarinic M1,M2,M3,M4,M5

 GLUTAMATE
Excitatory neurotransmission
Receptors
o NMDA(N-Methyl-D-Aspartate)
o AMPA (Amino methyl propionic Acid)
o Kainate
o Metabotropic

Glutamate ---activate NMDA- Ca+2 - depolarization of neuronExcitation of

neurons

GLUTAMATE PATHWAY

 Cortico –brain stem; --pyramidal cells of prefrontal cortex to brain stem

 Cortico-striatal;---------pyramidal cells of prefrontal cortex to stratum, N. Accumbens
 Thalamo-cortical; -----thalamus to pre frontal cortex
 Cortico-thalamic; ------pre frontal cortex to thalamus
 Cortico-cortical; --------Pre frontal cortex to other prefrontal cortex

49
  GABA;
Inhibitory neurotransmitter
GABA-BENZODIAZEPINE-CL-CHANNEL RECEPTOR COMPLEX;
GABAinflux of chloride ions -hyper polarization of neuronsinhibitory effect

 HISTAMIME; -SLEEP,APPETITE
H1brain
Receptors
H2GUT

 RECEPTORS

 CLASS-I- Inotropic receptors

 CLASS-IIG-protein coupled receptors
 ENZYMATIC RECEPTORS
 REGULATING GENE EXPRESSION

CLASS-I- RECEPTORS; inotropic /ligand gated receptors

Or membrane permeability or ions-excitation or inhibition

CLASS-II- G-Protein coupled receptors

 Adenyl-cyclase pathway
 Phospholipase (IP3/DAG)pathway
 Ion-channel regulation

ADENYL-CYCLASE PATHWAY

ATP -------- cAMP----------------5 AMP

Adenyl cyclase phosphodiesterase

cAMP-----Excitation
cAMP pathway
cAMP- ----Inhibition

50
IP3/DAG PATHWAY/PHOSPHOLIPASE-C PATHWAY

Activation of phospholipase- C hydrolysis of phospholipid

Inositol triphosphate (IP3) Diacyl glycerol (DAG)

Mobilize Ca+2 ions from activate protein kinase

Intracellular storage

Ca+2 Excitation

FUNCTIONS OF RECEPTORS

 To propagate regulatory signals from outside to within the effector cell

 To amplify the signals
 To integrate the various extracellular/intracellular signals
 To adapt the short term and long term changes and maintain the homeostasis

 NEUROTRANSMISSION;
Action potential at dendrtic site---------open ion channels at synapse ----------
postsynaptic

Electrical neurotransmission Chemical neurotransmission

Types of neurotransmission;
 Anterograde; pre synaptic to post synaptic
 Retrograde ; post synaptic to pre synaptic Eg; NO, cGMP, NGF
 Volumetric; Diffusion into adjacent neurons

 Neurotransmitter; Chemical signal that flows between neurons.

 Neuromodulator; Modulates the response of neuron to neuron.

 SECOND MESSENGER SYSTEM ; contain 4 elements

 Neurotransmitters (first messengers)
 Receptors
 G-protein
 Enzyme
Eg. Second messengers: cAMP,cGMP,IP3,DAG,Ca+2,NO,and CO

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 NEURONAL CIRCUITS
Cortico-cortical; prefrontal cortex to another prefrontal cortex

Cortico-striato-thalamo-cortical

Circuit for executive function-

Planning, judgement ,problem solving, cognitive function

Dorsolateral prefrontal cortex

Striatum

Thalamus

Circuit for Emotion/Fear/Depression

Ventral anterior cingulate gyrus

N. Accumbens

Thalamus

Circuit for attention

Dorsal anterior cingulate gyrus

Bottom of striatum

Thalamus

Circuit for impulsivity/compulsivity

Orbito frontal cortex

Caudate

Thalamus

52
 Circuit for motor activity

Prefrontal cortex

Putamen

Thalamus

 ION CHANNELS
Voltage gated ion channels
Ligand gated ion channels

K+ Channel opens Cl- channel opens

K+ Efflux Cl- ions influx

Membrane hyperpolarisation Membrane hyperpolarisation

Inhibitory effect Inhibitory effect

Ca+2 channel opens Na+ channel opens

Ca+2 influx Na+ influx

Membrane depolarisation Membrane depolarisation

Excitatory effect Excitatory effect

EFFECTS OF VARIOUS RECEPTORS AGONISM/ANTAGONISM

M1 receptor antagonism;

o Dry mouth,
o Constipation,
o Urinary retention,
o Blurring of vision,
o Cognitive impairment,
o Worsened tardive dyskinesia,
o Increases seizure, Delirium
o Paralytic ileus,

53
 1receptor antagonism;

o Postural hypotension,
o reflex tachycardia
H1 receptor antagonism;

o Sedation,
o Cognitive impairment,
o Weight gain.
Nor-epinephrine reuptake inhibition;

o Dry mouth,
o Constipation ,
o Urinary retention,
o Blurring of vision,
o Tachycardia ,
o Insomnia,
o Hypertension.
5HT2 Antagonism;

o Nervousness,
o Insomnia,
o anorexia,
o Sexual dysfunction,
o akathisia,
o Parkinsonism,
o Dystonia.
Serotonin reuptake inhibition;

o Diarrhoea,
o headache,
o Drowsiness.
5HT2cAntagonism;

o weight gain
5HT1 Agonism (serotonin syndrome);

o Diarrhoea,
o Disorientation,
o Diaphoresis,
o Hyperreflexia,
o Myoclonus,
o Ataxia,
o Labile mood,
o Tremor.

54
 SUBSTANCE RELATED DISORDER
 Drug Abuse; Maladaptive pattern of substance use leading to clinically significant
impairment or distress.
 The effect which any drug of abuse has on an individual depends on a number of
variables
o Dose
o Potency and purity of drug
o Route of administration
o Past experience of user
o Present circumstances
o Personality and genetic predisposition of user
o Age and clinical status of user

 Drug metabolites detected in urine

o Amphetamines can be positive for up to 5days
o Marijuana (THC) can be positive 2-4 days after acute use, 1-3 months after
chronic use.
o Cocaine is positive in urine 1.5 days after I.V use, up to 1 week for other
routes.
o Heroin is positive in urine 1.5 days

 REWARD CENTERS IN BRAIN

o Nucleus accumbens
o Ventral tegmental area of mid brain
o Locus coerulous

 ALCOHOL
Single drink
o 12gm of ethanol
o 12 OZ of beer
o 4 Oz of wine
o 1-1.5Oz of brandy/whiskey/rum

Absorption
o 10%---- stomach
o 80-90% --- small intestine
o Peak concentration - 30-90min

Metabolism
o 90%--- oxidation through liver
o 10%---Unchanged excretion through kidney
o Rate of metabolism ------15mg /dl/hour

55
 o Acute alcohol intake decreases hepatic metabolism of co-administrated drugs
by competition for microsomal enzymes.
o Chronic alcohol intake increases hepatic metabolism of co-administrated
drugs by increases for microsomal enzymes.

NEUROCHEMICAL EFFECTS OF ALCOHOL

 CNS depression ------ through membrane fluidity

 Sedation
 Sleep inducing Benzodiazepine GABA receptor complex
 Anti-convulsion
 Muscle relaxant

 Mute during intoxication through NMDA glutamate receptors

 Hyperactive during withdrawal

 Addiction
 Tolerance opioid receptors and reward centres
 Dependence
 Craving; increased dopamine at limbic system and orbito frontal cortex

TOLERANCE;
Need for a marked increased amount of substance to achieve intoxication or desired
effect. Or
Markedly diminished effect with continued use of the same amount of substance.

TYPES OF TOLERANCE

Behavioural tolerance; Ability of the person to learn how to perform tasks

effectively despite the effects of alcohol.

Pharmacokinetic tolerance; Adaption of the metabolic system.

Pharmacodynamic tolerance/cellular tolerance; Adaptation of nervous system to

perform function despite of high amount of alcohol.

Cross tolerance; once tolerance is developed to one brain depressant an individual

is likely to develop similar response to second class drug.
Eg Alcohol, benzodiazepine

Reverse tolerance; Increased sensitivity and sensitization of neuro chemical

adaptors due to brain damage/old age that leads to increase reaction to substance.

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ALCOHOL AFFECTS ON SLEEP
o Decrease REM sleep
o Decrease stage IV sleep
o More fragmented
o Long period of awakening
o Decrease sleep latency

BIOCHEMICAL MARKERS OF ALCOHOLISM

 Gama- Glutamyl transferase-------------------------------->30IU/L

 SGOT ------------------------------------------------------>45 IU/L
 SGPT ------------------------------------------------------->45 IU/L
 MCV --------------------------------------------------------->91 µm3
 Carbohydrate deficit transferrin ------------------- >20 mg/L

 Uric acid ----------------------------- Male ---->6.4 mg/dl

Female-->5 mg/dl

 Triglycerides --------------------------------------------->160 mg/dl

 Adenyl cyclise in platelets and reticulocytes

ALCOHOL SCREENING SCALES

 Michigan Alcohol Screening test (MAST)
 Alcohol Used Disorder Identification Test (AUDIT)
 CAGE Questionnaire

 Cut down
 Annoyed
 Guilty
 Eye opener/early morning drinking

 Clinical institute withdrawal assessment alcohol scale(CIWA-A)

 Addiction severity index (ASI)

SIGNS OF ALCOHOL INTOXICATION;

 Slurred speech
 In-coordination
 Unsteady gait
 Nystagmus
 Impaired attention
 Stupor/Coma

57
BEHAVIOURAL EFFECTS OF ALCOHOL INTOXICATION (depends upon blood
alcohol concentration)

 0.05% or 20-30 mg/dl ---------- decreased thinking and psychomotor

activity

 0.1% or 30-80 mg/dl---------- motor and cognitive problems

 0.1-015% or 80-200 mg/dl ------(legal drinking/intoxication)

Slurred speech In-coordination
Unsteady gait Nystagmus
Impaired attention Stupor/Coma

 0.2% or 200-300 mg/dl -------- marked CNS depression

 0.3% or 300-400 mg/dl ------- stupor

 0.4% or > 400mg/dl ---------- coma, death

ALCOHOL DEPENDENCY
Features of dependency
 Tolerance
 Withdrawal
 Craving

Types of dependency

Classification –I) type –A ,and type-B

Type-A Type- B
 Late onset Early onset
 Few childhood risk factors High childhood risk factors
 Mild dependence Severe dependence
 Few alcohol related problems Many alcohol related problems
 Less psychopathology More psychopathology
 May or may not family history Strong family history
 No polysubstance abuse Poly substance abuse

Classification –II)

 Early stage problem drinking;- not much depended.

 Affiliative drinking;- daily moderate amount of social drinking.
 Schizoid drinking; - isolated drinking, binge drinking, severe dependence.

58
 Classification-III)

 Gamma-dependence; - the person unable to stop drinking once they start.

 Delta- dependence;- must drink certain amount each day and are unaware of
lack of control.

Classification-IV
 Type-I (Similar to type -A)
 Type -II(similar to type-B)

Classification-V
 Anti-social alcoholism(similar to type-A)
 Developmentally cumulative
 Negative effect of alcoholism (women)
 Developmentally limited

ALCOHOL WITHDRAWAL
 Autonomic hyperactivity
 Hand tremors
 Nausea/vomiting
 Transient visual, auditory, and tactile hallucination
 Psychomotor agitation
 Anxiety
 Grand-mal seizures

Alcohol withdrawal

6-8 hours (Tremors, Shakes)

8-12 hours (Psychosis, Perceptual abnormality)

12-24 hours- seizures

72 hours ---Delirium tremens (risk up to one week)

NON PSYCHOLOGICAL/ SYSTEMIC COMPLICATIONS DUE TO ALCOHOLISM

 Features of intoxication
 Features of withdrawal
 Blackouts
 Alcohol hallucinations
 Withdrawal seizures
 Delirium tremens

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 Nutritional problems
o Wernicke s encephalitis
o Korsakoff psychosis
o Peripheral neuropathy
o Optic neuropathy
o Pellagra and vit B12deficiency

 Gastrointestinal complications
o Esophagitis
o Gastritis
o Hepatitis
o Fatty liver
o Cirrhosis of liver
o Hepatocellular cancer
o Hepatic encephalopathy
o Chronic hepatocellular degeneration
o Pancreatitis
o Pancreatic cancer
o Gallstones
o Mal absorption syndrome
o Post gastrectomy

 CVS complications
o Hypertension
o Cardiovascular disease
o Dilated cardio myopathy
 Haematological complications
o Anaemia
o leucopenia
o Thrombocytopenia
o Haemorrhagic disorder
 CNS complications
o Cerebral atrophy
o Alcohol dementia
o Neuropathy
o Central pontine myelinosis
o Marchiafava bignami
o Myopathy

 Electrolytes imbalance
o Hypoglycemia
o Hyperglycemia
o Hypo natremia
o Hyper calcemia
o Hypo phosphataemia
o Hypo/hyperthermia

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  Other complications
o Myelopathy
o Foetal alcohol syndrome
o Risk of trauma
o compressive neuropathy

FOETAL ALCOHOL SYNDROME

 Mental retardation
 Microcephaly
 IUGR
 Cranio facial malformation
 Limb abnormalities
 CVS abnormalities (ADS)
 Short stature
 Hyper telorism
 Short palpebral fissure
 Inner epicanthal fold
 Short turned nose
 Learning disorders

WERNICKE S ENCEP(ALOPAT(Y GOA

 Global confusion
 Ataxia
 Opthalmoplegia (6th nerve palsy/ Lateral rectus muscle palsy)
 Horizontal Nystagmus
 Neurological lesions at thalamus, hypothalamus, mid brain, pons, medulla, and
cerebellum.

Treatment
 Thiamine 100mg orally 2-3 times /day and continued for 1-2 weeks or even longer
KORSAKOFF PSYCHOSIS
 Impaired memory (recent > remote)
 Confabulation
 Ataxia
 Peripheral neuropathy
 Neurological lesions at thalamus, hypothalamus, mid brain, pons, medulla, and
cerebellum.

Treatment
 Thiamine 100mg orally 2-3 times /day orally and continued for 3-12 months or even
longer.
 20% recovers totally, 50% partial recovery and others remain with lifelong disability.

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BLACKOUTS;

 They are discrete episodes of anterograde amnesia that occurs in alcohol

intoxication.
 Impairment of recent memory with intact remote memory.
 Mainly involve hippocampus and related temporal lobe structures
 There are two types En-bloc and Fragmented.
Pathological drinking;
Severe behavioral syndrome develops rapidly after a person consume small amount of
alcohol that would have minimum behavioural effects on most of the persons.

Harmful use:
A pattern of psychoactive substance use that is causing damage to health either physical or
mental or both.

Abuse;
Maladaptive pattern of substance use leading to clinically significant impairment or distress.

Addiction;
Habituation to the use of substance, that on deprivation gives rise to symptoms of distress
and irresistible impulse to take the substance again.

TREATMENT OF ALCOHOL WITHDRAWAL/DEADDICTION

Goals ;

 Short term goals

o Manage intoxication
o Manage withdrawal
o Motivation enhancement
o Treat acute medical sequelae
o Crisis intervention
 Long term goals
o Relapse prevention
o Maintain abstinence
o Occupational rehabilitation
o Social reintegration
o Improve quality of life

 Diazepam (20-60mg/day), chlordiazepoxide (50-150mg/day), or lorazepam (4-

24mg/day).
 Thiamine 50mg/TID/day orally or 100mg/day IM.
 Supportive measures; fluid replacement, electrolyte imbalance correction.
 Other drugs for alcohol withdrawal ; Barbiturates, clonidine, carbamazepine,
neuroleptics.

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  De addiction /deterrent/alcohol sensitising agents
 DISULFIRAM (250-750MG/DAY)
 CALCIUM CARBIMIDE
 DISULFIRUM
o Approved by FDA in 1951
o Aversive agent. Only drug used for complete abstinence from alcohol
dependence
o Dese 250 mg/day for 1 year (no specific guidelines)

Anti-craving drugs

o Acamprosate ; 666 mg TID/day (6-12 months)

o Naltrexone 25-50 mg/day for 3 months/ 6 months
o Baclofen 10 – 60 mg/day
o Fluoxetine ; 60mg/day
o Topiramate 25-300 mg/ day for 3 months
o Ondansetron; 4mg/day for 3 month
Combination regimens
 Disulfiram + Naltrexone
 Acamprosate + Naltrexone
Depot preparations
 Implanted Disulfiram
 Depot Naltrexone
PSYCHOLOGICAL TREATMENT FOR ALCOHOL ABUSE

GOALS

 Enhance efficacy of pharmacotherapy.

 Achieving sustained drug free states.
 Providing the relationship.
 Change of life style
 Improved quality of life
MODALITIES

 Brief intervention
 Extended intervention
 Relapse prevention
 Cognitive and behavioural therapy
 Group therapy
 Family therapy
 Self help groups (Alcohol Anonymous)

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  SEDATIVE –HYPNOTICS ABUSE
o Approximate therapeutic equivalent doses of benzodiazepine
 Alprazolam 0.5 mg
 Chlordiazepoxide 25 mg
 Clonazepam 0.5 mg
 Diazepam 10 mg
 Lorazepam 1 mg
 Nitrazepam 10 mg
 Oxazepam 20 mg
 Management of benzodiazepine intoxication
o Gastric lavage not recommended due to risk of aspiration
o Assisted ventilation
o FLUMAZENIL competitive benzodiazepine antagonist. Dose: intravenous
injection of 0.1mg to 0.6mg over a period of 30 sec maximum dose 2mg-5mg.
 Management of benzodiazepine dependence
o Therapeutic dose dependence: gradual dose reduction/ switching to a long
half-life from short half-life drug.
o Prescribed high dose dependence / recreational use ; convert into diazepam
(6mg alprazolam is approximately equivalent to 120 mg diazepam) gradually
shifted to diazepam and then stopped.

 PSYCHOSTIMULANTS
o Amphetamines
o Methyl phenidate
o Diethyl propion
o Methylene dioxy methamphetamine(MDMA/Ecstasy)
o Modafinil
o Benzphentamine
o Pimoline
o Methylene ethyl amphetamine (MDE/Eve)

Mechanism of action;
o Increase dopamine, serotonin, nor-epinephrine from storage sites.

INTOXICATION

 Tachy/ bradycardia
 Respiratory depression
 Pupillary dilatation
 Cardiac arrhythmia
 Hypo/hyper tension
 Confusion
 Nausea/ vomiting
 Seizure
 Muscle weakness
 Chest pain
 Withdrawal of psycho stimulants

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 Fatigue
 Vivid unpleasant dreams
 Insomnia/hypersomnia
 psychomotor agitation/retardation
 Increase appetite
 Usually resolves in 24-48 hours
 Amphetamine psychosis usually remits within one week.

 PHENCYCLIDINE INTOXICATION(PCP);

o Nystagmus
o Motor Inco-ordination
o Cognitive impairment

 CLUB DRUGS

o LSD
o Ketamine
o Gama-hydroxy butyrate
o Methamphetamine
o MDMA/Ecstasy

 DATE RAPE DRUGS

o Ketamine
o Gama-hydroxy butyrate
o Rohypnol

 CAFFEINE RELATED DISORDER

 It is methyl xanthine contain Theo bromine and theophylline.
 Peak plasma concentration within one hour
 Metabolised by liver.
 Inhibits phosphodiesterase

ATP--------- cAMP---------------5AMP

Adeny cyclase Phosphodiesterase

Caffeine -
o Increases BP
o Increases gastric secretions
o Increases epinephrine and nor-epinephrine
o Increases renin
o Increases free fatty acid

65
 CAFFEINE INTOXICATION CAFFEINE WITHDRAWAL

o Restlessness/agitation Headache
o Nervousness Lethargy/fatigue
o Excitement Sleepiness
o Insomnia Dysphoric mood
o Flushed face Difficulty to concentrate
o Diuresis Depression
o GI disturbance
o Anxiety/irritability
o Muscle twisting
o Nausea/vomiting
o Rambling flow of thoughts and speech
o Muscle ache
o Tachycardia/cardiac arrhythmia
o Impaired cognitive performance

 CANNABIS RELATED DISORDERS

o Active form is Delta- 9 tetrahydrocannabinol(THC)
o Acts on cannabinoid receptors (Anandamide)
o These are G-protein coupled receptors found in basal ganglia, hippocampus,
and cerebellum.
o Concentration of THC varies across different parts of the plants: leaves
(Bhang) contain 1-3%, female flowering tops (Ganja) contain 3-5%, and
resinous extract (Charas) contain 5-10% of THC.
o Cannabis preparations can be smoked or ingested orally
o When smoked, effects usually last for 3-4 hours, effects may last longer up to
42-72 hours when ingested orally.

INTOXICATION
o Increased appetite
o Dry mouth
o Conjunctival injection
o Flash back phenomenon
o Tachycardia
o Euphoria/ disinhibition, Reversible cognitive impairments
o Anxiety/ agitation, Stimulation of brain reward area
o Suspiciousness
o Impaired judgement
o Hallucinations
o Depersonalization
o Derealisation
o Dronabinol ; synthetic tetra hydro cannabinol for treatment of cancer
patients.
o Suggested treatment: Benzodiazepine (preferably shortacting), and
antipsychotics (preferably second generation) for psychosis or paranoia.
o Propranolol 60-120mg for anxiety
o Duration of treatment : 1-2 days

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 Treatment of cannabis withdrawal syndrome
o Symptoms: irritability, anger, depressed mood, restlessness, insomnia,
tremor, decreased appetite. Mostly transient, mild and self limiting.
o In severe cases benzodiazepines, dronabinol (20-60mg/day), baclofen
40mg/day.
o Duration of treatment is around 7days
 Treatment of cannabis dependence
o Psychological intervention is the mainstay of treatment
 Motivational enhancement treatment(MET)
 Cognitive behavioural therapy (CBT)
 Combined MET & CBT
 Family therapy
o Pharmacotherapy
 Buspirone (up to 60mg/day)
 Baclofen (40-60mg/day)
 Fluoxetine (20-40mg/day)
 Entacapone (200mg/day)
 N-acetyl-cysteine (1200mg/day)

COCAINE

 Increase dopamine by blocked dopamine transporters.

 Intoxication and withdrawal are similar to psycho stimulants.
 Crack is a free base and a more potent form of cocaine
 Used with heroin(dynamite/speedballs)morphine (whiz-bang) marijuana
(cocoa puffs)

 HALLUCINOGENS

o LSD
o Mescaline
o Ketamine
o Psilocybin
o MDMA (ecstasy)

 INHALANTS
o Use mostly reported by children and adolescent
o Can be classified as 4 types
 Volatile solvents: paint thinners, Gasoline, Correction fluids, Nail polish,
glue, petrol etc..
 Aerosols; paints and deodorants
 Gases: refrigerants, and medical anaesthetics
 Nitrites

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 o Can be used by various modes of administration;
 Huffing (soaking a rag and placing it on the mouth to inhale) most
common
 Sniffing /Snorting; inhaling through nose
 Bagging( inhaling from a bag that contain substance)
 Dusting (spraying directly in to the mouth)

 NICOTINE
 It modulates the dopamine and glutamate release due to stimulation of
nicotine receptors on the ventral tegmental area.
 Half-life 2 hours.

WITHDRAWAL

o Dysphoric /depressive mood ,Head ache

o Insomnia/irritability ,Dizziness
o Anxiety/anger ,Abdominal pain
o Difficulty to concentrate
o Palpitations, Restlessness, Sweating
o Bradycardia , Weakness

Treatment; Bupropion, Nicotine patch/gum/nasal spray, clonidine, nortryptiline

and varenicline (nicotine receptors agonist)

 OPIOIDS
Natural
o Opium
Semi synthetic;-
o Heroin,
o Pholcodeine

Synthetic;-
o Pethidine,
o Fentanyl,
o Methadone,
o Dextropropoxyphene,(proxivon)
o Tramadol,
o Ethoheptazine.
Agonist;-
o Nalorphine,
o Pentazosin,
o Nalbuphine.

Partial agonist;
o Buprenorphine

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 Pure antagonist;
o Naltrexone,
o Naloxone,
o Nalmefene

OPIOID RECEPTORS
o Mu-receptors
o Kappa- receptors
o Delta-receptors
OPIOID PEPTIDES
o Dynorphins
o Met-enkephalin
o Leu-enkephalin
o Beta-endorphin

OPIOID WITHDRAWAL OPIOID INTOXICATION

 Dysphoric mood Behavioural problems
 Nausea/vomiting Pupillary constriction
 Muscle aches /cramps Drowsiness/ coma
 Lacrimation Slurred speech
 Rhinorrhoea Impaired concentration and memory
 Diarrhoea
 Sweating
 Piloerection
 Papillary dilation
 Yawning
 Fever
 Insomnia

Treatment of opioid withdrawal/dependence

 Pure agonist (methadone)

 Partial agonist (buprenorphine)

 Antagonist (naltrexone)

 Clonidine reduces adrenergic firing in opioid withdrawal

 DRUG SCREENING TESTS

o Liquid /gas chromatography

o Radio immune assay
o Spectroscopy

69
 PSYCHOPHARMOCOLOGY
 Modern psychopharmacology is largely-
o To understand the actions of drugs on the brain,
o To grasp the impact of diseases on the central nervous system (CNS), and
o To interpret the behavioural consequences of psychiatric medicines,

 NARCOTICS; The drugs which are naturally occurring/cultivable substances.

 PSYCHOTROPICS; The drugs which are synthetic substances /non cultivable

substances.
o Antipsychotics
o Antidepressants
o Mood stabilizers
o Hypnotics
o Anxiolytics
o Stimulants
o Cognitive enhancers
 Tranquilizer; the drug which calms patient without inducing sleep.

 Pharmacokinetics; what the body does to the drug.

 Pharmacodynamics; What the drug does to the body

 DRUG MECHANISMS

 Agonist; it activates a receptor to produce an effect.

 Inverse agonist; it activates a receptor to produce an opposite effect.

 Antagonist; it inactivates a receptor and does not produce an effect.

 Partial agonist; it activates a receptor to produce sub maximal effect.

 Ligand; it selectively attaches to particular receptors.

 THERAPEUTIC INDEX; the ratio of mean toxic dose to mean effective dose.

low therapeutic index

o Lithium
o Carbamazepine
o Sodium valproate
o Phenytoin

High therapeutic index

o Haloperidol
o Antidepressants

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 Therapeutic window phenomenon;
Optimal therapeutic affect is exerted only over a narrow range of plasma
concentration or drug doses, both below and above this range, beneficial effects are
suboptimal.

 Eg; TCAs exerts maximal antidepressant effect when their plasma

concentration is maintained between 50-150µg/ml.

 Clonidine decrease BP when plasma concentration 0.2-2 µg/ml and increase

BP >2 µg/ml.

 Potency; the amount drug that is required to achieve therapeutic effect.

 Auto induction;
Dose dependent induction of its own metabolism, with a subsequent decrease in the
plasma concentration.
Eg; carbamazepine

 Auto inhibition;
Dose dependent inhibition of its own metabolism, with a subsequent increase in the
plasma concentration.
Eg; paroxetine

 TREATMENT OUTCOME ;
 RESPONSE; 50% decrease symptoms in standard rating scale.
 REMISSION; symptoms improvement that has last for < 2months.
 RECOVERY; symptoms improvement that has last for>2months.
 RELAPSE; symptoms occur in remission period.
 RECURRENCE; symptoms occur in recovery period.

 2 –ADRENERGIC RECEPTOR AGONISTS

o CLONIDINE
o GUANFACINE

MECHANISM OF ACTION OF CLONIDINE

Stimulate presynaptic receptors

Reducing adrenergic neurons firing

Decrease nor-epinephrine release

INDICATIONS
o Opioid, alcohol, benzodiazepine, and nicotine withdrawal
o Tourette s disorder
o ADHD
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 o PTSD
o Other anxiety disorder

 DOSAGE; 0.1 to 0.2mg up to 1.4 mg/day in divided doses, regular monitoring

of the BP if BP < 90/60 withhold the next dose

OVERDOSAGE
o Constricted pupil
o Coma
o Fatigue
o Respiratory depression
o Hypotension
o Behavioural problems
ADVERSE EFFECTS

o Constipation
o Depression
o Anxiety
o Vivid dreams
o Nightmares
o Hallucinations
o Dry mouth/eyes
o Sedation/insomnia
o Hypotension
o Dizziness

CONTRA INDICATIONS
o Heart disease
o Rebound hypotension
o Vascular disease
o Renal disease
o Raynaud disease
o H/O depression

CLONIDINE WITHDRWAL
o Anxiety
o Restlessness
o Tremor
o Abdominal pain
o Palpitations
o Headache

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 - ADRENERGIC BLOCKERS (NAPAL-PM)
o N-Nadolol
o A-Atenolol
o P-Pindolol
o A-Acebutolol
o L-labetolol
o P-Propranolol
o M-Metoprolol

Pindolol can be used as augmentation of antidepressant.

Propranolol
Pindolol some antagonist activity of 5HT1A receptors
Nadolol

Metoprolol
Atenolol 1 > 2
Acebutolol

INDICATIONS

 Definitively effective indications

o Performance anxiety
o Lithium induced tremors
o Neuroleptic induced akathisia

 Probably effective indications

o Adjuvant therapy of alcohol/other substance withdrawal
o Adjuvant therapy of aggressive /violent patient.

 Possibly effective indications

 Antipsychotic augmentation
 Antidepressant augmentation

ADVERSE EFFECTS

 Nausea
 Congestive heart failure
 Vomiting
 Bronchial asthma
 Diarrhoea
 Worsened hypoglycaemia in diabetic pts

73
  Hypotension
 fatigue
 Bradycardia
 insomnia and vivid dreams
 Dizziness
 Depression,
 Psychosis

CONTRAINDICATIONS;
 Asthma
 Persistent angina
 Vascular disorders
 Congestive heart failure
 AV block
 Thyrotoxicosis
 Insulin dependent DM.

DOSAGE OF PROPRANOLOL; 10-20 mg up to 180 mg/day in divided doses. BP and Pulse

rate should be strictly monitored.

Pulse rate
<50/min – no Propranolol
50-79/min-50 mg propranolol
>80/min – 100 mg propranolol
BP <90/60 withhold dose

 ANTICHOLINERGICS (BOBPET)

 B-benzatropine -----------1-4mg one to three times daily

 o-orphenadrine----------- 50-100mg tid/day
 B-biperiden -------------- 2mg 1-3times/day
 P-procyclidine ---------- 2.5mg -5mg tid/day
 E –ethopropazine ------- 50 mg -100mg 1-3 times/day
 T –trihexyphenidyl ------- 2- 5 mg 2-4 times/day

INDICATIONS
 Neuroleptic induced dystonia
 Neuroleptic induced parkinsonism

ADVERSE EFFECTS
o Tachycardia
o Dry mouth
o Nausea

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 o Constipation
o Paralytic ileus
o Confusion
o Disorientation
o Memory impairment
o Blurred vision
o Dilated pupil
o Urinary retention
o Mild mood elevating
Toxicity of anticholinergics
o Delirium
o Coma
o Agitation
o Seizures
o Hallucination
o Severe hypotension
o SPVT
o Hyperthermia
o Dilated pupil
o Paralytic ileus
o Dry skin

Contraindications
o Urinary retention
o Prostatic hypertrophy
o Narrow angle glaucoma

 AMANTADINE
 t1/2-12-18 hrs.

Mechanism
Augment the dopamine neurotransmission
o Blocks reuptake
o Agonist of post synaptic receptors
o Increased presynaptic release

INDICATIONS
 Neuroleptic induced parkinsonism and akathisia
 SSRI induced sexual dysfunction

 Dosage – 100-200mg/day

75
 Adverse effects –
o Arrhythmia
o Delirium
o Psychosis
o livido reticularis of legs

 ANTICONVULSANTS (BD-HIS-ABNM)
o Barbiturates ---------- Pheno-barbitone, Pentobarbitone.
o Deoxybarbiturates------- Primidone
o Hydantoins ---------------- Phenytoin
o Iminostilbenes ------------ Carbamazepine, Oxcarbamazepine.
o Succinamides ------------- Ethosuccimide
o Aliphatic acids ------------ Sodium valproate
o Benzodiazepines -------- Diazepam, Lorazepam, Midazolam
o Newer anticonvulsants-- (Pre-Ga Ti Top Zo Le La)
o Miscellaneous ------------ Acetazolamide.

Doses
o Phenobarbitone ---- 3-5 mg/kg body wt
o Phenotoin ----------- 5-10 mg/kg body wt
o Carbamazepine ----- 10-20 mg/kg body wt
o Valproate ------------ 20-40 mg/kg body wt

 NEWER ANTICONVULSANTS (Pre-Ga Ti Top Zo Le Lo La)

 Pregabalin--------75-300 mg/day
 Gabapentin---- ---300-900 mg/day
 Tiagabine------
 Topiramate-------25-200mg/day(max : 400 mg/day)
 Zonisamide------100 -400 mg/day
 Leviteracetam---- 250-1000mg/day
 Lamotrigine ---- 25 – 200 mg/day
 Lacosemide -----250-1000 mg/day

Gabapentin & pregabalin

 Increase GABA levels

Uses
 Anxiety disorders
 Postherpetic neuralgia
 Trigeminal neuralgia
 Central pain syndrome

76
  Diabetic neuropathy
 Carpal tunnel syndrome
 Radiculopathies
 Meralgia paresthetica

Topiramate
 Glu AMPA receptors
 Blocks NA receptors
 Indirect GABA activity
 Dosage : 25-200mg/day(max : 400 mg/day)

Uses
 Anxiety
 Alcohol craving

Adverse effects (overall)

 Ataxia
 Dizziness
 Memory impairment
 Psychosis (zonisamide,levetiracetam)
 Paraesthesia

Zonisamide &Levetiracetam
 Enhance GABA activity
Uses
 Acute mania
 Add on antidepressant
 Anxiolytic
 Dose : 250-1000mg/day

 ANTIHISTAMINICS USED IN PSYCHIATRY (Direct-PHC)

o Direct—Diphenhydramine—25-50mg 3-4 times/day
o P---- Promethazine ------ -----25-100mg 3-4 times/day
o H----Hydroxyzine ------ -------25-100mg 3-4 times/day
o C ----Cyproheptadine---- ---4-20mg/day in divided doses
o Cyproheptadine is not metabolised in liver
INDICATIONS
o Neuroleptic induced dystonia, parkinsonism, akathisia
o Cyproheptadine
o SSRI induced sexual disturbances
o Anorexia nervosa
o Serotonin syndrome

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 Adverse effects
 Sedation
 Dizziness
 Hypotension
 GI disturbances

BARBITURATES
Long acting
Phenobarbitone
Mephobarbitone

Short acting
Butobarbitone
Secobarbitone
Pentobarbitone

Ultra short acting

Hexobarbitone
Methohexitone
Thiopentone

INDICATIONS
o Electro convulsive therapy
o Epilepsy
o Hypnosis
o Narcolepsy
o Withdrawal from sedatives/hypnotics

ADVRESE EFFECTS
o Steven-Johnson syndrome
o Megaloblastic anemia
o Neutropenia
o Teratogenicity
o Cognitive impairment

NON BENZODIAZEPINE HYPNOTICS

o Zolpidem
o Zopiclone
o Eszopiclone
o Zaleplon

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  BENZODIAZEPINES

HYPNOTICS
 Diazepam
 Flurazepam
 Nitrazepam Zaleplon
 Temazepam
 Triazolam
 Midazolam

ANTI ANXIETY (D-COLA)

 D-Diazepam
 C-Clonazepam
 O-Oxazepam
 L-Lorazepam
 A-Alprazolam

ANTI CONVULSANT
o Diazepam
o Clonazepam
o Clobazam
o Midazolam

INDICATIONS
o Insomnia
o Generalized anxiety/other anxiety
o Social phobia
o Mixed anxiety disorders
o Bipolar –I
o Akathisia
o Parkinsonism
o Alcohol withdrawal

WITHDRAWAL
o Anxiety/irritable
o Insomnia
o Difficulty to concentrate
o Tremors
o Depersonalisation
o Hyperesthesia
o Myoclonus and seizures
o Delirium

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 FLUMAZENIL; Specific benzodiazepine antagonist.
 Used in benzodiazepine overdose
 Blocks the benzodiazepine receptors at GABA-A ligand gated-chloride
channels.--> prevent benzodiazepine binding
 Onset of action 1-2min, peak effect 6-10min.
 Dizziness ,sweating, headache,

 BUSPIRONE ; It act as agonist, partial agonist ,and antagonist of 5HT1A receptors

 CALCIUM CHANNEL BLOCKERS

 Nifedipine
 Nimodipine
 Amlodipine

INDICATIONS

 Augmentation of mood stabilizers

 Augmentation of antidepressants
 Ultra rapid cycling bipolar disorder

 COGNITIVE ENHANCERS
Cholinesterase inhibitors
 Donepezil -------- 5-10mg/day
 Rivastigmine-----3-6mg/day
 Galantamine-----4-16mg/day

NMDA receptor antagonist

 Memantine ------5-10mg/day

o ADVERSE EFFECTS
Nausea/vomiting
Diarrhoea
Dizziness
Postural hypotension
Muscle cramps
Insomnia

 DANTROLENE; 1mg/kg body wt

It is a central muscle relaxant
Indications
 Catatonia
 Neuroleptic induced malignant syndrome
 Serotonin syndrome

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 ADVERSE EFFECTS
o Slurred speech
o Headache
o Confusion
o Hallucinations
o Depression hepatitis
o Seizures
o Pleural effusion
o Pericarditis

 DISULFIRAM
Aldehyde dehydrogenase
It inhibits ---------- Alcohol dehydrogenase
Dopamine beta hydroxylase

Alcohol --------------- Acetaldehyde---------- Acetic acid

Alcohol dehydrogenase Aldehyde dehydrogenase

Half-life -------60-120 hours.

Used in alcohol de sensitising therapy.
Dose ------250-500mg/day(max 750mg/day)

CONTRAINDICATIONS
Hepatic disease
Renal disease
Refractory seizure
Psychosis
Pregnancy
Cerebrovascular disorders
Cardiovascular disease
Peripheral neuropathy

ADVERSE EFFECTS
GI upset
Dermatitis
Hepatitis
Peripheral neuropathy
Sexual side effects
sedation

DISULFIRAM-ETHANOL REACTION
o Nausea/vomiting
o Throbbing headache
o Hypo/hyper tension
o Flushing, Sweating /thirst
o Tachycardia, Chest pain
o Vertigo, Blurring of vision

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Treatment; mild to moderate usually subside within 2 hours.

In severe cases
Proper rehydration
Hypotension Dopamine infusion
Vit-C bolus(1-2gm)
Methylpyrazole blocks the formation acetaldehyde but not used.

 Patient on disulfiram may need to avoid alcohol 1-2 weeks after last dose.
 Patient on alcohol may need to avoid disulfiram at least 12hours after last
drink
 Disulfiram aggravate psychosis due to blockaed dopamine beta hydroxylase
(it is responsible to conversion of dopamine to nor-epinephrine) that leads to
increase of dopamine.

 ACAMPROSATE
 Antagonism of NMDA glutamate receptors
 Anti-craving drug for alcohol.

DOSAGE
o 666mg three times a day.
o Mild to moderate renal failure 333mg 2-3 times a day. In severe renal failure
is contraindicated.

ADVERSE EFFECTS
o Headache
o Diarrhoea/flatulence
o Abdominal pain
o Parasthesia
o Skin reaction

 DOPAMINE RECEPTOR AGONISTS

 Bromocriptine ------2.5 -5mg/day

 Apomorphine
 Ropinirole -------- 0.25-5mg/day
 Levodopa -------- 100-500mg/day
 Pramipexole

INDICATIONS
 Parkinsonism
 Extrapyramidal symptoms
 Focal perioral tremors
 Hyperprolactinemia
 Galactorrhoea
 Neuroleptic malignant syndrome
 Restless leg syndrome
 Sexual dysfunction

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 ADVERSE EFFECTS
o Nausea/vomiting
o Postural hypotension
o Headache
o Dizziness
o Cardiac arrhythmias

 LAMOTRIGINE

Half life is 24 hours.

Mechanism of action
o
Block voltage sensitive Na+ channel
o Block Ca+2 channels
o Weak inhibitor of 5HT3 receptors

Used as mood stabilizer in bipolar depression

Lamotrigine Dose with CBZ with Valproate

 WEEK 1 & 2 25mg/day 50mg/day 12.5mg/day

 WEEK 3 & 4 50mg/day 100mg/day 25mg/day
 WEEK 5 100 mg/day 200mg/day 50mg/day
 TARGET DOSE 200mg/day 400mg/day 100mg/day
 MAXIMUM 400mg/day 800mg/day 200mg/day
 Steven-Johnson syndrome is life threatening complication.

 CARBAMAZEPINE

Mechanism of action
o Na+ channel block
o NMDA Glutamate antagonism
o Adenosine A1 antagonism
 Potent enzyme inducer.
 Half-life------ 18-54 hours
 Steady state 2-4 days
 Maximum enzyme induction reached in 3-5 weeks.

INDICATIONS

 Acute mania
 Acute depression
 Prophylaxis of bipolar –II
 Alcohol withdrawal
 Control of aggression

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ADVERSE EFFECTS
o Nausea/vomiting
o Constipation/diarrhoea
o Ataxia
o Drowsiness
Idiosyncratic reaction of CBZ
o Agranulocytosis
o Steven-Johnson syndrome
o Aplastic anaemia
o Hepatic failure
o Pancreatitis

 Dosage : 10-20mg/kg body wt

CONTRAINDICATIONS
 Haematological abnormalities
 Hepatic disease
 Cardiac diseases

LABORATORY EXAMINATION
o Complete blood count
o Liver function tests
o Serum electrolytes
o ECG > 40 years
(For every 3, 6, 9, & 12 months)

 OXCARBAZEPINE

 Sedation/nausea more common

 Hyponatremia
 Less haematological complications
 Dose: 10-20 mg/kg body wt

 LITHIUM;

 Monovalent ion
 Does not bind plasma protein
 Does not undergo metabolism
 Excreted unchanged through kidney
 Plasma half life 1,3 days in early days ,2.4 days in long period.
 Steady state reached after 5-7days of regular use
 Thyroid and renal concentrations are higher than in plasma.

84
 Mechanism of action;

 Alteration of ion channel

 Effects on neuro transmitters and neuropeptides
 Alteration of signal transduction pathway
 Activation of second messenger system
 Inhibition of inositol monophophatase
 Reduction of protein kinase –C activity
 Activation signalling cascade
Serum levels

o 0.8- 1.2 mEQ/L -------Therapeutic

o 0.6-1.0 mEQ/L -------Prophylactic
o > 1.5 mEQ/L -------Toxic

ADVERSE EFFECTS

Gastro intestinal

 Nausea / vomiting
 Decrease appetite
 Thirst
 Diarrhoea

Prevention
Dividing the dose
Administration with food
switching to another preparation (lithium citrate)

 Weight gain due to

Lithium induced hypothyroidism

Lithium induced edema
Excessive consumption of fluids due to increase thirst

Neurological

 Fine tremors - 8-12 Hz and most by seen on outstretched hands

Prevention
Dividing daily doses
Using sustained preparation
Decrease caffeine intake
Reassessing the concomitant use of other medications
Treatment
Propranolol (30-120mg/day in divided doses)
Primidone (50-250mg/day in divided doses)

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  Mild parkinsonism
 Ataxia /Dysarthria
 Periphral neuropathy
 Benign intracranial neuropathy

Cognitive
o Dysphoria
o Lack of spontaneity
o Slowed reaction time
o Impaired memory

Renal complications

 Poly urea with secondary to polydipsia

 Nonspecific interstitial fibrosis
 Nephrotic syndrome late complications
 Renal failure

Prevention
o Adequate fluid replacement
o Use of lowest effective dose
o Use single effective dose
o High salt intake and proper rehydration
Cardiac complications

o ECG- T wave flattening/inversion

o Sinus dysrhythmias due to decrease pacemaker act of SA node
o Episodes of syncope
Dermatological complications

o Follicular, maculo papular eruptions

o Peritibial ulceration
o Worsening of psoriasis
o Alopecia

LITHIUM TOXICITY

Mild to moderate (1.5-2mEQ/L)

Gastrointestinal complications
Nausea /vomiting
Dryness of mouth

Neurological complications
Ataxia
Dizziness
Slurring of speech
Lethargy/ Excitement
Muscle weakness

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Moderate to severe (2-2.5 mEQ/L)

o Anorexia
o Persistent nausea/vomiting
o Blurring of vision
o Course tremors
o Hyperreflexia
o Muscle fasciculation s
o ECG changes
o Severe ataxia
o Confusion
o Delirium
o Stupor/ coma
o Circulatory failure /Death

Severe toxicity (>2.5 mEq/l)

o Generalised convulsions
o Oliguria
o Renal failure
o Death

Management of lithium toxicity

o Discontinue lithium
o Complete investigations
o Serum lithium levels
o Unabsorbed lithium is removed by ingestion of polyethylene glycol
o Haemodialysis

Indications of lithium

o Manic episode
o Bipolar depression
o Maintenance of bipolar disorder (usually second episode)
o Major depressive episode
o Schizoaffective psychosis and schizophrenia

First episode maintenance therapy

o Adolescent mania
o Presence of family history
o High suicidal risk
o Sudden onset of manic episode
o Poor social support

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 Contraindications of lithium

o Pregnant Ebstein s anomaly

o Renal disorders
o Thyroid disorders
o Cardiac diseases
Dose ; 300-1800 mg/ day

Laboratory monitoring
Cardiac profiles
Renal profiles
Thyroid profiles

Methods of lithium estimation

Flam phototherapy
Atomic absorption spectrophotometry
Ion selective electrode analysis

SODIUM VALPROATE
USFDA approved in 1997 for treatment of manic episode associated with bipolar-1 disorder

Mechanism of action

Prolongation of Na+ channel Facilitation of GABA mediated Cl- channels

Decrease Na+ influx Influx of Cl- ions

Decrease firing of neurons Hyper polarization of neurons

Inhibitory effect Decrease firing of neurons

Inhibitory effect

Inhibit NMDA mediated Ca+2channels Inhibition of GABA transaminase enzyme

Decrease influx of Ca+2 ions Decrease metabolism of GABA

Decrease depolarization of neurons Increase concentration of GABA

Decrease firing of neurons Opening of GABA mediated Cl- channel

Inhibitory effect Influx of Cl- ions

Hyper polarization of neurons

Inhibitory effect

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Pharmacokinetic and dynamics of valproate

o Completely absorbed orally

o 90% bioavailability
o Peak concentration orally in 4-5hours
o Plasma half-life 10-16 hours
o Highly protein bound
o Metabolised by hepatic glucuronidation and mitochondrial beta oxidation
o Dose 20-40mg/kg body wt
o Serum therapeutic levels 50 -100µg/ML

Adverse effects

Common complications
o Nausea
o Sedation
o GI irritation
o Tremor
o Weight gain
o Hair loss
Uncommon complications
o Vomiting
o Diarrhoea
o Ataxia
o Dysarthria
o Hepatic transaminase

Rare complications
o Fatal hepatotoxicity
o Reversible Thrombocytopenia
o Platelet dysfunction
o Coagulation disturbance
o Oedema
o Hemorrhagic pancreatitis
o Agranulocytosis
o Encephalopathy and coma
o Respiratory failure

INDICATIONS OF SODIUM VALPROATE

o Acute mania
o Rapid cycling bipolar disorder
o Bipolar depression
o Augmentation of antidepressant

 Dose ;20-40 mg/kg body wt(max 2400mg/day)

 Therapeutic level 50 -125µg/ml

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 CONTRAINDICATIONS OF SODIUM VALPROATE

o Pregnancy---- Neural tube defects

o Hepatic diseases
o Haematological disorder

ANTIDEPRESSANTS

MONOAMINE OXIDASE INHIBITORS

MAOA inhibitors

Irreversible inhibitors
 Phenelzine
 Tranylcypromine
 Isocarboxazid

Reversible inhibitors
 Meclobemide
 Clorgyline

MAOB inhibitors
 Selegiline

Adverse effects of MOAs

 Orthostatic hypotension

Prevention
Decrease caffeine intake
Increase salt intake
Increase fluid intake
Treatment
Sodium chloride tablets
Fludrocortisone (0.1-0.2 mg)
Nor-epinephrine
 Tyramine induced hypertensive crisis most serious adverse effect: treatment iss sub
lingual captopril 25mg or parenteral
 Insomnia
 Weight gain
 Sexual dysfunction
 Oedema

 Note; - patient on MAO inhibitors should not add/switch to other antidepressant

within 2 weeks.

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TRICYCLIC ANTIDEPRESSANTS (MAD CAT IN Desi Pro)

 M-Maprotiline Tetracyclics
 A-Amoxapine

 D-Doxepin/Dothiepin
 C-Clomipramine
 A-Amitriptyline Tertiary amines
 T-Trimipramine
 I-Imipramine

 N-Nortriptyline
 Desi-Desipramine Secondary amines
 Pro-protriptyline

 Mechanism of action ; blocks the 1, H1, M1 receptors and serotonin, nor-epinephrine

reuptake inhibition.

INDICATIONS Of TCAs
o Major depressive episode
o Panic episode with Agoraphobia
o Generalized anxiety disorders
o Neuropathic pain (effects through blockade of sodium channels)

SPECIFIC INDICATIONS OF TCAs

o Major depressive episode -------- All TCAs
o OCD ------- Clomipramine
o Panic attacks --------- Imipramine
o Neuropathic pains ------- Amitriptyline
o Mixed anxiety and depressive episode ---- Amitriptyline+ chlordiazepoxide
o Enuresis ----------- Imipramine
o Peptic ulcer ---------------- Doxepin
o Premature ejaculation -------- Clomipramine
o Depression with OCD ---------- Clomipramine

 Amitriptyline
 Trimipramine Highly sedative TCAs
 Doxepin
 Amoxapine has dopamine receptor blocking property, it produces extra pyramidal
symptoms .
 Nortriptyline ---- least orthostatic hypotension.
 Doxepin-------- high anticholinergic activity

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ADVERSE EFFECTS
o Anticholinergic affects
o Orthostatic hypotension
o Sedation
o Seizures
o Tachycardia
o Conduction abnormality
o Allergic reactions
o Haemorrhagic reactions
o Increase hepatic transaminases
o Lethal dose is about 3 times the maximum therapeutic dose; activated charcoal 1-
2mg/kg initially followed by 2 or 3 more doses several hours apart will decrease
absorption of TCAs
o Physostigmine salicylate 1mg/IM counteracts both central and peripheral
anticholinergic effect use only coma, arrhythmia, or convulsions resistant to standard
treatment.

DOSAGE

o Amitriptyline –---------- 10-300 mg/day in divided doses

o Clomipramine ---------- 10 -150 mg/day in divided doses
o Dothiepin /Doxepin ------ 25-225 mg/day in divided doses
o Imipramine -------------- 10-200 mg/day in divided doses
o Nortriptyline ------------ 10-125 mg/day in divided doses
o Lethal dose of TCAs ---------- 1000mg

 SELECTIVE SEROTONIN REUPTAKE INHIBITORS(SSRIs)

Drug----------------- Half-life ------------------ dose

o Fluoxetine ------------ 5-7 days ----------------- 20-80mg/day
o Paroxetine ----------- 21 hours ----------------- 20-60 mg/day
o Fluvoxamine --------- 15 hours --------------- 50-300 mg/day
o Sertraline ------------- 3-5 days -------------- 50-200mg /day
o Citalopram ---------- 30-35 hours ---------- 20-60 mg/day
o Escitalopram -------- 30-35 hours ----------- 10-40 mg/day

o SSRIs having metabolites ---------- Fluoxetine and Sertraline

o High plasma protein bound SSRIs ------ Fluoxetine , paroxetine and Sertraline
o Highly selective serotonin reuptake SSRIs------- Escitalopram and Citalopram
o Anticholinergic SSRI-------- paroxetine
o High drug interaction-------- fluvoxamine
o Insomnia ------------- Fluoxetine
o Sedation ------------- Citalopram, Escitalopram, and Paroxetine
o Equally insomnia and sedation --------- Fluvoxamine and sertraline

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 INDICATIONS OF SSRIs

 Depression (childhood ---- Fluoxetine)

 Depression during pregnancy (except paroxetine-----cardiac anomalies )
 Depression during postpartum
 Depression in elderly/medically ill (except paroxetine)
Adults-------Fluoxetine, Fluvoxamine, Sertraline, paroxetine
 OCD Children--- Fluvoxamine and Sertraline
 OCD spectrum disorder
 Generalised anxiety and social anxiety disorders
 Premenstrual dysphoric syndrome (fluoxetine, paroxetine, sertraline)
 PTSD ( paroxetine, sertraline)
 Eating disorders( fluoxetine, sertraline)
 Panic disorders -------Paroxetine and Sertraline
 Dysthymia and atypical depression
 Dementia and borderline personality
 Smoking cessation
 Chronic fatigue syndrome
 Body dysmorphic disorders
 Pervasive developmental disorders
 Pain management (diabetic neuropathy, arthritis), phantom limb pain fibromyalgia
(fluoxetine)
 Trichotillomania
 Premature ejaculation
 Hot flushes in women at menopause

 SSRIs have been associated with increased suicidal ideation, hostility, and
psychomotor agitation in clinical trials involving in children and adolescent and
young adults (up to 24 years old). This effect was not seen in those aged 24 -65.
 SSRIs have flat dose response curve, do not increase the dose till steady state is
reached (4 weeks for fluoxetine and 1-2 weeks for other drugs.)
 Therapeutic effect seen after 7-28 days

ADVERSE EFFECTS OF SSRIs

 Sexual problems ;- anorgasmia , decreased libido, ejaculatory disturbances

Treatment;
o Bupropion
o Sildenafil
o Tadalafil
o Amantadine
o Cyproheptadine
o Mirtazapine
o Drug holidays (not effective with fluoxetine)

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 Gastrointestinal side effects ;
Sertraline and Fluoxetine have high gastric complications
Nausea /vomiting
Anorexia
Diarrhoea
Dyspepsia/Flatulence
Increased GI bleeding along with NSAIDs

 CNS effects
o Headache , worsening of migraine
o Seizures mainly in underlying seizure disorders
o Both activation and sedation occurs in initial treatment
o Insomnia: decrease in REM sleep, prolonged sleep onset latency, increased
awakening, and increased dreaming. May respond to clonazepam or
Cyproheptadine
o Precipitation mania and hypomania
o Lethargy, apathy; may respond to amantadine, bupropion, buspirone,
Modafinil.
o Cognitive impairment : donepezil 2.5- 10mg/day may be benefit
o Fine tremors may respond to propranolol
o Akathisia may respond to propranolol or benzodiazepine
o Dystonia, dyskinesia, parkinsonism in older people
o Nocturnal bruxism may respond to buspirone up to 50mg/day
o Paraesthesia /electric shock like sensation may be caused by pyridoxine
deficiency (pyridoxine 50-150mg/day)

o Paroxetine produces constipation due to anticholinergic activity.

o Weight gain----- Paroxetine
o Weight loss---- fluoxetine
o Headache ---- Fluoxetine
o Anxiety high in Fluoxetine low in Paroxetine and Escitalopram.
o Insomnia --- Fluoxetine
o Sedation ---- Paroxetine and Escitalopram
o Sleep bruxism
o Emotional blunting in long term use
o Seizure ---- Fluoxetine > 100mg
o Anticholinergic effects ------- Paroxetine
o Haematological complication ;- Easy bruising and prolonged bleeding time due to
functional impairment of platelet agglutination.
o Dilutional hyponatraemia
o Paroxetine and fluvoxamine have more withdrawal effects due to short half life.
o Fluoxetine ----- least/no withdrawal effects.

SEROTONIN SYNDROME

 IN 1960 Oates and Sjoerdsma first identified serotonin syndrome

 Serotonin is synthesised from the aminoacid Tryptophan.
 Tryptophan is transported into brain from the plasma.

94
  Tryptophan cannot be synthesised in the body it must be ingested with food and diet
which contains rich serotonin dairy products, beef, poultry, barley, fish, legumes and
peanuts.
 Adults require tryptophan 720-960mg/day.
 Once tryptophan enters the brain is converted to serotonin
 Serotonin dose not cross the blood brain barrier.

Pathophysiology

 5HT1A and 5HT2 receptors have been implicated in the serotonin syndrome
 Hyper stimulation of brain stem and spinal cord 5HT2 receptors by combining
serotonergic agents with MAO inhibitors.
 The beta adrenergic and dopaminergic system also thought to play a role.

Drugs increasing the serotonin levels

 Increase serotonin synthesis

L- tryptophan

 Decrease serotonin metabolism

Isocarboxazid
Tranylcypromine
Phenylzine
Meclobemide
Selegiline
 Increase serotonin release
Amphetamine
Cocaine

 Inhibit serotonin reuptake

TCAs
SSRIs
 Serotonin receptor agonists
Buspirone
LSD
Sumatriptan

 Dopamine agonists
Bromocriptine
Levodopa

CLINICAL FEATURES

Cognitive and behavioural symptoms

 Confusion /disorientation
 Agitation/irritability
 Coma/stupor
 Anxiety

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  Hallucinations
 Labile mood

 Autonomic symptoms
 Hyperthermia
 Diaphoresis
 Sinus tachycardia
 Hypertension
 Dilated pupil
 Flushing
 Nausea
 Diarrhoea

 Neuro muscular symptoms

o Myoclonus
o Hyper reflexia
o Rigidity
o Tremor
o Ataxia
o Extensor plantar response

STERNBACH criteria for serotonin syndrome

1. Coincidence with the addition of /increased in a known serotonergic agent. Aleast 3

of the following symptoms Diarrhoea, Diaphoresis, Rigidity, myoclonus, hyperreflexia
and Ataxia.
2. Other etiological factors (infection, metabolic ,substances abuse… have been ruled
out .
3. The neuroleptics had not been started / increased in dosage prior to the onset of
signs and symptoms.

SEROTONIN- NOREPINEPHRINE REUPTAKE INHIBITORS (SNRIs)

o Venlafaxine ---------- 75-375mg/day (XR 75-225mg/day)

o Desvenlafaxine------ 50-200mg/day
o Duloxetine ---------- 60-120mg/day
o Milnacipran ---------
o Subitramine -------- 10-15mg/day

INDICATIONS OF SNRIs

o Depression,
o GAD
o Social anxiety and anxiety disorders
o Diabetic neuropathy and
o Stress urinary incontinence ---- Duloxetine

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ADVERSE EFFECTS

o Nausea
o Somnolence
o Dry mouth
o Dizziness
o Constipation
o Blurring of vision
o Increased intraocular pressure
o Increased blood pressure

WITHDRAWAL EFFECTS

o Dizziness
o Nausea
o Anxiety
o Somnolence
o Insomnia

 Milnacipran is FDA approved for treatment of fibromyalgia

NOREPINEPHRINE REUPTAKE INHIBITORS (NRI)

 Reboxetine -----------2-8mg/day
Indication---------- Depression in adult

NOREPINEPHRINE -DOPAMINE REUPTAKE INHIBITORS (NDRIs)

BUPROPION

o Norepinephrine reuptake inhibition

o Dopamine reuptake inhibition
o Blockade of nicotine receptors
o Lower switch rate(to hypomania or mania)than other antidepressants

INDICATIONS

 Hypoactive sexual disorders

 Depression
 Seasonal affective disorder(FDA approval )
 Smoking cessation
 ADHD (children and adult)
 Cocaine detoxification
 Bipolar disorder
 Neuropathic pain

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ADVERSE EFFECTS

o Headache
o Nausea
o Dry mouth
o Tremor
o Insomnia
o Psychosis
o Hypertension
o Seizures (>300mg) risk 100-300mg-0 .1%, 300-450mg 0.4%, >450mg 2.2%
o Dose ------ 75-300mg/day (max 450mg/day) children 1-6mg/kg/day

SEROTONIN ANTAGONIST AND REUPTAKE INHIBITORS (SARIs)

 Trazodone -------------50-300mg/day
 Nefazodone ---------- 300-600mg/day

INDICATIONS

o Depression
o Insomnia
o Erectile disorder
o PTSD
o Secondary depression in other mental illness (schizophrenia, dementia)

ADVERSE EFFECTS

o Sedation
o Orthostatic hypotension
o Headache
o Nausea
o Priapism due to prominent alpha1 receptor blockade in absence of anticholinergic
activity.
o Jaundice and hepatic toxicity

ADRENERGIC ALPHA 2 RECEPTOR ANTAGONISTS

Mianserin and Mirtazapine

MIRTAZAPINE
o Pre synaptic 2 receptor blockade
o Post synaptic 5HT2 receptor blockade
o Postsynaptic 5HT3 receptor blocked

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More suitable in elderly depression/Melancholia /Endogenous depression
Least /no gastric side effects
No significant interaction with other antidepressants
Depression in negative schizophrenia

ADVERSE EFFECTS

o Somnolence
o Dry mouth
o Increased appetite
o Constipation
o Weight gain
o Dizziness
o Myalgia

Dose ----- 15-45mg/day

SERATONIN PARTIAL AGONIST AND REUPTAKE INHIBITORS (SPARI)

 Vilazodone
o Dose 20-40mg/day
o No dose adjustment in moderate renal and hepatic impairment
o Less sexual dysfunction than with other antidepressants

ANTIDEPRESSANT AUGMENTATION STRATEGIES

 Advantages
o May have rapid onset of response
o Response >50% with most combinations
o No need to taper first agent or have a washout
 Disadvantages
o Increase potential for side effects
o Increased risk for drug interactions
o Increased cost
 Antidepressants combinations
o RIMA+TCA (DO NOT COMBAINE irreversible MAOI with any other
antidepressant)
o RIMA+SSRI
o SSRI+TCA
o NDRI+SSRI
o NDRI+ SNRI
o SSRI+SARI
o SSRI+MIRTAZAPINE
o ANTIDEPRESSANT+THYROID HORMONE
o ANTIDEPRESSANT+LITHIUM
o ANTIDEPRESSANT+ANTICONVULSANTS
o ANTIDEPRESSANT+BUSPIRONE
o ANTIDEPRESSANT+PSYCHOSTIMULENTS/MODAFINIL
o ANTIDEPRESSANT+ECT
99
 o ANTIDEPRESSANT+TRYPTOPHAN
o ANTIDEPRESSANT+PINDOLOL
o ANTIDEPRESSANT+TESTOSTERONE
o ANTIDEPRESSANT+SECOND GENERATION ANTIPSYCHOTICS
o ANTIDEPRESSANT+REPETITIVE INTRACRANIAL MAGNETIC STIMULATION
o ANTIDEPRESSANT+OMEGA-3-FATTY ACIDS
o ANTIDEPRESSANT+FOLATE

TYPICAL ANTIPSYCHOTICS

 Also called as first generation anti-psychotics, Traditional antipsychotics,

conventional antipsychotics.
 Chlorpromazine was introduced in the mid 1950 by Delay and Deniker.

Mechanism of action

o Block the dopamine D1, D2,and D3 receptors

o Block 1 adrenergic receptors
o Block M1 muscarinic receptors and H1 histaminic receptors

Classification of typical antipsychotics

 PHENOTHIAZINES
o Aliphatic side chain
 Chlorpromazine
 Triflupromazine
 Perphenazine
o Piperidine side chain
 Thioredazine
 Misoridazine
o Piperazine side chain
 Trifluperazine
 Fluphenazine

 BUTYROPHENONES
o Haloperidol
o Droperidol
o Penfluridol

 THIOXANTHENES
o Thiothixene
o Flupenthixol

 DIPHENYLPIPERIDINS
o Pimozide
o Loxapine

100
High potency drugs

o High dopamine blockade

o Low sedation
o Low anticholinergic
o High EPS
o Low peripheral complications
o Low orthostatic hypotension
o Low cardiotoxicity
o Low seizure potential
o Eg. Haloperidol

Low potency drugs

o Low dopamine blockade
o High sedation
o High anticholinergic
o Low EPS
o High peripheral complications
o High orthostatic hypotension
o High cardiotoxicity
o High seizure potential
o Eg . CPZ

 Half-life of these drugs is nearly about 24 hours

 Penfluridol is long acting oral antipsychotic agent used once a week.

INDICATIONS

o Acute psychotic episodes in schizophrenia and schizoaffective psychosis

o Maintenance treatment of schizophrenia and schizoaffective psychosis
o Mania
o Depression with psychosis
o Delusional disorders
o Borderline personality disorders
o Substance induced psychosis
o Delirium and Dementia
o Mental disorders due to medical conditions
o Childhood schizophrenia
o Pervasive disorders
o Touretts syndrome

Doses

o Haloperidol------ 5-30mg/day (max—100mg/day)

o CPZ------------ 50 -1000 mg/day (max 1000mg/day)
o Flupenthixol ---- 4-18 mg/day(max 18mg/day)
o Sulpiride ------ 100 -2400 mg/day(2400mg/day)
o Pimozide ----- 2-20mg/day (20mg/day)

101
Adverse effects of typical antipsychotics
Extra pyramidal side effects
o Parkinson s syndrome TRAP ; Tremor, Rigidity, Akinesia, postural instability
o Akathisia
o Acute dystonia
o Neuroleptic malignant syndrome
o Tardive dyskinesia and dystonia
o Thioridazine , sulpiride have least EPS

Seizure

 High potency drugs ------ low epileptogenic

 Low potency drugs ------ least epileptogenic
 Molindone is least epileptogenic

Anticholinergic effects

Peripheral
o Dry mouth
o Constipation
o Urinary retention
o Decrease bowel sounds/paralytic ileus

Central
o Agitation
o Disorientation/ Delirium
o Hallucinations
o Seizures
o Dilated pupil
o Stupor/coma

Cardiac side effects; due to 1 adrenergic blockade

o Hypotension
o Reflux tachycardia
o Cardiac arrhythmia
o Orthostatic hypotension
o ECG changes ; T wave inversion, QT prolongation

Weight gain

o High in low potency drugs

o Low in high potency drugs
o Molindone and Loxapine have least weight gain

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Endocrine side effects ; due to blockade of D2 receptors at tubero-infundibular tract

o Increase prolactin
o Decrease GnRH
o Amenorrhoea
o Galactorrhoea
o Breast enlargement

Sexual side effects

o Anorgasmia
o Decreased libido
o Thioridazine has high sexual complications
o Retrograde ejaculation and Priapism

Other side effects

o Allergic dermatitis low potency drugs

o Photosensitivity
o Bluish discoloration of skin--------CPZ
o Reversible pigmentation at cornea and lens ------ CPZ
o Obstructive/cholestatic jaundice ---- CPZ
o Irreversible retinal pigmentation-------- thioridazine (>1000mg)

Over dose of typical antipsychotics

o CNS depression
o EPS
o Mydriasis
o Rigidity
o Restlessness
o Hypotension
o Decreased deep tendon reflexes
o Tachycardia
o Respiratory depression
Treatment

o Airway. Breathing, and Circulation

o Fluid rehydration
o Electrolyte correction
o Seizures-----------Diazepam IV
o Hypotension------- Dopamine/Nor epinephrine
o Gastric lavage with activated charcoal

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ATYPICAL ANTIPSYCHOTICS/SECOND GENERATION ANTIPSYCHOTICS

 Also called as serotonin –dopamine antagonists/ second generation antipsychotics

Drug ---------------Half life -----------------Dose----------------- FDA approval

 Risperidone ----20 hours ----------2-16 mg/day------- 1993

 Olanzapine ----31 hours ---------- 2.5-20 mg/day----- 1996
 Quetiapine ----7 hours --------- 25-800 mg/day---- 1997
 Clozapine ------12 hours ---------- 12.5-900mg/day--- 1970
 Ziprasidone ----5-10 hours ---------- 20-160 mg/day----- 2001
 Paliperidone ---20 hours ----------- 3-12 mg/day-------- 2006
 Aripiprazole -- 75 hours --------- 5-30 mg/day------- 2002
 Asenapine ----------- 5-20 mg/day------ 2007
 Iloperidone ---------- -------- 4-24 mg/day ------ 2007
 Sertindole ---------- ---------- 6-24 mg/day
 Zotepine ------------ ----------- 50-300 mg/day
 Amisulpride------------------ 200-1200 mg/day
 Bifepruox--------------- ------- 5-20 mg/day
 Melperone
 lurasidone
Mechanism of action

o Blockade of dopamine D1, D2, D3 and D4

o Blockade of 1, 2 adrenergic receptors
o Blockade of M1, M2 muscarinic receptors
o Blockade of 5HT1A, 5HT2C, 5HT2A, 5HT6,and 5HT7
ADVERSE EFFECTS

o Sedation /Dizziness
o Syncope
o Tachycardia
o Hypotension
o Weight gain
o lipid abnormality/Metabolic syndrome
o EPS
o Hyperprolactinemia

Side effects of clozapine

o Sailorrhoea
o Sedation
o Seizure
o Agranulocytosis
o Total cell count -------- < 3000 cells/cumm
o Neutrophils count ------ < 1500 cells/cumm clozapine should not to be give
o Polymorphs -------------- <40%

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LEAST/NO-EPS ATYPICAL ANTIPSYCHOTICS
o Aripiprazole,
o Olanzapine ,
o Quetiapine,
o Clozapine,
o Risperidone(<6mg)
o Ziprasidone

LEAST/NO DYSLIPIDAEMIA
o Amisulpride
o Aripiprazole
o Ziprasidone

LEAST/NO IMPAIRMENT OF GLUCOUSE TOLERANCE

o Amisulpride
o Aripiprozole
o Ziprasidone
o Risperidone

LEAST/NO HYPERPROLACTINAEMIA
o Aripiprazole,
o Olanzapine ,
o Quetiapine,
o Clozapine,
o Ziprasidone

LEAST / NO POSTURAL HYPOTENSION

o Amisulpride
o Aripiprazole
o Haloperidol
o Sulpiride
o Trifluperazine

LEAST/ NO QT PROLONGAT)ON
o Aripiprazole

LEAST/NO SEXUAL DYSFUNCTION

o Aripiprazole
o Quetiapine
o Clozapine

LEAST/NO SEDATION
o Amisulpride
o Aripiprazole
o Risperidone
o Sulpiride
o Haloperidol
o Trifluperazine
o Ziprasidone

105
LEAST /NO TARDIVE DYSKINESIA

o Clozapine
o Aripiprazole
o Olanzapine
o Quetiapine

LEAST/NO WEIGHT GAIN

o Amisulpride
o Aripiprazole
o Risperidone
o Sulpiride
o Haloperidol
o Trifluperazine
o Ziprasidone
o Quetiapine

ANTIPSYCHOTICS EQUIVALENT DOSES

o Chlorpromazine ------------------------------------------ 100 mg/day

o Haloperidol------------------------------------------------- 3 mg/day
o Fluphenazine ---------------------------------------------- 2 mg/day
o Fluphenthixol---------------------------------------------- 3 mg/day
o Zuclopenthixol -------------------------------------------- 25 mg/day
o Trifluperazine --------------------------------------------- 5 mg/day
o Sulpiride --------------------------------------------------- 200 mg/day
o Pimozide -------------------------------------------------- 2 mg/day
o Loxapine -------------------------------------------------- 10 mg/day
o Fluphenazine depot ---------------------------------- 10 mg/week
o Flupenthixol depot ---------------------------------- 5 mg/weeek
o Haloperidol depot------------------------------------ 15 mg/week
o Zuclopenthixol depot -------------------------------- 100mg/week

DEPOT ANTIPSYCHOTICS

o Haloperidol decanoate------- 12.5-75 mg/4weekss

o Fluphenthixol decanoate ---- 12.-400 mg/4weeks
o Fluphenazine decanoate ---- 6.25-50 mg/4weeks
o Fluphenazine enanthate --- 6.25-50 mg/4weeks
o Zuclopenthixol decanoate -- 100-600 mg/4 weeks
o Risperidone consta---------- 12.5-50 mg/ 2 weeks
o Olanzapine pamoate ------- 75-150 mg/ 4weeks

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STIMULANTS

Amphetamine 0.15 -0.5 mg/ body wt

Dextroamphetamine

Methylphenidate 0.3-1mg/kg body wt

Dexmethylphenidate

Pimoline
Modafinil ------100- 400 mg/day

INDICATIONS OF STIMULANTS

o Narcolepsy
o Hypersomnolence
o Depressive disorder
o Obesity
o Encephalopathy
o Fatigue
o ADHD

ADVERSE EFFECTS OF STIMULANTS

 Hypertension
 Tachycardia
 Hyperthermia
 Seizure
 Psychosis
 Delirium
 Dry mouth
 Pupillary dilatation

ATOMOXETINE

 Increase norepinephrine by selective inhibition of the pre synaptic norepinephrine

transporter.
 Half-life -----------5 hours

INDICATIONS

 ADHD
 Cognitive enhancer in schizophrenia
 Add on to antidepressant

 DOSE:---- 0.5-1.8 mg/kg body wt

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ADVERSE EFFECTS

 Abdominal discomfort
 Decrease appetite
 Weight loss
 Sexual dysfunction
 Dizziness/Vertigo
 Mood swings

THYROXIN IN PSYCIATRY

INDICATIONS
o Augmentation of antidepressant
o Lithium induced hypothyroidism

CONTRAINDICATIONS
o Hypertension
o Cardiac diseases
o Angina

Adverse effects
 Headache
 Palpitations
 Weight loss
 Diarrhoea
 Abdominal cramps
 Nervousness
 Increase blood pressure
 Tremor insomnia
 Osteoporosis

PHOSPHODIESTERASE INHIBITORS s

 Sildenafil ------------- 25-100mg/day

 Vardenafil ---------- 2.5 -20 mg/day increase cAMP
 Tadalafil -----------5-20mg/day

ATP/GTP----------------cAMP/cGMP ------------5AMP/5GMP

Phosphodiesterase

Sexual stimulus --NO - cAMP--- blood flow of penis---- Erection of penis

Phosphodiesterase inhibitors are not effective in absence of sexual stimulus

108
Indications

o Impotency
o Pulmonary hypertension

Contraindications
o Hypertension
o Atherosclerosis
o Diabetes
o Cardiac diseases
o Recent myocardial infarction
o Patient on nitrates
Adverse effects

o Myocardial infarction
o Headache
o Flushing
o Stomach pain
o Nasal congestion
o Diarrhoea
o Dizziness

PSYCHOTROPICS IN SPECIAL PATIENT GROUPS

1) EPILEPSY

ANTIPSYCHOTICS ANTIDEPRESSANTS

 Haloperidol SSRIs
 Sulpiride Meclobimide
 Risperidone Low dose of lithium
2) PREGNANCY

Antidepressant (I-FAN) antipsychotics

 I-Imipramine Atypical antipsychotics

 F-Fluoxetine Haloperidol
 A-Amitriptyline CPZ
 N-Nortriptyline Trifluperazone

Mood stabilizers sedatives

 Olanzapine Promethazine
 Quetiapine

109
3) BREAST FEEDING

Antidepressants antipsychotics

 Paroxetine Sulpiride
 Sertraline Olanzapine

Mood stabilizers sedatives

o Olanzapine Lorazepam
o Sodium valproate Zolpidem

4) RENAL IMPAIRMENT

Antipsychotics antidepressants

Haloperidol citalopram
Olanzapine sertraline
Avoid high anticholinergic drugs
Avoid Sulpiride and Amisulpride

Mood stabilizers
Sodium valproate
Carbamazepine
Lamotrigine

Anxiolytics /sedatives
Lorazepam
Zolpidem

5) HEPATIC IMPAIRMENT

Antipsychotics

 Haloperidol
 Sulpiride
 Amisulpride

Antidepressants
Imipramine
Paroxetine
Citalopram

Mood stabilizers

Lithium

110
 anxiolytics/sedatives(LOT)
Lorazepam
Oxazepam
Temazepam
6) PARKINSONS DISEASE

Antipsychotics
Olanzapine
Quetiapine

Antidepressants
SSRIs

 BENZODIAZEPINES EQUIVALENT DOSES

Diazepam 5mg-Chlordiazepoxide 15mg-Oxazepam 15mg

 CLINICAL GUIDELINES

o Indian psychiatric society guidelines (IPS)

o National institute of health and clinical excellence (NICE)
o Maudsley prescribing guidelines

 CATIE study:- Clinical Antipsychotic Trail for Intervention and Effectiveness

 CUtLASS study: cost utility of the latest antipsychotic drugs in schizophrenia study.

 EUFEST study: European First Episode Schizophrenia Trial found that 7% of first

episode patients had persistent negative symptoms.

 FDA- APPROVED MEDICATIONS FOR BIPOLAR DISORDERS

Drug acute mania - maintenance treatment

o Lithium 1970 1974

o Olanzapine 2000 2004
o Carbamazepine 2004 NO
o Divalproex 1996 NO
o Risperidone 2003 NO
o Quetiapine 2004 NO
o Ziprasidone 2004 NO
o Lamotrigine NO 2003

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PSYCHOTROPIC DRUG DOSAGE RANGE
DRUG DOSE RANGE

1. Alprazolam --------------------- 0.25 – 10 mg

2. Acamprosate ----------------------- 333 – 1998 mg
3. Agomelatine --------------------- 25 – 50 mg
4. Amitriptyline ---------------------- 10 – 300 mg
5. Amisulpride ----------------------- 50 – 800 mg
6. Amoxapine ---------------------- 50 – 600 mg
7. Aripiprozole ---------------------- 5 – 30 mg
8. Asenapine ----------------------- 5- 20 mg
9. Atomoxetine ---------------------- 10 – 100 mg
10. Bupropion ---------------------- 150 – 450 mg
11. Buspirone ---------------------- 15 – 60 mg
12. Carbamazepine ---------------------- 200 – 1600 mg
13. Chlordiazepoxide --------------------- 10 – 150 mg
14. Chlorpromazine ---------------------- 30 – 800 mg
15. Citalopram ---------------------- 20 – 60 mg
16. Clomipramine ----------------------- 25 – 250 mg
17. Clonidine ------------------------ 0.1 – 1.8 mg
18. Clonazepam ----------------------------- 0.25 – 4 mg
19. Clozapine ------------------------------ 2.5 – 800 mg
20. Desipramine ------------------------------ 25 – 300 mg
21. Desvenlafaxine ------------------------------ 50 – 400 mg
22. Dexmethylphenidate ------------------------ 2.5 – 20 mg
23. Dextroamphetamine + amphetamine ----- 10 – 40 mg
24. Diazepam ------------------------------- 5 – 40 mg
25. Donepezil ------------------------------- 5 – 20 mg
26. Doxepin -------------------------------- 25 – 300 mg
27. Dothipin -------------------------------- 25 – 300 mg
28. Duloxetine -------------------------------- 20 – 120 mg
29. Escitalopram ------------------------------- 10 – 40 mg
30. Estazolam ------------------------------- 1–2 mg
31. Eszopiclone ------------------------------- 1–3 mg
32. Fluoxetine ------------------------------- 20 – 80 mg
33. Fluphenazine ------------------------------- 1 – 40 mg
34. Flurazepam -------------------------------- 15 – 30 mg
35. Fluvoxamine -------------------------------- 25 – 300 mg
36. Gabapentin --------------------------------- 300 – 3600 mg
37. Galantamine --------------------------------- 8 – 24 mg
38. Haloperidol --------------------------------- 1- 100 mg
39. Imipramine --------------------------------- 50 – 300 mg
40. Isocarboxazid -------------------------------- 20 – 60 mg
41. Iloperidone --------------------------------- 1 – 24 mg
42. Lamotrigine --------------------------------- 25 – 400 mg
43. Lithium --------------------------------- 300 – 1800 mg
44. Lorazepam ---------------------------------- 1 – 10 mg
45. Loxapine --------------------------------- 20 – 250 mg

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46. Maprotiline ---------------------------------- 25 – 250 mg
47. Memantine ---------------------------------- 5 – 20 mg
48. Mesoridazine -------------------------------- 30 – 400 mg
49. Methylphenidate ----------------------------- 10 – 60 mg
50. Milnacipran ------------------------------- 50 – 100 mg
51. Mirtazapine ------------------------------- 15 – 45 mg
52. Molindone -------------------------------- 15 – 225 mg
53. Modafinil --------------------------------- 50 – 800 mg
54. Nefazodone -------------------------------- 200 – 600 mg
55. Nortriptyline -------------------------------- 75 – 150 mg
56. Naltrexone --------------------------------- 25 – 100 mg
57. Olanzapine --------------------------------- 5 – 20 mg
58. Oxazepam -------------------------------- 30 – 120 mg
59. Oxcarbazepine ------------------------------- 300 – 2400 mg
60. Paliperidone -------------------------------- 6 – 12 mg
61. Paroxetine -------------------------------- 20 – 60 mg
62. Paroxetine CR -------------------------------- 12.5 – 62.5 mg
63. Perphenazine -------------------------------- 12 – 64 mg
64. Phenelzine -------------------------------- 15 – 90 mg
65. Pimozide ------------------------------------ 1 – 10 mg
66. Prazepam ------------------------------------ 20 – 60 mg
67. Pregabalin ------------------------------------ 50 – 600 mg
68. Protriptyline --------------------------------- 15 – 60 mg
69. Quetiapine --------------------------------- 25 – 800 mg
70. Ramelteon ---------------------------------- 8 – 16 mg
71. Risperidone ----------------------------------- 2 – 16 mg
72. Rivastigmine ----------------------------------- 3 – 12 mg
73. Sertraline ----------------------------------- 50 – 200 mg
74. Selegiline ----------------------------------- 5 – 30 mg
75. Sulpiride ---------------------------------- 200 – 2400 mg
76. Sertindole ---------------------------------- 4 – 20 mg
77. Temazepam --------------------------------- 15 – 30 mg
78. Thioridazine ----------------------------------- 20 – 800 mg
79. Thiothixene ------------------------------------ 6 – 60 mg
80. Tiagabine ----------------------------------- 4 – 56 mg
81. Topiramate ----------------------------------- 50 – 400 mg
82. Tranylcypromine ----------------------------- 30 – 60 mg
83. Trazodone ----------------------------------- 150 – 600 mg
84. Triazolam ----------------------------------- 0.125 – 0.5 mg
85. Trifluoperazine -------------------------------- 2 – 40 mg
86. Trimipramine -------------------------------- 50 – 300 mg
87. Valproic acid -------------------------------- 500 – 4200 mg
88. Venlafaxine --------------------------------- 75 – 375 mg
89. Varenicline --------------------------------- 0.5 – 2 mg
90. Zaleplon ---------------------------------- 5 – 20 mg
91. Ziprasidone --------------------------------- 20 – 160 mg
92 Zolpidem ------------------------------------ 5 - 20 mg

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 PHYSICAL METHODS OF TREATMENT IN PSYCHIATRY

1) ELECTRO CONVULSIVE THERAPY

Milestones in the History of Convulsive Therapy

1500s Paracelsus induced seizures by administering camphor (by mouth) to treat

psychiatric illness.

1785 First published report of the use of seizure induction to treat mania, again using
camphor.

1934 Ladislas Meduna begins the modern era of convulsive therapy using intramuscular
injection of camphor for catatonic schizophrenia. Camphor is soon replaced with
pentylenetetrazol.

1938 Ugo Cerletti and Lucio Bini conduct the first electrical induction of a series of seizures
in a catatonic patient and produced a successful treatment response

1940 ECT is introduced to the United States.

Curare developed for use as a muscle relaxant at ECT.

1951 Introduction of succinylcholine.

1958 First controlled study of unilateral ECT.

Indications of ECT

o Depression with suicidal risk

o Depressive stupor
o Resistant depression
o Melancholia /Endogenous depression
o Depression in pregnancy
o Depression in medical disorders
o Schizophrenia acute exacerbation
o Schizophrenic stupor
o Catatonia
o Resistant schizophrenia
o Schizoaffective disorder
o Postpartum psychosis

Adverse effects

o Headache
o Vomiting
o Confusion
o Amnesia (anterograde and retrograde )
o Fractures/Dislocations

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Prevention of adverse effects

o Using unilateral ECT

o Oxygenation before and after seizure
o Minimal voltage
o Proper spacing
o Brief pulse type

Mechanism of action

o Changes in neurotransmitter receptors

o Changes in second messengers

Anaesthetics agent: Thiopental (2-3mg/kg body wt) IV

Muscle relaxant : Succinylcholine o.5 to 1mg/kg body wt

Atracurium

Atropine: 0.6mg

Basic investigations before giving ECT

o X-ray chest
o X-ray skull
o Fundus examination
o Full physical examination
o ECG

EEG changes during ECT: Flatting---- Delta activity----- Theta activity

Electrical stimulus

o Sine wave
o Brief pulse
o Ultra brief pulse

 Plantar extension is monitored in partially relaxed patients and EEG is monitoring In

fully relaxed patients.
 Minimum 25 sec seizure is effective
 Empty stomach 6 hours prior to giving ECT
 Site : 1 inch above the midpoint of the imaginary line between tragus of the ear to
inner canthus of the eye.
 Prolonged and tardive seizures ----- seizure >180 sec(RX iv diazepam)
 Number of ECTs ------6-12 (max 20)
 Maintenance treatment ----- weekly, bi weekly, monthly

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 2) VAGAL NERVE STIMULATION

o Left vagal nerve

o Refractive epilepsy
o Resistant depression
3) DEEP BRAIN STIMULATION

 Parkinson s disease
 OCD
 Tourette syndrome
4) TRANS CRANIAL MAGNETIC STIMULATION

 1.5 – 2.0 TESLA

 Resistant depression
 OCD
 PTSD
 Parkinson s
5) PYSCHOSURGERY ( Jacobsen and John Fulton )

 Resistant depression
 OCD--cingulotomy
 Chronic anxiety
6) OTHER METHODS

 Insulin coma therapy

 Atropine coma therapy
 Sleep deprivation
 Co2 inhalation therapy
 Nitrous oxide therapy

PSYCHOTHERAPIES

PSYCHOANALYSIS; - Proposed by Sigmund Freud

PSYCHOANALYTIC PSYCHOTHERAPY
 Insight orientation psychotherapy
 Supportive psychotherapy

BRIEF PSYCHOTHERAPY
o Brief focal psychotherapy
o Time limited psychotherapy
o Short term dynamic psychotherapy
o Short term anxiety provoking psychotherapy

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GROUP PSYCHOTHERAPIES

o Supportive group therapy

o Analytically oriented psychotherapy
o Psychoanalysis of group
o Transactional group therapy
o Behavioural group therapy

FAMILY THERAPY

o Psychodynamic –experimental method

o Bowen model
o Structural method
o General system method

DIALECTICAL BEHAVIOURAL THERAPY

o Borderline personality disorder

o Suicidal risk

BIO-FEEDBACK

o Electromyogram (EMG)
o Electro encephalogram (EEG)
o Galvanic skin response (GSR)
o Thermistor

BEHAVIOURAL THERAPY
o Systematic desensitization
Relaxation training
Hierarchy construction
Desensitization of the stimulus
o Therapeutic graded exposure (no relaxation training)
o Flooding (no hierarchy construction)
o Modelling
o Aversion therapy
o Eye movement desensitization and processing for childhood PTSD
o Positive reinforcement
o Shaping
o Response prevention
o Thought stopping

117
 GENERAL PSYCHIATRY

SCHIZOPHRENIA

 Benedict Morel ------- Dementia precoce

 Emil Kraepelin---------Dementia precox , paranoea
 Eugen Bleuler --------coined schizophrenia
A s------- Autism, Association, Ambivalence, Affect

 Karl Jaspers ------ Existential psychoanalysis

 Adolf Meyer -- schizophrenia in reaction to life stress
 Gabriel –Langfeldt- schizophreniform psychosis

Prevalence of schizophrenia
 General population -------------------------------- 1%
 Non twin sibling of schizophrenic patient -----8%
 Child with one parent schizophrenia -----------12%
 Child with two parent schizophrenia -----------40%
 Dizygotic twin of schizophrenic patient --------12%
 Monozygotic twin of schizophrenic patient ---47%

 GENES : 1q,5q,6p,6q,8q,10p,13q,and 15q are strongly associated with schizophrenia .

 Candidate genes for schizophrenia ----DISC1, GRM3,COMT,NRG,RGS4 and G72.

PSYCHODYNAMIC & NEURODYNAMIC THEORIES OF SCHIZOPHRENIA

PSYCHODYNAMIC MODELS

A) Classical psychoanalytic models

I. Sigmund Freud
II. Paul Federn
III Heinz Hartmann

B) Interpersonal model

C) object-relations model
1. Melanie Klein
2. WD Fairbairn
3. Margaret Mahler
4. Ping-Nie Pao

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MODEL ON FAMILY DYNAMICS
1. Fromm et al
2. Bateson and Jackson
3. Theodore Lidz
4. Wynne and singer
5. Vaughn and Leff and brown et al

NEURODYNAMIC THEORIES
1. Biological or neuronal network model
2. Adoption studies
3. Stress-diathesis model
4. Vulnerability-Stress model

The Psychodynamic models thus developed as classical, interpersonal and Object relations
models. These were followed by family models.

The final shift was attributed to the neurodynamic models with the advent of biological,
adoption studies, stress-diathesis and vulnerability stress hypothesis.

The amalgamation of all these led to the biopsychosocial model.

CLASSICAL PHYCHOANALYTIC MODELS

Sigmund Freud.
Freud states that schizophrenia is also a state generated due to internal conflicts.

This can be explained by the structural model of the mind. That is id, ego, and superego.
The id is the storehouse of primary impulses of the mind, like sexual and aggressive. This is
the primitive mind and is entirely unconscious.

On the other hand the superego is that which is largely learned It symbolizes the rules,
regulations and values inherited from parents and society at large. It is mostly also in the
unconscious and its presence is felt through guilt and shame.

The ego is the middle man. It is the agent between the id and superego.

These are activated by anxiety as a response to the danger signal generated by the internal
conflicts. He described the causation of schizophrenia is due to 2 reasons.
1. The conflict-defence model.
2. The deficit or deficiency model.

119
 The conflict-defence model
A conflict leading to an anxiety leading to defence.

The regression is to an earlier stage of development where fixation or arrest occurred prior
to the oedipal stage ie., before the development of an integrated ego.

The primary defences used here are denial and projection. Here due to denial of the
unfulfilled wish, there is projection onto the object .

This is classically described in the explanation for latent homo-sexual impulses.

) love him A man s impulse .
) don t love him Denial hence, ) hate him
(e hates and hence persecutes me Projection

Thus the person develops an entire delusional system based on such conflicts.

This can be extrapolated to any case where ambivalence towards any love object exists.

The Deficit or Deficiency model

Here the defence mechanisms do not come into play. Due to the existing conflict, there is a
withdrawal of libidinal energy into the self. This energy, now directed towards the self, leads
to the grandiosity seen or primary narcissism.

This continuous process of withdrawal leads to a break from reality. This leads to a
diversion of the libidinal impulses away from the real world and towards inter-nailed,
fantasized objects and hence emerges the positive symptoms of schizophrenia Viz, delusions
and hallucinations.

Paul Federn
He was the one who studied the ego in more detail. He believed that the ego developed at
such a high level of consciousness, that it developed its own feeling , i.e., that of the self or
) . (ence., probably originated the use of the term ego as it is used in common parlance
today, and not strictly in the psychodynamic sense.

Now Federn believed that the ego exhibited boundaries—both internal and external. When
the internal boundary was transgressed it leads to internal regression to an earlier stage of
development.

The external boundary could be intact—in which case the person can function well in the
world despite presence of symptoms; whilst when the external boundary is broken, the
person stops functioning even with others, i.e., there is overall decline in functioning.

120
Heinz Hartmann
He believed there was a premorbid ego, and one that developed after the onset of the illness.
Due to the illness, there is regression to the primary ego state. This ego, due to the generated
conflicts, perceives narcissistic injury to it and responds to this with aggressive impulses.

This he explained with the use of defences-initially intellectualization and sublimation

followed by denial and projection.

He believed that the ego was a dynamic system which constantly expanded its horizon, to
adapt to the stresses faced by the individual.

It is when this dynamic equilibrium gets upset, that the above mechanisms act and lead to
schizophrenia

INTERPERSONAL MODEL

The interpersonal model was described by Harry Stack Sullivan According to this model
man is a social being who depends on his development largely on the interaction with his
environment, and society at large.

In Freudian psycho-dynamics, the id impulses are primary, and subsequently modified by

the ego and superego.

In sullivanian psychodynamics, the self is a product of the existing world. He described the
very first relationship to be that of a mother and child.
.
They initially exist as a symbiotic dyad. Gradually the self separates to realize the mother as
an independent entity.

It is at this crucial stage that the process of pathological development can start. In case of an
over-anxious mother, the child forms a template (some thing like that seen in the
reduplication of the DNA) for the anxiety to develop.

In fact, he believed that schizophrenia was an outcome of the struggle that the child faces
due to early exposure to anxiety.

The child who is trying to establish a self-system of equilibrium, now faces three states the
good me (flow anxiety), the bad me (high anxiety) and the not me (apocalyptic anxiety of
schizophrenia).
During adolescence especially due to the introduction of previously alien sexual drives, the
state of anxiety heightens and reaches abnormal proportions. This is when florid psychotic
symptoms develop.

The remission occurs during the process of reorganization of the self into the pre-existing
state of equilibrium. Sullivan thus believed the schizophrenic process to thus begin as an
external one (with the mother) and subsequently gets internalized.

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 OBJECT-RELATIONS MODEL

Melanie klein
She attributed the importance of love and hate in all relationships. She described the
concept of the self as in context to other, and this was termed as internal object relations.

During development, one uses the defences of splitting and projective identification for
adaptation and healthy development of these internal object relations. However, the same
defences used in adults could have disastrous outcomes.

She went on to describe two positions in infancy the paranoid position and the depressive
position.

In the paranoid position, the individual splits the hate or bad experiences, and projects them
onto others who thus appear to be persecutory.

The infant thus develops with a pre-existing substrate for the genesis of schizophrenia. It
then responds to stresses, especially in adolescence, by going to either of the above
positions, and obviously in schizophrenics regresses to the paranoid position.

Wd Fairburn
Fairburn again believed that human contact was the basis of development, even If that
contact was not pleasant. According to him, the absence of a mother.

During the stage of the paranoid position, gave rise to ambivalent feelings towards love.
Hence the schizoid thinking of to love or not developed, and these feelings surfaced during
periods of stress, usually the first time being during adolescence.

Margaret Mahler
She is credited for mainly describing the stages of development , viz., autism, symbiosis and
separation individuation.

Autism is the early infantile stage where the infant largely resides in his or her own fantasy
world.

The symbiotic relationship is one set up with the mother and child during the early
formative years. It is during the last phase of development, the separation-individuation
phase of adolescence, in which the stress may become over whelming, and there is a
regression to the earlier stage of autism and fantasy.

Ping-nie pao
He was the first to describe the onset of psychosis due to either a stressful situation (acute)
or due to genetic loading (chronic).

He believed that abnormal development due to mixed signals emanating from a mother
acting upon a child with a pre-existing vulnerable constitution lead to distress.

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There was an attempt to neutralize this distress and in the process was born the state he
called organismic panic. The ego tries to correct this and reintegrate the individual, only to
yield symptoms such as delusions, hallucinations and an altered personality.

MODEL ON FAMILY DYNAMICS

These models might as well be comparable to the object relation theory, except for the fact
that instead of individual, the relations between all the members of the family come into
play.

Fromm et al
Fromm-Reichmann-first described the theory of a schizophrenogenic mother.

According to this theory, the presence of a cold indifference and non-reactive mother lead to
poor development of socially adaptive behaviors in children. This further led to
development of poor social skills and abnormal communication, ultimately a pattern of
schizophrenic behavior gradually emerged in these children.

Bateson and Jackson

They explained what is now called that double bind theory. Gregory Bateson and Donald
Jackson studied that often in families with a schizophrenic patient, the parents might be
giving the children conflicting messages. When a child receives two messages of opposite
meanings, it leads to a double bind.

The inability to interpret this difference leads to a feeling of guilt. Subsequently the child
may have ambivalent feelings which if generated would lead to an altered pattern of
thinking.

For, example a mother telling her child / you don t love me enough and at the same time
indicating that hugging, kissing or showing any form of affection was not acceptable. This
kind of a conflict leads to ambivalent feelings in the child and a subsequent schizoid thing
pattern.

Theodore lidz & R. lidz

They described the theories of marital schism and marital skew.

Schism, as the name suggests, it indicates a dichotomous or extreme pattern of existence.

Basically, two individuals who do not get along with each other, have completely contrasting
views and ideas, yet stay under the same roof.

These individuals, as parents could send conflicting messages to their offspring, and be
fertile ground to yield a schizophrenic mind.

This pattern is often seen in countries like ours, where arranged marriages bring together
contrasting individuals, bound together by marriage.

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Skew, on the other hand, as in statistics, is an extreme form, or at the extreme end of
deviation.

In this case there is a chronic disagreement, within an outwardly calm family. Here, one
parent usually does not fulfil the parental role. As a result, a single parent dominates, and
the child subsequently assumes the parent role.

There is over-dependence, and ambiguity regarding family boundaries and individual

responsibilities. This leads to a lot of confusion and conflict in the child, thus again
generating schizophrenic thinking patterns.

Wynne and singer

They described the family communications model. Here, there are basically two types of
communications between families.
a) Amorphous
b) Fragmented

Amorphous: Here there is vague and indefinite communication. The parents themselves
lack concrete ideas and emotions. Their thoughts are ill-defined. The communication
between the members thus is not definitive.
This probably leads to more of loosening of thoughts and formal though disorder.

Fragmented: Here there is poor integration of language and disruption of phrases. The
meaning to be conveyed does not get across to the different members. In short the
communication is often conflict-laden.

Lidz found that where the families had both parents with high communication skills, the
chances were of developing normal and neurotic offspring;

in families with both parents having poor communication skills the chances were of
developing offspring with schizophrenia;

in families with one parent having good skills and the other having poor skills, the chances
of either were 50 – 50.

Vaughn Leff and Brown et al.

They described a very powerful tool in today s view of the prognosis of a schizophrenic
patient; a concept which is called expressed emotions . (ere the attitude of the family
towards an affected individual can lead to further relapses and a poorer prognosis.

According to some, the initial precipitation of the illness too, could be attributed to
expressed emotions.
There are in all 5 emotions described:
a) Hostility
b) Criticism
c) over-involvement
d) Guilt induction
e) Intrusiveness

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Of these the first 3 are found to predict high relapse rates within the first 9 months itself.

A structured interview using the scale Camberwell Family )nterview can be used
during the in-patient stay to explore these areas.

Families can be classified as those with high EE and those with low EE . The data suggests
that families with high EE require a contact of 35 hours only, between affected patient and
family. These individuals are usually in day-care centres and half-way homes.

NEURODYNAMIC THEORIES

1. Biological or neuronal network model

2. Adoption studies
3. Stress-diathesis model
4. Vulnerabilty-Stress model

Biological or Neuronal Network Model

This states that it is basically an erroneous development in neuro-anatomy that yields to
aberrant connections with grey matter.
This leads to generation of various pathological symptoms of schizophrenia. We would
reach a better understanding if the following concepts are understood.

a) Parallel processing model. The neurons in the cerebral cortex exist by the multiple
connections with each other.

There are exciting synaptic connections between these neurons. Hence from one neuron,
multiple connections can go to other neurons, via the synapses, and vice-versa. This sets up
a neuronal pool or network.
There exist at a given time many such networks simultaneously in the brain, setting up what
is called the parallel processing . Thus various inputs can be assimilated at a given time, and
stored at different points.

This is where the memory circuits come into play. The hippocampus forms the storehouse
of memory. Now retrieval of memory occurs in perceiving a cue. This triggers off the
neuronal circuitry to get back the stored memory from the hippocampus.

An example: A person looking for a building on the street, assimilates a variety of inputs.
He sees a bank opposite the building, a lady walking in red, the street lights, boys playing in
the park, the buildings around, and the colour and dimensions of the particular building that
he was looking of these various bits of information, fire thousands of neurons and set up
many parallel memory circuits.

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These are stored as various bits of information to be used later if required. Now, if asked by
someone else about the building, the person concerned will give landmarks that he retrieves
from his memory, and hence accurately reduplicates his experience.

Now let us say that this neuronal pool misfires. Instead of retrieving information only from
this memory circuit, it also retrieves memories from other circuits simultaneously.

The resultant would be a chaotic response which would lead to disordered thinking, and
what is now hypothesized as the neuronal basis for delusions and hallucinations.

b) Parasitic memories: Along with formation of memory circuits that are formed from self-
experiences, at times there are spurious memories which develop, i.e., these form de-novo.

Here, each memory has a certain energy level. Depending on the existing energy fluxes there
are signals set up whereby these memories get attracted to various circuits.

These may get drawn into circuits not originally attached to them and form something called
parasitic memories i.e., they are unwanted and add to the circuit. )t is these parasitic
memories that contribute to the vague and often bizarre symptoms of schizophrenia.

c) Aberrant brain circuitry: The formation of neuronal plates and synapses itself may be
faulty. These may occur in a pre-existing faulty brain, thereby implying that the brain
development in utero is in itself erroneous.

During development, with the input from the environment, and certain experiences; or
perhaps an inherent latency to form faulty circuits, the brain starts forming erroneous
connections.

Another aspect is the pruning of synapses. When there is either an increase or decrease in
the synaptic pruning, this can lead to alteration in the memory storage and trivial.

The generation of hallucinations, is attributed to synaptic pruning, as it seen not only in

schizophrenia, but also in dementia and other organic states, where pruning has been
studied in more detail.

Adoption Studies
The most classical genotype model studied was the Finnish Adoption Model done by Pekka
Tienari et al. Here the genetic loading was studied, along with environmental contribution.
Basically, the groups studied were of 3 types, divided as follows:

1) Progeny of an affected schizophrenic in an adopted family wherein the environment

was relatively stress-free.

2) Progeny of an affected schizophrenic in an adopted family with a stressful

environment, viz., abnormal communication, emotional over-involvement.

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 3) Progeny of an unaffected individual in an adopted family with a stressful
environment, viz., abnormal communication, emotional over-involvement etc.

Of all the groups studied, it was found that children in group (2) had the maximum chances
of developing schizophrenia.

Group (1) though having an obvious genetic vulnerability, adapted due to a healthy
environment.

Similarly group (3) having a healthy genetic make-up, did not succumb, but could cope up
with the on-going stresses.

This study was a landmark in suggesting that both genes and an unhealthy environment
contribute to the full-blown schizophrenic syndrome.

Stress-Diathesis Model
This may also be termed as the nature-nurture model. The pioneers of this model are:
a) Sandor Rado and
b) Paul Meehl

Sandor Rado: According to Rado, there is an inherited factor in the genesis of

schizophrenia which constitutes the genotype.
When this genotype interacts with the environment, it gives rise to phenotype called as
schizotype.

This schizotype has often aberrant cognitive processes and a deviant style of communication
with family members.
When this person is exposed to a stressful environment, then this schizotype manifests as
delusions, hallucinations and bizarre behaviour.

Paul Meehl: Meehl believed that it was the faulty neural development that was inherited as
a phenotypic trait.

This manifested as schizotaxia or the inherent ability to develop the illness

When this schizotaxic individual interacted with an asocial environment, she/he tended to
develop faulty cognitive processing. She/he thus in turn tended to become ambivalent,
anhedonic, and aversive to human relations.

These theories further corroborated the contribution of a stressful environment, in the

genesis of schizophrenia.

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Vulnerability-Stress Model

Vulnerability may be defined as the inherited tendency towards developing schizophrenia .

At best it is a trait, which is present pre-morbidly.

However, it is unique, in that it is not a fixed trait. It is dynamic, and its characteristics and
contribution in the illness process may change from time to time, and with each ensuing
episode.

Vulnerability, although largely genetic, may also add an acquired component during the
antenatal or postnatal period. It may or may not be contributed by birth order, season and
social environment.

The following are the commonest vulnerabilities seen in schizophrenia:

a) Cognitive deficits which lead to an inability to filter out information. As a result there
is excessive storage of unrequired information which adds to the schizophrenic
process.

b) Actual deficits in neuronal connections and neurophysiology, leading to the inability

in the censoring or filtering mechanism as mentioned above.

c) Poor social skills development. It reflects an inability to communicate, have eye to

eye contact and set up meaningful relationships.

d) Poor psychological development and excessive use of few defenses like denial,
splitting and projection

 CLASSIFICATION OF SCHIZOPHRENIA

ICD-10 (PHC-UPR-SOS)
o Paranoid schizophrenia
o Hebephrenic schizophrenia
o Catatonic schizophrenia
o Undifferentiated schizophrenia
o Post schizophrenic depression
o Residual schizophrenia
o Simple schizophrenia
o Other schizophrenia
o Unspecified schizophrenia

DSM-IV
o Paranoid schizophrenia
o Disorganized schizophrenia
o Catatonic schizophrenia
o Undifferentiated schizophrenia
o Residual schizophrenia

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Crows classification
Type -1(positive)
Type -2 (negative)

Domains of schizophrenia
Thinking/thought
Affect
Perception

CRITERIAS OF SCHIZOPHRENIA

o Kurt Schneider criteria(First rank symptoms)

o Gabriel Langfeldt criteria
o New-Haven schizophrenic index
o Flexible system
o Research diagnostic criteria
o Saint Louis criteria
o Present state examination
o Tsuang-Winokur criteria
o Domain classification

Minimum duration of schizophrenia

ICD-10------- 1month
DSM-IV------ 6 months

BOUFFEE-DELIRANTE

o It is acute delusional state

o Duration less than 3 months according to DSM-IV

ONEIROID STATE

o It is a dreamlike state in which patient is deeply perplexed and not fully oriented to
time, place and person.

PARAPHRENIA :- synonym for paranoid schizophrenia

PSEUDO NEUROTIC SCHIZOPHRENIA

 Initially the symptoms are anxiety, phobia, obsessions, and compulsions later thought
disorder and psychosis.
 Symptoms: pan anxiety, pan phobia, pan ambivalence and sometimes chaotic
sexuality.
 Currently it is called as borderline personality disorder according to DSM-IV.

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SCHIZOPHRENIC ILLNESS

According ICD-10(duration)

 Less than 2 weeks ----------- Acute transient psychosis

 Two weeks – less than 1 month--------- Schizophrenia like illness
 More than 1 month ----------- schizophrenia

According DSM-IV (duration)

o Less than 1 month ---------- Brief psychotic disorder

o 1 month to 6 months ------- schizophreniform disorder
o More than 6 months --------- schizophrenia

Age of onset

o Male ---- 15-25 years

o Female ------ 15 -35 years
o Female shows bi-model age presentation
o Late onset schizophrenia------- > 45 years

 Cenesthetic hallucination: - Sensations of altered states in bodily organs

o Ex; burning sensation in the brain, pushing sensation in the blood

vessels, cutting sensation in the bone marrow.
 Suicide rate in schizophrenia --------- 10%

 DELUSIONAL DISORDER

o Non bizarre delusions present at least one month (DSM-IV) or three

months (ICD-10) without other symptoms of schizophrenia or mood
disorder.

 WHO international pilot study of schizophrenia found the incidence of schizophrenia

o.7-1.4% per 1000 aged 15-45 years.

POSITIVE SYMPTOMS :- due to mesolimbic dopamine hyperactivity

o Delusions
o Hallucinations
o Disorganised behaviour
o Disorganised Speech

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NEGATIVE SYPTOMS:- due to decreased dopamine activity in prefrontal cortex
Anderson 7As
o Apathy
o Alogia
o Avolition
o Asocialization
o Anhedonia
o Attention deficit
o Affect flattening

TREATMENT OF SCHIZOPHRENIA

Pharmacological
Acute phase
Stabilization phase
Maintainance phase

Non-pharmacological treatment:-

Psychotherapy:
Individual
Group
Family psychotherapy

Vocational skill training:

Receiving skill
Processing skills
Sending skills

Vocational rehabilitation:
Self-help groups
Boston-university model
Transitional employment programme
Supportive employment

Community rehabilitation:
Crisis centres
Half-way homes
Foster care
Day care centres

COURSE OF SCHIZOPHRENIA
o Continuous course
o Episodic with progressive deficit
o Episodic with stable deficit
o Episodic remittent
o Incomplete remission
o Complete remission

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  POOR PROGNOSTIC FACTORS OF SCHIZOPHRENIA

 Young age onset

 No predisposing factor
 Insidious onset
 Poor premorbid social and supportive system
 Withdrawn/Autistic behaviour
 Negative symptoms
 Family history of schizophrenia
 Neurological signs and symptoms
 No remission in 3 years
 Many relapses

RESISTANT SCHIZOPHRENIA :-
 Not responding with two antipsychotics (at least one atypical antipsychotic) with full
dose and full duration.
 Clozapine is the drug of choice for resistant schizophrenia.

SCHIZOAFFECTIVE DISORDER:
One month duration of schizophrenia symptoms and an uninterrupted period of illness
during at some time either there is a major depressive episode or manic episode or mixed
episode concurrent with symptoms that meet criteria A for schizophrenia.

 Jacob Kasanin------- coined term schizoaffective disorder

 It is also called atypical schizophrenia, Good prognosis schizophrenia, Remitting
schizophrenia, and Cycloid psychosis.
 Prevalence of schizoaffective disorder-------0.5-0.8%

 Paranoid pseudo community----------- coined by Norman Cameron

OTHELLO SYNDROME:- conjugal paranoia/ Delusions of infidelity /pathological jealousy or

morbid jealousy.

DECLERAMBAULT SYNDROME;
Psychose passionelly
Erotomania (delusions of love)

 MONO SYMPTOMATIC HYPOCHONDRIACAL DELUSIONS

 Delusions of infestation (Parasitosis)
 Delusions of dysmorphophobia
 Delusions of body odour/halitosis (olfactory reference syndrome/ Bromosis)

 MEGALOMANIA:- Delusions of grandiosity.

 COTARD SYNDROME:- Nihilistic delusions

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  CAPGRASS SYNDROME:- the belief that familiar person has been replaced by an
imposter and is called as Illusion of doubles/ Illusion dessocies.

 FREGOL) S P(ENOMENON:- familiar person can assume the disguise of strangers.

 INTERMETAMORPHOSIS:- Familiar person can change themselves into an other

person at will.

 SHARED PSYCHOTIC DISORDER:- shared paranoid disorder or induced psychotic

disorder or Double insanity.

 Foliea deux------ 2 persons

 Foliea trios-------3 persons
 Foliea quatre----4 persons
 Foliea famille----family
 Foliea simultanee---- two persons simultaneously

MOOD DISORDERS
MOOD:- pervasive and sustained feeling tone that is experienced internally and that in
extreme can influence a person s behaviour and perception of the world.

UNIPOLAR DEPRESSION:- only depressive episodes.

BIPOLAR DISORDERS: Both depression and manic episodes

Bipolar -1;------ major depression and Manic episode

Bipolar – 11: ---- major depression and Hypo manic episode

DYSTHYMIA:- mild depression (not MDD) at least 2 years.

CYCLOTHYMIA: Mild depression (not MDD) and hypo manic episode at least 2 years.

DOUBLE DEPRESSION: Dysthymia superimposed with major depression.

CHRONIC DEPRESSION ; Major depressive episode continuous for at least 2years.

SEASONAL AFFECTIVE DISORDER: At least 2 consecutive years regular temporal

relationship between onset of major depression and season.

RAPID CYCLING: at least 4 episodes of mood disturbance within 12 months period.

RECURRENT DEPRESSION:- 2 or more major depressive episodes.

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MELANCHOLIC DEPRESSION:
o Severe anhedonia
o Early morning awakening
o Weight loss
o Profound feelings of guilty
o Endogenous depression
o Changes in autonomic nervous system
o Absence of external stressors or precipitants

 ATYPICAL DEPRESSION :
o Reversed vegetative symptoms
o Also called as hysteroid dysphoria
 Jean Falret------ Folie cieculaire

 Karl Kahlbam---- cyclothymia

 Emil Kraepelin--- manic depressive psychosis and involutional malencholia.

MINIMUM DURATIONS
 Depressive episode--------2 weeks
 Manic episode ------------- 1 week
 Hypomania----------------- 4 days
 Cyclothymia --------------- 2 years
 Dysthymia ----------------- 2 years
 Chronic depression ------ 2 years
 Brief depression -------- < 2 weeks

LIFE TIME PREVALENCE

o Major depression-------------- 5-17%
o Dysthymia ----------------------- 3-6%
o Minor depression-------------- 10%
o Recurrent depression--------- 16 %
o Unipolar depression ---------- 20- 25%
o Bipolar-1------------------------- 0-2.4%
o Bipolar-II-------------------------0.3-4.8%

SEX PREDOMINANCE
o Major depression---------- female >male
o Bipolar-I ---------------------- female=male
o Bipolar-II --------------------- female > male
o Manic episode ------------- female< male
o Depression ------------------ female > male
o Mixed episode ------------- female<male
o Rapid cycling --------------- female>male

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  Chromosomes 18, 21, 22 are responsible for bipolar disorders
 Bipolar -1 earlier onset then bipolar-II
 ¾ of bipolar –I starts with depression
 Untreated depressive episode last 9-12 months
 Untreated manic episode lasts for 6- 9 months

MOOD CONGURENT DELUSIONS: content of thought is harmonious to expression of mood.

GOOD PROGNOSTIC FACTORS OF MOOD DISORDER.

o Mild episode
o Late age of onset
o Acute onset
o Absence of family history
o Absence of psychosis
o Good social support
o Absence of substance abuse
o Less number of episodes

RESISTANT DEPRESSION: treatment failure with two classes of antidepressants with full
dose and duration.

ATYPICAL PSYCHOSIS:

 Motility psychosis: Akinetic and Hyperkinetic psychosis

 Confessional psychosis: more anxiety and less distractibility.

 Anxiety-blissfulness psychosis: Anxiety, paranoid ideas/Hypochondrial ideas, and

depression.

DELIRIOUS MANIA: Mania with disorientation of time, place, person with clear
consciousness.

ANXIETY DISORERS
 ANXIETY: Diffuse, unpleasant, vague sense of apprehension often accompanied by
autonomic symptoms.

FEAR
o Known
o External
o Definite
o Non conflictual threat
ANXIETY
o Unknown
o Internal
o Vague
o Conflictual threat

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 CLASSIFICATION OF ANXIETY DISORDER

 Panic disorder with or without agoraphobia

 Agoraphobia with or without panic disorder
 Specific phobia
 Social phobia
 Obsessive compulsive disorder
 Post traumatic stress disorder
 Acute stress disorder
 Generalised anxiety disorder

 Domains of anxiety
o Thinking
o Perception
o Learning

 EPIDEMIOLOGY:
o Prevalence -----20-30%
o Female>male
o High socioeconomic >low socioeconomic

 PANIC DISORDER: Acute intense attack of anxiety accompanied by feeling of

impending death

Clinical features
 Palpitations/sweating
 Shaking
 Shortness of breath
 Chest pain/discomfort
 Nausea/reeling sensation
 Light-headedness/fainting
 Derealisation/depersonalization
 Fear of death
 Persistent concern of further attack

 PHOBIA: excessive fear of specific object/ situation.

o Acrophobia------------- heights
o Cynophobia----------------- dog
o Agoraphobia ---------- open places
o Mysophobia-------------- dirt/germs
o Allurophobia ------------ cats
o Pyro phobia ---------------- fire
o Hydrophobia ---------- water
o Xenophobia---------------- strange
o Claustrophobia-------- closed place
o Zoophobia --------------- Animal

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  OBSESSION: recurrent and persistent thoughts, impulse, or images that are
experienced as intrusive and inappropriate .
Eg; contamination, repeated doubts, orders, impulse, sexual images

 COMPULSIONS: repetitive behaviour or mental acts whose goal is to prevent or

reduce the anxiety or distress.
Ex: hand washing, checking, prying, counting, repeating words.

 TREATMENT OF OCD
Pharmacological
 Clomipramine ----------------- 75-300mg/day
 Fluoxetine ----------------------- 20-80 mg/day
 Fluvoxamine --------------------- 50-300 mg/day
 Paroxetine ------------------------ 20- 60 mg/day
 Sertraline --------------------------50-200 mg/day
 Citalopram ------------------------ 20-60 mg/day
Non pharmacological:
 Systematic desensitization
 Reinforcement procedure
 Aversion
 Thought stopping
 Flooding/ implosion
 Exposure and response prevention
 Cognitive behavioural therapy
 Psychosurgery

 POOR PROGNOSTIC FACTORS OF OCD

 Yeilding to compulsion
 Childhood onset
 Bizarre compulsions
 Need for hospitalization
 Co-existing depression/psychosis
 Presence of personality disorder

SPECTRUM DISORDERS;
These are etiologically, genetically, treatment, and symptomatically closely related
disorders.

SCHIZOPHRENIC SPECTRUM DISORDERS

o Schizophrenia
o Schizoid personality disorder
o Schizotypal personality disorder
o Schizotaxia

BIPOLAR SPECTRUM DISORDER.

o Bipolar-I
o Bipolar-II
o Hypomania
o Cyclothymia

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 o Dysthymia
o Schizoaffective disorder
OCD SPECTRUM DISORDER
 Gambling
 Paraphilia
 Body dismorphic disorder
 Trichotillomania
 Hypochondriasis
 Somatoform disorders
 Tourette disorder
 Autism
 Schizotaxia
 Aspergers syndrome
 Impulse control disorders
 Bulimia/Anorexia nervosa
 Psychogenic excoriation

SOMATOFORM DISORDERS

DEFINITION : it is an illness of multiple somatic complaints in multiple organ systems that

occurs over a period of several years and result in significant impairment or treatment
seeking or both.

CLASSIFICATION

ICD-10
Somatization disorder
Undifferentiated somatoform disorder
Hypochondriacal disorder
Somatoform autonomic dysfunction
Heart and cardiovascular system
Upper gastrointestinal tract
Lower gastrointestinal tract
Respiratory system
Genitourinary system
Persistent somatoform pain disorder
Other and unspecified disorder

DSM-IV
Somatization disorder
Conversion disorder
Hypochondriasis
Body dysmorphophobia
Pain disorders
Undifferentiated somatoform
Not otherwise specified

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BRIQUET S SYNDROME /SOMAT)ZAT)ON D)SORDER: At least 4 pain symptoms, 2
gastrointestinal symptoms, one sexual symptom, and one pseudo neurological symptoms.
None of which is completely explained by physical and laboratory examination.
Histrionic personality is seen as somatisation disorder.

CONVERSION DISORDER: Symptoms/ deficits of motor or sensory functions which suggest

another medical condition but that is judged to be caused by conflicts or other symptoms.
Conversion term coined by Sigmund Freud

PRIMARY GAIN: achieve the primary gain keeping internal conflicts outside their
awareness.

SECONDARY GAIN: patients accrue tangible advantages and benefits as a result of being
sick.

LABELLE INDIFFERENCE: patient is inappropriate cavalier attitude towards serious

symptoms.

ASTASIA-ABASIA: gait disturbance seen in conversion disorder

HYPOCHONDRIAC DISORDER:
Six months or more non-delusional preoccupation with fears of having/idea that one has
serious disease based on the persons misinterpretation of bodily symptoms.

BODY DYSMORPHIC DISORDER:

Preoccupation with an imagined defect in appearance that causes clinically significant
distress or impairment in important areas of functioning.

AUTONOMIC AROUSAL SYNDROME:

Somatic symptoms that are limited to body functions innervated by the autonomic nerves
system.

PSEUDOCYESIS: a false belief of being pregnant that is associated with objective signs of
pregnancy.

CHRONIC FATIGUE SYNDROME:

Six months or more of severe debilitating fatigue often accompanied by myalgia, headache,
pharyngitis, low grade fever, cognitive complaints, GI symptoms and tender lymph nodes.

FACTITIOUS DISORDERS:
Intentional production of or feigning of physical or psychological symptoms.

MUNCHAUSEN SYNDROME:
In which the patient with embellish their personal history, chronically fabricate symptoms
to gain hospital admission and more from hospital to hospital.

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DISSOCIATIVE DISORDER:
Disruption in the usually integrated functions of consciousness, memory, identity, or
perception of world.

Classification
DSM-IV
 Dissociative identity disorder
 Dissociative amnesia
 Depersonalization disorder
 Dissociative fugue
 Not otherwise specified

DISSOCIATIVE AMNESIA:
Inability to recall important personal information usually of a traumatic or stressful nature
that is too extensive to be explained by normal forgetfulness.

DEPERSONALIZATION DISORDER:
There may be a sensation of being an outside observer of one s mental process, one s body
or parts.
The patient has a sense of an absence of control over his or her action.
Patient has persistent or recurrent feelings of detachment or estrangement from one s self.

CLINICAL FEATURES:
Feeling of bodily changes
Duality of self as observer or actor
Being cut off from others
Being cut off from one s own emotions

DISSOCIATIVE FUGUE:
Sudden unexpected travel away from home or one s customary place of daily activities with
inability to recall some or all one s past.

DISSOCIATIVE IDENTITY DISORDER:

The presence of two or more distinct identities or personality states that recurrently takes
control of individual s behaviour accompanied by an inability to recall important personal
information that is too extensive to be explained by normal forgetfulness.

DISSOCIATIVE TRANS DISORDER:

Temporarily or marked alteration in the state of consciousness or loss of customary sense of
personal identity without the replacement by an alternative sense of identity.

DISSOCIATIVE POSSESSION DISORDER:

Temporarily or marked alteration in the state of consciousness or loss of customary sense of
personal identity and replacement by an alternative sense of identity.

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GANSER SYNDROME:
The giving of approximate answers together with clouding of consciousness and frequently
with hallucinations, other somatoform/conversion symptoms.

NORMAL SEXUALITY AND SEXUAL DISORDERS

NORMAL SEXUALITY: determined by

o Anatomy
o Physiology
o Culture in which person lives
o Relationship with others
o Developmental level
o Perception of being male /female
o Private thoughts/fantasies

PSYCHOSEXUAL FACTORS
o Sexual identity
o Sexual orientation
o Gender identity
o Sexual behaviour

SEXUAL IDENTITY:
Chromosomes, external genitalia, internal genitalia, hormonal composition, gonads, and
secondary sexual characters.

SEXUAL ORIENTATION: objects of person sexual impulse (homosexuality/heterosexuality)

GENDER IDENTITY: psychological aspects of behaviour related to masculinity, feminity.

SEXUAL BEHAVIOUR:
o Orbitofrontal cortex------------ controls emotions
o Left anterior cingulate gyrus------controls hormones and sexual arousal
o Right caudate nucleus ----------controls sexual activity following sexual arousal
o Limbic system -------------------------- controls elements of sexual activity
o Brain stem ----------------controls inhibitory and excitatory spinal sexual reflex
Inhibition ---------- through serotonin
Excitation --------- through nor epinephrine
Brain stem: sexual arousal and climax at spinal level

Hormones in sexual behaviour:

 Dopamine -------- increase desire
 Serotonin -------- decrease desire
 Testosterone ----- increase libido
 Oestrogens --------- increase lubrication in female sexual arousal
 Progesterone----- decrease libido
 Oxytocin ----------- increase pleasure in sexual act

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Physiological stages by Master and Johnson
 Phase-I /Desire phase
 Phase-II /Excitement phase
 Phase-III / orgasm phase
 Phase-IV / Resolution phase

SEXUAL DISORDERS

SEXUAL DESIRE DISORDERS

 Hypoactive sexual disorder
 Sexual arousal disorder

SEXUAL AROUSAL DISORDERS

 Female sexual arousal disorder
 Male erectile disorder

ORGASM DISORDERS
 Female orgasm disorder
 Male orgasm disorder
 Premature ejaculation disorder

SEXUAL PAIN DISORDERS

 Dyspareunia
 Vaginismus
 Post coital headache

PSYCHOLOGICAL TREATMENT

o Dual sex therapy by Master and Johnson

o Vaginismus -------- dilate vaginal orifice by finger or graded dilator
o Premature ejaculation ------ squeeze technique and stop-start technique
o Orgasm disorders------------- masturbation
o Hypnotherapy
o Behavioural therapy
o Group therapy
o Analytically oriented psychotherapy

PHARMACOTHERAPY

Sildenafil ------- 25-100mg/day

Vardenafil ----- 5-20mg/day not effective in absence of sexual stimulus
Tadalafil -------- 5-20mg/day

OTHER PHARMACOLOGICAL AGENTS.

o Prostaglandins
o Aminophylline
o Isosorbide dinitrate
o Antiandrogens

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 o Antiestrogens
o Trazadone
o Bromocriptine
o Yohimbine
o Hormonal therapy
NON-PHARMACOLOGICAL TREATMENT---------- vaccum pump

SURGICAL TREATMENT
 Male prosthesis semi ridged, inflated
 Vascular surgery

PARAPHILIAS

PARAPHILIA or perversions are sexual stimuli or acts that are deviations from normal
sexual behaviour but some persons experience arousal or orgasm.

EXHIBITIONISM:-exposure of one s genitals to unsuspecting strangers.

FETISHISM:- use of non-living objects for sexual orgasm

FROTTEURISM:-touching or rubbing against an unconsenting woman

PEDOPHILIA:- sexual act with a prepubescent child

MASICHISM:- an act of being humiliated, beaten, and made to suffer for sexual gratification.

SADISM:- psychological or physical suffering of the victim for sexual orgasm

VOYEURISM/SCOPOPHILIA:- the act of observing an suspecting person who is naked

TRANSVESTIC FETISHISM: - sexual orgasm by involving the cross dressing.

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 SLEEP AND SLEEP DISORDERS

PHYSIOLOGY OF SLEEP:

REM SLEEP
o Paradoxical sleep
o Decrease Physiological function
o High levels of brain activity
o Normal REM latency – 90 min
o Brain O2 use increased
o Thermoregulation is altered
o Partial or full penile erection
o Near total paralysis of skeletal muscles
o Dreams are abstract or surreal
o Most REM sleep occurs in last 3rdof night
EEG
o Rapid conjugate eye movements
o Low voltage, random fast activity with
o saw tooth waves
o Marked reduction of muscle tone in EMG

NREM SLEEP
o Slow wave sleep & Orthostatic sleep
o Decreased Physiological function
o Low levels of brain activity
o Blood flow to most of the tissues is decreased
o Dreams are typically lucid & purposeful
o Most NREM occurs in first 3rdof night
EEG
o Vertex waves on stage-I
o K- complexes & sleep spindles in stage-II
o Low amplitude & slow waves in stage III & IV
o Episodic, involuntary body movements in EMG

Supra chiasmatic nucleus of hypothalamus regulates sleep

Normal sleep: NREM sleep—75%

Stage-I --- 5%
Stage –II-45%
Stage-III- 12%
Stage-IV13%

REM sleep—25%

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CLASSIFICATION OF SLEEP DISORDERS

DYSSOMNIA

1) INSOMNIA
Primary insomnia
Inadequate sleep hygiene
Psychological insomnia
Sleep state misinterpretation
Idiopathic insomnia

2) HYPERSOMNIA
Narcolepsy
Primary hypersomnia

3) BREATHING RELATED
Obstructive sleep apnoea
Central alveolar hypoventilation

4) CIRCADIAN RHYTHM DISORDERS

 Delayed sleep phase type
 Jet-lag type
 Shift work type
 Advanced sleep phase type
 Disorganised type

PARASOMNIAS

 Nightmare disorders
 Sleep terror
 Sleep walking (somnambulism)
 Sleep related bruxism
 REM-sleep behaviour disorders
 Sleep related head banging
 Sleep paralysis

SLEEP LATENCY:
The period of time from turning out the light until the appearance of stage 2 sleep.

REM LATENCY:
The period of time from onset of sleep until the first REM period of the night.

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TETRAD OF NARCOLEPSY:
- Sleep Attacks
- Cataplexy
- Sleep paralysis
- Hypnogogic and Hypnopompic hallucinations

Modafinil is the Drug of Choice.

HLA D2 associated disorder.
Responsible neurotransmitter is Hypocretin.

RESTLESS LEG SYNDROME:

- Otherwise known as EKBOM Syndrome or Creepy crawly syndrome
- Subjective sensation of vague pains.
- Rx Ropinirole, L-Dopa, Bromocriptine and other Dopamine agonists.

PERIODIC LIMB MOVEMENT:

Stereotyped abrupt contractions of certain leg muscles during sleep.
Rx – Benzodiazepines, Levo Dopa, Quinine, Opioids.

IMPULSE CONTROL DISORDERS:

- Intermittent Explosive disorder
- Kleptomania
- Pyromania
- Trichotillomania
- Pathological gambling

PERSONALITY DISORDERS:

An enduring pattern of inner experience and behaviour that developed markedly

from the expectations of individual s culture.

Alloplastic: Able to adapt and alter to external environment.

Ego syntonic: Acceptable to ego.

Classification of Personality Disorders (DSM IV):

Cluster A: (SSP)
- Schizoid personality disorder
- Schizotypal personality disorder
- Paranoid personality disorder

Cluster B: (H-BAN)
- Histrionic personality disorder
- Borderline personality disorder
- Antisocial personality disorder
- Narcissistic personality disorder

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Cluster C: (OCD)
- Obsessive Compulsive personality disorder
- Dependent personality disorder

PARANOID PERSONALITY DISORDER:

- Long standing suspiciousness
- Mistrust of persons in general
- Preoccupied with unjustified doubts
- Hostile, Irritable and angry
- Pathologically jealous spouses
- Ideas of reference
- Defense mechanism – Projection

SCHIZOID PERSONALITY DISORDER:

- Lifelong pattern of social withdrawal
- Discomfort with human interactions
- Introversion
- Constricted affect
- Avoid spontaneous conversation
- Unable to express anger directly

SCHIZOTYPAL PERSONALITY DISORDER:

- Introverted, odd and strange behaviour
- Magical thinking or sixth sense
- Ideas of reference
- Peculiar notions, illusions
- Inappropriate or constricted affect
- Their inner world filled with vivid imaginary relationships
- Child like fears and fantasies
- Derealizations

ANTISOCIAL PERSONALITY DISORDER:

- Psychopathic PD
- Dissocial PD (ICD 10)
- Lying, Truancy, Running away from home, thefts, fights and illegal activities
- Failure to conform social norms
- Impulsivity or failure to plan ahead
- Reckless disregard for safety of self and others

BORDERLINE PERSONALITY DISORDER:

- Ambulatory Schizophrenia or As- )f personality or Pseudo neurotic

Schizophrenia or Emotionally unstable PD )CD
- Unstable affect, mood, behaviour, object relations and self image
- Females more common than males
- Micro psychotic episodes
- Recurrent suicidal behaviour, gestures or self mutilating behaviour
- Defense mechanism – Projective identification

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HISTRIONIC PERSONALITY DISORDER:

- Excitable, emotional, colorful, dramatic, extroverted fashion

- High degrees of attention seeking behaviour
- Seductive behaviour
- Self dramatization and exaggerated expression of emotion
- Defense mechanism – Repression and Dissociation

NARCISSISTIC PERSONALITY DISORDER:

- Heightened sense of self importance

- Grandiose feeling of uniqueness
- Preoccupied with fantasies of unlimited success, power, ebullience and beauty
- Sense of entitlement
- Lack of empathy
- Arrogant behaviour or attitudes

AVOIDANT PERSONALITY DISORDER:

- Anxious PD )CD
- Sensitivity to rejection
- Social withdrawal
- Preoccupied with being criticized or rejected social situation

DEPENDENT PERSONALITY DISORDER:

- Difficulty in making every day decisions without advise of others

- Dependent in every issues with others
- Feels uncomfortable or helpless when alone

OBSESSIVE COMPULSIVE PERSONALITY DISORDER:

- Anankastic PD )CD
- Emotional constructions, orderliness, perseverance, stubbornness,
indecisiveness, preoccupied with details, rules & regulations
- Defense mechanisms – Isolation, Intellectualization, Reaction formation, undoing,
rationalization

PASSIVE AGGRESSIVE PERSONALITY DISORDER:

- Covert obstructionism, Procrastination, stubbornness, inefficiency

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DEPRESSIVE PERSONALITY DISORDER:

- Pessimistic, anhedonic, duty bound, self-doubting, chronically unhappy

PSYCHOSOMATIC MEDICINE
ALEXITHYMIA:
Inability to express ones feelings because they are unaware of their mood.

HISTORY
History of psychosomatic thinking:
o Heinroth, 1818: the term „psychosomatic
o Jacobi, 1822: the term somatopsychic
o Schafer, 1966: sociopsychosomatics
o Sifneos, 1973: alexithymia
o Locke, 1981: psychoneuroimmunology

2005-American board of medical specialties, American board of psychiatry and neurologists

approved a separate board to be called the American board of psychosomatic medicine.

Psychosomatic medicine became the 7th sub-speciality in psychiatry.

Psychosomatic medicine is an area of scientific investigation concerned with the relation

between psychological factors and physiological phenomena in general and disease
pathogenesis in particular.

Integrates mind and body into a psychobiological unit; to study psychological and biological
processes as dynamic interacting systems.

It emphasizes the unity of mind and body and the interaction between them.

Two basic assumptions:

o There is a unity of mind and body (reflected in the terms of mind-body
medicine)
o Psychological factors must be taken into account when considering all disease
states.

The concepts of psychosomatic medicine also influenced the field of behavioural medicine
which integrates the behavioural sciences and the biomedical approach to the prevention,
diagnosis, and treatment of diseases.

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DSM-IV Diagnostic Criteria for Psychological Factors Affecting Medical Conditions

A. A general medical condition (coded on Axis III) is present.

B. Psychological factors adversely affect the general medical condition in one of the
following ways:

(1) The factors have influenced the course of the general medical condition as shown by a
close temporal association between the psychological factors and the development or
exacerbation of, or delayed recovery from, the general medical condition.

(2) The factors interfere with the treatment of the general medical condition.

(3) The factors constitute additional health risks for the individual.

(4) stress-related physiological responses precipitate or exacerbate symptoms of a general

medical condition.

Mental disorder affecting medical condition (e.g., an Axis I disorder such as major
depressive disorder delaying recovery from a myocardial infarction)

Psychological symptoms affecting medical condition (e.g., depressive symptoms delaying

recovery from surgery; anxiety exacerbating asthma)

Personality traits or coping style affecting medical condition (e.g., pathological denial of
the need for surgery in a patient with cancer, hostile, pressured behavior contributing to
cardiovascular disease)

Maladaptive health behaviors affecting medical condition (e.g., lack of exercise, unsafe
sex, overeating)

Stress-related physiological response affecting general medical condition (e.g., stress-

related exacerbations of ulcer, hypertension, arrythmia, or tension headache)

Other unspecified psychological factors affecting medical condition (e.g., interpersonal,

cultural, or religious factors)

Excluded are:

1) Classic mental disorders that have physical symptoms as part of the disorder (e.g.,
conversion disorder)
2) somatization disorder
3) Hypochondriasis
4) Physical complaints that are frequently associated with mental disorders (e.g.,
dysthymic disorder)
5) Physical complaints associated with substance-related disorders

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STRESS THEORY

Stress can be described as a circumstance that disturbs, or is likely to disturb, the normal
physiological or psychological functioning of a person.

In the 1920s, Walter Cannon (1875–1945) conducted the first systematic study of the
relation of stress to disease.

In the 1950s, Harold Wolff (1898–1962) observed that the physiology of the
gastrointestinal (GI) tract appeared to correlate with specific emotional states.

William Beaumont (1785–1853), an American military surgeon, had a patient named

Alexis St. Martin, who became famous because of a gunshot wound that resulted in a
permanent gastric fistula.
Beaumont noted that during highly charged emotional states the mucosa could become
either hyperemic or blanch, indicating that blood flow to the stomach was influenced by
emotions.

Hans Selye (1907–1982) developed a model of stress that he called the general adaptation
syndrome.
It consisted of three phases:
(1) the alarm reaction
(2) the stage of resistance, in which adaptation is ideally achieved
(3) the stage of exhaustion, in which acquired adaptation or resistance may be lost.

Selye believed that stress, by definition, need not always be unpleasant. He called unpleasant
stress distress. Accepting both types of stress requires adaptation.

Franz Alexander´s general scheme of the interaction of conflict and overdrive in autonomic
nervous system
Life Events or situation, favourable or unfavourable often occurring by chance, generates
challenges to which the person must adequately respond.

Thomas Holmes and Richard Rahe constructed a social readjustment rating scale after
asking hundreds of persons from varying backgrounds to rank the relative degree of
adjustment required by changing life events.

Fight or Flight response is mediated by hypothalamus, the sympathetic nervous system,

and the adrenal medulla.
If chronic, this response can have serious health consequences.
The hypothalamus, pituitary gland, the adrenal cortex mediate the second facet.

Neurotransmitter Responses to Stress

o Stressors activate noradrenergic systems in the brain and cause release of
catecholamine from the autonomic nervous system.
o Stressors also activate serotonergic systems in the brain, as evidenced by increased
serotonin turnover.
o Stress also increases dopaminergic neurotransmission in mesoprefrontal pathways.

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Endocrine Responses to Stress
o CRF is secreted from the hypothalamus.
o CRF acts at the anterior pituitary to trigger release of ACTH.
o ACTH acts at the adrenal cortex to stimulate the synthesis and release of
glucocorticoids.
o Promote energy use, increase cardiovascular activity, and inhibit functions such as
growth, reproduction, and immunity.
o High level of Cortisol results in suppression of immunity which can cause
susceptibility to infections and possibly also in many types of cancer.

Immune Response to Stress

o Inhibition of immune functioning by glucocorticoids.
o Stress can also cause immune activation through a variety of pathways including the
release of humoral immune factors (cytokines) such as interleukin-1 (IL-1) and IL-6.
o These cytokines can themselves cause further release of CRF, which in theory serves
to increase glucocorticoid effects and thereby self-limit the immune activation.

Specific versus Nonspecific Stress Factors

o Some investigators have suggested that specific personalities and conflicts are
associated with certain psychosomatic diseases.
o Researchers first identified specific personality types in connection with coronary
disease.
o An individual with a coronary personality is a hard-driving, competitive, aggressive
person who is predisposed to coronary artery disease.

Meyer Friedman and Ray Rosenman first defined two types:

1) Type A personalities ---similar to the coronary personality
2) Type B personalities—calm, relaxed, and not susceptible to coronary disease

Franz Alexander was a major proponent of the theory that specific unconscious conflicts
are associated with specific psychosomatic disorders.
For example, persons susceptible to having a peptic ulcer were believed to have strong
ungratified dependency needs.
Persons with essential hypertension were considered to have hostile impulses about which
they felt guilty.
Patients with bronchial asthma had issues with separation anxiety.

Gastrointestinal System
o Gastrointestinal disorders rank high in medical illnesses associated with psychiatric
consultation.
o Psychological and psychiatric factors commonly influence onset, severity, and
outcome in the functional GI disorders.
o Sympathetic autonomic responses can be generated in the lateral hypothalamus, a
region with neural interactions within the limbic forebrain.

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 o Acute stress can induce physiological responses in several GI target organs.
o In the oesophagus, acute stress increases resting tone of the upper oesophageal
sphincter and increases contraction amplitude in the distal oesophagus.
o Such physiological responses may result in symptoms that are consistent with globus
or oesophageal spasm syndrome.

Peptic Ulcer Disease

o Peptic ulcer refers to mucosal ulceration involving the distal stomach or proximal
duodenum.
o Early studies of peptic ulcer disease suggested a role of psychological factors in the
production of ulcer vulnerability.
o This effect was believed to be mediated through the increased gastric acid secretion
associated with psychological stress.
o Recent evidence for a primary role of H. pylori in peptic ulcer initiation suggests that
psychosocial factors may play a role primarily in the clinical expression of symptoms.
o Stressful life events reduce the immune responses resulting in higher vulnerability to
infection with H.pylori.

o Ulcerative Colitis
Ulcerative colitis is an inflammatory bowel disease affecting primarily the large
intestine. The cause of ulcerative colitis is unknown.
o For individual patients, psychiatric factors may play a key role in the presentation
and complexity of the disorders such as ulcerative colitis.
o Some workers have reported an increased prevalence of dependent personalities in
these patients.

Irritable bowel syndrome

o Irritable Bowel Syndrome (IBS) is a classical example of psychosomatic illness
because of the thick interlacement among the bio-psycho-social factors that
characterize its onset and its evolution.
o Various researches point out a role of the so-called brain-gut interactions and of the
infectious and inflammatory factors.
o Besides, many studies have demonstrated a high percentage of personality disorders
in the IBS patients.

Cardiovascular Disorders
Cardiovascular disorders are the leading cause of death in the United States and the
industrialized world.

o Depression, anxiety, type A behavior, hostility, anger, and acute mental stress have
been evaluated as risk factors for the development and expression of coronary
disease.
o Studies of patients with preexisting coronary artery disease (CAD) also demonstrate
a near doubling of risk for adverse coronary disease-related outcomes, including
myocardial infarction (MI), revascularization procedures for unstable angina, and
death, in association with depression.

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Hypertension
o Some patients have labile blood pressure e.g., white coat hypertension, in which
elevations occur only in a physician's office and are related to anxiety).
o Personality profiles associated with essential hypertension include persons who have
a general readiness to be aggressive, which they try to control, albeit unsuccessfully
o The psychoanalyst Otto Fenichel observed that the increase in essential
hypertension is probably connected to the mental situation of persons who have
learned that aggressiveness is bad and must live in a world for which an enormous
amount of aggressiveness is required.

o Respiratory System
Asthma is a chronic, episodic illness characterized by extensive narrowing of the
tracheobronchial tree.
o Patients with asthma are characterized as having excessive dependency needs,
o Up to 30 % of persons with asthma meet the criteria for panic disorder or
agoraphobia.
o The fear of dyspnoea can directly trigger asthma attacks, and high levels of anxiety
are associated with increased rates of hospitalization and asthma-associated
mortality

Hyperventilation Syndrome
o Patients with hyperventilation syndrome breathe rapidly and deeply for several
minutes, often unaware that they are doing so.
o They soon complain of feelings of suffocation, anxiety, giddiness, and light-
headedness.
o Tetany, palpitations, chronic pain, and paraesthesia around the mouth and in the
fingers and toes are associated symptoms.
o The attack can be aborted by having patients breathe into a paper (not plastic) bag or
hold their breath for as long as possible, which raises the plasma PCO2.
o Cognitive symptoms include a short attention span, impaired recent memory, and an
exaggerated startle response.

Endocrine system

Hypothyroidism
o Psychiatric symptoms of hypothyroidism include depressed mood, apathy, impaired
memory, and other cognitive defects.
o Also, hypothyroidism can contribute to treatment-refractory depression.
o A psychotic syndrome of auditory hallucinations and paranoia, named myxedema
madness, has been described in some patients
o Psychotropic agents should be given at low doses initially, because the reduced
metabolic rate of patients with hypothyroidism may reduce breakdown and result in
higher concentrations of medications in blood.

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Cushing's Syndrome
o Psychiatric symptoms are common and vary from severe depression to elation with
or without evidence of psychotic features.

Hypercortisolism
o Psychiatric symptoms are myriad. Most patients experience fatigue and
approximately 75 % report depressed mood.
o In cases of iatrogenic Hypercortisolism and adrenal carcinomas, however, mania and
psychosis may predominate.
o The psychiatric disturbances in prednisone-treated patients tend to appear within
the first 2 weeks of treatment and occur more commonly in women than in men.

Skin Disorders

Psychogenic Excoriation
o Psychogenic excoriations (also called psychogenic pruritus) are lesions caused by
scratching or picking in response to an itch or other skin sensation or because of an
urge to remove an irregularity on the skin from pre-existing dermatoses, such as
acne.
o The behavior in psychogenic excoriation sometimes resembles obsessive-compulsive
disorder in that it is repetitive, ritualistic, and tension reducing, and patients attempt
(often unsuccessfully) to resist excoriating.
o The skin is an important erogenous zone, and Freud believed it susceptible to
unconscious sexual impulses.

Psoriasis
o Psoriasis is a chronic, relapsing disease of the skin, It is difficult to control the
adverse effect of psoriasis on quality of life. It can lead to stress that, in turn, can
trigger more psoriasis.
o Patients who report that stress triggered psoriasis often describe disease-related
stress resulting from the cosmetic disfigurement and social stigma of psoriasis,
rather than stressful major life events.
o Psoriasis-related stress may have more to do with psychosocial difficulties inherent
in the interpersonal relationships of patients with psoriasis than with the severity or
chronicity of psoriasis activity

Hyperhidrosis
o States of fear, rage, and tension can induce increased sweat secretion that appears
primarily on the palms, the soles, and the axillae.
o The sensitivity of sweating in response to emotion serves as the basis for
measurement of sweat by the galvanic skin response (an important tool of
psychosomatic research), biofeedback, and the polygraph (lie detector test).

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Musculoskeletal System

Rheumatoid Arthritis
o Stress can predispose patients to rheumatoid arthritis and other autoimmune
diseases by immune suppression.
o Depression is comorbid with rheumatoid arthritis in about 20% of individuals.
o Individuals with rheumatoid arthritis and depression commonly demonstrate poorer
functional status, painful joints, health care use, bed days, and inability to work than
do patients without depression.

Low Back Pain

o Many instances are psychosomatic.
o Examining physicians should be particularly alert to patients who give a history of
minor back trauma followed by severe disabling pain.
o Patients with low back pain often report that the pain began at a time of
psychological trauma or stress.
o The pain distribution rarely follows a normal neuroanatomical distribution.
o According to Sarno, the pathophysiology involved is vasospasm of blood vessels that
supply the involved muscle, nerve, or tendon.
o Vasospasm is mediated by the autonomic nervous system, which is extraordinarily
sensitive to changes in emotional tone, chronic emotional stress, and unconscious
affects.
o The ischemia and oxygen deprivation cause pain in the areas involved.
o Treatment includes educating patients about the physiological component
(vasospasm) and helping them understand the working of the unconscious mind and
conflicts that arise from unconscious affects, especially that of rage.

Headaches

Migraine
o Stress is a precipitant, and many persons with migraine are overly controlled,
perfectionists, and unable to suppress anger.

Tension Headaches
o Tension headaches are frequently associated with anxiety and depression.
o Tense, high-strung, competitive personalities are especially susceptible to the
disorder.
o Psychotherapy is an effective treatment for persons chronically afflicted by tension
headaches.
o Biofeedback using electromyogram (EMG) feedback from the frontal or temporal
muscles may help some patients.

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TREATMENT OF PSYCHOSOMATIC DISORDERS

A major role of psychiatrists and other physicians working with patients with
psychosomatic disorders is mobilizing the patient to change behavior.

Aaron Lazare described specific negotiating strategies to achieve behavioral changes:

1) Direct education. Explain the problem, goals, and methods to achieve goals.

2) Third-party intervention. Family members, friends, and other clinicians can

provide support and encourage the patient to follow a course of action.

3) Exploration of options. There may be alternative methods for achieving a desired

goal. For example, quitting smoking can be done with support groups, nicotine patches or
gums, psychotropic drugs, etc.

4) Provision of sample treatment. If a patient fears a particular course of action or

considers change impossible, a treatment trial can be implemented.

5) Control sharing. Some patients resent any approach that appears to be

authoritarian. They may wish to set the pace of a withdrawal program or titrate their
medication depending on adverse effects.

6) Concession making. The clinician may grant the patient something that he or she
wants (e.g., medication) as a bargaining chip to get the patient to comply with advice.

7) Empathic confrontation. The doctor can try to step into the patients' shoes in an
effort to raise their level of awareness.

8) Stress Management and Relaxation Therapy

 Self-Observation
 Cognitive Restructuring
 Relaxation Exercises
 Hypnosis
 Biofeedback
 Time Management
 Problem-Solving

9) Cognitive-behavioral therapy methods are increasingly used to help individuals

better manage their responses to stressful life events.

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STRESS MANAGEMENT TECHNIQUES:

- Self-observation
- Cognitive restructuring
- Relaxation technique Jacobson s muscle relaxation technique, Bio-feedback,
yoga)
- Time management
- Problem solving

CONSULTATION-LIASON PSYCHIATRY:
It is the study, practice and teaching of the relation between medical and psychiatric
disorders.

PSYCHIATRIC RATING SCALES

Diagnostic Scales in Psychiatry
1. Present State Examination -Ninth Edition (PSE-9)
2. Schedules for Clinical Assessment in Neuro psychiatry (SCAN)
3. Diagnostic Interview Schedule (DIS)
4. Schedule for Affective Disorders and Schizophrenia (SADS)
5. Structured Clinical Interview for Axis I DSM-IV Disorders (SClD)
6. Composite International Diagnostic Interview (CIDI)

Depression Rating Scales

1. Hamilton Rating Scale for Depression (HAM-D, HRSD)
2. Montgomery-Asberg Depression Rating Scale (MADRS)
3. Beck Depression Inventory (BDI)
4. Zung Depression Scale (SDS and DSI
5. Depression Outcomes Module (DOM)
6. Carroll Depression Scale (CDS-R, CRS).
7. Raskin Depression Rating Scale.
8. Cornell Dysthymia Rating Scale (CDRS)

Obsessive-Compulsive Symptoms
1. Yale-Brown Obsessive Compulsive Scale (Y-BOCS)
2. Leyton Obsessional Inventory (LOI)

Panic Disorder
1. Sheehan Patient-Rated Anxiety Scale (SPRAS)
2. Acute Panic Inventory (API)

Post-Traumatic Stress Disorder

1. Davidson Trauma scale {DTS]
Mania Assessment Scales
1. Young Mania Rating Scale (YMRS)
2. Manic State Rating Scale (MSRS)

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Functional Level Scales
1. Global Assessment of Functioning Scale (GAF and GAS)
2. Clinical Global Impressions (CGI)

General Health Assessment Scales

1. The Duke Health Profile (DUKE)
2. The Short Form 36 Health Survey (SF-36)
3. The COOP Charts for Adult Primary Care Practice.

Insight Assessment Rating Scales

1. Scale to Assess Unawareness of Mental Disorder (SUMD)
2. Insight and Treatment Attitude Questionnaire (ITAQ)
3. Schedule for Assessment of Insight (SAI)

Involuntary Movements Assessment Scales

1. Abnormal Involuntary Movement Scale (AIMS)
2. Simpson Angus Scale (SAS)
3. Barnes Akathisia Scale (BAS, BARS)
4. Extrapyramidal Symptom Rating Scale (ESRS)
5. Udvalg for Kliniske Undersogelser (UKU) Side Effect Rating Scale

Patient Satisfaction Scales

1. The Client Satisfaction Questionnaire (CSQ)
2. The Service Satisfaction Scale (SSS-30)
3. Drug Attitude Inventory (DAI)

Quality of life scales:

1. Lehman Quality of Life Interview (QOLI).
2. Psychological General Well Being Schedule (PGWB)
3. The Nottingham Health Profile (NHP)
4. Quality of Life Scale
5. The Sickness Impact Profile (SIP)
6. The Quality of Well Being Scale (QWB)

Substance Abuse Rating Scales

1. CAGE Questionnaire
2. Michigan Alcohol Screening Test (MAST)
3. Inventory of Drug-Taking Situations (IDTS)
4. Addiction Severity Index (ASI)
5. Fagerstrom Test for Nicotine dependence (FTND)

Suicide Risk Assessment Scales

1. Beck Scale for Suicide Ideation (BSS
2. California Risk Estimator for Suicide
3. Beck Hopelessness Scale (BHS)
4. Suicide Probability Scale (SPS)

159
Impulsivity/Aggression Rating Scales
1. Barratt Impulsiveness Scale (BIS-11)
2. Buss-Durkee Hostility Inventory (BDHI)
3. Overt Aggression Scale - Modified (OAS-M)
4. State-Trait Anger Expression Inventory (STAXI-2)

Geriatric Rating Scales

1. Alzheimer's disease Assessment Scale (ADAS)
2. Behavioral Pathology in Alzheimer's Disease (BEHAVE-AD)
3. Relative's Assessment of Global Symptomatology (RAGS-E)
4. Burden Interview (Bl)
5. Geriatric Depression Scale (CDS)
6. The Mini-Mental State Examination (MMSE)
7. Blessed Dementia Scale (BLS-D)
8. The Cambridge Mental Disorders of the Elderly Examination (CAMDEX)
9. Neuropsychiatric Inventory (NPI)

Psychosis Rating Scales

1. Brief Psychiatric Rating Scale (BPRS)
2. Positive and Negative Symptom Scale for Schizophrenia (PANSS)
3. Nurses' Observation Scale for Inpatient Evaluation (NOSIE)
4. Scale for Assessment of Positive Symptoms (SAPS)
5. Scale for Assessment of Negative Symptoms (SANS)
6. Comprehensive Psychopathological Rating Scale (CPRS)

Anxiety Rating Scales

General Anxiety
1. Hamilton Rating Scale for Anxiety (HAM-A)
2. Covi Anxiety Scale
3. The State-Trait Anxiety Inventory (STAI)
4. Sheehan Disability Scale.

Phobias/Social Anxiety
1. Liebowitz Social Anxiety Scale (LSAS)
2. Social Phobia and Anxiety Inventory (SPAI)
3. Fear Questionnaire (FQ)

Rating Scales for Children

1. Children's Depression Inventory (CDI)
2. Children's Depression Rating Scale (CDRS)
3. Revised Children's Manifest Anxiety Scale (RCMAS)
4. Child Behavior Checklist (CBCL)
5. Conners' Rating Scale (CRS, CRS-R, and CASS)
6. Comprehensive Behavior Rating Scale for Children (CBRSC).
7. Adaptive Behavior Scale (AAMR ABS)

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 DELIRIUM

- Acute onset of fluctuating, cognitive impairment.

- Disturbance of consciousness with reduced ability to attend.
- Perceptual abnormalities.
- Sleep wave cycle disturbances.
- Disorganized thought process
- Abnormal psychomotor activity.

PREVALENCE:
1% - General
10% - Emergency
40% - Terminal ill patients

DOMAINS OF DELIRIUM:
- Consciousness
- Attention
- Cognition
- Perception

PATHOPHYSIOLOGY OF DELIRIUM:
- Decreased oxidative metabolism
- Reduced cholinergic functions
- Dopamine excess
- Norepinephrine excess
- Glutamate excess
- Serotonin imbalance
- GABA imbalance
- Decreased beta endorphins
- Abnormal signal transduction
- Abnormal second messenger
- Change in blood brain barrier
- Endocrine abnormality
- Decreased Somatostatin like reactivity
- Inflammatory hypothesis

DELIRIUM SUBTYPES:
Hyperactive Delirium
Hypoactive Delirium

COURSE OF DELIRIUM:
- Usually last 3 to 5 days.
- Persistent symptoms 6-8 weeks.
- % of patient s up to months.

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TREATMENT:
- Find the cause and give specific treatment for the reversible cause.
- Ensure patient safety while educating the patient, family and staff.
- Symptomatic treatment:
 Psychosis & Agitation – Haloperidol, Inj Ziprasidone, ECT
 Sleep disturbance – Oxazepam, Zolpidem
 Non-pharmacological – Orientation cues, restrains, family or parent
education

Treatment of specific etiology of delirium:

 Anticholinergic intoxication: Physostigmine

 Wernicke s encephalopathy – Thiamine
 Benzodiazepine toxicity – Flumazenil
 Opioid toxicity – Naloxone, Naltrexone
 Alcohol withdrawal – Benzodiazepine, Thiamine
 Parkinsonism – Clozapine, Quetiapine

DEMENTIA

It is an acquired, global or multifocal impairment of cognitive functions involving

decline in intellect, memory and personality in presence of normal consciousness.
(Impairment of at least one of the following)

- Language, memory, visuo spatial skills, personality, emotion and cognition.

*Components of Cognition:
- Orientation,
- Consciousness,
- Attention,
- Perception,
- Language,
- Visio spatial functions
- Memory
- Mood
- Personality
- Thought & Problem Solving

*causes of pseudo dementia:

- Depression
- Mania
- Schizophrenia
- Hysteria

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Screening tests:
- Mini Mental status examination
- Blessed Mental Status Test

MINI MENTAL STATUS EXAMINATION: By Folstein

Total score30 (553539) - ORARL
- Orientation (Time-5, Place-5)
- Registration (3)
- Attention (5)
- Recall (3)
- Language (9)

Score:
>23 – Normal
23 – Mild
12-23 – Moderate
<12 - Severe

SIGNS OF CORTICAL DEMENTIA: (4A)

- Aphasia
- Alexia
- Agnosia
- Amnesia
SIGNS OF SUB CORTICAL DEMENTIA:

- Forgetfulness
- Slow thoughts
- Depression
- Apathy

CLASSIFICATION OF DEMENTIA:

CORTICAL:
- Alzheimer s disease
- Pick s disease
- Crutzfeldt Jacobs disease
- Large vessel strokes

SUBCORTICAL:
- Parkinson s disease
- (untington s disease
- Progressive supranuclear palsy
- Wilsons disease
- Normal pressure hydrocephalus
- Depression
- Lacunar infarcts
- Binswangers syndrome

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MIXED:
- Vascular
- Infections
- Trauma
- Tumours
- Metabolic

INVESTIGATIONS:

All cases:

- Blood count
- ESR
- Serum electrolyte
- Liver profile
- Kidney profile
- Thyroid function tests
- Serum B12 & Folate
- Chest X Ray
- ECG
- CT & MRI

In selected cases:
- CSF Examination
- Neuropsychological tests
- HIV
- Auto antibody screening
- Serum copper and ceruloplasmin
- Drug and toxin screening
- Blood gas analysis-ABG
- Cerebral angiography

In suspected cases:
- WBC Enzyme screening
- Urine and plasma amino acids
- Plasma pyruvate and lactase
- Bone marrow, liver, brain, nerve and muscle biopsy

CLASSIFICATION (DSM IV)

- Alzheimer s dementia
- Vascular dementia
- Due to other medical conditions
- Due to multiple etiology
- Substance induced
- Not otherwise specified

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ALZHEIMERS DEMENTIA:
Risk factors:
- Increased age
- Family history
- Female gender
- Low education status
- Head injury

Protective factors:
- Antioxidants
- NSA)D s
- Smoking
- Estrogens

Genetics:
- Presenilin 1 (Chromosome 14)
- Presenilin 2 (Chromosome 1)
- Amyloid precursor (Chromosome 21)
- Apo E (Chromosome 19)

Histopathology:
- Senile plaques
- Neurofibrillary tangles
- Granular vascular changes
- Hirano bodies
- Lipofuschin depositions
- Lewy bodies
- Congophillic angiopathy

Clinical features:
- Forgetfulness
- Poor self-care
- Amnesia (Recent Events)
- Disorientation (mainly time)
- Aphasia (both receptive and expressive)
- Apraxia
- Agnosia
- Visuo spatial skill defects
- Impaired executive functions
- Spastic Paraparesis
- Psychiatric (Delusions, hallucinations, depressive behaviour and personality
changes)
Treatment:
- Tacrine (High hepatotoxicity)
- Donepezil (5-10mg/day, Max 30mg)
- Rivastigmine (3-6 mg/day, Max 12mg)
- Galantamine (4-8 mg/day, Max 16mg)
- Memantine (5-10 mg/day, Max 30mg)

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Neuroprotectors
- Piracetam
- Citicholine
- Methylcobalamine
- NSA)D s
- Estrogen replacement
- Statins

Poor prognostics factors:

- Male gender
- Age > 65 years
- Parietal lobe damage
- Prominent behaviour problems
- Severe focal cognitive defects
- Comorbid depression

VASCULAR DEMENTIA

- Arteriosclerotic Dementia or Multi infarct dementia

- Step wise decline of cognitive functions
- Focal neurological defects
- Cerebro vascular defects
- HACH)NSK) S )schemic Score (To differentiate vascular dementia from
Alzheimer s dementia
- BinsWanger s Disease:
Subcortical atherosclerotic encephalopathy
Micro infarctions of white matter with sparring of grey matter
Ischemic periventricular leucoencephalopathy

CADASIL:
Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and
Leucoencephalopathy (Chromosome 19 abnormality)

DEMENTIA WITH LEWY BODIES:

- Senile dementia with lewy body type

- Lewy body variant of Alzheimer s disease
- Lewy body dementia
- Diffuse Lewy body disease
- Cortical Lewy body disease
Core clinical features:

- Fluctuating levels of attention and alertness

- Recurrent visual hallucinations
- Parkinson s features TRAP
Tremor
Rigidity
Akinesia
Postural Instability

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(UNT)NGTON S DEMENT)A

- Trinucleotide repeat sequence abnormality (Chromosome 4)

- Neuronal loss in Caudate and Putamen
- Symptoms (Psychiatric, Cognitive & Movement Disorders)
CREUTZFELDT JACOB DEMENTIA
- Prion Disorder
- Progressive dementia
- Myoclonus
- Ataxia
- Muscle rigidity
- Death within one year
- Spongy form appearance in cortex, striatum and thalamus

NORMAL PRESSURE HYDROCEPHALUS

Triad:
Cognitive impairment (Dementia)
Urinary Incontinence
Frontal Ataxia

- Enlarged lateral ventricles but little increased CSF pressure

- Communicating hydrocephalus with patent Aqueduct of Sylvius

PROGRESSIVE SUPRA NUCLEAR PALSY

- Vertical Supra nuclear Gaze palsy

- Rigidity
- Dementia
- Vertical Optico kinetic Nystagmus
WERN)CKE S - KORSAKOFF S SYNDROME – (GOA)

Global confusion
Ophthalmoplegia (6th nerve)
Ataxia

- Thymine deficiency
- Damage medial thalamic nuclei and mammillary bodies

VITAMIN B 12 DEFICIENCY

- Megaloblastic Anaemia
- Posterior Column damage (Positive sense & Vibration sense lost)
- Myelopathy
- Peripheral Neuropathy
- Hyper deep tendon reflex
- Ataxia
- Dementia

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PELLAGRA(3D)

- Dementia
- Diarrhoea
- Dermatitis
NEUROPSYCHIATRIC ASPECTS OF CEREBRO-VASCULAR DISORDERS

SYNDROME SITE OF LESION

Vascular Dementia --- Multiple Ischemic lesions

Major Depression --- Left frontal lobe & Left basal ganglia
Minor Depression --- Lt Post Parietal & Occipital region
Mania --- Rt Baso temporal & Rt Orbito frontal
Anxiety --- Lt Dorso lateral frontal cortex
Psychotic Disorders --- Rt temporo Parieto occipito junction
Apathy --- Post internal capsule & cingulate gyrus
Catastropic Reaction --- Lt anterior sub cortical
Pathological Laughing & Crying --- Bilateral hemispherical lesions

NEUROPSYCHIATRIC ASPECTS OF BRAIN TUMOURS

Primary Tumours: Originate within brain & meninges.

Secondary Tumours: Metastasis at distant site.

ANATOMICAL CLASSIFICATION:

Supratentorial Tumours:

- Frontal lobe tumours

- Parietal lobe tumours
- Temporal lobe tumours
- Occipital lobe Tumours
- Diencephalic Tumours
- Pituitary tumours

Infratentorial Tumours:

- Brain stem tumours

- Cerebellar tumours

PSYCHIATRIC MANIFESTATIONS OF FRONTAL LOBE TUMOURS:

- Psychosis
- Mania / Hypomania
- Depression
- Catatonia
- Hallucinations or Delusions

168
 - Personality changes
- Apathy
- Impaired executive functions
- Abulia
- Lack of spontaneity
- Psychomotor retardation
- Akinetic Mutism
- Expressive aphasia
- Dysprosodic aphasia

PSYCHIATRIC MANIFESTATIONS OF TEMPORAL LOBE TUMOURS:

- Viscosity
- Increased emotionality with depression, elation and irritability
- Hostility and aggression
- Humorlessness
- Excessive philosophical concern
- Hyper religiosity
- Hypo sexuality
- Hypergraphia

PSYCHIATRIC MANIFESTATIONS OF PARIETAL LOBE TUMOURS:

- Depression
- Paranoid delusions
- Cotards syndrome
- Impairment of cortical senses:
Two point discrimination
Joint position sense
Stereognosis
Vibration sense
Graphasthesia

- Gerstmann Syndrome:
 Finger Agnosia
 Dysgraphia
 Left to right confusion
 Acalculia
 Hemi neglect
 Apraxia
 Receptive aphasia

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PSYCHIATRIC MANIFESTATIONS OF OCCIPITAL LOBE TUMOURS:

- Visual hallucinations
- Homonomous hemianopia
- Visual Agnosia
- Behavioural problems

PSYCHIATRIC MANIFESTATIONS OF DIENCEPHALIC TUMOURS:

- Depression
- Mood lability or Euphoria
- Personality changes
- Subcortical dementia
- Hypersomnia
- Akinetic Mutism
- Anorexia nervosa like illness
- Schizophrenia like illness
NEUROPSYCHIATRIC ASPECTS OF HEAD INJURY

ACUTE:

- Post traumatic Amnesia

- Retrograde Amnesia
- Post traumatic Delirium

CHRONIC:

- Cognitive impairment:
Dementia / Amnesia
Impaired executive functions
Catastrophic Reactions
- Psychosis
- Personality changes
- Post-Traumatic Stress Disorder / Anxiety Disorders
- Punch-Drunk Syndrome

- Post Traumatic Syndrome:

 Headache
 Dizziness
 Irritability
 Emotional lability
 Increased Sensitivity to noise & light
 Poor concentration

Factors that increase psychiatric morbidity following head injury:

- Increased duration of loss of consciousness

- Increased duration of post traumatic amnesia
- Increased duration of post traumatic delirium

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 - Increased age, arteriosclerosis, alcoholism
- Increased area of brain damage
- Increased neurological sequelae
- Dominant / Bilateral Hemisphere involvement

NEUROPSYCHIATRIC ASPECTS OF HIV:

HIV VIRUS:

- Single strand RNA Virus

- Lenti virus family
- Rhinovirus group
- It infects T-lymphocyte (CD 4) and macrophages
- Contains Reverse transcriptase enzyme (RNA Dependent DNA Polymerase)
- Normal CD 4 cell count (800 – 1000 cells/cu mm)
- CD 4 count dropped approx. 100 cells/cu mm/year
- Immune system quite compromised, CD 4 count less than 200 cells/cu mm.

AIDS:
When CD 4 count < 200 cells/cu mm with or without symptoms or CD 4 count > 200 with
symptoms.

Psychiatric complications:

- Delirium
- Dementia
- Minor cognitive motor disorders
- Major depression
- Bipolar illness
- Schizophrenia like illness
- Personality changes

TREATMENT:

- Nucleoside reverse transcriptase inhibitors

- Non nucleoside reverse transcriptase inhibitors
- Nucleotide reverse transcriptase inhibitors

SECONDARY INFECTIONS:

- Toxoplasmosis: Characterized by multiple ring enhancing lesions in the basal

ganglia, grey-white matter junction.
Rx – Pyrimethamine + Sulfadiazene or Clindamycin

- Cytomegalo Virus:
- Cryptococcal meningitis
- Progressive multifocal leucoencephalopathy

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 - CNS lymphoma
- Gullian Barre syndrome
- Myelopathy

NEUROPSYCHIATRIC ASPECTS OF HERPES SIMPLEX ENCEPHALITIS

- Caused by HSV 1 &2

- Abrupt onset of fever, personality changes & headache followed by cognitive
changes and focal neurological signs (Aphasia, Hemiparesis, Seizure etc.,), coma
and death within 2 weeks
- Rx – Acyclovir & Vidarabine

NEUROPSYCHIATRIC ASPECTS OF SUB ACUTE SCLEROSING PAN ENCEPHALITIS

- Slow infection with Measles virus

- Progressive inflammation and sclerosis of Brain
- Onset – 7 to 12 years after Measles infection
- Decreased intelligence, reading, writing & visuo spatial abilities.
- Myoclonus
- Hallucinations
- Apraxia
- Agnosia
- Balints Syndrome
 Optic Ataxia
 Simultagnosia
 Sticky fixation
- Cerebral Ataxia
- Cortical blindness or Optic atrophy
- Stupor, coma, death
- EEG Changes – High amplitude, bilateral stereotyped complexes that repeat every
3-5 secs.
- Rx- Interferon, GAMA

PRION DISEASES
Proteinaceous, infectious particle and capable of replication without the benefit of
Nucleic acid.

- Creutzfeldt-Jacob Disease
- Gerstmann-straussler syndrome
- Variant of CJD
- Fatal familial insomnia
- Kuru
- Bovine spongiform disease
- Chronic wasting disease
- Transmissible Mink encephalopathy

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NEUROPSYCHIATRIC ASPECTS OF EPILEPSY

SEIZURE:
Paroxysmal, abnormal, excessive firing of group of neurons that leads to motor, sensory,
autonomic and psychic activity.

EPILEPSY:
Two or more unprovoked seizures with or without underlying cause.

Classification of Epilepsy: (International League of Epilepsy)

- Partial Seizures
 Simple Partial
 Complex Partial
 Partial seizures with secondary generalization
- Generalized Seizures
 Absence Seizures
 Tonic-Clonic seizure
 Tonic Seizure
 Atonic Seizure
 Myoclonic Seizure
- Unspecified Seizures
 Neonatal Seizures
 Infantile Spasms

SIMPLE PARTIAL SEIZURES:

- Seizure occur within discrete region of brain

- Consciousness fully preserved
- Associated with focal defects
- Jacksonian march
- Todd s Palsy
- Epilepsia Partialis Continua

COMPLEX PARTIAL SEIZURES:

- Focal seizure activity with transient impairment of the patient s ability to

maintain normal contact with environment.
- Motion less staring combined with simple automatism or automatic behaviour
(Lip-smacking, chewing, swallowing, picking movements of hand, sometimes
running).
- Usually lasts less than 1 minute.

GENERALIZED SEIZURES:
The seizure from both the hemispheres simultaneously.

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ABSENCE SEIZURES:
- Petit-mal epilepsy
- Sudden, brief loss of consciousness without loss of postural control.
- Repetitive short lasting, usually 10 to 20 sec.
- EEG 3 per sec, spike and wave pattern.

TONIC-CLONIC EPILEPSY:
- Grandmal epilepsy
- Contractions of all muscles of the body (Tonic phase) followed by Clonic Phase
with impairment of consciousness.

ATONIC SEIZURES:
- Sudden loss of postural muscle tone lasting 1 to 2 seconds.

MYOCLONIC SEIZURES:
- Sudden and brief muscle contraction that may involve part of the body or total
body.

TWILIGHT STATES:
- Protracted period of intermixed Ictal and Post Ictal changes.

PHASES OF EPILEPSY:
- Pre Ictal
- Ictal
- Post Ictal
- Inter Ictal

PRE ICTAL:
Prodromal Symptoms (Hours to Days):

- Tension
- Dysphoria
- Insomnia
Aura (Just prior to onset of seizure-Minutes to Hours):

- Most common in Temporal lobe complex partial seizures.

- Autonomic or visceral aura (Epigastric Discomfort)
- Derealization or Depersonalization.
- Cognitive symptoms
Forced thinking
Déjà vu
Jamais vu
Deja pense
Deja entendu
Fugue
- All modalities of hallucinations
- Twilight states

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 - Illusions
- Affective symptoms (Anxiety & Euphoria)
ICTAL: (Seizure itself produces)
- Automatism
- Behavioural problems
- Psychosis
- Cognitive & perceptual symptoms
- Aggressive behaviour

POST ICTAL:
- Delirium
- Post ictal psychosis
Variable psychosis & affective symptoms
Usually lasts from 1 day to 1 month.
- Depression (Most common)

INTER ICTAL:

- Not dependent on seizure.

- Brief Interictal psychosis
Anxiety
Insomnia
Hallucinations
Depression
Affective symptoms
- Forced normalization (Landolts Phenomenon)
When psychosis occurs the subsequent EEG s are normalized

Chronic Inter Ictal Or Schizophrenic Like Psychosis.

6 to 12 times more common in epileptic individuals
Risk factors:
Early onset
Refractory seizures
Left temporal focus
Female gender
Long duration
No family history of Schizophrenia
Absence of premorbid schizophrenic traits
Rx – Antipsychotic along with Anticonvulsants

Personality changes (Gestalt -Geschwind syndrome)

Interpersonal stickiness or viscosity
Increased emotionality with depression, elation and irritability
Hostility and aggression
Humorlessness
Excessive philosophical concern
Hyper religiosity
Hypo sexuality
Hypergraphia

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Kluver-Bucy Syndrome:
Bilateral damage of amygdala
Aggression
Hyper orality
Hyper sexuality
Hyper metamorphosis
Impulsivity
Reduced inhibitions
PSEUDO SEIZURES:
- Absence of neurological disorders
- No specific aura
- Seizure may be induced or provoked
- Inconsistency in clinical presentation
- Seizure may differ from attack to attack
- Only occurs in presence of others
- Gradual onset and prolonged duration
- Asymmetrical movement
- Rare whole body rigidity
- Rare incontinence, tongue bite, injuries
- Vocalization may occur through out ictus
- Normal ictal & post ictal EEG
- No post ictal confusion or delirium
- No increase in prolactin
- Subsequent recall of events during ictus.
- No relationship of ictal frequency to anti convulsant medication

MOVEMENT DISORDERS

HYPOKINETIC DISORDERS
- Akinesia
- Hypokinesia
- Bradykinesia

HYPERKINETIC DISORDERS
- Dystonia
- Chorea
- Tics
- Myoclonus
- Tremors

NEUROLEPTIC INDUCED MOVEMENT DISORDERS

- Parkinson s Symptoms
Tremor
Akinesia
Rigidity
Postural instability

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 - Akathisia
- Dystonia
- Tardive dyskinesia
- Neuroleptic Malignant Syndrome

** Nigrostriatal dopamine tracts:

- Increased Dopamine: Hyperkinetic movements
- Decreased Dopamine: Hypokinetic movements
STUPOR

- Catatonic stupor
- Organic stupor
- Depressive stupor
- Manic stupor
- Hysterical stupor

NEUROLEPTIC MALIGNANT SYNDROME (3D Hyper MART)

- Delirium
- Diaphoresis
- Dysarthria / Dysphasia
- Hyper Reflexia
- Myoclonus
- Autonomic instability
- Rigidity
- Tremor

Rx of NMS: (ABCDE S)
- Amantidine
- Bromocriptine / Benzodiazepine
- Carbidopa / Levodopa
- Dantroline
- ECT
- Supportive measures

SEROTONIN SYNDROME(3D Hyper MALT)

- Delirium
- Diaphoresis
- Diarrhoea
- Hyper Reflexia
- Myoclonus
- Ataxia
- Labile mood
- Tremor

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NEUROPSYCHIATRIC ASPECTS OF HEADACHE

CLASSIFICATION (International Headache Society)

1. Migraine
2. Tension type headache
3. Cluster headache
4. Other primary headaches
5. Due to Head & neck trauma
6. Due to Cranial & cervical disorder
7. Due to Cerebro vascular disorder
8. Due to Substance Induced or withdrawal
9. Due to Infections
10. Due to disorders of Neck, Eye, Ear, Tongue Disorders
11. Due to disorders of Homeostasis
12. Due to Psychogenic
13. Due to Cranial Neuralgia
14. Due to Other types

DIAGNOSTIC CRITERIA FOR MIGRAINE:

- At least 5 episodes (With Aura – 2 episodes)

- Headache lasting 4 – 72 hrs
- Unilateral location
- Pulsating type
- Moderate to severe
- Photophobia / Phonophobia

CLUSTER HEADACHE:
- At least 5 attacks
- Severe retro orbital pain
- Ipsilateral conjunctival injection or lacrimation
- Ipsilateral lateral congestion or Rhinorrhea
- Ipsilateral eye lid oedema
- Ipsilateral fore hand and facial swelling
- Ipsilateral miosis or ptosis
- Restlessness or agitation

TENSION TYPE HEADACHE:

- Headache occurring ≥ days per month or ≥ days per year

- Bilateral location
- Pressing or tightening quality
- Not aggravated by routine physical activity
- No nausea, no vomiting, no photophobia, no Phonophobia

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 CHILD PSYCHIATRY
CHILD & ADOLESCENT PSYCHOLOGICAL ASSESSMENT INSTRUMENTS:

INTELLECTUAL ABILITY
- Wechsler Intelligence scale for children 3rd edition (6-16yrs)
- Wechsler Adult Intelligence scale (16-Adolescent)
- Wechsler preschool and primary care of intelligence (3-7yrs)
- Kaufmann Assessment battery of children (2.6-12.6yrs)
- Kaufmann Adolescent & Adult intelligent test (11-85yrs)
- Stanford-Binet intelligence scale (2-23yrs)
- Peabody picture vocabulary test- III (4-adult)

ACHIEVEMENT ABILITIES
- Woodcock Johnson Psychoeducational battery
- Wide range achievement test
- Kaufmann test of Educational achievement test
- Wechsler individual achievement test

ADAPTIVE BEHAVIOUR
- Vineland Adaptive Behaviour Scale
- Scales of Independent Behaviour-Revised

ATTENTIONAL CAPACITY
- Trial making test
- Wisconsin Card Sorting Test
- Behavioural Assessment System for children
- Home Situation Questionnaire
- ADHD Rating Scale
- School Situational Rating Scale
- Child Assessment Profile

PROJECTIVE TESTS
- Rorschach s Test
- Thematic Apperception Test
- Draw a Person Test

MENTAL RETARDATION
It is defined as significantly sub average general intellectual functioning resulting in
or associated with concurrent impairment in adaptive behaviour and manifested during
developmental period before the age of 18 years.

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CLASSIFICATION BASED ON IQ:

Profound MR - < 20
Severe MR - 20 – 34
Moderate MR - 35 – 49
Mild MR - 50 – 69
Borderline - 70 – 90
Normal - 90 – 110
Above Normal - > 110
Genius - > 120

EPIDEMIOLOGY:
- General Population 1-3%
- Peak age – 10 to 14 years
- Mild MR 85%
- Moderate MR 10%
- Severe MR 4%
- Profound MR 1%

ETIOLOGY:
- Genetic Factors
- Developmental factors
- Acquired factors

GENETIC FACTORS
- Autosomal Dominant/Recessive
- X-linked Dominant/Recessive

Down Syndrome:
- Also called Mongoloid facies
 Slanted eyes
 Epicanthal fold
 Flat nose
- 3 types of chromosomal abnormalities
 Trisomy – 21
 Non dysjunction occur after fertilization
 Translocation between 21 & 15
- Clinical features:
 Mild to Moderate MR (Normal development up to 6 months)
 Child is Placid, cheerful, co-operative & easily adapt at home
 Emotional disorders
 Language disorders
 Behavioural disorders
 Social skill problems
 Memory skill problems
 Self-skill problems
 (igh incidence of Alzheimer s disease
 Patient does not live beyond 40 years

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 - Signs of Downs syndrome:
 Hypotonia
 Oblique palpebral fissure
 Abundant neck skin
 Small, flattened skull
 High cheek bones
 Protruding tongue
 Hands broad, thick with single palmar transverse crease
 Little fingers short & curved
 Moro s reflex weak or absent

Fragile X Syndrome:
- Second most common cause of MR
- Mutation in X chromosome is known as Fragile site (Xq 27.3)
- Large long Head
- Long ears
- Short stature
- Hyper extensible joints
- Post pubertal macroorchidism
- Psychiatric Symptoms:
 Moderate to severe MR
 ADHD
 Learning disorders
 Pervasive developmental disorders
 Speech disorders

Prader-Willi Syndrome:

- Small deletion in chromosome 15

- 1 in 10000 births
- Compulsive eating
- Small stature
- Obesity
- Mental retardation
- Hypogonadism
- Hypotonia
- Small hands and feet

Cats cry syndrome:

- Deletion at 5th chromosome

- Microcephaly
- Oblique palpebral fissure
- Hypertelorism
- Cats like cry

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Phenylketonuria:

- Autosomal recessive disorder

- Phenylalanine hydroxylase deficiency
- Increased phenylalanine levels
- Diagnosis by Guthrie test & Ferric chloride test
- Severe MR
- Eczema
- Vomiting
- Hyperactive bizarre body movements
- Low phenylalanine diet to protect the disabilities

Rett s Syndrome:

- X-linked dominant
- Only in females
- Child normal up to 6 months
- Deterioration of communication skills, motor skills and social functioning.
- Autistic like behaviour
- Ataxia
- Facial grimacing
- Stereotyped hand movements
- Scoliosis
- Seizures
- Cerebral atrophy with pigmentation at substantia nigra
- Moderate MR

Neurofibromatosis:

- Von Reckling Hausen Disease

- Autosomal dominant disorder
- Café-au-lait spots on the skin
- Optic glioma
- Acoustic neuroma
- Mild MR

Tuberous Sclerosis:

- Autosomal dominant
- Mental Retardation
- Seizures VOGT S TR)AD
- Adenoma Sebacium
- Ash-leaf spots in the Eye
- Rhabdomyoma of the kidney

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Lesch Nyhan syndrome:

- X-linked recessive
- Abnormality in Purine metabolism
- Mental Retardation
- Seizure
- Choreoathetosis
- Spasticity
- Self mutilation

Adenoleucodystrophy
- Diffuse demyelination of cerebral white matter
- Mental retardation
- Seizures
- Spasticity
- Ataxia

ACQUIRED & DEVELOPMENTAL FACTORS

- Prenatal period
 Uncontrolled diabetes
 Anemia
 Hypertension
 Preeclampsia
 Alcohol use

- Rubella (German Measles)

 Mental Retardation
 Congenital heart diseases
 Cataract
 Deafness
 Microcephaly
 Microophthalmia

- Cytomegalo virus
 Still births
 Mental retardation
 Microcephaly
 Hepato-splenomegaly
 Intra cerebral calcification

- Toxoplasmosis
 Severe MR
 Microcephaly
 Choreoretinitis
 Seizures

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 - Herpes simplex virus
 Microcephaly
 Moderate MR
 Intra cranial calcification
 Ocular problems

- Fetal Alcohol Syndrome

 Hypertelorism
 Microcephaly
 Short palpebral fissure
 Shortened nose
 Mild to moderate MR
 ADHD
 Learning disorders
- Prenatal drug abuses
- Pregnancy complications
- Acquired childhood infections and disorders

MANAGEMENT OF MR:

- Physical examinations for various signs & symptoms

- Chromosomal studies (Amniocentesis, Chorionic villi sampling)

- Urine and blood analysis for:

 Lesch-Nyhan syndrome
 Galactosemia
 Phenylketonuria
 Hurler syndrome
- EEG & Neuroimaging techniques
- Psychological assessments

- Primary prevention:
 Education and awareness about developmental disorders
 Upgrade public health policies
 Improve maternal and child health care
 Family and genetic counseling
 Supplementary enrichment programs

- Secondary prevention:
 Shorten the course of illness
 Hormonal replacement therapy
 Dietary replacement
 Early diagnosis and treatment of psychiatric disorders
 Behavioural therapy
 Cognitive therapy
 Family therapy

184
 - Tertiary prevention:
 Prevention of disabilities
 Rehabilitations
o Day care centers
o Integrated schools
o Vocational training centers

- Organizations of Mental Retardation:

 American Association on Mental Retardation
 National Information Center for children and youth with disabilities
 National organization for rare disorders
 Sibling information network
 Association for children with Down syndrome
 National Down syndrome congress
 National Fragile X Syndrome Association
 Prader-Willi Syndrome Association

LEARNING DISORDERS

Learning disorders in children and adolescents are characterized by academic under

achievement in reading, written expression and mathematics in comparison of overall
intellectual capacity of the child.

- Also known as academic skills disorder

- 5 % of School age children
- Types:
 Reading Disorders
 Mathematic Disorders
 Disorders of written expression

- Comorbid conditions
 ADHD
 Communication disorders
 Conduct disorder
 Depressive disorder

- Etiology:
 Genetic factors
 Perinatal injuries
 Neurological disorders
 Lead poisoning
 Fetal alcohol syndrome
 Utero drug exposure

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READING DISORDERS:

- Also called as
o Word blindness
o Reading backward
o Learning disability
o Alexia
- 4 % of School age children

- Clinical features:
 Impaired ability to recognize word
 Slow and inaccurate reading
 Poor comprehension
- Males more common than female (4:1)
- 6, 15 & 8 chromosomal abnormality

- Diagnostic tests:
 Standardized spelling test
 Written composition
 Processing and using language
 Design copying
 Woodcock-Johnson psychoeducational battery – Revised
 Peabody individual achievement test – Revised
- Treatment:
 DISTAR-Direct Instructional System for Teaching And Remediation
 Bridge Reading Program
 Psychotherapy

MATHEMATIC DISORDERS:

- Also called as
o Dyscalculia
o Congenital arithmetic disorder
o Acalculia
o Gerstmann syndrome
o Developmental arithmetic disorder
- 1 % of School age children
- Poor achievement in linguistic skills, perceptual skills, mathematic skills and
attention skills

- Clinical features:
 Difficulty in learning to count meaningfully
 Difficulty to learn cardinal and ordinal system
 Difficulty to perform arithmetic operations
- Diagnostic test: KEYMATH Diagnostic Arithmetic Test
-

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DISORDERS OF WRITTEN EXPRESSION:

- Also called as
o Dysgraphia
o Spelling dyslexia
- 4 % of school age children
- Diagnostic tests:
 TOWL – Test Of Written Language
 TEWL – Test of Early Written Language

COMMUNICATION DISORDERS

o Domains of language
o Phonology
o Language
o Semantic
o Pragmatic

- Language Disorders
o Expressive disorder
o Mixed expressive and receptive disorder

- Speech Disorders
o Phonological disorders
o Stuttering
Etiology ;
o Subtle cerebral damage
o Maturational lag in cerebral development
Assessment tool; Carter neurocognitive assessment

MOTOR SKILLS DISORDER/ DEVELOPMENTAL COORDINATION DISORDERS

o Clumsy child syndrome : awkward motor behaviors that could not be correlated with
any specific neurological disorder or damage.
o Strongly associated with speech and language disorder
o Specialized tests for motor coordination disorders are
 Bender gestalt visual motor gestalt test
 Frostig movement skills test battery
 Bruininks-oseretsky test of motor development

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PERVASIVE DEVELOPMENTAL DISORDERS

Characterized by impaired reciprocal social interactions, aberrant language

development and restricted behavioural repertoire.

CLASSIFICATION:

- Autistic Disorders
- Rett s Disorder
- Childhood disintegrative disorder
- Asperger s Disorder

Common Clinical Features:

- Qualitative impairment in social interactions
- Qualitative impairment in communication skills
- Repetitive or stereotyped behavior

Autism:

- Also called:
o Early infantile Autism
o Childhood Autism
o Kanners Autism / Syndrome

- Diagnostic Scale:
 ADOS – G: Autism Diagnostic Observation Schedule – Generic

Childhood disintegrative Disorder:

- Child normal up to 2 years

Rett s Syndrome:
- X-linked dominant
- Only in females
- Child normal up to 6 months
- Deterioration of communication skills, motor skills and social functioning.
- Autistic like behavior
- Ataxia
- Facial grimacing
- Stereotyped hand movements
- Scoliosis
- Seizures
- Cerebral atrophy with pigmentation at substantia nigra
- Moderate MR

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Asperger s Syndrome:

- Also called Autistic Psychopathy

- Marked impairment in social communication rather than cognitive and language
skills

ADHD (ATTENTION DEFICIT / HYPERACTIVE DISORDER)

- Characterized by pattern of diminished sustained attention and higher levels of

impulsivity in child and adolescent than expected for someone of that age and
developmental level

- Types:
o Inattentive type
o Hyperactive or impulsive type
o Combined

- Diagnostic criteria: (66627)

 At least 6 features in inattention
 At least 6 features in hyperactivity and impulsivity
 At least 6 months duration
 At least 2 settings (house & school)
 Onset below 7 years
- Clinical features:
 Inattention
 Careless with detail
 Fails to sustain attention
 Appears not to be listening
 Fails to finish tasks
 Poor self organization
 Looses things
 Forgetful
 Easily distracted
 Avoid task requiring sustained attention

 Hyperactive
 Fidgets with hands and feet
 Leaves seat in the class
 Runs / climbs
 Cannot play quietly
 Always on the go

 Impulsivity
 Talks excessively
 Burst out answers
 Cannot wait turn
 Interrupts others

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 - Etiology:

o Biological
 Neurochemical factors
 Neurophysiological
 Neuroimmunology

o Structural
 Neurodevelopmental
 Neuroimaging

- Comorbid disorders
 Learning disorders
 Motor coordination problems
 Autistic spectrum disorders
 Tic disorders
 Conduct disorders
 Substance abuse
 Anxiety
 Depression
 Bipolar disorders

- Management of ADHD:

o Pharmacological

 Stimulants
 Methyl Phenidate – 0.3 to 1mg/kg body wt.
 Dexmethyl Phenidate – 0.3 to 1mg/kg body wt.
 Dextro amphetamine – 0.15 to 0.5mg/kg bd wt.
 Dextro amphetamine plus amphetamine salt preparations
 > 3 yrs. of age Dextro amphetamine is preferable
 > 6 yrs. Methyl Phenidate is preferable

 Non stimulants
 Atomoxetine – 0.5 to 1.8mg/kg bd wt.
 Bupropion – 3 to 6mg/kg bd wt.
 Venlafaxine – 25 to 150mg/day
 Clonidine – 0.1 to 0.3 mg/day

o Non Pharmacological
 Behavioural therapies
 Positive reinforcement
 Family therapy
 School interventions
 Group therapy

*** UTAH Criteria – For Adult ADHD

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 DISRUPTIVE BEHAVIOURAL DISORDERS

Types:

1. Oppositional Defiant Disorder

2. Conduct Disorder

OPPOSITIONAL DEFIANT DISORDER:

Enduring pattern of negativistic, disobedient and hostile behaviour towards
authority figures as well as inability to take responsibility for mistakes, leading to placing
blame on others.

CONDUCT DISORDER:
Characterized by repetitive and persistent pattern of antisocial, aggressive or defiant
behaviour, in which age appropriate social norms are violate.

ETIOLOGY:

- Social factors
 Poverty
 Low socio economic status
 Overcrowding
 Homelessness
 Social isolation
 Truancy
 Unemployment

- Family factors
 Parental criminality
 Parental psychotic disorders
 Parental conflict
 Divorce
 Single parenting

- Childhood factors
 Low IQ
 Epilepsy
 Neurological disorders
 Brain damage

- Neurobiological factors
 Low levels of beta hydroxylase

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CLINICAL FEATURES:
- Aggression
- Cruelty to people or animals
- Destruction of property
- Deceitfulness
- Theft
- Fire setting
- Truancy
- Running away from home
- Disobedient behaviour
- Serious violation of rules

COMORBID CONDITIONS:

- ADHD
- Autistic spectrum disorders
- Substance abuse
- Anxiety
- Depression
- Learning disorders

TREATMENT:

- Parent management training

- Functional family therapy
- Multi systemic therapy
- Child interventions
 Social skill training
 Problem solving
 Anger management
- Treat comorbid conditions
- Address child protective centers

EMOTIONAL DISORDERS IN CHILDREN

ANXIETY DISORDERS
- Separation anxiety
- Over anxiety
- Avoidant disorder

DISORDERS DUE TO MOVEMENT

- Head banging
- Breath holding problems
- Temper tantrums
- Hyperkinetic syndromes
- Tic disorders

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HABIT DISORDERS
- Thumb sucking
- Nail biting
- Pica
- Rumination disorders

PROBLEMS OF TOILET TRAINING:

- Enuresis
- Encopresis

PROBLEMS OF SPEECH:
- Stammering
- Selective Mutism

PROBLEMS AT SCHOOL:
- School phobia
- Impaired school performance

SLEEP DISORDERS:
- Nightmares
- Night terrors
- Somnambulism

EATING DISORDERS:
- Anorexia nervosa
- Bulimia nervosa
- Obesity
- Pica
- Ruminating disorders

TIC DISORDERS

Rapid and repetitive muscle contractions resulting in movements or vocalizations

that are expressed involuntarily.

TYPES:

SIMPLE MOTOR TICS:

- Eye blinking
- Neck jerking
- Shoulder shrugging
- Facial grimacing

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COMPLEX MOTOR TICS:
- Smelling of objects
- Jumping
- Touching
- Grooming behavior
- Echopraxia
- Copropraxia

SIMPLE VOCAL TICS:

- Coughing
- Throat clearing
- Grunting
- Sniffing
- Shouting
- Barking

COMPLEX VOCAL TICS:

- Repetitive words or Phrases
- Palilalia
- Echolalia

TOURETTE S D)SORDER:

- It is characterized by multiple motor tics and one or more vocal tics.

- Life time prevalence 4-5 per 10000
- Onset: Motor tics less than 7 years, Vocal tics around 11 years.
ETIOLOGY:

- Genetic
- Neuroanatomical
 Abnormality in frontal cortex, caudate nucleus, putamen and
thalamus

- Neurochemical
 Increased dopamine
 Endogenous opioids
- Neuro Immunological
 Infection of Beta hemolytic streptococcus

Activates the immune system

Inflammation of basal ganglia

Disruption of cortico striato thalamo cortical circuit

Tic/OCD/ADHD

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TIC RATING SCALE:

- Tic Symptom Self Report

- Yale Global Tic Severity Scale

TREATMENT:

- Pharmacological
 Haloperidol
 Pimozide
 Atypical antipsychotics
 Clonidine
 Atomoxetine
 SSR) s
- Nonpharmacological
 Habit reversal technique
 Promonitory urge phenomenon

ELIMINATION DISORDERS

ENEURESIS
Repeated voiding of urine into clothes or bed, whether the voiding is involuntary or
intentional.

- Child s chronological or developmental age must be at least years

- Types:
o Nocturnal
o Diurnal
o Both

ETIOLOGY:
- Genetic factors
 First degree relatives more common

- Psychological
 Separation from parent
 Disturbed family
 Death or illness of parent
 Social phobia
 Anxiety
 Depression
 Anger or Rejection from care taker

- Physiological
 Improper toilet training

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 - Organic factors
 Metabolic (Diabetic)
 Worm infestation
 Urinary obstruction
 Epilepsy
 Sleep disorders
 Spina bifida
 Weak bladder musculature

TREATMENT:
- Non pharmacological
 Proper toilet training
 Fluid restriction at bed time
 Treat constipation
 Behavioural therapy
o Bell and Pad method
o Reinforcement method
 Psychotherapy
- Pharmacotherapy
 Imipramine – 25 to 50mg/day
 Reboxetine – 4 to 8mg/day
 Desmopressin
ENCOPRESIS
Pattern of passing of feaces at inappropriate places whether the passage is
involuntary or intentional.

- Child chronological or developmental age must be at least 4 years.

CHILD ABUSE
- Physical abuse
- Sexual abuse
- Neglect
- Emotional abuse

PHYSICAL ABUSE:
- Hurting
- Shaking
- Throwing
- Poisoning
- Drowning
- Munchausen Syndrome by proxy

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SEXUAL ABUSE:
- Penetrating / Non Penetrating physical acts
- Watching sexual activities
- Encouraging sexual behavior

EMOTIONAL ABUSE:
- Rejection
- Repeated separation
- Mis-socialization

NEGLECT:
- Failure to provide adequate food, clothing, shelter and supervision.
- Failure to protect from harm or danger
- Failure to assess appropriate medical care

PREVALENCE OF ABUSE:
- Neglect – 62 %
- Physical abuse – 18 %
- Sexual abuse – 10 %
- Emotional abuse – 7 %

ETIOLOGY:
- Violent home lives
- Over crowding
- Low poverty
- Social isolation
- Poor supportive system
- Unemployment
- Financial problems
- Problem families
- Unwanted children
- Childhood development disorders
PSYCHIATRIC OUTCOME OF CHRONIC ABUSE:
- PTSD
- Dissociative disorder
- Borderline PD
- Paraphilia s
- Substance abuse
- Fear or anxiety
- Emotional problems

TREATMENT:
- Ensuring child safety and well being
- Removal from abusive and neglect family
- Proper investigations to rule out any physical or psychological disorder
- Treat comorbid conditions
- Psychotherapy
- Trauma focused cognitive behavioral therapy
- Family therapy

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 FORENSIC PSYCHIATRY
It is a sub specialty of psychiatry, which usually deals with the application of
psychiatric knowledge to legal issues (Psychiatry in law) & application of legal knowledge to
psychiatric issue.

DEFINITION OF MENTAL ILLNESS

A mentally ))) person means a person who is in need of treatment by reason of any Mental
Disorder other than Mental Retardation
- Mental Health Act 1987

Mental Disorders are disorders of the Mind that result in partial or complete disturbance in
the persons thinking, feeling and behavior, which very often results in recurrent or
persistent inability or reduced ability to carry out activities of daily living, self-care,
education, employment and participation in social life
-Disabilities Act

MAGNITUDE OF MENTAL HEALTH PROBLEMS IN INDIA

o 1% of the general population suffers from Major Mental Disorders.

o 10-15% of the population suffers from mild mental health problems.

o 5-10% suffers from ill-effects of alcohol and other addiction forming substances.

o 1-2% suffers from mental retardation (subnormal intellectual functioning).

o 10% of elderly suffer from clinical depression and 5-6% of persons aged 60 yrs,
suffer from dementia.

o 5-10% of Children and adolescents suffer from some emotional and behavioral
problems.

Insanity Defense
Can a person commit a crime and plead Unsound Mind as a defense for escaping
punishment?
Yes! If he could prove that he was of unsound mind at the time of committing the
crime
Can be raised in several ways :
Guilty but Insane
Diminished Responsibility
Incapacity to form an intent because of automation.

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Evolution of the Standards

o Wild beast Test

o The McNaughten Test
o Irresistible impulse / loss of control test
o Durham Test (product rule)
o The model penal code (ALI Test)
o APA / Federal court test
o Sec. 84 (IPC) - in India

CRIMINAL LAW:
It defines certain acts as offences against the state, and in doing so, makes them
punishable.

CIVIL LAW:
It defines the rights and duties of individuals in relation to each others.

CRIMINAL RESPONSIBILITIES:
According to criminal law, committing an act that is socially harmful is not sole
criterion of whether a crime has been committed.

Two components:
Voluntary conduct
Evil intent

Mc Naughten Rule: Sec 84 IPC

Durham s Rule:
An accused is not criminally responsible if his unlawful act was the product of mental
damage or mental defect.

INTOXICATION: Sec 85 & 86 IPC

SUICIDE: Sec 309 IPC
CONSENT: Sec 90 IPC
SEXUAL PERVERSION: Sec 377 IPC
ALCOHOL DEPENDENCE: Sec 510 IPC
MURDER: Sec 302 IPC
RIGHTS OF PRIVATE DEFENSE AGAINST AN INSANE PERSON: Sec 98 IPC

CIVIL RESPONSIBILITY:

1. CONTRACT: It is an agreement enforceable by law according to Indian Contract Act

(Act No 9 of 1872)

2. MARRIAGE:
 Hindu Marriage Act (Act No 25 of 1955)
 Special Marriage Act (Act No 43 of 1954)
 Muslim marriage act (Act 1929)

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 3. ADOPTION: Under the Hindu adoption and maintenance act (Act 78 of 1956)

4. WITNESS: Under the Indian Evidence Act (Act 1872)

A lunatic is not competent to give evidence

5. Testamentary Capacity:
A capacity to give valid will. Regulated by Indian Sessions act. (Act No 39 of 1925)

6. Rights to vote and to stand for election

Vote: Act No 326 of Constitution of India
Stand for election: Act No 102 of Constitution of India

7. Civil proceedings

FITNESS TO STAND TRIAL

In ascertaining fitness plead; it is necessary to determine whether the person :

1. Is oriented to place, person and time.

2. Understands the questions asked.
3. Understands the nature of the charge.
4. Understands the difference between guilty and not guilty
5. Is able to instruct his advocate
6. Is able to follow the evidence presented in the court, and
7. It able to challenge the selection of jurors.
A person may be suffering from severe mental disorder but still be fit to stand trial

INDIAN LUNACY ACT:

- Year 1912, Act No 4,

- Contains 8 chapters
- LUNATIC: An Idiot person of unsound mind (Including MR)
- No provision for separate hospital for different categories of patients
- No provision to establish Central and State authorities.
- No definite guidelines for license to establish or maintain hospital
- No definite guidelines for penalties for improper establishment and maintenance
of hospitals
- No definite provisions or guidelines for OPD treatment facility
- Visitors board:
 Minimum 3 members
 Definite role in admission, care, treatment & discharge
 No provisions for inclusion psychiatrist and social worker
- Voluntary admission: medical officer can admit voluntary patient with opinion
from at least two of board visitors.
- No provision for involuntary admission/under special circumstances
- Less flexible guidelines for leave of absence.

200
 - No provision to delay discharge of voluntary patient if they need further
hospitalization.
- No specific guidelines for judicial safeguards/property management.
- No provision for protection of human rights of mentally ill patient.
- No provision for inspecting officer.

INDIAN MENTAL HEALTH ACT-1987

EVOLUT)ON OF M(A,
Lunatic Asylum – A British concept

o 1st Indian Lunacy Act 1858; Modified in 1883

o 2nd ILA, 1912

o B(ORE COMM)TTEES draft – )ndian Mental (ealth Act Pre )ndependence

o Mental Health Bill Introduced in parliament 1980, 1981, 1986.

o MHA – Enacted in May 1987.

o MH Authority Rules framed in 1990.

o M(A Enforced from st April

An Act to consolidate and amend the law relating to the treatment and care of
mentally ill person, to make better provision with respect to their property and affairs and
for matters connected therewith or incidental thereto.

- Year 1987, Act No 14.

- It contain 10 chapters & 98 Sections
- MENTALLY ILL PERSON: Any person who is in need of treatment for any reason
other than MR
- Provision for separate hospitals for children, drug addicts and mentally ill
prisoners.
- Clear provisions to establish Central & State Mental Health Authorities
- Definite guidelines for license to establish or maintenance of hospital
- Definite guidelines for penalties for improper establishment and maintenance of
hospitals.
- Definite provisions or guidelines for OPD treatment facility
- Visitors board:
 Minimum 5 members
 No role in admission, care, treatment & discharge.

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  Provisions for inclusion of psychiatrist and social worker.
- Voluntary admission: Medical officer is empowered to admit voluntary patient.
- Provision for involuntary admission/under special circumstances.
- No flexible guidelines for leave of absence.
- Provision to delay discharge of voluntary patient if they need further
hospitalization.
- Specific guidelines for judicial safeguards/property management.
- Provision for protection of human rights of mentally ill patient.
- Provision for inspecting officer.

RECEPTION ORDER:
An order made under the provision of Mental Health Act for the admission and
detention of mentally ill person in a psychiatric hospital.

CENTRAL AUTHORITY FOR MENTAL HEALTH SERVICES:

- Controlled by Central Government

- Regulation, development, direction & coordination of Mental Health Services
- Supervise the psychiatric hospitals or psychiatric nursing homes and other
mental health agencies
- Advise all matters relating to central health
- Discharge matters relating to mental health
- State authority for mental health services control above matters by state
government
 Establishment & Maintenance of psychiatric hospitals or nursing homes – Sec 6
 Application for license for psychiatric hospital or nursing home – Sec 7
 Grant or refusal of license – Sec 8
 Duration and renewal of license – Sec 9
 Removal of License – Sec 11
 Treatment of outpatients – Sec 14
- Maximum duration for leave of absence is 60 days

ADMISSION & DISCHARGE PROCEDURES UNDER MENTAL HEALTH ACT

- ADMISSION ON VOLUNTARY BASIS

Request by major – Sec 15
Request by guardian (Minor) – Sec 16
Discharge Request by Major or by guardian – Sec 18 (Discharge within 24
hours of such request.)

- ADMISSION UNDER SPECIAL CIRCUMSTANCES(SEC 19)

 If mental ill patient do not or cannot give consent, medical officer. can
admit such a patient on application by relatives or friends with two
medical certificates.
 Maximum period of admission 90 days.

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 - TEMPORARY ADMISSION ORDER
 Issued by Magistrate for patient who is at risk of his or her own life or of
others.
 Only one Medical certificate is required.
 This order is valid for 6 months. (>6 months, Medical officer should apply
to the Magistrate for permission to continue the treatment under Sec 20.

- ADMISSION WITH RECEPTION ORDER

A. On Application (Sec 20); An application for a reception order may be made by

1. The relative (husband, wife, neighbor or friend) can apply to the magistrate in
written supported with two medical certificates.
2. The medical officer in charge of psychiatric hospital or psychiatric nursing.
- Every application shall be accompanied by two medical certificates
from two medical practitioners of whom one shall be a medical
practitioner in the service of government.

- Sec 21: form and contents of medical certificates.

- Sec 22: procedure upon application for reception order

B. Reception order on production of mentally ill persons before magistrate

- Sec 23: powers and duties of police officers in respect of certain mentally ill
persons. ( wandering lunatics)
- Sec 24: procedure on protection of mentally ill person
- The magistrate may pass reception order, stating the detention of the said
person as an inpatient in a psychiatric hospital.
- sec 25: order in case of mentally ill person cruelly treated or not under
proper care and control.

C. Further provisions regarding admission and detention of certain mentally ill

persons
- Sec 26: Admission as inpatient after inquisition(severe interrogation)
- Sec 27: Admission and detention of mentally ill prisoner
 Convicts-Under Sec of the Prisoner s Act .
 Under trial- Under Sec 330 of Code of Criminal Procedures.
 Cruelty but mentally ill prisoner (Under Sec 335 of Code of Criminal
Procedures.

Admission of Military Person

o Under Sec 144 of Air Force Act 1950

o Under Sec 145 of Army Act 1950
o Under Sec 143 & 144 of Navy Act 1957
-

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Admission in Emergencies

- If mentally ill patient is in danger and medical officer in charge thinks he needs
admission. The medical officer can admit the patient, but within 72 hours the
patient should be produced before the magistrate.
- If the patient cannot be shifted, the magistrate is asked to come to the psychiatric
hospital/psychiatric nursing home and get the patient examined and pass a
reception order (The magistrate may extend time period for 72 hours)

NDPS (NARCOTIC DRUGS & PSYCHOTROPIC SUBSTANCES) ACT – 1985

Naturally occurring substances are Narcotics

- Ganja
- Cocaine
- Opium
- Poppy straw

Synthetically produced substances are Psychotropics

- Heroine
- Brown Sugar
- Synthetic Opioids

- The Opium Act – 1857

- The Opium Act – 1878
- The Dangerous Drug Act – 1930
- NDPS Act – 1985

- The Opium Act exclusively with the matters related to opium.

- The Dangerous Drug act which deals with other drugs like Cannabis & Cocaine
- The maximum punishment under The Dangerous Drug act for the various
offences related to drugs is Simple imprisonment with or without fine.

NDPS Act contain 6 chapters and 83 sections

- 1st Chapter – Preliminary

- 2nd Chapter – Narcotic Authorities (State & Central)
- 3rd Chapter – Deals with prohibition, control, regulation according to Sec 8 of
NDPS Act (No person shall cultivate or consume coca, opium, and cannabis)
- 4th Chapter – Deals with offences and penalties
 Punishment for cultivation in relation to poppy straw, coca plant or leaves,
opium and cannabis.
 1st Offence – Imprisonment 10yrs (may extend upto 20yrs) and fine
rupees one lakh (may extend upto two lakhs)
 2nd or more offences – Imprisonment 15yrs (may extend upto 30yrs)
and fine rupees one and half lakh (may extend upto three lakhs)

204
  Punishment in relation to ganja and cultivation of cannabis.
 1st Offence – Imprisonment 5yrs and fine rupees fifty thousand.
 2nd or more offences – Imprisonment 10yrs and fine rupees one lakh.

 Punishment in relation to any controlled substances – Imprisonment 10yrs

and fine of rupees one lakh

 Punishment in relation to small quantities – 6 months imprisonment and

fine.

 Death penalty – For large quantities.

- 5th Chapter – Deals with procedures

- 6th Chapter – Miscellaneous

LAWS RELATING TO PSYCHIATRY IN INDIA

- Mental Health Act 1987

- Persons with Disability Act 1996
- Rehabilitation council of India Act 1992
- Juvenile Justice Act 1986
- Consumer Protection Act 1986

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 COMMUNITY PSYCHIATRY

DEFINITION: Community psychiatry is a psychiatry focusing on the detection, prevention,

and treatment of mental disorders and social deviance as they develop in the community
rather than as they are perceived and encountered at large psychiatric facilities.

Thus the first mental asylum was established in Bombay in 1745,

The second in Calcutta (1781),
The third in Madras (1794) and
The fourth in Monghyr (Bihar).

These asylums had acquired all the bad qualities and treated mentally ill at par with
criminals.

The administrative set up resembled the jail system and absence of medical personnel
contributed a lot for the dismal state of affairs in the asylums.

Adolf Meyer, in 1909, advocated management of mentally ill patient outside the
institutions and proposed a comprehensive community mental health approach in which
psychiatrists, family physicians, police, teachers and social workers would work together to
organize primary, secondary and tertiary preventive measures in the community.

Though the first General Hospital Psychiatric Department was started at Bombay and
Culcutta way back in 1933, more and more such units and departments started working in
1960s and 1970s.

In 1957, Dr. Vidya sagar, the then Superintendent of Amritsar Mental Hospital, involved the
family allowing them to stay with their patients in open tents pitched in the hospital campus

- Philippe Pinel & William Tuke – Movement against the Mentally Ill patient in the
asylum and started moral treatment which includes.
 Human Care
 Avoid physical restraint
 Better staff patient interaction
 Open door systems

CLIFFORD BEERS – Mental Hygiene Movement

INDIAN PSYCHIATRIC SOCIETY – 1939

 1960 – First Superintendents conference, mental hospitals in India.

 1963 – Community Psychiatry Movement
 1971 – Work shop on priorities in Mental Health Care
 1982 – National Mental Health program

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 NATIONAL MENTAL HEALTH PROGRAMME

o Adapted for implementation in India – 1982

o Aim: Integral part of total health programme.
o Reviews Mental Health situation: Needs, Facilities, Services

Objectives
o Availability; Accessibility of Mental Health Services
o Application of Mental Health Knowledge to General Health Care
o Promote Community Participation

Approaches
o Mental Health skills to periphery
o Appropriate tasks in Mental Health Care
o Integrate Mental Health Care into General Health Services.
o Linkage of community development and mental health care
o Service: Treatment; Rehabilitations and Prevention.

Initial Goals
o Mental Health Skill training to Medical Officers and Health Staff at PHC
o 5000 target non-medical professionals 2 week training
o 20% PHC Physician – 2 week training – 5 years
o 1 Psychiatrist post – 50% District Level
o Appropriate Psychotropic usage at PHC
o Psychiatry units with I.P Beds in all Medical College Hospitals.

Achievements
o DMHP- 25 Districts – 20 States
o Human Resource Development
o Increase Public Awareness

Legislation Supporting Mental Health Care

o NDPS Act 1985
o MHA 1987
o PDA 1995
o NHRC- recognition of Human Rights of Mentally Ill -1999
o NHP- Recognition of Mental Health as part of General Health

Barriers
o Emphasis on curative; not preventive
o Community resources – not given importance
o Poor funding (280 millions/9th plan)
o Uneven Distribution of Resources
o Non-implementation of MHA 1987
o Limited UG Training

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Restrategisation
o Redesignation – DMHP around nodal institution
o Strengthening Medical Colleges
o Streamlining and Modernizing Mental Hospitals.
o Strengthen Central & State Mental Health Authorities
o Research & Training
o Funding 1900 millions in 10th Five Year Plan

Revised Goals
o Strengthening Community and Families
o Mental Health Initiatives to support individuals and families
o Rebuilt social cohesion, community development; rights of Mentally Ill.

Plan of action
o Organizing Services- Primary Physicians and Psychotropic Drugs
o Community Mental Health Facilities
o Support to Families
o Human Resource Development
o Public Mental Health Education
o Private sector mental health care
o Support to Voluntary Organisations
o Promotion and Preventive Activities
o Administration Support.

Strategies 11th Five Year Plan

o DMHP- All Districts of all States
o Direct funding of Districts
o Private Medical Colleges as Nodal Institutions
o Training District Medical Officer in Mental Health & Administration
o Encourage Private Psychiatrists/ Practitioners in Psychiatric Care.
o Public Private Participation
o Increase Budget – 10% of total Health Budget.

IDEAS Scale:

 Indian Disability Evaluation and Assessment Scale.

 Developed by the rehabilitation committee of Indian Psychiatric Society, 2002
 Duration – Total duration of illness should be atleast 2 years.
 Disorders
 Schizophrenia
 Bipolar Disorders
 Dementia
 OCD
 Items: (4 items)
 Self Care
 Inter personal activity
 Communication and understanding
 Work

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  Scores of each item:
0 – No
1 – Mild
2 – Moderate
3 – Severe
4 – Profound
Total Score 0 – 20.
 Add Score: How many months in last two years patient exhibits symptoms.
< 6 months – Add 1
7 to 12 months – Add 2
12 to 18 months – Add 3
>18 months – Add 4

 Global Disability Score: Total Score + Add Score (Range 1-20).

 Percentage:
 For the purpose of welfare benefits 40% will be the cutoff point.
 The score above 40% have been categorized as Moderate, Severe and
Profound based on the global severity score.
Global Scores:
0 - No Disability
1-7 - Mild Disability
8-13 - Moderate
14-19 - Severe
20 - Profound

 Recertification of IDEAS – Every 2 years reassessed and recertified.

THERAPEUTIC COMMUNITY:
The treatment setting that provides an effective environment for behaviour changes
in patients through re-socialization and rehabilitation.
- Established by Maxwell Jones
- E.g., Opioid Dependence

TOKEN ECONOMY PROGRAM:

- It is derived from experimental psychology – Operant Conditioning
- The token rewards used as positive reinforcement for desired behaviour.

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 PSYCHIATRIC CASE SHEET
IDENTIFICATION DATA
 Name
 Age
 Sex
 Religion
 Address
Low
 Socioeconomic status Middle KUPPUSWAMI SCALE
High
 Occupation
 Identification marks
INFORMANT DETAILS
 Name
 Age
 Sex
 Relation to the patient
 Educational status
 How long annoyed with patient

Reliable information
 Contact (more than two contacts
 Consistency
 Credibility
 Adequacy
 Intelligence
 Verifiability

HISTORY OF PRESENT ILLNESS

Details of each and every compliant

 Onset
Acute (hours to weeks)
Sub acute (1 to 6 months)
Insidious ( > 6 months)

 Duration (total duration/ recent aggravation)

 Precipitating factor
 Direct / indirect relation to illness
 Time interval between precipitating factor and onset of illness
 Whether temporally related or not
 Reaction of the patient at the time of precipitating event

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  Course of illness
 Deteriorating
 Fluctuating
 Stable
 Improving

 Symptoms occurrences
 Throughout the day/ sometimes of the day
 When alone/ any people observing
 How it is controlled

WANDERING
 Purposeful / purposeless
 Return back alone / taken by any person
 Day time/night time/during sleep
 Is there any collection of waste material? (hoarding sign)
 Is there any disorientation at that time?
 Psychomotor activity at that time
 Personal hygiene at that time
 Is there any begging / eating road side edible material

SLEEP
 Increased/decreased/irregular
 Early insomnia
 Mid insomnia
 Late insomnia
 Day time sleeping
 Any sleep related disorders
 Sleep walking
 Sleep terror
 Nightmares
 Reaction to sleep disturbance (Distress/ decreased need of sleep)
 Premorbid sleep pattern
 Any history of epilepsy during sleep
 What are the activities during insomnia?
 Talking/ muttering to self
 Watching TV/ reading/ wandering / disturbing others …..etc.
 Is there any medication use for sound sleep?

APPETITE
 Increased/decreased
 Weight loss/gain

TREATMENT HISYORY OF PRESENT EPISODE

 Psychiatrist/physician
 Details of drugs and doses and ECT
 Compliance (reason of noncompliance)

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DAILY ROUTINE WORKS
 Personal hygiene
 Social activities
 Domestic tasks
 Leisure activities

HISTORY OF SUBSTANCE ABUSE (alcohol)

 How long
 Any episodic use (binge type/non binge type)
 Amount
 H/O early morning drinking
 H/O tolerance
 H/O withdrawal features
 H/O craving
 Social drinker/ problem drinker
 Drinking alone /with friends
 H/O legal problems during intoxication
 H/O amnesia after intoxication
 H/O alcohol related physical problems
 H/O head injury/physical injuries during intoxication
 H/O drunken driving
 H/O motivation for abstinence
 H/O behavioural abnormalities during intoxication
 H/O disturbed social, occupational, functional relations due to alcoholism
 H/O negligence of family needs due to alcohol

H/O SUICIDE
 An idea /motive to commit suicide
 Duration of suicidal ideas
 Onset of suicidal ideas
 Lethality of attempt
 Intention /plan

Assessment of suicide

(Questions related to suicidal intention)

o When did you experience suicidal thought?
o Were there any recent events that brought these thoughts?
o How often these thoughts cross your mind?
o Have you felt that you were being burden?
o Have you felt that life Is not worth living?
o What if life makes you feel better?
o What if life makes you feel worse?
o Do you have any plan to end your life?
o How much control of your suicidal ideas do you have?
o Can you supress them or call someone to help?
o What stops you from killing yourself? (Family, religion ,beliefs )

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Questions related to suicidal plan
o Do you own a gun or have access to a firearm?
o Do you have access to potentially harmful medication?
o Have you imagined your funeral and how people will react to your death?

Risk assessment(SADPILLS)
o S- Schizophrenia and other psychotic disorders
o A-Affective disorders
o D-Despair/ Hopelessness
o P-Plan/positive suicidal ideas
o I-Impulsivity
o L-Lethality of suicidal attempt
o L-Losses
o S-Substance abuse

Warning signs(IS PATH WORM)

o I-Ideation
o S-Substance abuse
o P-Purposelessness
o A-Anxiety
o T-Trapped
o H-Hopelessness
o W-Withdrawal
o A-Anger
o R-Recklessness
o M-Mood changes

Assessment of suicidal cues

Verbal cues
o They are better off without me
o The world would be a better place without me
o ) can t take it and more
o I am no good any way
o ) don t know how ) feel
Behavioural cues
o Suicidal note
o New purchase of weapon/poison/rope…etc.
o Relapse of alcohol behaviour
o Recklessness
Situational cues
o Prior history of suicidal cue
o H/O sexual abuse
o H/O recent loss
o Rapid decline of social, occupational, and functional relations
o Serious illness

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Assessment and quantification of suicidal risk
o Beck s scale for suicidal ideation
o Beck s hopelessness scale
o California suicidal risk assessment scale
o Colombia suicidal severity assessment

NEGATIVE HISTORY (rule out organic aetiology)

Head injury
How long the illness occured after head injury
Impairment of consciousness
Post traumatic amnesia
<5min----- very mild
1-hour----- mild
1-day ----moderate
1-week--- severe
1-month – very severe

Epilepsy
o Onset
o Duration of illness
o No of attacks
o Duration of each attack
o Consciousness level
o Any injuries /tongue bite
o Similar/variable attacks
o Simple/complex/generalised
o Any aura
o Post ictal confusion/behavioural problems
o Any prolonged prodromal symptoms
o Treatment details
Fever
o High grade/low grade
o Associated with chills and rigors
o Continuous/step ladder pattern
o Toxic or altered sensorium
o Any meningeal signs
o Any fits

Headache
o Onset/duration
o Continuous/intermittent
o Photophobia/phonophobia
o Unilateral/bilateral
o Nausea/vomiting
o Associated with altered sensorium
o Aggravating /reliving factors
o Any focal deficits
o Any blurring of vision

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H/O severe vomiting/diarrhoea
H/O jaundice
H/O other medical disorders

PAST HISTORY

Physical history
Any h/o chronic medical illness (DM/TB/HTN/HIV)
Mental history
H/o previous episodes
Onset
Duration
Course
Treatment response

FAMILY HISTORY
o Nuclear /joint family
o Family type
o H/o consanguinity
o Details of family members
o H/o any family stress, details of the patients reaction to that event
o H/o mental illness
o H/o alcoholism/substance abuse
o H/o suicidal deaths
o H/o DM/Epilepsy
o H/o congenital abnormalities
o Details of interpersonal relations

PERSONAL HISTORY

Mother antenatal history (fever, infections, drugs, and medical illness)

Birth history
o Preterm/term/post term delivery
o Home/hospital delivery
o Normal/CS/forceps delivery
o H/o birth asphyxia
Developmental milestones
Motor /sensory/ speech
Motor development
 Neck holding --------------- 3 months
 Sitting with support ------ 5 months
 Sitting without support--- 8 months
 Standing with support --- 9 months
 Walking with support ---- 10 months
 Crawling ------------------ ---- 11 months
 Standing without support -- 12 months

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  Walking without support ----- 13 months
 Running ------------------------- 18 months
 Upstairs --------------------------- 2 years
 Tricycle --------------------------- 3 years
 Downstairs ----------------------- 4 years
 Jumping --------------------------- 5 years

H/O Child health and adjustment Problems

Educational history
o Age at beginning of schooling
o Type of school attended
o Relationship with peers and teachers
o Any h/o truancy/ other difficulties of schooling
o Qualification achieved
o Age on leaving school
o Higher educations

Occupational history
o Age at starting work
o H/o frequent changes of job
o Performance (adequate/inadequate)
o Performance after illness started
o Duration of any period of unemployment

Sexual history
o Age at menarche/menstrual history
o Sexual orientation/Gender identity
o Masturbation/fantasies
o Relationship with members of opposite sex
o H/o any extra marital relationships
o H/o homosexual feelings/ experiences
o H/o sexual perversions
o H/o sexual abuse
o H/o pregnancies/stillbirths/BOH
o H/o menopause

Marital history
o Age at marriage
o Details of spouse
o Marital life (satisfactory/unsatisfactory)
o Sexual adjustment (satisfactory/unsatisfactory)
o Details about (pregnancies, stillbirths, miscarriages, terminations, live births)
o H/o separation or divorce

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PREMORBID PERSONALITY

Social relations
 Well maintained/not
 Leader/follower
 Aggressive type/submissive type/ambitious type
 Dependent/independent

Interests and hobbies

General mood
 Bright and cheerful
 Worrying
 Calm and relaxed
 Stable/self-depreciative

Morales and religious attitudes

Attitude to work and responsibility

Predominant trait
o Hysterical
o Hypomanic
o Cyclothymic
o Introverted
o Extroverted
o Depressive
o Dependent
o Anankastic
o Antisocial
o Schizoid
Others
o Sleep
o Food habits
o Bowel/bladder
o Fantasies

GENERAL PHYSICAL EXAMINATION

o Built and nourishment
o Anaemia/jaundice/goitre/pedal oedema
o Injuries/scars
o Any relevant history top to bottom of the body

VITAL DATA
o Temperature
o Pulse
o Blood pressure
o Heart rate
o Respiratory rate

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SYSTEMIC EXAMINATION
o CNS
o CVS
o GIT
o Respiratory system
MENTAL STATUS EXAMINATION (ABCSTPM)
APPEARANCE
o Normal
o Unkempt
o Over dressed

BEHAVIOUR
o Co-operative/not co-operative
o Eye contact (maintain/not maintain/fleeting)
o Psychomotor activity
 Normal
 Increased (restlessness/excitement)
o Rapport (communicative/emotional)
o Tics/mannerisms
o Any compulsions
o Any motor behaviour (catatonic signs and symptoms)

CONSCIOUSNESS
o Clear/fluctuations
o Drowsy
o Delirium
o Stupor
o Coma

SPEECH
o Sample of speech in patient language
Intensity
o Audible
o Soft
o Excessive/ loud
Reaction time
o Normal
o Decreased ------ Mania
o Increased ------ Depression
o Variable -------- schizophrenia
Response time
o Normal
o Decreased ------ Depression
o Increased ------ Mania
o Variable -------- schizophrenia
Productivity
o Normal
o Garrulous
o Laconic

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Pitch
o Monotonous
o Normal fluctuations
o Other abnormalities
Ease
o Spontaneous
o Hesitant
o Mute
Deviations
o Rhyming
o Punning
o Echolalia
o Neologisms
o Others
Relevant/irrelevant
Coherent/incoherent

THOUGHT EXAMINATION
Form of thought
o Dereistic thinking
o Autistic thinking
o Incoherence
o Wold salad
o Verbigeration
o Loosening of association
o Clang association
o Echolalia
o Palilalia
o Perseveration
o Stereotype
o Illogical thinking
o Concretism
o Thought block
o Condensation
o Neologism
o Asyndesis
o Metonyms
o Substitution
o Drivelling
o Desultory thinking
Stream of thought
o Pressure of speech
o Flight of ideas
o Prolexity (ordered flight of ideas)
o Circumstantiality
o Tangentiality

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Content of thought
o Overvalued ideas
o Fantasies
o Ideas of reference
o Obsessions
o Phobias
o Hypochondrical ideas
o Bizarre ideas
o Delusions
 Primary /secondary
 Systematised/non-systematised
 Partial/complex
 Simple /complex
 Type of delusion
 Reference
 Grandiose
 Control/influence
 Nihilistic
 Persecutory
 Bizarre
 Infidelity
 Guilty
 Love
 Jealousy
 Shared delusion
 Somatic
 Delusions of doubles
Possession of thought
o Thought insertion
o Thought broadcast
o Thought withdrawal
o Thought echo

PERCEPTION
o Illusions
o Derealisation
o Depersonalisation
o Déjà vu
o Jamais vu
o Hallucinations
- Auditory hallucinations
1st person: patient hears one s own thoughts thought eco/audible thought
2nd person: the voice is directly talking to the patient.
3rd person: two or more people discuss themselves about the patient.
Running commentary type.
- Visual hallucinations
- Olfactory hallucinations
- Tactile hallucinations

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 - Gustatory hallucinatory
- Others
o Somatic
o Kinesthetic
o Functional

MOOD
Subjective
Objective
o Range
o Reactivity
o Lability/incontinence
o Appropriate
o Communicable

EXAMINATION OF HIGHER MENTAL FUNCTIONS

 Attention and concentration

1. Digit span test

2. Serial subtraction test
3. Days or months forward to backward

Digit span test: Forward is attention, backward is concentration

Forward: patient is given the following instructions

 I will be saying some digits, listen carefully.
 When I finish saying them, you will have to repeat them in the same order.
 The examiner after instructing the patient.
- Give an example (for eg if i say 3,7 you say 3,7).
- Read digits at the rate of one per second to the patient.
- Note whether the immediate response of the patient is correct or not.
- The same digit should not be presented more than once.
- If the patient cannot repeat a particular number of digits on one trial, a
2nd trial with the same number of the digits is given and credit is given if
;the response is correct.
- The following digits may be used
5–7–3
5–3–8–7
1–6–4–9–5
3–4–1–7–9–6
7–2–5–9–4–8–3
4–7–2–9–1–6–8–5
Backward: patient is given the following instructions
 I will be saying some digits, listen carefully.
 When I finish saying them, you will have to repeat them in the reverse order.

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  The examiner after instructing the patient.
- Give an example (for eg if i say 3,7 you say 7,3.).
- Read digits at the rate of one per second to the patient.
- Note whether the immediate response of the patient is correct or not.
- The same digit should not be presented more than once.
- If the patient cannot repeat a particular number of digits on one trial, a
2nd trial with the same number of the digits is given and credit is given if
the response is correct.
- Same digit should not be used as for the forward test

The following digits may used

-
4–1–7
6–1–5–8
2–9–7–6–3
6–3–5–8–4–6
4 – 7 –1 – 5 – 3 – 8 – 6
9–2–5–8–3–1–7–4
Serial subtraction test
o Increasingly difficult tests are presented.
o Instruct the patient.
o Gives an example of have to perform the task.
o Notes the response verbatim and note the time taken in seconds.

TASK correct response and time limit

20 – 1 20 to 0 reversed in 15 sec
40 – 3 40, 37, 34, 31, etc. in 60 sec
100-7 100, 93, 86, 79, etc. in 120 sec

MEMORY (immediate, recent, and remote memory.)

 Immediate memory : tested by digit span test

 Recent memory : tested by

A. Address test: An address consisting of about 4-5 facts. Which is not known
to the patient is slowly read to the patient after instructing him to attend
to the examiner and is engaged in conversation and the response is noted
in verbatim. Recall is asked after 3-5 minutes.
B. Asking the patient to recall events in the last 24 hours, details of time and
amount in the meal or visitors in the hospital from in the inpatient.

 Remote memory : tested by information of life events

o Date of birth or age
o Number of children
o Name and number of family members
o Time since marriage or death of any family member
o Year of completing education
o Facts may be asked relevant to the patient is background.

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ORIENTATION
 Time
 Approximately what time of the day is it?
 Is it morning, evening, or night?
 Approximately how long is it since you had your breakfast/lunch/dinner?
 Approximately how long have I been talking to you?
 What is the day today?(day of week)
 What is the date today? (day of moth)

 Place
 What place is this?
 Is this a school, office, hospital, restaurant etc.?
 Person
 Asking the identity of patient
 )nquiring about the identity of the patient s relatives or family members

INTELLIGENCE
 This includes the areas of general information, comprehensive, arithmetic, and
vocabulary.

 General information

o )nformation relevant to the patient s literacy, age, or occupation may be

asked.

o Literates
- Name of the prime minister
- Name of the chief minister
- Capitals of countries
- Current events
o Illiterates
- Seasons
- Crops or fruits grown in particular seasons
- Price of food grains or food items
- Prices of land

 COMPREHENSION

The ability to understand questions asked during an interview is one s index.

Specifically the following questions of increasing difficulty may be asked
- What will you do when you feel cold?
- What will you do if it rains, when you start for work?
- What will you do when you miss the bus when you are on the journey?
- What will you do when you find on your way that it will be late by the time
you reach your work spot?
- Why should we be away from bad company?

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  ARITHMETIC
The following questions may be asked with increasing time units.
1. How much is 4 rupees and 5 rupees
2. I borrowed 6 rupees from a friend and returned 2 rupees, how much
do I still owe him?
3. If a man buys clothes for 12 rupees and gives a shop keeper 20 rupees,
how much change would he get back?
4. How many pencils can you buy for two rupees if one pencil costs 25
paisa?
5. If 18 boys are divided into 6 groups, how many groups will there be?

Correct answers: 1) 9, 2) 4, 3) 9, 4) 8, 5) 3
Time limit 1 to 3 ---- 15 sec
4 to 6 ----30 sec-

 ABSTRACTION
Tested by similarities, differences and proverbs.

Similarities:
The patient is given the following instructions:
I will be giving you some pair of words, you have to tell me in what way they are
alike, what is common between them or what is the similarity between them?
1. Orange – Banana (Fruits)
2. Dog – Lion (Animals)
3. Eye – Ear (Sense organs)
4. North – West (Directions)
5. Table – Chair (Furniture)
Correct responses that is Abstract responses are given in brackets. Differences being an
easier task is always presented before similarities.

Differences:
The instructions are as follows:
I will be presenting to you some pair of words, listen carefully and tell me in what
way they are different from each other?
1. Stone – Potato (Not edible – edible , Hard - Soft)
2. Fly – Butterfly (Small – Large, Not colourful – Colourful)
3. Cinema – Radio (Audio visual – Audio)
4. Iron – Silver (Heavy – Light, Dull – Bright)
5. Prize – Punishment (Positive – Negative, Pleasant – Unpleasant)

Proverbs:
Patient is asked the following questions:
1. Whether he knows what a proverb is?
2. An example of a proverb and what it means?

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If it is clear that the patient has the concept of a proverb, the following may be asked:
1. Slow and steady wins the race
2. A barking dog never bites
3. As you sow, so shall you reap
4. All that glitters is not gold or all that is white is not milk
5. Where there is a will there is a way
6. Empty vessels make more noise
7. Every potter praises his pot
8. It is useless to cry over spilt milk
The response of the patient is to be noted verbatim & the answer is judged to be correct or
incorrect

JUDGEMENT:
It is assessed in the following areas:
1. Personal
2. Social
3. Test

Personal: Judgement is assessed by inquiries about the patients future plans.

Social: Judgement is assessed by observing behaviour in social situations.

Test judgement: The following 2 problems are presented to the patient in a manner in
which he can comprehend.

1. Fire problem: In the house in which you are , catches fire,

What is the first thing you will do?

(Correct answer – Try to put it off with water)

2. Letter problem: If when you are walking on the roadside you see a stamped & sealed
envelope with an address on it which someone had dropped, what will you do?

(Correct answer – Post it in a letter box or give it to a post man)

INSIGHT:
Six Grades:
1. Complete denial of illness
2. Slight awareness of being sick and needing help but denying it at the same time
3. Awareness of being sick but blaming it on others, on external factors or organic
factors
4. Awareness that illness is due to something unknown to the patient
5. Intellectual insight, admission that the patient is ill and that symptoms or failure in
social adjustment are due to the patient s own particular irrational feelings or
distresses without applying this knowledge to future experience
6. True emotional insight. Emotional awareness of the motives and feelings within the
patient and important persons in his life which can lead to basic changes in
behaviour

** POL )NS)G(T RAT)NG SCALE

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SUMMARY:
Concise description of all the important aspects of the case to enable others who are
unfamiliar with the patient to grasp the essential features of the problem. The summary
should be presented in the same format as described in the previous pages.

DIAGNOSTIC FORMULA:
A concise description suggested towards the diagnosis, plan of management and estimation
of the prognosis.

Components of diagnostic formula – (S-A-D-F-P-P)

o Statement of Problem
o Aetiology
o Differential diagnosis
o Further investigations
o Plan of management
o Prognosis

PROVISIONAL DIAGNOSIS: Should be in ICD-10 format

- Points favouring the diagnosis
- Points not in favour of the diagnosis
-

DIFFERENTIAL DIAGNOSIS:

MANAGEMENT:

Hospitalization:
- Severe suicidal ideas
- Homicidal ideas
- Command delusions
- Severely aggressive and unmanageable patients
- For diagnostic clarification

Investigations:
Confirmative/Supportive:
 Psychological:
o Projective Tests Rorschach s
o Organic test batteries
 Neuroimaging:
o CT
o MRI
o EEG

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Routine Investigations:

Special investigations: (LFT, Renal functions, cardiac, thyroid)

- For treatment and monitoring of drugs
- For identification of medical disorders
- For functional status of vital organs

**Note:
Indications of Neuroimaging techniques in psychiatry:
- Atypical age of onset
- Atypical presentation
- Associated with focal defects
- Confusion or dementia of unknown cause
- Presence of abnormal EEG
- First episode of psychosis with unknown etiology
- Movement disorders of unknown etiology
- Prolonged catatonia
- First episode of major affective disorder
- Diagnosis of anorexia nervosa
- Associated with seizures
- Personality changes over 50 years of age
- History of alcohol or other substance abuse
- History of cerebro vascular trauma
- Impaired cognition on MSE
- Absence of family history
- Resistance to treatment

TREATMENT:

Pharmacological management:
 Acute phase
 Stabilisation phase
 Maintenance phase
Non-pharmacological management:
 Behavioural therapy
 Cognitive behavioural therapy
 Psychotherapy

Prognosis:
Good prognostic factors:
Poor prognostic factors:

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 EXAMINATION OF NON-COOPERATIVE OR STUPOROSE PATIENTS (Kirby, 1921)

The difficulty of getting information from non-cooperative patients should not

discourage the physician from making and recording certain observations. These may be of
great importance in the study of various types of cases and give valuable data for the
interpretation of different clinical reactions. It is hardly necessary to say that the time to
study negativistic reactions is during the period of negativism, the time to study a stupor is
during, the stuporose phase. To wait for the clinical picture to change or for the patient to
become more accessible is often to miss and opportunity and leave a serious gap in the
clinical observation. The following guide is devised to cover in a systematic way the most
important points for purposes of clinical differentiation.

GENERAL REACTION AND POSTURE:

a) Attitude: voluntary or passive
b) Voluntary postures comfortable, natural, constrained or awkward
c) What does the patient do if placed in awkward or uncomfortable positions.
d) Behaviour towards physicians and nurses: resistive, evasive, irritable, apathetic,
complaining.
e) Spontaneous acts: Any occasional show or playfulness, mischievousness or
assaultiveness. Defence movements when interfered with or when pricked with a pin.
Eating and dressing. Attention at bowels and bladder. Do the movements show only
initial retardation or are they consistent throughout?
f) To what extent does the attitude change? Is the behaviour constant or variable from
day to day? Do any special occurrences influence the condition?

FACIAL EXPRESSION:
Alert, attentive, placid, vacant, solid, sulky, scowling, averse, perplexed, distressed, etc. Any
play of facial expression or signs of emotional tears, smiles, flushing, perspiration. On what
occasions?

EYES:
Open or closed. If closed, resist having lid raised. Movement of eyes absent or obtained on
request, give attention and follow the examiner or moving objects, or show only fixed
gazing, furtive glances or evasion.

DEFINITIONS IN MSE:

EXCITEMENT: Agitated, purposeless motor activity influenced by external stimuli.

AGITATION: Severe anxiety associated with motor restlessness.

AGGRESSION: Forceful, goal directed action that can be verbal or physical.

PSYCHOMOTOR ACTIVITY: Motor activity correlated to psychic activity.

POVERTY OF SPEECH: Restriction in the amount of speech used.

PRESSURE OF SPEECH: Increased amount of spontaneous speech.

228
RHYMING: Identifying sounds between words or their endings.

PUNNING: Harmonious use of words with two or more meaning.

RELEVANT: Appropriate answer to question

COHERENT: Understandable speech (there is a sequential connection between one idea and
another idea.

THOUGHT: Ideational component of mental activity.

IDEA: It is a suggestion about a possible course of action.

DELUSION: False, unshakable belief that is out of keeping with the patient s social and
cultural background.

OBSESSION: Recurrent and persistent thoughts, impulse or images that are experienced as
intrusive and inappropriate. E.g. Contaminations, Repeated doubts, Orders, Impulse, Sexual
images.

COMPULSIONS: Repetitive behaviour or mental acts whose goal is to prevent or to reduce

the anxiety or distress. E.g. Hand washing, Ordering, Checking, Praying, Counting, Repeated
words.

JUDGEMENT: Ability to understand a situation correctly and act appropriately.

INSIGHT: Conscious awareness and understanding ones own psychodynamic and

symptoms of maladaptive behaviour.

MOOD: Pervasive and sustained feeling tone that is experienced internally and that, in the
extreme can markedly influence virtually all aspects of persons behaviour and perception of
the world.

MOOD CONGRUENT DELUSIONS: The content of the delusion is harmonious to the

expression of mood.

ORIENTATION: State of awareness of ones self and ones surroundings in the term of time,
place and person.

PRIMARY DELUSIONS (Autochthonous delusions):

Three components:
DELUSIONAL MOOD: Patient thinks that something is going on around him that concerns
him but he does not know what it is.

DELUSIONAL PERCEPTION: Giving a new meaning usually in the sense of self reference to a
normally perceived object.

DELUSIONAL IDEA: Sudden revelation or well formed idea appears in the thinking .

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TRANSFERENCE
Transference is the tendency we all have to see someone in the present as being like an
important figure from our past.

COUNTERTRANSFERENCE
The physician also superimposes the past on the present. This is called countertransference,
the physician transference to the patient.

Types of Countertransference

Concordant countertransference
The physician experiences and empathizes with the patient s emotional experience and
perception of reality.

Complementary countertransference
The physician experiences and empathizes with the emotional experience and perception of
reality of an important person from the patient s life.

KURT SC(NE)DER S CR)TER)A FOR SC()ZOP(REN)A

FIRST RANK SYMPTOMS:

1. Audible thoughts
2. Voices arguing or discussing or both
3. Voices commenting
4. Somatic passivity experience
5. Thought withdrawal and other experiences of influenced thought
6. Thought broadcasting
7. Delusional perception
8. All other experiences involving volition made affect and made impulse
SECOND RANK SYMPTOMS:

1. Other disorders of perception

2. Sudden delusional idea
3. Perplexity
4. Depressive and euphoric mood changes
5. Feeling of emotional impoverishment
6. … and several others as well
***For Practicals

Inj HPL 1ml = 5mg (1amp = 1ml)

Inj PHENERGAN 1ml = 25mg (1amp = 2ml)
Inj LORAZEPAM 1ml = 2mg (1amp = 2ml)
Inj DIAZEPAM 1ml = 5mg (1amp = 2ml)
Inj FLUDECON 1ml = 25mg (1amp = 1ml)
Inj FLUANXOL 1ml = 20mg (1amp = 2ml)
Inj ATROPINE 1ml = 0.5mg (1amp = 1ml)

230
Inj SCOLINE 1ml = 50mg (1vial = 10ml)
Dilution 2ml + 8ml distilled water
10ml = 100mg
1ml = 10mg
Inj PENTATHAL = 500mg vial + 20cc water
1ml = 25mg

Dosage: General ECT

Scoline 1 to 2mg/kg bd wt 0.5 to 1mg/kg bd wt

Pentathal 5 to 7mg/kg bd wt 2 to 3mg/kg bd wt

THINKING & THOUGHT DISORDER

THINKING
Refers to ideational components of mental activity, processes used to imagine , evaluate,
forecast, plan, create, and will.

Schneider suggested that there were three features of healthy thinking, which are

 Constancy:- This is the characteristic persistence of a completed thought whether or

not complication in its content.
 Organization:- The contents of thought are related to each other in consciousness
and do not blend with each other, but are separated in an organized way.
 Continuity:- There is a continuity of the sense continuum, so that even the most
heterogeneous subsidiary thoughts, sudden ideas or observations which emerge are
arranged in order in the whole content of consciousness.

Styles of thinking

• Cognitive style:-One s predominant manner of information processing and decision

making, the particular biases and distortions that thinking processes make by means
of augmenting, elaborating, or minimizing incoming information.

• Obsessional style:-of thinking is marked by attention to detail and hyper vigilance

concerning the possible implication of a particular thought or event.

• Obsessional style may be highly adaptive in certain situations, as in professions

requiring meticulous detail such as library science, computer programming, and
surgery.

• Hysterical style:-of thinking is characterized by global, diffuse, impressionistic,

emotionally laden evaluations of situations where lack of attention is given to detail
and nuances.

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Types of Thinking :-According to Freud s division

1) Primary process thinking

2) Secondary process thinking

According to non-Freudian typology

1) Fantasy thinking

2) Imaginative thinking

3) Rational or conceptual thinking

Primary process thinking:- is typically seen in dreams but also prominent in young
children and in psychotic state.

• This type of thinking disregards logic, permits contradiction to exit simultaneously,

disregards the linear notion of time, and is dominated by wish and fantasy.

• Primary process thinking represent what has been loosely and metaphorically called
right brain thinking , associate with visual image and creative thought.

Secondary process thinking:-the ability to think abstractly and to think in detail about
future plans and also characterized by predictability, coherence, and redundancy.

• Ideas follow one another in a sequence that is understandable to listener.

Fantasy thinking:-the person to escape from, or deny, reality, and can be seen in normal as
well as pathological thinking.

Everyone occasionally uses fantasy thinking when day dreaming

Imaginative thinking:-Memory in order to generate plans for the future.

Rational or conceptual thinking:-Uses logic to solve problems.

DISORDERS OF THOUGHT

1) Disorders of form of thought

2) Disorders of progression (stream)

o Disorders of productivity (volume)

o Disorders of tempo (speed)
o Disorders of direction
3) Disorders of content thought

4) Disorders of possession thought

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Disorders of form of thought

Dereistic thinking:-
o Dereism refers to digression from reality.
o Autism refers to preoccupation with fantasies, delusions and hallucinations to the
exclusion of reality.In common usage both terms are synonymous.
Incoherence:-

• The sequential connection between one idea and the next is lost so that the talk
seems to be muddled up and incoherent.

• In extreme cases the speech is full of jargon and is meaningless and is termed word
salad and verbigeration .

Word salad: - describes the stringing together of words that seem to have no logical
association.

Verbigeration:- describes the disappearance of understandable speech, replaced by string

of incoherent utterances.

Loosening of association:- flow of thought in which ideas shift from one subject to another
in a completely unrelated way.

Clang association :-Refers to a sequence of thought stimulated by the sound of a preceding

word .For example a patient with mania said, ) ll kill with a drill or a pill--God, ) m ill-what
swill

Echolalia:- the patient repeats a sentence just uttered by the examiner.

Palialia:- repetition of only the last uttered word or phrase. a symptom found most often in
pt with ch. schizophrenia.

Perseveration :- The pt continues to respond to previous question and is unable to break

free from the first response. It is commonly seen in delirium and other organic metal
disorder.

Stereotypy: - Refers to the content repetition of a phrase or a behavior in many different

settings, irrespective of context.

Concretism:- Because of the bizarreness of thinking the patient is unable to form concepts,
and to abstract common properties of a situation.

Illogical thinking: - (ere the thought is totally illogical, e.g. Ramu has a moustache. ) have a
moustache .So ) am Ramu .

Over inclusion:- Themes which are irrelevant to the context and which are only distantly
related to the main theme are included in thinking.

233
Intellectualization:- It is preoccupation with abstract and philosophical issues and riddles
which often do not carry a definite answer, e.g. a pt s preoccupation with a question why is
it that death has no death?

Condensation:- Many ideas are compressed into one or two words like a portmanteau —
two meanings packed into one word.

Neologism:-Refers to coining new words– which almost always have a private meaning
known to the patient alone. Several words are condensed to from single word.

Other formal thought disorders

 Asyndesis :- Lack of adequate connection between successive thought.

 Metonyms:- Imprecise expression or use of substitute term or phrase instead of
more exact one (e.g. for a pen –writing stick ).

 Substitution:- A major thought is replaced a subsidiary one.

 Omission:- Senseless omission of a thought or part of it.

 Fusion:- Heterogeneous elements of thoughts are interwoven.

 Drivelling:- Disorganized intermixture of constituent parts of one complete thought.

 Desultory thinking:-Speech is grammatically and syntactically correct but sudden

ideas force their way from time to time.

 Thought Blocking:- Abrupt interruption in train of thought before a thought or idea

is finished: after a brief pause, person indicates no recall of what was being said or
was going to be said (also known as thought deprivation).

 Glossolalia:- Expression of a revelatory message through unintelligible word (also

known as speaking in tongues); not considered with practices of specific Pentecostal
religions; also known as cryptolalia, a private spoken language.

DISORDER OF PROGRESSION (stream)

 Disorder of productivity:- High productivity gives rise to crowding of thought and

pressure of speech. And low productivity gives rise to poverty of ideas.

 Disorder of tempo:-
o Flight of ideas:-Here the thoughts flows each other rapidly, there is no general
direction of thinking and connection between successive thoughts appear. The pts
speech is easily diverted to external stimuli and internal superficial association.

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  )n hypomania so called ordered flight of ideas occurs in which, despite many
irrelevance, the pt is able to return to the task in hand. in this condition clang
and verbal association are not so marked and the speed of emergence of
thought is not as fast as in flight, so that this marginal variety of flight of ideas
has been called prolexity .

 In acute mania, flight of ideas can become so severe that incoherence occur,
because one thought is formulated into words another forces it way forward.
 Flight occasionally occurs in excited schizophrenics and in organic states,
especially resulting from lesion of the hypothalamus.
 Flight of ideas without pressure of speech occurs in some mixed affective
states.
Disorders of direction:-

• Circumstantiality:- Here thinking proceeds slowly with many unnecessary trivial

details but finally the point is reached.

• Tangentiality:- The person s thought wanders further and further away from the
intended point, without ever returning, so that the person may not even remember
what the original point was supposed to be.

DISORDERS OF CONTENT OF THOUGHT

 Overvalued ideas:- Abnormal beliefs, unique to the individual which dominates his
life. They differ from delusions in being less intense and less unbelievable .

 Fantasies:- Vivid imaginations with a wishful content perceived as unreal by the

individual.

 Ideas of reference:- False interpretations with a self-referential quality. All

happenings around are interpreted as having special reference to the individual.

 Obsessions and compulsions:-

• Obsessions are recurrent ideas or images or impulses that enter the person s mind
again and again in which are disturbing to him and which he tries to resist without
success.

Obsessions are perceived as his own thoughts unlike delusions of passivity

where an external agent appears to be controlling his thoughts.
However, he is unable to stop their recurring nature and their emergence
which causes severe discomfort to the pt.
Obsessions may take several forms like thoughts, ruminations, doubts and
impulses.
• Compulsions are rituals or stereotyped behavior which follows obsessive ideas is
disturbing to the pt.

235
Strange experiences:-

• Sometimes the thought contents are nonverbal experiences which the pt is unable to
recount to others.

• An example is the mystic experience with its noetic quality where the person feels
that the doors of revelation are suddenly thrown open to him.

• These may occur fleetingly in a normal individual or in religious mystics.

• Pathologically it occurs in schizophrenia and in substance abuse.

Delusions:- Irrational false unshakeable beliefs which are not shared by others, and are out
of keeping with one s educational, social and cultural background.

Classification of delusions

Parameter Type

o Depending on origin --------------------- primary and secondary

o Depending on organization ----------------Systematized and non-Systematized
o Depending on the reality value ---------- Partial and complete
o Depending on complexity ------------- Simple and complex
o Depending on the theme --------------- Grandiose, persecutory, ..etc.

Primary delusions spring up suddenly with no preceding mental events, for example, the
patient has a sudden revelation that his neighbor has plans to kill him.

Three other types of primary delusions

• Delusional percept:- The experience of interpreting a normal perception with a

delusional meaning.

• Delusional mood:-Is a state of perplexity, a sense that something odd is going on

that involves the pt, but in unspecified ways.

• Delusional memory:-The elaboration of false memories and their subsequent fixed

beliefs may assume delusional proportions.

Secondary delusions can be understood in the light of happenings which preceded the
delusion.

Systematized delusions are well organized and several interrelated belief are logically
woven into them.

Non systematized delusions are fragmented and poorly organized.

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Partial delusions are those in which the patient entertains doubts about the delusional
beliefs.

Complete delusions are those held utterly without doubt.

Simple delusions are containing relatively few elements.

Complex delusions may contain extensive elaborations of people, spirits, motives, and
situations.

Classification of delusions depending on the theme

• Theme of delusions is influenced by the pt s educational and cultural background as

well as to a great degree by the type of illness. However, a particular theme is not
specific or pathognomic of a particular disease. A pt may have several different types
of delusions at the same time.

1) Persecutory delusions:-

• They refer to the pt s conviction that he is being persecuted and harassed by others.

• He accuses them of trying to poison him or harm him through black magic, x-rays or
modern gadgets or through physical force.

• They are common in delusional disorders and in schizophrenia.

2) Delusions of references:-

• All happenings around the pt are interpreted as directed at him.

• Thus persons talking to each other, their actions or gestures, or newspaper reports
all are taken as having special significance for him.

3) Delusions of jealousy:-

• This is common in marital partnership where one member is convinced that the
other is unfaithful.

• Attempts are made to catch the partner red-handed and to exhort a confession
through persuasion or violence. Seen in Othello syndrome .

4) Delusions of love:-

• They are more common among females and involve strong convictions that a
particular male usually of a higher social background in love with her and wants to
marry her. (delusion of erotic attachment)

• This often leads to her writing amorous letters to the individual, who in fact may not
even be aware of her intensions. Seen in Declerambault s syndrome

237
5) Delusions of control:-

• The pt holds that his thoughts or actions or behavior are not his own but are those of
an external agency which controls him.

• It is common in schizophrenia.

6) Shared delusions:-

• Abnormal beliefs are shared more than one person. e.g. delusion occur in couples
(folie a deux) and in families (folie en famille).

7) Delusions of grandeur:-

• They are exalted beliefs about his self-importance –where the pt believes that he is
endowed with supernatural powers, immense wealth and other possessions.

• They are seen in schizophrenia, mania and in some organic conditions.

8) Delusions of sin and guilt:-

• These are common in depression and involve the pt s conviction that he has
committed unpardonable sins.

9) Delusions of worthlessness and poverty:-

• These are also common in depression. The pt believes that he is a ruined man, has no
worth and has no useful functions in the world.

10) Nihilistic delusions:-

• The pt holds that he is doomed and no more alive and that his organs have rotted
away. Usually seen in depression but can occur in schizophrenia.

11) Hypochondriacal delusions:-

• They are delusions of ill health and are commoner in the elderly pt and in depression
and psychosis.

• The pt believes that he has an incurable illness or grave bodily defects.

12) Somatic delusions:-

• They involve delusional beliefs of one s own body parts or the body functioning.

• They are also common in depression.

(13) Delusion of doubles:- The patient believes that someone close to him has been
replaced by an exact double. (Capgras's syndrome)

238
(14)Fregoli's phenomenon:- Strangers are identified as familiar person in the patient s life
(delusion of disguise).

(15)Bizarre delusions:- A delusion that involves a phenomenon that the person s culture
would regard as totally implausible.

(16)Nihilistic delusions:-These are beliefs that some person or thing has ceased, or is
about to cease, to exist. E.g. pt s delusion that he has no money. That the world is about to
end. these are seen in severe depression.

• Occasionally, nihilistic delusions concern failures of bodily function, often that the
bowels are blocked, and often called Cotard's syndrome .

Disorders of possession of thought

(1)Thought insertion:-

• The delusion that certain thoughts are not pt s own but implanted by an outside
agency. Often there is an associated explanatory delusion.

• For example, those persecutors have used radio waves to insert the thoughts. This
experience must not be confused with that of the obsessional pt who may be
distressed by thoughts that he feels are alien to his nature but who never doubts that
these thoughts are his own.

(2)Thought withdrawal:-

• The delusion that thoughts have been taken out of the mind.

• The delusion usually accompanies thought blocking: the pt experiences a sudden

break in the flow of thoughts and believes that the missing thoughts have been
taken away by some outside agency.

(3) Thought broadcasting:-

• The delusion that unspoken thoughts are known to other people through radio,
telepathy, or in some other way.

• Some pts also believe that their thoughts can be heard out loud by other people, a
belief which also accompanies the experience of hearing one s own thoughts spoken.

(4) Others:-Thought control, Thought echo

239
THOUGHT ABNORMALITIES IN VARIOUS PSYCHIATRY DISORDERS

SCHIZOPHRENIA:-

• Schneider s first rank symptoms:- delusional perception, thought insertion,

withdrawal, broadcasting, echo.

• Schneider claimed that five features of formal thought disorder could be isolated, viz.
derailment, omission, fusion, substitution and drivelling.

• He claimed that schizophrenics shows three types of thought disorder, viz. Transitory
thinking, Drivelling thinking, Desultory thinking. These occur separately or in
combination.

• Depending on these disorders he divides three groups, viz. Desultory group, Thought
withdrawal group and drivelling group.

Desultory group:- Affective blunting, lack of drive, somatic hallucination and

desultory thinking. Occurs in hebephrenic-paranoid or in catatonic one.

Thought withdrawal group:- Transitory thinking, thought withdrawal,

delusional inspiration, experience of passivity religious and cosmic experience
and perplexity. Occurs in paranoid schizophrenia with projection symptoms.

Drivelling group:-primary delusional experience, loss of interest in things and

values, inadequate affective responses and drivelling thinking. Occurs in
paranoid schizophrenia with systematized delusions.

• Bleuler regarded schizophrenia as a disorder of association and pointed out that the
outstanding feature of schizophrenic formal thought disorder was the lack of
connection between associations, which gave rise to changeable and unclear
concepts.

• Bleuler believed that this incompleteness of ideas was the result of condensations,
displacement and the misuse of symbols.

• In condensation two ideas of something in common are blended into a false concept,
while in displacement one idea is used for an associated idea.

• The faulty use of symbols consists in using the concrete aspects of the symbol instead
of the symbolic meaning.

• Cameron also stresses the lack of adequate connections between successive

thoughts and calls this asyndesis .

240
 • He points out that the pt uses clusters of more or less related thoughts in place of
well-knit sequences and he is unable to eliminate unnecessary material and focus on
the problem which he has to solve.

• The pt uses imprecise approximations in which some substitute term or phrase is

used instead of a more exact one.

• Cameron calls these imprecise expressions metonyms and points out that the pt
develops his own private mode of speech which is full of personal idioms.

• The schizophrenic is therefore able to generalize and shift from one hypothesis to
another, but his generalizations are too inclusive and too much entangled with
private fantasy.

• Goldstein claimed that in schizophrenia and in coarse brain disease there was loss of
the abstract attitude, so that thinking became concrete, i.e. the pt was unable to free
himself from the superficial concrete aspects of thinking.

• Goldstein held that the difference between the concrete thinking in coarse brain
diseases and schizophrenia was that in the latter condition the pt had not lost his
fund of words.

• In early stage of schizophrenia the first signs of thought disorder may appear as a
peculiar Woolliness . The pt talks about himself but uses the words in such a vague
way that it is impossible to make out what he is getting at.

Neurological conditions shows delusions

• Alzheimer's disease, vascular dementia, Huntington's disease, temporal lobe epilepsy,

and multiple sclerosis.

• They also occur in posttraumatic encephalopathy, Wilson's disease and other

degenerative extrapyramidal disorders, and brain tumors, but they are not common
in these conditions.

• Delusions are frequent in delirium. When delusions occur with focal lesions, the
injury is usually in the left or right temporo-parietal region.

• In left-sided brain lesions, delusions occur in conjunction with Wernicke's aphasia;

with right-sided lesions, prominent visual hallucinations commonly accompany the
delusional disorder.

• Delusions are most common in diseases affecting the temporal lobe cortex or the
basal ganglia, particularly the caudate nucleus. Delusions are more frequent in
disorders with bilateral than unilateral damage.

241
 DISORDERS OF PERCEPTION

SENSORY DISTORTIONS
A constant real perceptual object which is perceived in a distorted way which is the result of
a change in the intensity, quality and spatial form of the perception.

SENSORY DECEPTIONS
A new perception occurs which may or may not be in response to external stimuli.

ILLUSIONS
Misinterpretations of stimuli arising from an external object

In the illusions stimuli from a perceived object are combined with a mental image to
produce a false perception.
FANTASTIC ILLUSIONS
The patients saw extraordinary modifications of his environment.
Eg. The patient who looked in the mirror and instead of seeing his own head, he saw that of
pig.

PAREIDOLIA
In which vivid illusions occurs with out the patient making any effort. These illusions are the
result of excessive fantasy thinking and a vivid impressive visual imagery.
The subject sees vivid pictures in the fire or in the cloud, without any conscious effort on his
part and sometimes even against his will.

HALLUCINATIONS
A perception without an object has the advantage of being brief and to the point, but it does
not quite cover the functional hallucination. Definition by Esquirol s

A false perception, which is not sensory distortion or misinterpretation, but which occurs at
same time as real perceptions. Definition by Jaspers.

Jaspers distinguished between true perceptions and mental images

True perceptions
Complete
Substantial
Appears in objective space
Clearly delineated
Constant and independent on the will
The sensory elements are full are fresh
Mental images
Incomplete
Not substantial
Appears in subjective space
Not clearly delineated
Dependent on the will
Inconstant and have to be re-created
Pseudo hallucinations
Type of mental images

242
 DEFINITIONS

Abreaction
A process by which repressed material, particularly a painful experience or a conflict, is
brought back to consciousness; in this process, the person not only recalls, but also relives
the repressed material, which is accompanied by the appropriate affective response.

Abstract thinking
Thinking characterized by the ability to grasp the essentials of a whole, to break a whole into
its parts, and to discern common properties. To think symbolically.

Acting out
Behavioural response to an unconscious drive or impulse that brings about temporary
partial relief of inner tension; relief is attained by reacting to a present situation as if it were
the situation that originally gave rise to the drive or impulse.

Affect
The subjective and immediate experience of emotion attached to ideas or mental
representations of objects. Affect has outward manifestations that can be classified as
restricted, blunted, flattened, broad, labile, appropriate, or inappropriate.

Akathisia
Subjective feeling of motor restlessness manifested by a compelling need to be in constant
movement; may be seen as an extrapyramidal adverse effect of antipsychotic medication.
May be mistaken for psychotic agitation.

Akinesia
Lack of physical movement, as in the extreme immobility of catatonic schizophrenia; can
also occur as an extrapyramidal effect of antipsychotic medication.

Akinetic mutism
Absence of voluntary motor movement or speech in a patient who is apparently alert (as
evidenced by eye movements).Seen in psychotic depression and catatonic states.

Alexithymia
Inability or difficulty in describing or being aware of one's emotions or moods.

Ambivalence
Coexistence of two opposing impulses toward the same thing in the same person at the same
time.Seen in schizophrenia, borderline states, and obsessive-compulsive disorders (OCDs).

Amnesia
Partial or total inability to recall past experiences; may be organic (amnestic disorder) or
emotional (dissociative amnesia) in origin.

243
Anhedonia
Loss of interest in, and withdrawal from, all regular and pleasurable activities.Often
associated with depression.

Anosognosia
Inability to recognize a physical deficit in oneself (e.g., patient denies paralyzed limb).

Anterograde amnesia
Loss of memory for events subsequent to the onset of the amnesia; common after trauma.
Compare with retrograde amnesia.

Apperception
Awareness of the meaning and significance of a particular sensory stimulus as modified by
one's own experiences, knowledge, thoughts, and emotions.

Appropriate affect
Emotional tone in harmony with the accompanying idea, thought, or speech.
.
Blackout
Amnesia experienced by alcoholics about behavior during drinking bouts; usually indicates
reversible brain damage.

Catalepsy
Condition in which persons maintain the body position into which they are placed; observed
in severe cases of catatonic schizophrenia.Also called waxy flexibility and cerea flexibilitas.

Cataplexy
Temporary sudden loss of muscle tone, causing weakness and immobilization; can be
precipitated by a variety of emotional states and is often followed by sleep. Commonly seen
in narcolepsy.

Catatonic posturing
Voluntary assumption of an inappropriate or bizarre posture, generally maintained for long
periods of time. May switch unexpectedly with catatonic excitement.

Catatonic stupor
Stupor in which patients ordinarily are well aware of their surroundings.

chorea
Movement disorder characterized by random and involuntary quick, jerky, purposeless
movements. Seen in Huntington's disease.

Circumstantiality
Disturbance in the associative thought and speech processes in which a patient digresses
into unnecessary details and inappropriate thoughts before communicating the central idea..

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Clang association
Association or speech directed by the sound of a word rather than by its meaning; words
have no logical connection; punning and rhyming may dominate the verbal behavior. Seen
most frequently in schizophrenia or mania.

Cognition
Mental process of knowing and becoming aware; function is closely associated with
judgment.

Command automatism
Condition associated with catalepsy in which suggestions are followed automatically.

Conation
That part of a person's mental life concerned with cravings, strivings, motivations, drives,
and wishes as expressed through behaviour or motor activity.

confabulation
Unconscious filling of gaps in memory by imagining experiences or events that have no basis
in fact, commonly seen in amnestic syndromes; should be differentiated from lying.

Deja entendu
Illusion that what one is hearing one has heard previously.

Deja pens
Condition in which a thought never entertained before is incorrectly regarded as a
repetition of a previous thought.

Deja vu
Illusion of visual recognition in which a new situation is incorrectly regarded as a repetition
of a previous experience.

Delirium
Acute reversible mental disorder characterized by confusion and some impairment of
consciousness; generally associated with emotional liability, hallucinations or illusions, and
inappropriate, impulsive, irrational, or violent behavior.
Depersonalization
Sensation of unreality concerning oneself, parts of oneself, or one's environment that occurs
under extreme stress or fatigue. Seen in schizophrenia, depersonalization disorder, and
schizotypal personality disorder.

Derealization
Sensation of changed reality or that one's surroundings have altered.
Ego-alien
Denoting aspects of a person's personality that are viewed as repugnant, unacceptable, or
inconsistent with the rest of the personality. Also called ego-dystonia.

Egocentric
Self-centred; selfishly preoccupied with one's own needs; lacking interest in others.

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Ego-syntonic
Denoting aspects of a personality that are viewed as acceptable and consistent with that
person's total personality.

Formication
Tactile hallucination involving the sensation that tiny insects are crawling over the skin.Seen
in cocaine addiction and delirium tremens.

Hypnosis
Artificially induced alteration of consciousness characterized by increased suggestibility and
receptivity to direction.

Jamais vu
Paramnestic phenomenon characterized by a false feeling of unfamiliarity with a real
situation that one has previously experienced.

La belle indifference
Inappropriate attitude of calm or lack of concern about one's disability.May be seen in
patients with conversion disorder.

Labile affect
Affective expression characterized by rapid and abrupt changes, unrelated to external
stimuli.

Mood
Pervasive and sustained feeling tone that is experienced internally and that, in the extreme,
can markedly influence virtually all aspects of a person's behavior and perception of the
world.

Mood-congruent delusion
Delusion with content that is mood appropriate (e.g., depressed patients who believe that
they are responsible for the destruction of the world).

Mood-congruent hallucination
Hallucination with content that is consistent with a depressed or manic mood (e.g.,
depressed patients hearing voices telling them that they are bad persons and manic patients
hearing voices telling them that they have inflated worth, power, or knowledge).
Mood-incongruent delusion
Delusion based on incorrect reference about external reality, with content that has no
association to mood or is mood inappropriate (e.g., depressed patients who believe that they
are the new Messiah).

Mood-incongruent hallucination
Hallucination not associated with real external stimuli, with content that is not consistent
with depressed or manic mood (e.g., in depression, hallucinations not involving such themes
as guilt, deserved punishment, or inadequacy; in mania, not involving such themes as
inflated worth or power).

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 NEUROLOGY
ANATOMY OF BRAIN

 DEVELOPMENT OF BRAIN

EctodermNeural plateNeural tube

3 primary vesicles (PMR)

Procencephalon Rhombencephalon

Mesencephalon
Secondary vesicles (MM)
Secondary vesicles (TD) Midbrain

Telencephalon & Diencephalon Metencephalon Myelencephalon

RT & LT hemisphere Pons & Cerebellum Medulla

Corpus striatum Spinal cord
Thalamus and hypothalamus
Optic stalk
Pituitary stalk

 ORGANIZATION OF BRAIN
 Receptors;-specialised to react the stimulus
 Synapses;-Storage of information
 Neurons;- conduction stimulus
 Effectors;- for response

 PARTS OF NEURON
 Dendrites
 Body/soma
 Axon
 Axon terminals

 TYPES OF NEURON
 Pseudo unipolar
 Unipolar
 Bipolar
 Multipolar

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 TYPES OF GLIAL CELLS
 Oligo dendrocytes;-formation of myelin in CNS
 Schwan cells;- formation of myelin in PNS
 Astrocytes;- removal of neuro transmitters from synaptic cleft
 Microglia; scavengers(macrophages)

 STRUCTURE OF BRAIN
 Cortical;-Frontal, Parietal, Temporal, and Occipital.
 Sub cortical;-Basal ganglia and Diencephalon
 Brain stem; Mid brain, Pons, Medulla.
 Cerebellum

 FRONTAL LOBE (4 subdivisions)

 Motor area
 Supplementary motor area
 Broca s area
 Pre frontal cortex
o Orbito frontal cortex
o Medial frontal cortex
o Dorsolateral frontal cortex

Functions of frontal lobe

 Executive functions; judgement, planning and organizations
 Voluntary movements
 Language production (Lt lobe)
 Motor prosody (Rt lobe)
 Memory (working memoryleft prefrontal cortex)
 Motivation
 Learning

 TEMPORAL LOBE
 Hippocampus
 Para hippocampal gyrus
 Amygdala
 Wernicke s area
Functions
 Audition
 Language comprehension (Lt lobe)
 Sensory prosody (Rt lobe)
 Memory (medial and lateral lobe and hippocampus)
 Emotion (Amygdala)

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 PARIETAL LOBE
 Cortical sensations
o Two point discrimination
o Stereognosis
o Position sense
o Joint sense
 Visio-spatial functions(Rt lobe)
 Calculations (Lt lobe)

 OCCIPITAL LOBE
 Vision
 Visual perception

 CEREBELLUM
 Cerebellar Nucleus
o Dentate
o Globose
o Emboliform
o Fastigial
Functions
o Equilibrium
o Co-ordination of muscular activity
o Maintenance of tone
o Memory
o Speech co-ordination

 DIENCEPHALON STRUCTURES
 Epithalamus
 Subthalamus
 Metathalamus
 Thalamus
 Hypothalamus

 HYPOTHALAMUS
 Preoptic nuclei
 Supra optic nuclei
 Para ventricular nuclei
 Ventromedial nuclei
 Dorsal nuclei
 Mammillary nuclei

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 Functions of hypothalamus
 Temperature control
 Neuro endocrine control
 Appetite control
 Control of body rhythms
 Sleep control
 Memory
 Motivation
 Emotion

 LIMBIC SYSTEM (H2 CAP MN)

 H-Hypothalamus
 H-Hippocampus
 C-Cingulate gyrus
 A-Amygdala
 P-Prefrontal cortex
 M-Mammillary body
 N-Nucleus accumbens
Functions
 Emotions
 Learning
 Motivation
 Addiction
 Memory
 Sexual behaviour

 BASAL GANGLIA
 Corpus striatum
o Caudate nucleus
o Lentiform nucleus (Putamen, Globus pallidus)
 Amygdaloid body
 Claustrum
 Subthalamic nucleus
 Substantia nigra
Functions
 Control muscle tone
 Automatic movements
 Emotional expression
 Implicit memory
 Chorea  Caudate nucleus
 Parkinson s disease; -substantia nigra
 Hemiballismus;-Sub thalamic nucleus
 Athetosis Globus pallidus
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  RETICULAR FORMATION; the network of grey and white matter of medulla, pons
and midbrain.
Functions
 Somatomotor and sensory control
 Visceromotor control
 Neuroendocrinal control
 Biological rhythms
 Sleep and arousal perception

 PYRAMIDAL TRACT (UPPER MOTOR NEURON)

Pyramidal cells in area 4 of cerebral cortex

Corona radiata

Posterior limb of internal capsule

Rostral part of midbrain

Rostral end of pons

Pyramidal part of medulla

80% crossed/decussating

Ventral cortico spinal tract lateral cortico spinal tract

 EXTRAPYRAMIDAL TRACT
 Corpus striatum
 Substantia nigra
 Subthalamus
 Red nucleus
 LOWER MOTOR NEURON
 Anterior horn cell
 Nerve root
 Nerve
 Myoneural junction
 Muscle
CRANIAL NERVES

1. OLFACTORY NERVE
2. OPTIC NERVE
3. OCCULOMOTOR NERVE

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 4. TROCHLEAR NERVE
5. TRIGEMINAL NERVE
6. ABDUCENS NERVE
7. FACIAL NERVE
8. AUDITORY NERVE
9. GLOSOPHARYNGEAL NERVE
10. VAGUS NERVE
11. SPINAL ACCESSORY NERVE
12. HYPOGLOSSAL NERVE

 OLFACTORY NERVE(sense of smell)

Olfactory receptors (superior aspect of nasal cavity)

Olfactory nerve

Olfactory bulb

Olfactory tract

Primary olfactory cortex

Uncus
Hippocampal gyrus
Amygdaloid complex
Entorhinal cortex
Olfactory nerve examination

 The olfactory nerve, begin with an assessment of the patency of the nasal
breathing passages.
 The patient should occlude a nostril & demonstrate that air passes freely
through the open nostril with both inspiration and expiration. Then, the
demonstration should be repeated for the other nostril.
 The test itself involves occlusion of a single nostril while the eyes of the
patient are closed.
 The patient should inhale gently through the open nostril in close proximity to
a common odorant (e.g., vanilla, ground coffee, fresh orange, etc.).

INTERPRETATION
 The failure to detect & identify odorants (anosmia) unilaterally often indicates
damage to the central nervous system, commonly involving cranial nerve I itself, the
thalamus, the frontal lobe or connections among these structures. but peripheral
causes must be excluded.

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  Common peripheral sources of anosmia are the smoking of tobacco, colds, flues,
allergies, & the nasal consumption of cocaine.

*gadolinium-Enhanced MRI for evaluation intracranial causes of olfactory dysfunction.

 Anosmia: absence of smell

 Hyposmia: decrease sense of smell .
o Causes of hyposmia
 Congenital
 KALLMANNS SYNDROME
o Congenital hypoplasia or absent of olfactory bulb.
o Anosmia
o Hypogonodotropic hypogonadism
 Acquired causes
o Upper respiratory tract infections
o Nasal and Para nasal diseases
o Head injury
o Olfactory groove meningioma (unilateral anosmia)
o Parkinson disease
o Alzheimer s disease
o Lewy body disease
o Normal aging
o Olfactory hallucinations(uncal fit)
o Depression
o Schizophrenia
o Alcohol withdrawal
o Drug abuse (cocaine, heroin, morphine)
o Medications (carbamazepine, phenytoin, )
o Radiation

OPTIC NERVE: for sense of vision

Ganglion cell layer of internal retina

Optic nerve

Optic chiasm

Optic tract

Optic radiation

Occipital cortex

Examination of optic nerve

1) Visual Acuity
 Visual acuity refers to the visual ability to discriminate and recognize subtle
geometric variations.

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  The most common standardized test of visual acuity involves the reading of a wall-
mounted or hand-held Snellen Eye Chart. To begin the test, the patient should cover
one eye under conditions of favorable lighting.

INTERPRETATION
 The numbers recorded for each eye serves as the denominator in a ratio for which
the numerator is fixed at 20 feet or 6m. For example, an index of 20/200 indicates
that, for the tested eye, the patient can discern at a distance of 20 feet what
neurologically intact persons should be able to discern at a distance of 200 feet.

 Defects may involve the cornea, pupil, lens, fluidic media of the eye, central retina,
optic nerve, optic chiasm, and optic tract, lateral geniculate body of the thalamus,
optic radiations, or occipital pole.

2) Color Vision
 Snellen Charts may include colored spots (red, green, blue, yellow), which the
clinician may ask the patient to identify.

 Clinician may ask the patient to articulate the color of other objects that may be
available (e.g., paper, pens, books, clothes, instruments)

 More rigorous testing of color vision may involve the use of Ishihara Plates, special
graphical instruments designed specifically for the assessment of color vision.

INTERPRETATION
 When visual acuity fails, color vision also often suffers, as, from the anatomical
perspective, mechanisms that process visual detail overlap considerably with those
that process color.

 On the other hand, color vision may suffer entirely independently of deficits in visual
acuity, usually in association with sex-linked genetic defects. Specifically, individuals
may fail to express certain retinal photo pigments, leading to bilateral color
blindness.

3) Visual fields
 Visual fields reflect the portions of space that one should be able to see with each eye.
Rapid assessments of the visual fields are best achieved through the method of
confrontation.

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  To begin, the clinician & patient should face each other at close proximity. Next, the
patient should be instructed to close one eye, using the other to stare directly into the
corresponding eye of the clinician.

 While the patient maintains a fixed gaze, the clinician will move objects (e.g.,
clinicians wiggling fingers) from points behind the patient directly forward and thus
into what should correspond to portions of the visual fields of the neurologically
intact patient. The patient should be instructed to indicate verbally when the moving
objects become visible. For each eye, the clinician should assess at least six
trajectories, corresponding to clock positions of 12:00, 2:00, 4:00, 6:00, 8:00, and
10:00.

INTERPRETATION
 The failure of the patient to observe the moving objects in peripheral portions of the
visual field may reflect pathology at virtually any point throughout the visual system,
from the cornea to the anterior portions of primary occipital cortex in the vicinity of
the calcrine sulcus.

 Prechiasmatic lesions which include fractures of sphenoid bone (transecting the optic
nerve), retinal tumors, or masses compressing the optic nerve result in unilateral
blindness and unilaterally unreactive pupil (although the pupil would react with light
shown in the contralateral eye).

 Bitemporal hemianopsia (tunnel vision) can be caused by pituitary adenoma,

craniopharyngioma or saccular Berry aneurysm at optic chiasm.

 Postchiasmatic lesions are associated with homonymous hemianopsia or

quadrantanopsia depending on location of the lesion.

4) Fundus examinations
--- The pulsations of the optic vessels,
---Check for a blurring of the optic disc margin &
---Change in the optic disc's color from its normal yellowish orange
 The initial change in the ophthalmoscopic examination in a patient with increased
intracranial pressure is the loss of pulsations of the retinal vessels. This is followed
by blurring of the optic disc margin and possibly retinal hemorrhages.

Optic nerve lesions:

 Intra ocular lesions
o Primary open angle glaucoma
o Acute angle closed glaucoma
o Central retinal artery occlusion
o Branch retinal artery occlusion
o Anterior ischemic optic neuropathy
o Papilledema
o Idiopathic intracranial hypertension
o Optic neuritis
o Optic nerve drusen

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 o Congenital dysplasia of optic nerve
o Diagnosis
 Fundus examination
 Fluorescein angiography

 Orbital or intracranial lesions

o Multiple sclerosis
o Optic neuritis
o Posterior ischemic optic neuropathy
o Traumatic optic neuropathy
o Metabolic or toxic optic neuropathy
 Leber hereditary optic neuropathy
 Congenital optic atrophy
 Hypovitaminosis (folic acid, thiamine, cyanocobalamin.)
 Methanol poisoning
 Ehambutal
 Isoniazid
 Para neoplastic optic atrophy
o Compressive optic neuropathy
 Central retinal vein occlusion
 Meningioma
 Cavernous hemangioma
 Optic nerve glioma
 Thyroid related orbitopathy
 Orbital cellulitis
 Idiopathic orbital inflammation
 Optic chiasm lesions
o Bilateral hemianopia
o Pituitary adenoma
o Glioma or glioblastoma
o Craniopharingioma
 Optic tract or optic radiation or lateral geniculate body lesions
o Contra lateral homonymous visual loss
o Stroke
o Demyelination
o Metastatis
 Primary visual cortex or visual association cortex lesion
o Homonymous hemianopia
o Posterior cerebral artery occlusion
o Middle cerebral artery occlusion

OCULOMOTOR, TROCHLEAR, ABDUCENS NERVES

 Oculomotr nerve (site-midbrain)
o Ocular muscles (SO-4, LR-6)
 Medial rectus, superior rectus, inferior rectus, inferior oblique, and
levator palpebral superioris.

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 3rd nerve damage
o Diabetes
o Stroke
o Hypertension
o Trauma
o Advanced age
o Expanding berry aneurysm
o Idiopathic
o Cavernous sinus thrombosis
o Myasthenia gravis
o Tolasa-hunt syndrome: painful ophthalmoplegia due to idiopathic cavernous
sinus inflammation.
o 3rd nerve palsy + severe headache  aneurysm of posterior communicating
artery
o Isolated 3rd nerve palsy with pupillary sparing  diabetic ophthalmoplegia
o Isolated medical rectus palsy  intra nuclear ophthalmoplegia
o Lesion at red nucleus + 3rd nerve palsy  Benedict s syndrome
o Benedict s syndrome + ipsilateral cerebellar ataxia  Claude syndrome
o 3rd nerve palsy + contralateral hemiplegia Webers syndrome

 Parasympathetic pathway
3rd Nerve

Edingerwestphal nucleus (cholinergic)

Ciliary muscle (pupillary constriction)

Lens accommodation
 Hutchinson pupil: in comatose patients unilateral mydriasis due to supratentorial
intracranial pressure increased  compression of uncus of temporal lobe  uncal
herniation  compression 3rd nerve  3rd nerve palsy
 Vongraefe s sign: lid lag in hyper thyroidism.
 Pseudo Vongraefe s sign: traumatic injury of LPS leads to lid lag
 Cavernous sinus thrombosis  3rd, 4th, 6th, and ophthalmic branch of 5th nerve palsy
 Superior orbital fissure syndrome  3rd, 4th, 6th, and ophthalmic branch of 5th nerve
palsy but sudden onset and painful.
 Orbital apex syndrome  orbital pain with both internal and external
ophthalmoplegia.

 TROCHLEAR NERVE (4th nerve)

o Lower part of midbrain
o Supplies superior oblique muscle
o Causes of 4th nerve palsy
 Trauma -demyelination
 Stroke -diabetic & hypertension
 Tumor -infection & idiopathic

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  ABDUCENS NERVE (6th nerve)
o Nucleus present at inferior pons
o Supplies lateral rectus muscle
o Main abduction of eye
o Causes of 4th nerve palsy
 Trauma -demyelination
 Stroke -diabetic & hypertension
 Tumor -infection & idiopathic
 Obstructive hydrocephalus
 Myasthenia gravis
 Para median basilar artery branch occlusion
 Millard-Gubler syndrome  6th nerve palsy +crossed hemiplegia +
ipsilateral facial palsy
 Gradenigo syndrome  painful 6th nerve palsy due to mastoiditis

EXAMINATION OF III, IV, VI NERVES

1) Extra & Intraocular Muscles

 The test should begin with simple observation of the eyes. When gazing at distant
objects, the eyes of the patient should operate in tandem. At rest, neither of the eyes
should deviate from the midline horizontal position.

 The clinician should also ensure that neither of the eyelids is drooping (i.e., exhibiting
ptosis) and that the pupils are equal in size but neither markedly dilated nor
constricted. Clinician should ensure that the head of the patient is oriented vertically
and in direct opposition to the head of the clinician.

 The clinician should then place his/her finger approximately 45 cm from a point
directly between the eyes of the patient. Subsequently, the clinician should move the
tip of the finger through space, forming a large capital-H. The patient should attempt
to follow the movements of the finger with the eyes, while keeping the head fixed.

 The H should be sufficiently large as to force the eyeballs to their extremes of motion.
At the completion of the H, the clinician should return the finger to the distant central
location (i.e., directly in front of the patient).

 Then the finger should be moved towards the patient, with the target being directly
between the eyes. This causes the eyes to cross, perhaps culminating in bilateral
constriction of the pupils (i.e., accommodation-related pupillary constriction)

INTERPRETATION
 Resting deviation of the eyes

 Problems with movements of the eyes can reflect damage anywhere between cortical
motor centers (frontal or occipital) and the rostral medulla (including the
cerebellum).

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  First the persistent tendency for the eyes to drift as a pair to one side may indicate
either ipsilateral frontal (or occipital) damage or contralateral pontine damage.

 The tendency for the eyes to drift & remain down commonly reflects damage to
diencephalon or midbrain.
 Patients exhibiting a persistent upward gaze are less commonly seen, involve the
midbrain.
 Outward and slightly downward deviation of the eye often reflects damage to cranial
nerve III. along with this sign is an enlarged pupil (which responds poorly to light)
and ptosis.
 Isolated ptosis or pupillary dilation may indicate partial dysfunction of cranial nerve
III.
 Damage to cranial nerve IV tends to cause a subtle upward & inward repositioning of
the eye.
 Defects affecting cranial nerve VI commonly cause the affected eye to drift medially.
 Unilateral or bilateral ptosis may reflect defects of cranial nerve III or central or
peripheral portions of the sympathetic nervous system Diseases such as myasthenia
gravis or multiple sclerosis may be implicated.

2) Light Reflexes & Intraocular Muscles

 Pupillary responses ---light is obliquely put into one of the eyes. The clinician should
observe that, in response to the light, both pupils will constrict followed by a partial
return to pretest diameter

 The response of the pupil ipsilateral to the light is called "direct," & the response of
the pupil contralateral to the light is called "consensual." The test should be repeated
such that the clinician may observe for direct & consensual responses from both
pupils.

INTERPRETATION
 Responses to light are varied, with the full expression of light-induced pupillary
constriction indicating a functional reflex arc involving cranial nerve II (afferent) &
cranial nerve III, the critical efferent component of the parasympathetic nervous
system.

 Deficits of light-induced pupillary constriction may thus reflect defects located within
the following pathway: Cornea -- retina -- cranial nerve II -- optic chiasm -- optic tract
-- pretectal area (mesencephalon) -- posterior commissure (diencephalon) -- nucleus
of Edinger-Westphal -- superficial cranial nerve III -- constrictor pupillae muscle.

 VTH CRANIAL NERVE

o Nucleus present at pons
o Major sensory nerve of the face, mouth, nasal cavity
o Two nucleus  sensory and motor
o Sensory nucleus
 Spinal tract nucleus  pain and touch
 Principal sensory nucleus  light touch
 Mesencephalic sensory nucleus  proprioception

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  Sensory divisions
o Ophthalmic nerve: upper 1/3rd of face.
o Maxillary nucleus: forehead, medial cheek, side of the nose, upper lip, palate,
upper teeth, nasopharynx, and meninges of anterior, middle cerebral fossa.
o Mandibular nerve: lower jaw, cheek, lower lip, chin, mucus membrane of
mouth, gum, inferior teeth, ant 2/3rd of tongue, side of head, anterior wall of
external auditory meatus, external wall of tympanic membrane, and temporo-
mandibular joint.
 Motor nucleus: supplies muscles of mastication
o Masseter muscle
o Temporalis
o Medial and lateral pterygoids
o Mylohyoid
o Anteroir digastic muscle
 Lesions of trigeminal nerve
o Trigeminal neuropathy
o Stroke
o Trauma
o Malignancy
o Metastasis
o Herpes zoster infection
o (ansen s disease
o Scleroderma

 EXAMINATION OF 5TH NERVE

1) General Sensation
 During this crude test of sensation, the clinician asks the patient to close the eyes,
following which the face will be touched with the fingers corresponding to the three
trigeminal dermatomes (i.e., ophthalmic, maxillary, mandibular).

 In particular, the intention is to determine whether the stimulus is detected and

whether it is perceived as the same on both sides of the face.

INTERPRETATION
 The test may be sensitive to general losses of sensation related to unilateral or
bilateral deficits affecting the trigeminal dermatomes.

2) Sharp and Dull

 This test assesses the ability of the patient to detect a noxious tactile stimulus
applied to the face, again according to the three-dermatomal framework of the
trigeminal nerve. The clinician is to stimulate the skin (with some measure of
randomness) with either a pointed or blunt object. Comparing one side of the face
to the other, each dermatome should be stimulated with either the sharp or dull
object. After each stimulus, the patient should report whether it was experienced
as sharp or dull.
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INTERPRETATION
 Failures to report the sharp stimuli as feeling sharp should be interpreted as
failures of the nociceptive system. Exact interpretation will depend on whether
this finding occurs in isolation or along with other sensory deficits involving the
trigeminal sensory system.

 Pathology leading to deficits in this system can arise anywhere within the
pathway between the face, pons, spinal tract and nucleus of the trigeminal nerve,
trigeminal lemniscus, thalamus, internal capsule, corona radiata, postcentral
gyrus, and the parietal lobe.

3) Hot/cold
 In this instance, the stimuli used during assessments of cranial nerve V are two vials
filled with water, one hot water and the other with cold. With the eyes of the patient
closed, the clinician should bilaterally assess each of the trigeminal dermatomes at
some distance from the midline. The patient must correctly report the stimulus as
being either hot or cold.

INTERPRETATION
 The neural pathway being assessed is the trigeminal nerve, spinal tract and nucleus
of the trigeminal nerve, trigeminal lemniscus, ventral posteromedial nucleus of the
trigeminal nerve, and primary and secondary somatosensory cortices.

4) Light Touch
 The stimulus for this test is brief light stroking of the face (using a wisp of clean
cotton, with assessments made of each of the trigeminal dermatomes with
comparisons between left and right sides of the face featuring prominently. The
objective is to determine whether the patient can detect the stimulus, as indicated by
a verbal report.

INTERPRETATION
 Pathology leading to deficits in this system can arise anywhere within the pathway
between the face, pons, main sensory nucleus of the trigeminal nerve, trigeminal
lemniscus, thalamus, internal capsule, corona radiata, postcentral gyrus, and the
parietal lobe.

5) Mastication
 To test masticatory function, the clinician should place his/her thumb over the
masseteric muscles bilaterally, with the remaining fingers distributed across the
temporalis muscles. At the same time, the patient should be instructed to clench the
teeth repeatedly. The clinician should feel the muscles contract strongly.

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INTERPRETATION
 Weakness affecting the biting muscles may arise following injuries of the frontal lobe
or connections between the frontal lobe and the pons, particularly when normal or
increased muscle tone is evident. Weakness with diminished muscle tone may reflect
defects involving the pontine motor nucleus of the trigeminal nerve, the mandibular
division of the trigeminal nerve, or the muscles themselves.

Cranial Nerve VII FUNCTION -- Facial Movement and Sensation of Taste (Anterior
2/3rd of Tongue)

1) Facial Expression
 The test involves simultaneous bilateral contraction of facial muscles. On command,
the patient should be able to raise the eyebrows and wrinkle the skin of the forehead.
Next, the patient must be able to maintain closure of the eyes while the clinician
attempts to open the eyes of the patient using the thumb and forefinger.
Subsequently, the patient must puff out the cheeks without permitting air to escape
through the lips, even with mild pressure applied to the cheeks by the fingers of the
clinician. The patient must show the teeth (perhaps while smiling) and scowl or
frown.

INTERPRETATION
 Unilateral loss of strength and skill affecting the entire half of the face is often
interpreted as facial nerve palsy. Other common features of this condition are facial
asymmetries, particularly affecting the eye and the mouth, with the affected eye
commonly appearing to be open more widely than the unaffected eye. Dryness of the
eye may also lead to corneal abrasion, and the patient may find perceive sounds as
unpleasantly loud when presented to the ear ipsilateral to the affected side of the
face.

2) Gustation
 The sense of taste, as it relates to the anterior 2/3 of the tongue. To assess this
function, the patient is asked to stick out the tongue, as the clinician announces that
he/she will place something on the tongue for identification by the patient.

INTERPRETATION
 Failure of the patient to identify the substance placed on the tongue should be
followed with an additional test (using a subjectively dissimilar substance). Note that
the tongues of tobacco users may be chronically insensitive to flavor. Also, superficial
burns of the tongue (e.g., stemming from excessively hot beverages) may transiently
impair gustation.

 It is best to test the anterior 2/3 of the tongue using sweet or salty substances, with
mildly acidic substance also being acceptable but suboptimal. Bitter substances,
however, are better detected from receptors located beyond the receptive field of
cranial nerve VII (i.e., on the back of the tongue or in the deep recesses of the mouth,
even down the throat). Complementing a formal test of the gustatory sense, the
history should include questions concerning persistent sensations of taste (e.g.,
metallic) in the absence of flavorful stimuli.

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Cranial Nerve VIII FUNCTION – Audition &Balance

1) Finger Rustling
 The clinician should, repeatedly rub the fingertips against the thumb, producing a
noise. The patient should then be asked to identify the ear through which a similar
noise is heard with the eyes closed. After the patient closes the eyes, the clinician
should place his/her fingers near the ears of the patient alternately making the noise
with either, both, or neither of the hands.

INTERPRETATION
 Unilateral or bilateral failure to detect the noise are causes for concern.

2) Weber Test
 The Weber Test involves placement of the stem of a vibrating tuning fork in the
center of the forehead of the patient. The patient should be asked to indicate whether
the tone is heard and whether it is heard equally well in through both ears. As the
intensity of the vibration fades, the patient may be asked to indicate when the tone is
no longer audible. The clinician may also wish to note the rate at which the vibrating
fork loses its ability to sustain the experience of sound bilaterally during the test.

INTERPRETATION
 Although marked lateralization (the tendency for the sound to be perceived as louder
in one ear as compared to the other) suggests a lateralized defect in the auditory
system, it does not aid in the localization of the lesion. The ear to which the sound
lateralizes may, for example, may be affected by a lesion peripheral to the cochlea. In
other words, the patient in this case, may suffer from unilateral conduction deafness.
On the other hand, the nervous component of the auditory system opposite to the
lateralization of sound may be implicated in the pathology, suggesting nerve
deafness.

 Damage to the cochlea, cranial nerve VIII, or the dorsolateral rhombencephalon is

frequently implicated (unilateral damage to higher centers may also produce
asymmetrical experiences of loudness, but the effects may tend to be more subtle in
such cases).

3) Rinne Test
 The Rinne Test involves placement of the stem of the vibrating tuning fork firmly in
contact with the mastoid process.

 The clinician should time the period during which the noise remains audible to the
patient. Once the patient indicates that the noise is no longer audible, then the tuning
fork should be repositioned, with the tips of the fork placed adjacent to the external
acoustic meatus (but not in contact with the pinna).

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  The patient should once again experience the sound, and the clinician should once
again time the period during which the noise remains audible to the patient. The test
should be repeated for the opposite ear.

INTERPRETATION
 Under normal circumstances, the noise produced by the tuning fork vibrating against
the mastoid process should be audible for several seconds (e.g., 6). Also under
normal circumstances, due to the amplifying properties of the bones of the middle
ear, the noise should be audible for at least as long, once the tuning fork is placed in
air next to the external acoustic meatus. Under such circumstances, air conduction is
deemed to be greater than bone conduction (AC > BC).

 When bone conduction exceeds air conduction, then the conductive problem
suggested by the Weber test is confirmed. When bone and air conducted sound are
evident for less time than would normally be expected (given the characteristics of
the tuning fork used), then the nerve problem suggested by the Weber test is
confirmed.

Cranial Nerve IX FUNCTION -- Sensory and Motor Control of Gag Response

1) Gag
 The gag response is a protective reflex designed to eject foreign objects from the back
of the mouth and throat. To initiate the gag response, the clinician should ask the
patient to open the mouth, where after the clinician will stimulate the side of the soft
palate with a clean instrument (e.g., a tongue depressor or a swab). With stimulation
of either side of the palate, palatal muscles should contract forcefully and bilaterally.
The response should be assessed bilaterally for the purposes of comparison.

INTERPRETATION
 Normal responses bilaterally suggest that both cranial nerves IX and X are intact.
However, interpretation of abnormal responses is best deferred until the functional
characteristics of cranial nerve X have also been determined.

Cranial Nerve X FUNCTION -- Motor Control of Gag Response and Speech

Ahh!!!
 The patient should utter a prolonged "AAAAAAAAHHHHHHHHH." This should cause
the tongue to flatten, thereby revealing a symmetrically rising soft palate with
posterior and upward movement of the uvula along the midline.

INTERPRETATION
 The unilateral failure of the soft palate to rise accompanied by a contralateral
deviating uvula may indicate a unilateral vagal nerve palsy. Bilateral damage may be
expressed as a bilateral motoric deficit in this domain. Often accompanying the vagal
nerve palsy will be dysarthria and hoarseness of the voice. Normal responses on this
test accompanied by diminished gag responses implicating defects involving cranial
nerve IX. Diminished responses on this test coupled with impaired gag responses
may reflect damage involving cranial nerve X in isolation (as it is responsible for
much of the motoric component of the gag response) or in combination damage to

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 cranial nerve IX. Dysarthric conditions may also arise consequent to damage to
higher centers.

Cranial Nerve XI (Spinal Part) FUNCTION -- Shoulder Shrugging and Head Turning

Shoulder Shrugging
 The clinician should palpate the trapezius muscles bilaterally to assess bulk and tone.
Subsequently the clinician should offer resistance against the tops of the shoulders
while the patient shrugs.

 The clinician should also place the palm of one hand across the cheek of the patient,
the patient should receive instruction to rotate the head about the longitudinal axis,
with the face turning in the direction of the hand of the clinician against some
resistance. At the same time, the opposite hand of the clinician should be placed
firmly over the sternocleidomastoid muscle of interest (i.e., located opposite to the
direction of movement of the face).

INTERPRETATION
 A significant loss of muscular mass and tone may reflect defects involving cranial
nerve XI, probably accompanied by weakness. Weakness with a loss of mass may also
arise with damage to higher centers, but the loss of mass tends to be less pronounced
in such cases and may be accompanied by elevated muscle tone.

Cranial Nerve XII FUNCTION -- Movements of the Tongue

Protrusion and other Movements

 The patient should be instructed to stick the tongue straight out. The tongue held in
this position allows the clinician to visually inspect for lateral deviation abnormal
muscular mass, and aberrant movements (e.g., fasciculations). Subsequently, an
assessment should be made of lateral and vertical movements of the tongue.

INTERPRETATION
 Lateral deviation of the tongue may indicate dysfunction of either cranial nerve XII or
higher centers. A pronounced loss of muscular mass with or without fasciculations
(often ipsilateral to the side of deviation upon protrusion) tends to suggest
dysfunction of lower motor neurons. The failure of the tongue to emerge fully from
the mouth suggests bilateral involvement.

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 NEUROLOGY CASE SHEET

NAME:
AGE:
SEX:
MARITAL STATUS:
RESIDENCE:
OCCUPATION:

CHIEF COMPLAINTS:

HISTORY OF PRESENTING ILLNESS:

WEAKNESS:
 Onset
 Duration
 Progression
 Distal hand
 Difficulty in mixing food
 Holding water in the palm
 Buttoning the shirt/jacket
 Proximal hand
 Lifting weights
 Combing the hair
 Reaching objects on a high shelf
 Distal leg
 Holding chappals
 Walking on toes/heels
 Is he aware of slipping away of his chappals while walking
 Proximal leg
 Getting up from a squat
 Climbing the up/down stairs
 Trunk
 Turning in bed
 Rising up from bed

STIFFNESS/HYPOTONIA/CLONUS/OTHER MOTOR SYMPTOMS:

 Onset
 Progression
 Duration
 Any dragging of one leg?
 Crossing over of both legs?
 Back or neck pain?
 Any buckling at the knees?
 H/o cramping, especially early morning in bed?
 H/o clonus – vibration of the foot on the ground?

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  H/o twitching of muscles – fasciculation?
 Any thinning of limbs?
 Wasting of hands/feet? Unilateral or Bilateral

SENSORY SYMPTOMS:

 Positive phenomena
 Tingling
 Paresthesias
 Dysesthesias
 Hyperparthia
o Band like sensation (Posterior column)
o Burning (Spinothalamic)
 Negative phenomena
 Numbness
 Feeling of clothes on the body?
 Loss of hot/cold water sense?
 Loss of mosquito bite sense?
 Not aware of slipping of chappals?
 Ascending Paresthesias? (Extramedullary)
 Descending Paresthesias? (Intramedullary)
 Sacral Sparing?
 Root pains?
 Girdle like sensation?
 Funicular pains?
 Hermite Sign?
 Cotton wool sensation?
 Washbasin attacks?

AUTONOMIC SYMPTOMS
 Bladder symptoms
 Hesitancy?
 Urgency?
 Retention?
 Overflow?
 Incontinence?
 Able to sense full bladder?
 Bowel – Incontinence? Constipation?
 Impotence? Retrograde ejaculation?
 Postural dizziness?

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HMF SYMTOMS

 Signs of raised ICT –

 Headache, nausea, vomiting, blurred vision

 Seizures?
 Altered sensorium?
 Memory impairment?
 Behavioral changes?
 Emotional liability?
 Loss of speech output?

CRANIAL NERVE SYMPTOMS

 Loss of smell?
 Blurring of vision:
 Sudden/Gradual
 Painful/painless?
 Night/day blindness?
 Photophobia
 Double vision:
 Mono/bi ocular
 Direction in which seen
 Worse with near/distant vision?
 Associated with drooping of eyelid?
 Retro-orbital pain?
 Any difficulty in climbing downstairs?
 Difficulty in chewing a food bolus?
 H/o of facial asymmetry
 Difficulty in closing the eyes?
 Drooping of the angle of mouth?
 Holding air in the cheeks?
 Sealing lips?
 Taste impairment?
 H/o hearing difficulty:
 Unilateral/bilateral?
 Tinnitus or vertigo?
 Any ear discharge?
 In case of vertigo:
 Onset
 Severity
 Illusion of spin?
 Continuous or intermittent?
 Frequency and timing of attacks?
 Precipitating factors – Head movement/Body position change?
 Change in voice – Nasal/Hoarse?

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  Any Dysphagia:
 Liquids/Solids
 Intermittent/Continuous?
 Nasal regurgitation of feeds? Any chocking episodes?
 Any Dyspnea or Stridor?
 Any difficulty coughing?
 Any difficulty in neck movements? Able to shrug the shoulders? Any dropping of the
head forwards/backwards
 Any difficulty in manipulating the food, bolus in the mouth? Any difficulty in
removing the food between the cheeks and the teeth on any side?

CEREBELLAR SYMPTOMS:

 Any shaking of the hand while holding a glass of water in either hand? Or difference
in getting the food bolus to the mouth?
 Any swaying of the body while walking? To which side? Is it worse in the dark?
Describe the way he walks?
 Any slurring of speech?
 Handwriting change?

MENINGEAL SYMPTOMS

 Any neck stiffness?

SPINE / CRANIUM SYMPTOMS:

 Headache:
 Site
 Onset
 Character
 Radiation
 Associated features
 Timing
 Exacerbating and relieving factors
 Severity
 Neck pain (same as headache) especially is the pain increasing on
coughing/sneezing/straining at stools?
o Increased on walking (Disc)
o Increased on resting (Tumor)
 Back pain (same as headache). Any morning stiffness?
 H/o Neurological claudication – In Cauda equina case

HISTORY FOR ETIOLOGY

 H/o fever/weight loss/hemoptysis/cough/expectoration etc.

 H/o trauma?
 H/o rash & arthralgia for ATM/GBS case c/o SLE
 H/o drug/toxin exposure? E.g. Intake of kesari dhal
 (/o STD s

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  H/o dog bite?
 H/o vaccination with older type of Rabies vaccine?
 H/o electrical shock
 H/o tick bite
 H/o radiation exposure
 H/o recent diphtheria (<2 weeks)

PAST HISTORY

 H/o similar complaints in the past

 H/o DM/HTN/TB/Epilepsy/Asthma/Stroke/CAD
 H/o previous operations and hospitalizations
 H/o previous operations and hospitalizations
 H/o spinal operations/anesthesia – Important in Cauda Equina case

FAMILY HISTORY

 Product of consanguinity?
 Siblings? Children? Parents? – Any H/o illness in the family?
 Pedigree chart

PERSONAL HISTORY

 Diet – Mixed?
 Appetite
 Sleep – Normal or disturbed?
 Habits
o Chews tobacco/smoke – chutta/cigarettes – Packs? Years? Alcohol intake?
 Menstrual history
o Age of Menarche? Cycles? Duration? Associated Dysmenorrhea?
Oligo/Polymenorrhea?
 Obstetric history
o Last child birth
o P-L-A
o H/o birth complications?

TREATMENT HISTORY

 Any drug? Procedure?

GENERAL EXAMINATION

 BUILT
 NOURISHMENT
 PALLOR ICTERUS
 CYANOSIS
o Central or Peripheral

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  CLUBBING
o Grade
o Unilateral/Bilateral
o Painful/Painless

 LYMPHADENOPATHY
o Site
o Size
o Surface
o Skin
o Consistency
o Tenderness
o Temperature
o Fixity
 EDEMA
o Pedal / Sacral
o Localized / Generalized – Important in paralysis case

VITALS

 PULSE
o Rate
o Rhythm
o Volume
o Character
o Condition of vessel wall
o Radio-radial or Radio-femoral delay
o All peripheral pulses felt
o Any pulse deficit

 BLOOD PRESSURE
 Important in autonomic neuropathy
 Take upright BP in GBS case
 Right unilateral – Supine
 RESPIRATORY
 Important in Cord injuries above C4
 SBC
 Chest expansion
o Rate
o Rhythm
o Type – Thoracic/Abdominal/Paradoxical?
o Depth – Shallow / Deep?
 TEMPERATURE

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OTHER SIGNS

 ANY TROPHIC ULCERS / BED SORES?

 PERIPHERAL STIGMATA OF TB
 PERIPHERAL NERVE THICKENING
o Great auricular nerve
o Ulnar nerve at elbow
o Radial nerve and Median nerve
o Common peroneal nerve
o Posterior tibial nerve at medial malleolus
 NEUROCUTANEOUS MARKERS
 MARKERS OF CONGENITAL DISEASE

SYSTEMIC EXAMINATION

 HANDEDNESS
 HIGHER MENTAL FUNCTIONS

MMSE: By Folstein s

 Orientation to Time – Day, Date, Month, Season, Year? – (5)

 Orientation of Place – Country, State, City, Hospital, Floor – (5)
 Registration – Name 3 objects – (3)
 Attention and Calculation – Serial 7s – (5)
 Recall – (3)
 Language:
o Name a pencil and watch – (2)
o Repetition – No ifs and Buts – (1)
o 3 step command – (3)
 Take the paper in Right hand
 Fold it into half
 Place it on the ground
o Read and obey sentence – (1)
o Write a sentence – (1)
o Copy design –(1)

SPEECH:

 Articulation
 Spontaneous speech – fluency
 Comprehension
 Repetition
 Naming
 Reading
 Writing

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CRANIAL NERVE EXAMINATION

1. OLFACTORY: Subjective

2. OPTIC:

 VISUAL ACUITY
o Distant vision at 6m
o Near vision at 35.5cm
 COLOUR VISION
 VISUAL FIELD – By Confrontation method
 FUNDUS

3. OCCULOMOTOR
4. TROCHLEAR
6. ABDUCENT

 ANY OCULAR MISALIGNMENT

 POSITION OF GLOBE IN ORBIT
 LID POSITION AND WIDTH OF PALPEBRAL FISSURES
 CORNEA / CONJUNCTIVA / SCLERA / IRIS
 PUPILS
o Size
o Shape
o Equality
o Position
o Reflexes
 Light – Direct / Consensual
 Accommodation
o Other reflexes
 OCULAR MOTILITY – Imp in GBS with MF variant
o Fixation
o pursuit movements
 NYSTAGMUS
o Direction of the movement that produces NYSTAGMUS
o Fine / coarse
o Horizontal / Vertical / Rotatory
o 1/2/3 degree
o Any fatigability/ latency / adaptability
o Effect of fixation / head shaking

5. TRIGEMINAL

 MOTOR
o Inspection
o Palpation
 SENSORY
 REFLEXES

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7. FACIAL: Most commonly affected in GBS.

 MOTOR
o Inspection
o Palpation
 TASTE
 SECRETORY
 REFLEXES

8. ACOUSTIC or AUDITORY NERVE

 COCHLEAR PART
o Whisper voice, ticking watch, finger rub
o Rinne s test
o Weber test
 VESTIBULAR PART
o Finger to target test
o Caloric test
o Fukuda s stepping test

9. GLOSSOPHARYNGEAL 10. VAGUS NERVE

 MOTOR – Movement with phonation

 SENSORY
 REFLEXES
o Gag reflex
o Salivary reflex

11. SPINAL ACCESSORY

 Sternomastoid
 Trapezius

12. HYPOGLOSSAL

 Tongue size / Fasciculation s

 Movement and power of tongue
 Percussion myotonia

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MOTOR SYSTEM

ATTITUDE

BULK
 Inspection and Palpation
 Measurements
o Upper limbs
o Lower limbs

TONE
 Upper limbs
 Lower limbs

POWER

 NECK
o Flexion
o Extension in prone
 SHOULDER
o Abduction
o Adduction
o Internal rotation
o External rotation
o Flexion
o Extension
 ELBOW
o Flexion
o Extension
o Supination
o Pronation
 WRIST
o Flexion
o Extension
 FINGERS
o Flexion at DIP, PIP, MCP
o Extension at DIP, PIP, MCP
o Adduction – Card test
o Abduction
 HYPOTHENAR MUSCLES
 THENAR MUSCLES
o Extension – Terminal phalynx, proximal phalynx
o Flexion – Terminal phalynx, proximal phalynx
o Abduction – Pen test
o Adduction – Card test
o Opponens
 THORAX
o Diaphragm – Sniff test, Paradoxical movements

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  ABDOMEN
o Beevor s sign
 SPINE
o Extension in prone
o Flexion

 HIP
o Flexion
o Extension
o Abduction
o Adduction
o Internal rotation in prone
o External rotation in prone

 KNEE
o Flexion in prone
o Extension
 ANKLE
o Plantar flexion
o Dorsiflexion
o Inversion
o Eversion
 FOOT/TOES
o Extension
o Flexion

INVOLUNTARY MOVEMENTS
REFLEXES:

 SUPERFICIAL
o Corneal
o Conjunctival
o Abdominal – Upper & Lower
o Cremastric
o Planter
 DEEP
o Jaw jerk
o Biceps
o Brachioradialis
o Triceps
o Finger flexion
o Knee
o Ankle

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  RELEASED REFLEXES
o Glabellar tap
o Snout reflex
o Rooting / Sucking reflex
o Palmomental reflex
o (offman s sign
o Wallenberg s sign

SENSORY EXAMINATION

PRIMARY:
 Touch
 Joint sense – (>15O)
 Position sense
 Vibration – (128Hz Distal, Proximal)
 Pain – Superficial, Deep (muscular) – (Calf muscle tenderness is an important sign in
Polyneuropathy)
 Temperature – (At 300 &440)
 Rhomberg s test
SECONDARY / CORTICAL:

 Two point discrimination – (>2mm separation)

 Tactile localization
 Stereognosis
 Graphesthesia
 Test for sensory inattention/neglect

CEREBELLAR SIGNS

1. Titubation
2. Nystagmus
3. Scanning dysarthria
4. Finger nose test
5. Finger to finger test
6. Intention tremor & past pointing
7. Decomposition
8. Dysdiadochokinesias
9. Rebound phenomenon
10. Truncal ataxia
11. Stance ataxias & Gait ataxia with lateropulsion
12. Hypotonia
13. Pendular knee jerk
14. Heel to shin test
15. Toe to finger test
16. Tandem walking
17. Isometrataxia

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GAIT:

 Straight line walking

 Tandem walking

SIGNS OF MENINGEAL IRRITATION:

 Neck stiffness
 Kernig s sign
 Brudenzki s sign

SPINE AND CRANIUM

 Tenderness / Deformity
 Straight Leg Raising Test (SLRT)

FINAL DIAGNOSIS:

Anatomy, Pathology, Etiology

*** Important points

APHASIA: Disturbance in the comprehension or production of language in written or

spoken form

DYSPHASIA: Difficulty in speech

DYSARTHRIA: Difficulty in articulation.

AGRAPHIA: Inability to write.

ALEXIA: Inability to read

DYSLEXIA: Difficulty to read.

APHONIA: Total loss of production of voice.

EC(OLAL)A: Repetition of examiner s words.

PALILALIA: Repetition of terminal words of his/her own speech.

SPEECH AREAS:
BROCAS AREA:
 Area 44
 Motor speech area
 Production of speech but no repetition
 Inferior frontal gyrus
 Maintain rhythm and fluency of speech
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  Damage:
o Expressive aphasia
o Motor aphasia
o Brocas aphasia
o Non fluent aphasia
 Comprehension is present
WERN)CKE S AREA:

 Area 22
 Sensory speech area
 Comprehension of speech but no repetition
 Superior temporal gyrus
 Damage:
o Wernicke s aphasia
o Sensory aphasia
o Receptive aphasia
o Impairment of comprehension
o Fluent aphasia
o Jargon aphasia
o Neologisms

CONDUCTIVE APHASIA
 Lesion in arcuate fascicles
 Loss of repetition with intact comprehension and outflow

TRANSCORTICAL SENSORY APHASIA

 Wernicke s aphasia with intact repetition

TRANSCORTICAL MOTOR APHASIA

 Brocas aphasia with intact repetition.

GLOBAL APHASIA
 Both Wernicke s and Brocas aphasia.
 Lesion in Middle cerebral artery or left internal carotid artery.

NOMINAL APHASIA
 Impairment in naming.
 Lesion in angle of gyrus.

DYSARTHRIA

Difficulty in articulation. Three types:

 SPASTIC DYSARTHRIA – Pseudo bulbar palsy and Motor neuron disorder

 EXTRA PYRAMIDAL DYSARTHRIA – Parkinsonism
 CEREBELLAR DYSARTHRIA – Alcohol intoxication, Multiple sclerosis, Phenytoin
toxicity.

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CRANIAL NERVE PALSY SITE OF LESION

Unilateral 5th, 7th& 8th - Cerbello-pontine angle

Unilateral 3rd, 4th, 5th& 6th - Cavernous sinus
Unilateral 9th, 10th& 11th - Jugular foramen
Bilateral 10th, 11th& 12th - Bulbar palsy
Pseudo bulbar palsy
3rd nerve palsy +
Contralateral hemiplegia - Mid brain
6th& 7th nerve +
Contralateral hemiplegia - Pontine lesion
9th, 11th& 12th +
Contralateral hemiplegia - Medullary lesion

THANK YOU FOR READING & ACCEPTING

DR. S. Nagaraju .M.D(psych)

Assistant professor of psychiatry
Govt. Hospital for Mental Care
Visakhapatnam
Mail: drnaag.sanjeevini@gmail.com

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