Psychi

Concept Based Learning
Video Companion on Each Chapter
Next GeNeratioN
Comprehensive review series
“PSYCHIATRY”
Active Recall Based
Integrated Edition
Published by Delhi Academy of Medical Sciences (P) Ltd.
HEAD OFFICE
Delhi Academy of Medical Sciences (P.) Ltd.
4-B, Grovers Chamber, Pusa Road,
Near Karol Bagh Metro Station,
New Delhi-110 005
Phone : 011-4009 4009
http://www.damsdelhi.com
Email: info@damsdelhi.com
ISBN : 978-93-89309-23-2
First Published 1999, Delhi Academy of Medical Sciences
© 2021 DAMS Publication

All rights reserved. No part of this book may be reproduced or transmitted in any form or by any
means, electronic, mechanical, including photocopying, recording, or any information storage and
retrieval system without permission, in writing, from the author and the publishers.
This book contains information obtained from authentic and highly regarded sources. Reprinted
material is quoted with permission. Reasonable efforts have been made to publish reliable data and
information, but the authors and the publishers cannot assume responsibility for the validity of all
materials. Neither the authors nor the publishers, nor anyone else associated with this publication,
shall be liable for any loss, damage or liability directly or indirectly caused or alleged to be caused
by this book.
Neither this book nor any part may be reproduced or transmitted in any form or by any means,
electronic or mechanical, including photocopying, microfilming and recording, or by any
information storage or retrieval system, without permission in writing from Delhi Academy of
Medical Sciences. The consent of Delhi Academy of Medical Sciences does not extend to copying
for general distribution, for promotion, for creating new works, or for resale. Specific permission
must be obtained in writing from Delhi Academy of Medical Sciences for such copying.
Trademark notice: Product or corporate names may be trademarks or registered trademarks, and are
used only for identification and explanation, without intent to infringe.
Typeset by Delhi Academy of Medical Sciences Pvt. Ltd., New Delhi (India).
Contents
Chapter 1 General Psychiatry 01 – 17
Chapter 2 Schizophrenia and Other Psychotic Disorders 18 – 39
Chapter 3 Mood Disorders 40 – 65
Chapter 4 Neurotic Disorders 66 – 83
Chapter 5 Organic Mental Disorders 84 – 98
Chapter 6 Substance Use Disorders 99 – 124
Chapter 7 Child psychiatry 125 – 136
Chapter 8 Sleep, Eating, Sexual
and Personality disorders 137 – 151
Chapter 9 Psychology, Psychotherapy
and Community Psychiatry 152 – 179
Chapter 10 Psychopharmacology 180 – 207
1 General Psychiatry
CONCEPTS
Â Concept 1.1 Classification in Psychiatry
Â Concept 1.2 Epidemiology of psychiatric disorders
Â Concept 1.3 Examination in psychiatry and basic

Terminologies
2 | Psychiatry
Concept 1.1: Classification in Psychiatry
LEARNING OBJECTIVE: To identify basic differences between 2 major systems of
classification in psychiatry.
Time Needed
1 reading
st
15 mins
2 look
nd
10 mins
ICD-10 DSM IV TR
(International (Diagnostic and statistical manual)
Classification of Diseases)
Disorders covered All Mental disorders
Published by WHO APA (American Psychological Association)
Commonly used as 3 axis (research domain Multi-axial approach
criteria) AXIS I: Clinical Psychiatric Diagnosis
I: Primary diagnosis AXIS II: Personality Disorders and Mental Retardation
II: Disabilities AXIS III: General Medical Conditions
III: Contextual factors AXIS IV: Psychosocial and Environmental Problems
AXIS V: Global Assessment of Functioning: Current
and in past one year
There are three major purposes of classification of psychiatric

disorders: (Ref : Niraj Ahuja) (NEET PG Q)
1. To enable communication regarding the diagnosis of disorders,
2. To facilitate comprehension of the underlying causes of these disorders, and
3. To aid prediction of the prognosis of psychiatric disorders.
Points to Remember:
1) DSM 5 is latest DSM, which does not recommend multi-axial approach to
diagnosis
2) There is no GAF score (Axis 5) in DSM 5, it rather uses WHO-DAS (WHO
Disability assessment scale)Q.
General Psychiatry | 3
Concept 1.2: Epidemiology
LEARNING OBJECTIVE: To be able to answer questions related to prevalence of
psychiatric disorders.
Time Needed
1 reading
st
10 mins
2 look
nd
5 mins
MENTAL HEALTH CENSUS

Census (Kaplan Textbook 10th edition)
Mental Health Census
Disorder Lifetime Disorder Lifetime
Prevalence (%) Prevalence (%)
Any anxiety disorder 28.8 Mood disorder 20.8
Panic disorder 4.7 Major depression 16 6
Agoraphobia without panic 1.4 Dysthymia 2.5
Specific phobia 12.5 Bipolar 1 or 11 3.9
Social phobia 12.1 Impulse-control disorder 24.8
Generalized anxiety disorder 5.7 Oppositional-defiant disorder 8.5
Posttraumatic stress disorder 6.8 Conduct disorder 9.5
Obsessive-compulsive 1.6 Attention-deficit hyperactivity 8.1
Separation anxiety 5.2 Intermittent explosive 5.2
Substance disorder 14.6
Alcohol abuse 13.2
Alcohol dependence 5.4
Drug abuse 7.9
Points to Remember:
(Psychiatric Epidemiology) (Ref: Kaplan textbook)
1) All answers to questions asked related to prevalence of psychiatric disorders,
should be as per above stated mental health census data (most reliable, 2003
data, published in Kaplan)
2) As a group Any Anxiety Disorder (28.8) > Mood Disorders (20.8), but if
individually asked than major depressive disorder (16.6) carries highest
prevalence.
3) Most DALY lost is due to depressionQ.
4 | Psychiatry
Concept 1.3:
LEARNING OBJECTIVE: To be able to understand basic psychiatric terminologies,
identify symptoms.
Time Needed
1 reading
st
60 mins
2 look
nd
30 mins
EXAMINATION IN PSYCHIATRY AND BASIC TERMINOLOGIES TO

REMEMBER (Ref: Kaplan synopsis of psychiatry)
A complete psychiatric work up of the patient needs to have following: (History +
Examination)
I. Psychiatric History:
A. Identification Data
“A comment should be made regarding the reliability of the information provided.
The reliability of the information provided by the informants should be
assessed on the following parameters: (AIIMS)
1. Relationship with patient,
2. Intellectual and observational ability,
3. Familiarity with the patient and length of stay with the patient
4. Degree of concern regarding the patient.”
B. Chief complaints
It is important to use patient’s own words and to note the duration of each
presenting complaint. Some of the additional points which should be noted include:
1. Onset of present illness/symptom.
2. Duration of present illness/symptom.
3. Course of symptoms/illness.
4. Predisposing factors.
5. Precipitating factors (include life stressors).
6. Perpetuating and/or relieving factors.
C. History of present illness
D. Past psychiatric and medical history
E. Family history
F. Personal history: Personal history can be recorded under the following
headings: (AIIMS)Q
Perinatal History
Childhood History.
Educational History
Play History
Puberty
Menstrual and Obstetric History
Occupational History
Sexual and Marital History
II. Mental Status Examination:
A. Appearance and Behavior
1. Personal identification
2. Behaviour and psychomotor activity
Motor activity (conation): This is the capacity to initiate action or motor
activity as expressed thought one’s behavior.
Hyperactivity means an increased motor activity. The activity may be goal
directed or purposeless. This may interfere with assessment and interviewing.
Hyperactivity seen in patients with mania is associated energy and is purposeful
but may not appear so, as the patient may be engaged in too many activities at
one time.
Increased activity seen in catatonia is purposeless and frenzied. Patients avoid
social contact and may have other associated abnormal movements such as
gesticulations, posturing.
Hyperactivity seen in attention-deficit hyperactivity disorder is more of
restlessness making it difficult for the patient to sit quietly.
StereotypiesQ are repeated movements that are regular and have in obvious
significance.
Mannerisms are also repeated movements but appear to have some functional
significance.
At some point of time, these movements must have been purposeful but now
have become stilted and distorted. For example, a smile turned into a grimace
with lips everted and nasal flaring.
Tics are irregular repeated movements involving, a group of muscles. For
example, nose sniffing, raising of one shoulder. (At times tics can be habit
forming also)Q
Psychomotor agitation is the restlessness associated with anxiety or irritability.
Patient may pace up and down, fidget in his seat or constantly wring his hands.
Psychomotor retardation is the profound slowing of thought process and
motor activity. Speech seems to be slow, monotonous and effortful and the
patient may sit motionless.
Catato‑nic symptoms include stupor i.e. markedly reduced reactivity to
the environment and reduction of spontaneous movements. This is typically
accompanied by muteness. However, a patient may be only mute i.e. not
speaking at all but moves around.
Posturing is the adoption of unusual bodily postures for unusually long time.
Waxy flexibility is a form of compliance in which the patient’s limbs can be
placed in any position and patient retains the position without being asked to do
so. The increased muscle tone feels like wax.
Echopraxia is the imitation of the others’ movements automatically even when
asked not to do so.
Echolalia is the imitation of others’ speech.
Ambitendency is evident hesitation to carry out the requested movement. For
example, when a hand is proffered to shake, the patient extends his hand and
then withdraws and the cycle is repeated many a time.
6 | Psychiatry
Negativism is the automatic resistance to all requests. It may be passive (e.g.
not protruding the tongue when requested to) or active i.e. doing the opposite
of what is requested (e.g. tightly clenching the jaw when asked to show the
tongue).
3. General description
B. Speech:
Rapid, slow, pressured, hesitant, emotional, monotonous, loud, whispered,
slurred, mumbled, stuttering, intensity, pitch, ease, spontaneity, productivity,
manner, reaction time, vocabulary, prosody(flow)
Emotion: It is a complex feeling state related to mood and affect, with psychological,
somatic and behavior components.
C. Mood and affect
1. Mood (a pervasive and sustained emotion that colours the person’s
perception of the world): How does patient say he or she feels; depth,
intensity, duration, and fluctuations of mood ; depressed, despairing, irritable,
anxious, terrified, angry, expansive, euphoric (normal mood), empty, guilty,
awed, futile, self-contemptuous, anhedonic (lack of interest in previously
pleasurable activities), alexithymic (inability to express emotions)
Mood: It is a pervasive and sustained emotional state.
f Euthymic mood: normal range of mood.
f Dysphoric mood: an unpleasant mood.
f Irritable mood: easily angered and annoyed.
f Euphoric mood: subjective sense of well-being and joy.
f Expansive mood: feelings expressed without restraint.
f Elated mood: feelings of joy and confidence associated with increased motor
activity.
f Exaltation: elation with feelings of grandeur.
f Ecstasy: feelings of intense rapture.
f Depression: sadness with a distinct quality.
f Anxiety: feeling of apprehension without apparent reason.
f Apathy: dulled emotional state associated with indifference.
Affect (the outward expression of the patient’s inner experiences) :
Objective assessment
Affect: It is the immediate emotional state and has outward manifestations.
f Appropriate affect: emotions in harmony with the associate idea or speech.
f Inappropriate affect: it is the incongruency between the affect and the
emotional state or the associated idea reported. This does not refer to an
affect that is socially inappropriate. For example, someone smiling at the
failure of his rival may be socially inappropriate but it is congruent to the
feeling inside. By contrast, someone crying while reporting the feelings of
joy shows incongruency between the affect and the inner emotional state
reported.
f Labile affect: rapid changes in the feeling tone unrelated to external stimuli.
f Emotional incontinence: in the involuntary and uncontrollable display of
emotions not in the keeping with the inner feelings. Persons with emotional
incontinence recognize the loss of control which is lacking in patients with
inappropriate affect.
f Blunted affect: is characterized by the severe reduction in the intensity and
reactivity of the externalized feeling tone.
f Flat affect: is characterized by the absence of signs of affective or emotional
display.
D. Thinking and perception
1. Form of thinking : neologisms (coining new words), loose associations
(the ideas expressed seem unrelated and idiosyncratically connected)
Incoherence (word salad): represents a disturbance of syntax so that the
sentences lack cohesiveness and are grammatically incorrect leading to a
meaningless whole.
Derailment (loosening of associations): is slow and progressive digression
from the original topic. The topics are not related to each other. However, the
chunks of speech covering various topics are syntactically correct and are
meaningful. For example, a person is asked about his family. He starts with the
number of family members and who they are but moves onto the description of
city he studies in, to the weather and then to the automobiles and so on, giving
some details for each topic before moving on to next topic.
Neologism: is the invention of new words or giving a new meaning to the words
or giving a new meaning to the old words.
2. Flow of thinking
a. Productivity: Overabundance of ideas, paucity of ideas, flight of ideas (A
succession of multiple associations so that thoughts seem to move abruptly
from idea to idea; often (but not invariably) expressed through rapid,
pressured speech), rapid thinking, slow thinking, hesitant thinking; does
patient speak spontaneously or only when questions are asked, stream of
thought, quotations from patient
b. Continuity of thought: Whether patient’s replies really answer questions
and are goal directed, tangential, circumstantial, perseverative (persistence
of same response beyond point of relevance), clang associations (linked
by rhyming)
Circumstantiality indicates the loss of capacity for goal-directed thinking;
in the process of explaining an idea, the patient brings in many irrelevant
details and parenthetical comments but eventually does get back to the
original point. Tangentiality is a disturbance in which the patient loses
the thread of the conversation, pursues divergent thoughts stimulated by
various external or internal irrelevant stimuli, and never returns to the
original point.
3. Content of thinking:
Thought content is essentially what thoughts are occurring to the patient.
This is inferred by what the patient spontaneously expresses, as well as
responses to specific questions aimed at eliciting particular pathology. Some
patients may perseverate or ruminate on specific content or thoughts. They
may focus on material that is considered obsessive or compulsive.
8 | Psychiatry
Obsessional thoughtsQ are unwelcome and repetitive thoughts that intrude
into the patient’s consciousness. They are generally ego alien and resisted
by the patient.
Compulsions are repetitive, ritualized behaviors that patients feel compelled
to perform to avoid an increase in anxiety or some dreaded outcome.
Another large category of thought content pathology is delusions.
Delusions are false, fixed ideas that are not shared by others and can be
divided into bizarre and non bizarre (nonbizarre delusions refer to thought
content that is not true but is not out of the realm of possibility). Common
delusions include grandiose, erotomanic, jealous, somatic, and persecutory.
Disorder of possession of thought: Normal, we are in control of our thoughts,
feeling and acts. Thought this is never on the forefront of our mind but we
recognize that own and not alien. But this sense of control is lost in many
disorders.
Thought insertion: where in the patient experiences thoughts being inserted
in to his mind and the thoughts are recognized as not being his own.
Thought withdrawal: wherein the patient feels that his thoughts are being
taken away by some external agency.
Thought broadcast: The thoughts leave the boundary of one’s mind and
become accessible to others without the patient telling these to others.
4. Perceptual disturbances
a. Hallucinations and illusions: Whether patient hears voices or sees visions;
content, sensory system involvement, circumstances of the occurrence;
hypnagogic or hypnopompic hallucinations (sleep related)
Illusion is a false sensory distortion of the real external sensory stimuli. For
example, a rope is mistakes for a snake.
Hallucination is a false sensory perception without adequate stimulus.
Depending upon the sense organ involved, hallucination can be auditory,
visual, tactile, gustatory or olfactory.
Auditory hallucinations are common in psychiatric disorders. Presence of
other types of hallucination in the absence of auditory hallucination requires
ruling out the organic nature of illness.
Pseudohallucinations have been defined in two ways; (i) the patient has
insight into perceptual disturbance (hallucination) and (ii) the percept is
arising from the subjective space.
Apart from these, there are functional hallucinations wherein a stimulus
in one sensory modality and the two are perceived independently, e.g. every
time the patient heard a bird chirping, he heard God talking to him.
Reflex hallucination (Synaesthesia): stimulus in one sensory modality
causes hallucination in other sensory modality, e.g. a patient felt pain in his
hand whenever someone sneezed.
Extracampine hallucination: one is able to perceive stimuli outside the
normal range of perception, e.g. a patient in Delhi heard voices coming from
England.
Somatic passivity phenomenon: Somatic passivity is the presence of
strange sensations described by the patient as being imposed on the body
by ‘some external agency’, with the patient being a passive recipient. It is
one of the Schneider’s first rank symptoms.
b. Depersonalization and derealization: Extreme feelings of detachment
from self or from the environment.
E. Sensorium
1. Alertness: Awareness of environment, attention span, clouding of consciousness,
fluctuations in levels of awareness, somnolence, stupor, lethargy, fugue state,
coma
Disturbances of Consciousness
There are five basic levels of consciousness:
1. Alertness: Patient is awake, and aware of internal and external stimuli, and can respond to them.
2. Lethargy (or somnolence): Patient is not fully alert, and if not actively stimulated, drifts into
sleep. Even when aroused, patients are not able to give close attention
3. Obtundation: Patient is difficult to arouse, and when aroused, patient appears confused. Constant
stimulation is needed to get even minimal cooperation from the patient
4. Stupor (or semicoma): In stupor, patient doesn’t show any spontaneous response and remains
akinetic (lack of movement) and mute. They may respond only to persistent and vigorous
stimulation, by groaning or mumbling.
5. Coma: Coma is a state of complete unawareness. The patient cannot be aroused with any kind of
external stimulation, and doesn’t respond to internal stimuli either. The patient remains with the
eyes closed.
Fig. 1.1: Levels or stages of diminished consciousness.
This term STUPOR should be reserved for the syndrome in which mutism and
akinesis occur; that is, the inability to initiate speech or action in a patient who
appears awake and even alert.
A twilight state is a well-defined interruption of the continuity of consciousness. It
is usually an organic condition and occurs in the context of epilepsy, alcoholism,
brain trauma and general paresis; it may also occur with dissociative states. It
is characterized by (a) abrupt onset and end; (b) variable duration, from a few
hours to several weeks; and (c) the occurrence of unexpected violent acts or
emotional outbursts during otherwise normal, quiet behaviour.
Dream‑Like (Oneiroid) State: The patient is disorientated, confused and
experiences elaborate hallucinations, usually visual. There is impairment
of consciousness and marked emotional change, which may be terror or
10 | Psychiatry
enjoyment of the hallucinatory experiences; there may also be auditory or
tactile hallucinations. The patient may appear to be living in a dream world.
Fig. 1.2: Three dimensions of unconsciousness
2. Orientation
a. Time: Whether patient identifies the day correctly; or approximate date,
time of day; if in a hospital, knows how long he or she has been there;
behaves as though oriented to the present
b. Place: Whether patient knows where he or she is
c. Person: Whether patient knows who the examiner is and the roles or
names of the persons with whom in contact
3. Concentration and calculation: Subtracting 7 from 100 and keep subtracting
7s (Serial 100‑7 subtraction test)
4. Memory:
a. Remote memory: Childhood data, important events known to have
occurred when the patient was younger or free of illness, personal
matters, neutral material
b. Recent past memory: Past few months
c. Recent memory: Past few days, what did patient do yesterday, the day
before, have for breakfast, lunch, dinner
d. Immediate retention and recall: Ability to repeat six figures after
examiner dictates them first forward, then backward, then after a few
minutes’ interruption
5. Abstract thinking: Disturbances in concept formation; manner in which
the patient conceptualizes or handles his or her ideas; similarities (e.g.,
between apples and pears), differences, absurdities; meanings of simple
proverbs (e.g., A rolling stone gathers no moss) answers may be concrete
(giving specific examples to illustrate the meaning) or overly abstract (giving
generalized explanation); appropriateness of answers
F. Insight: Degree of personal awareness and understanding of illness has 5
grades (Q)
Grade I : Complete denial of illness
Grade II : Slight awareness of being sick and needing help but denying it at the
same time
Grade III : Awareness of being sick but blaming it on others, on external factors,
on medical or unknown organic factors
Grade IV : Intellectual insight: Admission of illness and recognition that symptoms
or failures in social adjustment are due to irrational feelings or
disturbances, without applying that knowledge to future experiences
Grade V : True emotional insight: Emotional awareness of the motives and feelings
within, of the underlying meaning of symptoms; does the awareness
lead to changes in personality and future behavior; openness to new
ideas and concepts about self and the important persons in his or her
life
G. Judgment and Reasoning
1. Social judgment: Subtle manifestations of behavior that are harmful to the
patient and contrary to acceptable behavior in the culture; does the patient
understand the likely outcome of personal behavior and is patient influenced
by that understanding; examples of impairment
2. Test judgment: Patient’s prediction of what he or she would do in imaginary
situations (e.g., what patient would do with a stamped, addressed letter
found in the street)
Neuropsychological tests: Primarily used to assess cognitive functions of brain
a) Bender gestalt test (mc used screening test for organic dysfunction)QQ
Fig. 1.3
12 | Psychiatry
b) MMSE (mini mental status examination) total score is 30QQ, bed side
test for dementia (<24)
The Mini-Mental State Exam

Patient Examiner Date
Maximum Score
Orientation
5 ( ) What is the (year) (season) (date) (day) (month)?
5 ( ) What are we (state) (country) (town) (hospital) (floor)?
Registration
3 ( ) Name 3 objects: 1 second to say each. Then ask the patient all 3 after you
have said them. Give 1 point for each correct answer.
Then repeat them until he/she lerns all 3. Count trials and record.
Trials
Attention and Calculation

5 ( ) Serial 7's. 1 point for each correct answer. Stop after 5 answers.
Alternatively spell "world" backward.
Recall
3 ( ) Ask for the 3 objects repeated above. Give 1 ponit for each correct answer.
Language
2 ( ) Name a pencil and watch.
1 ( ) Repeat the following "No ifs, ands or buts"
3 ( ) Follow a 3 stage command:
"Take a paper in your hand, fold it in half, and put it on the floor."
1 ( ) Read and obey the following: CLOSE YOUR EYES
1 ( ) Write a sentence.
1 ( ) Copy the design shown.
Total Score
ASSESS level of conciousness along a continuum________
Alert Drowsy Stupor Coma
PROJECTIVE PERSONALITY TESTS
14 | Psychiatry
Some Investigations in Psychiatry (Ref: Niraj Ahuja)
Biological Investigations
• Haemoglobin: Routine screen.
• Total and differential leucocyte counts: Routine screen, Treatment with antipsychotics
(e.g. clozapine), lithium, carbamazepine.
• Mean Corpuscular Volume (MCV): Alcohol dependence (increased).
• Urinalysis: Routine screen; Drug screening.
• Peripheral smear: Anaemia.
• Renal function tests: Treatment with lithium.
• Liver function tests: Treatment with carbamazepine, valproate, benzodiazepines.
Alcohol dependence.
• Serum electrolytes: Dehydration, SIADH, Treatment with carbamazepine,
antipsychotics, lithium.
• Blood glucose: Routine screen (age>35 years), treatment with antipsychotics
• Thyroid function tests: Refractory depression, rapid cycling mood disorder. Treatment
with lithium, carbamazepine.
• Electrocardiogram (ECG): Age>35 years, Treatment with lithium, antidepressants,
ECT, antipsychotics.
• HIV testing: Intravenous drug users, suggestive sexual history, AIDS dementia.
• VDRL: Suggestive sexual history.
• Chest X-ray: Age>35 years, Treatment with ECT.
• Serum CK: Neuroleptic malignant syndrome (markedly increased levels).
Drug Levels Drug levels are indicated to test for therapeutic blood levels, for toxic
blood levels, and for testing drug compliance. Examples are lithium (0.6-1.0 meq/L),
carbamazepine (4-12 mg/ml), valproate (50-100 mg/ ml), haloperidol (8-18 ng/ml),
tricyclic antidepressants (nortriptyline 50-150 ng/ml; imipramine 200-250 ng/ ml),
benzodiazepines, barbiturates and clozapine (350- 500 μg/L).
Electrophysiological Tests
• EEG (Electroencephalogram): Seizures, dementia, pseudoseizures vs. seizures,
episodic abnormal behaviour.
• BEAM (Brain electrical activity mapping): Provides topographic imaging of EEG data.
• Video-Telemetry EEG: Pseudoseizures vs. seizures.
• Evoked potentials (e.g. p300 in schizophrenia): Research tool.
• Polysomnography/Sleep studies: Sleep disorders, seizures (occurring in sleep).
The various components in sleep studies include EEG, ECG, EOG, EMG, airflow
measurement, penile tumescence, oxygen saturation, body temperature, GSR
(Galvanic skin response), and body movement.
• Holter ECG: Panic disorder.
Brain Imaging Tests (Cranial)
• Computed Tomography (CT) Scan: Dementia, delirium, seizures, first episode
psychosis.
• Magnetic Resonance Imaging (MRI) Scan: Dementia.
• Positron Emission Tomography (PET) Scan: Research tool for study of brain function
and physiology.
• Single Photon Emission Computed Tomography (SPECT) Scan: Research tool.
• Magnetic Resonance (MR) Angiography: Research tool
• Magnetic Resonance Spectroscopy (MRS): Research tool
Neuroendocrine Tests
• Dexamethasone Suppression Test (DST): Research tool in depression (response to
antidepressants or ECT). If plasma cortisol is >5 mg/100 ml following administration
of dexamethasone (1 mg, given at 11 PM the night before and plasma cortisol taken
at 4 PM and 11 PM the next day), it indicates non-suppression.
• TRH Stimulation Test: Lithium-induced hypothyroidism, refractory depression. If the
serum TSH is >35 mIU/ml (following 500 mg of TRH given IV), the test is positive.
• Serum Prolactin Levels: Seizures vs. pseudo seizures, galactorrhoea with
antipsychotics.
• Serum 17-hydroxycorticosteroid: Organic mood (depression) disorder.
• Serum Melatonin Levels: Seasonal mood disorders.
Biochemical Tests
• 5-HIAA: Research tool (depression, suicidal and/or aggressive behaviour).
• MHPG: Research tool (depression).
• Platelet MAO: Research tool (depression).
• Catecholamine levels: Organic anxiety disorder (e.g. pheochromocytoma).
16 | Psychiatry
Worksheet
• MCQ OF “GENERAL PSYCHIATRY” FROM DQB
• EXTRA POINTS FROM DQB

Important Tables (Active Recall)
ICD-10 DSM IV TR
(International Classification of (Diagnostic and statistical manual)
Diseases)
2 Schizophrenia and
Other Psychotic Disorders
CONCEPTS
Â 2.1 Historical aspect schizophrenia
Â 2.2 Etiology
Â 2.3 Epidemiology
Â 2.4 Clinical features
Â 2.5 Diagnostic criteria
Â 2.6 Subtypes
Â 2.7 Prognostic factors
Â 2.8 Management
Â 2.9 Delusional disorders
Â 2.10 Schizoaffective disorder

chi hrenia an ther Psych tic is r ers
2.1: Historical aspect schizophrenia
LEARNING OBJECTIVE: To understand the historical origin of schizophrenia, basic
symptoms described first by stalwarts and answer its related MCQs.
Time Needed
1st reading 15 mins
2 look
nd
10 mins
Emil Kraepelin
• Kraepelin translated Morel’s “demence precoceQ” into dementia precoxQ, a term
that emphasized the change in cognition (dementia) and early onset (precox) of the
disorder.
• Patients with dementia precox were described as having a long-term deteriorating
course and the clinical symptoms of hallucinations and delusions.
• Kraepelin distinguished these patients from those who underwent distinct episodes
of illness alternating with periods of normal functioning which he classified as having
manic‑depressive psychosis.
Eugene Bleuler
• Bleuler coined the termQ schizophrenia, which replaced dementia precox in
the literature.
• He chose the term to express the presence of schisms between thought, emotion, and
behavior in patients with the disorder.
• Bleuler identified specific fundamental (or primary) symptoms of schizophrenia to
develop his theory about the internal mental schisms of patients.
• These symptoms included associational disturbances of thought, especially looseness,
affective disturbances, autism, and ambivalence, summarized as the four As:
associations, affect, autism, and ambivalence.
Psychiatry
Kurt Schneider
First-rank symptoms of schizophrenia (Kurt Schneider) are a group of symptoms
representing ego boundary disturbances, and usually an external agency is blamed.
These include.
1. Thought insertion: wherein the patient experiences thoughts being inserted in to
his mind and the thoughts are recognized as not being his own.
2. Thought withdrawal: wherein the patient feels that his thoughts are being taken
away by some external agency.
3. Thought broadcast: The thoughts leave the boundary of one’s mind and become
accessible to others without the patient telling these to others.
4. Thought echo: One’s own thoughts are heard aloud.
5. Voice arguing: This is a form of third person auditory hallucination where voices
discuss the patient in third person.
. oices giving running commentary: On whatever patient is doing.
7. Made affect: The emotions are recognized as alien, imposed on the patient. For
example, one patient admitted that the tears were rolling down but she did not feel
sad inside and felt that this was forced onto her.
8. Made act: The action carried out by the patient is not considered as his own but as
an imposed one.
9. Made impulse: A sudden urge to do something takes over the patient. The patient
recognizes the action involved in fulfilling the urge as his own but not the impulse.
For example, one patient suddenly got up and smashed his wrist watch. He described
the act as his own but that the urge was imposed upon him.
10. Somatic passivity: The patient is a passive recipient of bodily sensations caused
by an external agency
11. Delusional Perception
2.2: Etiology in Schizophrenia (#extraedge) (NIMHANS)
LEARNING OBJECTIVE: To understand the etiological basis of schizophrenia, which is
not very well known, and answer its related MCQs.
Time Needed
1 reading
st
20 mins
2 look
nd
10 mins
A. Genetic factors:
Schizophrenia has a genetic contribution as reflected by higher monozygotic
concordance rate than dizygotic concordance rate. Several genes appear to make
a contribution to schizophrenia and nine linkage sites have been identified: 1q,
5q, 6p, 6q, 8p, 10p, 13q, 15q and 22q. Deletions at chromosome 22q11.2 (22q11
deletion syndrome, velocardiofacial syndrome, DiGeorge symdrome) have been
associated with development of schizophrenia in around 30 cases.
Several candidate genes contributing to schizophrenia have been identified, and
they include 7 nicotinic receptor, DISC 1 (Disrupted in schizophrenia), COMT
(catechol-o-methyl transferase), NRG 1 (Neuregulin 1), GRM3 (Glutamate
receptor metabotropic), RGS4 (Regulator of G protein signaling) and DAOA (or
G72) (D-Amino acid oxidase activator).
There is increased risk of development of schizophrenia in family members of
patients with schizophrenia. Also, family members of patients with bipolar disorders
too have a slightly increased risk of development of schizophrenia.
B. Biochemical factors:
Neurotransmitters in Schizophrenia: (Ref : Kaplan)
1. Dopamine Hypothesis: Schizophrenia results from too much dopaminergic
activity.
2. Serotonin: Current hypotheses posit serotonin excess as a cause of both positive
and negative symptoms in schizophrenia.
3. Norepinephrine: A selective neuronal degeneration within the norepinephrine
reward neural system could account for anhedonia in schizophrenia.
4. GABA: patients with schizophrenia have a loss of GABAergic neurons in the
hippocampus.
5. Neuropeptide: substance P and neurotensin
6. Glutamate: Glutamate has been implicated because ingestion of phencyclidine,
a glutamate antagonist, produces an acute syndrome similar to schizophrenia.
7. Acetylcholine and Nicotine: Postmortem studies in schizophrenia have
demonstrated decreased muscarinic and nicotinic receptors
C. Neuropathological factors: The neuropathology of schizophrenia is still not clear.
Abnormalities have been found in various structures, such as:
Cerebral ventricles: Reduction in cortical gray matter volume and enlargement
of lateral and third ventricles has been consistently observed.
Limbic system: Abnormalities in limbic system components such as hippocampus
(smaller in size and functionally abnormal), amygdala (smaller size) and
parahippocampal gyrus (smaller size) have been observed.
Psychiatry
Prefrontal cortex: Anatomical abnormalities have been found.

Thalamus: Neuronal loss especially in medial dorsal nucleus of thalamus.
Basal ganglia and cerebellum: Abnormalities have been reported but findings
are not consistent.
D. Environmental factors: Apart from genetic factors, the following environmental
factors have also been associated with development of schizophrenia.
Obstetric complications and abnormalities in development: Patients
with schizophrenia are more likely to have history of obstetric complications
in comparison to general population. Similarly they more often have abnormal
development such as delayed milestones, poor motor coordination, etc.
Fig. 2.1: Neurodevelopmental Theory of Schizophrenia
Stressful life events: Early childhood trauma (including sexual abuse) is a risk
factor. Further more, studies have shown an excess of stressful life events in few
weeks prior to onset of schizophrenia.
Season of birth and maternal exposure to infection: Studies have shown
that people who are born in winters and early spring are more likely to develop
schizophrenia. Also prenatal exposure to influenza virus and prenatal malnutrition
also increase the risk.
Advanced paternal age: Advanced paternal age has been found to be strongly
associated with the risk of development of schizophrenia.
Immigration: Migrants have higher chances of developing schizophrenia than
natives. The risk is especially higher for the second generation who are born in the
new homeland (the country of migration).
Drug abuse: Studies have shown that cannabis use increases the risk of
development of schizophrenia.
Urban birth and upbringing: Birth and upbringing in urban areas have been associated
with increase in risk for schizophrenia, in comparison to rural settings
2.3: Epidemiology of Schizophrenia:
LEARNING OBJECTIVE: To note the basic points about epidemiology of schizophrenia
and answer its related MCQs.
Time Needed
1 reading
st
10 mins
2 look
nd
5 mins
1. In the United States, the lifetime prevalence of schizophrenia is about 1
percent
2. According to DSM-IV-TR, the annual incidence of schizophrenia ranges from
0.5 to 5.0 per 10,000
3. Schizophrenia is equally prevalent in men and women. In general, the outcome for
female schizophrenia patients is better than that for male schizophrenia patients.
When onset occurs after age 45, the disorder is characterized as late-onset
schizophrenia.
Prevalence of Schi ophrenia in Specific Populations

Population Prevalence {%)
General population 1
Non-twin sibling of a schizophrenia patient 8
Child with one parent with schizophrenia 12
Dizygotic twin of a schizophrenia patient 12
Child of two parents with schizophrenia 40
Monozygotic twin of a schizophrenia patient 47
Psychiatry
2.4: Clinical features (Ref : Niraj Ahuja)
LEARNING OBJECTIVE: To understand clinical presentation of schizophrenia, and
answer its related MCQs.
Time Needed
1 reading
st
30 mins
2 look
nd
15 mins
Schizophrenia is characterised by disturbances in thought and verbal behaviour,
perception, affect, motor behaviour and relationship to the external world. The diagnosis
is entirely clinical and is based on the following clinical features, none of which are
pathognomonic if present alone.
Thought and Speech Disorders

Autistic thinking is one of the most classical features of schizophrenia. Here thinking
is governed by private and illogical rules. The patient may consider two things identical
because they have identical predicates or properties (von Domarus Law); for example,
Lord Hanuman was celibate, I am celibate too; So, I am Lord Hanuman.
Loosening of associations is a pattern of spontaneous speech in which things said in
juxtaposition lack a meaningful relationship or there is idiosyncratic shifting from one
frame of reference to another. The speech is often described as being ‘disjointed’. If the
loosening becomes very severe, speech becomes virtually incomprehensible. This is
then known as incoherence.
Thought blocking is a characteristic feature of schizophrenia, although it can also be
seen in complex partial seizures (temporal lobe epilepsy). There is a sudden interruption
of stream of speech before the thought is completed. After a pause, the subject cannot
recall what he had meant to say. This may at times be associated with thought withdrawal.
Neologisms are newly formed words or phrases whose derivation cannot be understood.
These are created to express a concept for which the subject has no dictionary word.
Sometimes, normal words are used in an unconventional or distorted way but the
derivation can be under stood, even if bizarre. These are called word approximations
or paraphasias for example, describing stomach as a food vessel’.
A patient with schizophrenia may show complete mutism (with no speech production),
poverty of speech (decreased speech production), poverty of ideation (speech amount
is adequate but content conveys little information), echolalia (repetition or echoing by
the patient of the words or phrases of examiner), perseveration (persistent repetition
of words beyond their relevance), or verbigeration (senseless repetition of same words
or phrases over and over again). These are disorders of verbal behaviour or speech.
Delusions are false unshakable beliefs which are not in keeping with patient’s socio-
cultural and educational background. These are of two types: primary and secondary.
1. Primary delusions arise de novo and cannot be explained on the basis of other
experiences or perceptions. Also known as autochthonous delusions, these are though
to be characteristic of schizophrenia and are usually seen in early stages.
2. Secondary delusions are the commonest type of delusions seen in clinical
practice and are not diagnostic of schizophrenia as these can also be seen in other
psychoses. Secondary delusions can be explained as arising from other abnormal
experiences.
The commonly seen delusions in schizophrenia include:
1. Delusions of persecution (being persecuted against, e.g. ‘people are against me’).
2. Delusions of reference (being referred to by others; e.g. ‘people are talking about
me’).
3. Delusions of grandeur (exaggerated self-importance; e.g. ‘I am God almighty’).
4. Delusions of control (being controlled by an external force, known or unknown; e.g.
‘My neighbour is controlling me”).
5. Somatic (or hypochondriacal) delusions (e.g. ‘there are insects crawling in my scalp’).
The other clinical features of schizophrenic thought disorder include: overinclusion
(tending to include irrelevant items in speech), impaired abstraction (loss of ability to
generalise), concreteness (due to impaired abstraction), perplexity and ambivalence.
Schneider s rst ran symptoms (such as thought insertion, thought withdrawal,
thought broadcasting, ‘made’ feeling, ‘made’ impulses and ‘made’ volitions), may also
be present.
Disorders of Perception
Hallucinations (perceptions without stimuli) are common in schizophrenia. Auditory
hallucinations are by far the most frequent. These can be:
i. Elementary auditory hallucinations (i.e. hearing simple sounds rather than voices)
ii. ‘Thought echo’ (‘audible thoughts’)
iii. ‘Third person hallucinations’ (‘voices heard arguing’, discussing the patient in third
person)
iv. ‘Voices commenting on one’s action’.
Only the third person hallucinations’ are believed to be characteristic of
schizophrenia. Visual hallucinations can also occur, usually along with auditory
hallucinations. The tactile, gustatory and olfactory types are less common.
Disorders of A ect
The disorders of affect include apathy, emotional blunting, emotional shallowness,
anhedonia (inability to experience pleasure) and inappropriate emotional response
(emotional response inappropriate to thought).
Disorders of Motor Behaviour

There can be either a decrease (decreased spontaneity, inertia, stupor) or an increase in
psychomotor activity (excitement, aggressiveness, restlessness, agitation).
Mannerisms, grimacing, stereotypies (repetitive strange behaviour), decreased self-
care, and poor grooming are common features.
Negative Symptoms
The prominent negative symptoms of schizophrenia include affective attening or
blunting, attentional impairment, avolition-apathy (lack of initiative associated with
psychomotor slowing), anhedonia, asociality (social withdrawal), and alogia (lack of
speech output). There is poor verbal as well as nonverbal communication with poor facial
expression, decreased eye contact, with usually poor self-care and social interaction.
Psychiatry
Other Features
1. Decreased functioning in work, social relations and self-care, as compared to the
earlier levels achieved by the individual.
2. Loss of ego boundaries (feeling of blurring of boundaries of self with the environment;
uncertainty and perplexity regarding own identity and meaning of existence).
3. Multiple somatic symptoms, especially in the early stages of illness.
4. Insight (into the illness) is absent and social judgement is usually poor.
5. There is usually no clinically significant disturbance of consciousness, orientation,
attention, memory and intelligence.
6. There is usually variability in symptomatology over time which in some cases can be
marked.
7. There is no obvious underlying organic cause that can explain the causation of the
symptoms.
8. There is no prominent mood disorder of depressive or manic type.
Post-Schizophrenic Depression (25% cases)

Some schizophrenic patients develop depressive features within 12 months of an acute
episode of schizophrenia. The depressive features develop in the presence of residual
or active features of schizophrenia and are associated with an increased risk of suicide.
The depressive features can occur due to side-effect of antipsychotics, regaining insight
after recovery, or just be an integral part of schizophrenia. It is important to distinguish
the depressive features from negative symptoms of schizophrenia and extrapyramidal
side-effects of antipsychotic medication.
Suicide in Schizophrenia (10% as per DSM IV) (5-6% as per DSM 5)

Suicide can occur in schizophrenia due to several reasons. Some of the common reasons
can include the presence of co-morbid depressive symptoms, command hallucinations
commanding the patient to commit suicide, impulsive behaviour, presence of anhedonia,
and/or return of insight in the illness (with the painful aware ness that one has suffered
from schizophrenia or psychosis). It is important to be aware of possibility of suicide
whilst treating a patient with schizophrenia so that the various risk factors can be
addressed in management.
Pseudoneurotic Schizophrenia
In initial phases, there are predominant neurotic symptoms that last for years and show
a poor response to treatment. The three classical features described are pananxiety
(diffuse, free-floating anxiety which hardly ever subsides), pan-neurosis (almost all
neurotic symptoms may be present) and pansexuality (constant preoccupation with
sexual problems).
Oneiroid Schizophrenia
This is a subtype of schizophrenia with an acute onset, clouding of consciousness,
disorientation, dream-like states (oneiroid means ‘dream’), and perceptual disturbances
with rapid shifting.
Van Gogh Syndrome

Dramatic self-mutilation occurring in schizophrenia has been also called as Van Gogh
syndrome
Pfropf Schizophrenia
This is a syndrome of schizophrenia occurring in the presence of mental retardation.
2.5: Diagnostic Criteria of Schizophrenia
LEARNING OBJECTIVE: To understand diagnostic criteria (ICD and DSM) of
schizophrenia, and answer its related MCQs.
Time Needed
1 reading
st
20 mins
2 look
nd
10 mins
DSM-5 Criteria
A. Characteristic symptoms: Two (or more) of the following, each present for a
significant portion of time during a 1-month period (or less if successfully treated).
At least one of these must be (1), (2) or (3):
1. delusions
2. hallucinations
3. disorganized speech (e.g., frequent derailment or incoherence)
4. grossly disorganized or catatonic behavior
5. negative symptoms, i.e., affective flattening, alogia, or avolition
B. Social/occupational dysfunction: For a significant portion of the time since the
onset of the disturbance, one or more major areas of functioning such as work,
interpersonal relations, or self-care are markedly below the level achieved prior
to the onset (or when the onset is in childhood or adolescence, failure to achieve
expected level of interpersonal, academic, or occupational achievement).
C. Duration: Continuous signs of the disturbance persist for at least 6 months. This
6-month period must include at least 1 month of symptoms (or less if successfully
treated) that meet Criterion A (i.e., active-phase symptoms) and may include periods
of prodromal or residual symptoms. During these prodromal or residual periods, the
signs of the disturbance may be manifested by only negative symptoms or two or
more symptoms listed in Criterion A present in an attenuated form (e.g., odd beliefs,
unusual perceptual experiences).
D. Schizoaffective and mood disorder exclusion: Schizoaffective disorder and
mood disorder with psychotic features have been ruled out because either (1) no
major depressive, manic, or mixed episodes have occurred concurrently with the
active-phase symptoms; or (2) if mood episodes have occurred during active-phase
symptoms, their total duration has been brief relative to the duration of the active
and residual periods.
E. Substance/general medical condition exclusion: The disturbance is not due to
the direct physiological effects of a substance (e.g., a drug of abuse, a medication)
or a general medical condition.
F. Relationship to a pervasive developmental disorder: If there is a history
of autistic disorder or another pervasive developmental disorder, the additional
diagnosis of schizophrenia is made only if prominent delusions or hallucinations are
also present for at least a month (or less if successfully treated).
Psychiatry
NOTE:
1. IN DSM 5, there are no subtypes of schizophrenia
2. DSM-5 raises the symptom threshold, requiring that an individual exhibit at least two
of the specified symptoms. (In DSM-IV, that threshold was one.)
3. ICD-11 criteria specifies minimum duration to diagnose schizophrenia as 1 month
Acute Psychosis: 1 month of symptoms (ICD-10) (onset within 2 weeks)
Brief Psychotic Disorder: 1 month of symptoms (DSM)
Schizophreniform Disorder: 1-6 months of symptom (DSM)
ICD-11 Criteria of Diagnosis:

Schizophrenia is characterized by disturbances in multiple mental modalities, including
thinking (e.g., delusions, disorganization in the form of thought), perception (e.g.,
hallucinations), self-experience (e.g., the experience that one’s feelings, impulses,
thoughts, or behaviour are under the control of an external force), cognition (e.g.,
impaired attention, verbal memory, and social cognition), volition (e.g., loss of
motivation), affect (e.g., blunted emotional expression), and behaviour (e.g., behaviour
that appears bizarre or purposeless, unpredictable or inappropriate emotional responses
that interfere with the organization of behaviour).
Psychomotor disturbances, including catatonia, may be present.
Persistent delusions, persistent hallucinations, thought disorder, and experiences of
influence, passivity, or control are considered core symptoms.
Symptoms must have persisted for at least one month in order for a diagnosis of
schizophrenia to be assigned. The symptoms are not a manifestation of another health
condition (e.g., a brain tumour) and are not due to the effect of a substance or medication
on the central nervous system (e.g., corticosteroids), including withdrawal (e.g., alcohol
withdrawal).
General criteria for Paranoid, Hebephrenic, Catatonic and Undifferentiated type of
Schizophrenia: (ICD-10)
G1. Either at least one of the syndromes, symptoms and signs listed below under (1),
or at least two of the symptoms and signs listed under (2), should be present for most
of the time during an episode of psychotic illness lasting for at least one month (or at
some time during most of the days).
(1) At least one of the following:

a) Thought echo, thought insertion or withdrawal, or thought broadcasting.
b) Delusions of control, influence or passivity, clearly referred to body or limb
movements or specific thoughts, actions, or sensations; delusional perception.
c) Hallucinatory voices giving a running commentary on the patient’s behaviour,
or discussing him between themselves, or other types of hallucinatory voices
coming from some part of the body.
d) Persistent delusions of other kinds that are culturally inappropriate and completely
impossible (e.g. being able to control the weather, or being in communication
with aliens from another world).
(2) or at least two of the following:
a) Persistent hallucinations in any modality, when occurring every day for at least
one month, when accompanied by delusions (which may be fleeting or half-
formed) without clear affective content, or when accompanied by persistent
over-valued ideas.
b) Neologisms, breaks or interpolations in the train of thought, resulting in
incoherence or irrelevant speech.
c) Catatonic behaviour, such as excitement, posturing or waxy flexibility, negativism,
mutism and stupor.
d) “Negative” symptoms such as marked apathy, paucity of speech, and blunting
or incongruity of emotional responses (it must be clear that these are not due to
depression or to neuroleptic medication).
G2. Most commonly used exclusion criteria: If the patient also meets criteria for manic
episode (F30) or depressive episode (F32), the criteria listed under G1.1 and G1.2
above must have been met before the disturbance of mood developed.
G3. The disorder is not attributable to organic brain disease, or to alcohol- or drug-
related intoxication, dependence or withdrawal.
In ICD-11, the types of schizophrenia have been described according to the course of
illness and include:
a) Schizophrenia, first episode: If patient meets diagnostic criterion of schizophrenia
and there have been no past episodes
b) Schizophrenia, multiple episodes: If patient meets diagnostic criterion of
schizophrenia, and there has been at least one episode in the past. Between the last
and current episode, there was significant remission of symptoms
Schizophrenia, continuous: If patient has been fulfilling the diagnostic criterions of
schizophrenia for almost the entire duration of illness (duration should be more than
one year)
Psychiatry
2.6: Subtypes of Schizophrenia
LEARNING OBJECTIVE: To differentiate between major subtypes of schizophrenia,
Time Needed
1 reading
st
20 mins
2 look
nd
10 mins
DSM-IV Key Features

Paranoid type Persecutory; Most common form of schizophrenia
Hallucinations, usually auditory; Personality relatively preserved
Disorganized type Early onset; Odd behavior; Labile or inappropriate mood ; Poor prognosis
Mirror gazing, giggling, silly smiles; Disorganized speech and behavior(often silly/
shallow and at or inappropriate affect
Catatonic type Psychomotor disturbance viz stupor, mutism, excitement,
negativism, waxy exibility, automatic obedience, echopraxia.
best response to C but first line of treatment lora epam.
Simple Type Social withdrawal, only negative symptoms, worst prognosis
Type 1 schizophrenia Type 2 schizophrenia

Symptoms Positive(Delusion, hallucination) egative Affect attening, poverty
of speech, etc.
Type of illness Acute Chronic
Response to neuroleptics Good Poor
Outcome Reversible Long standing
Intellectual impairment Absent Sometimes present
Etiology ncreased opamine in rain Structural changes in rain ilated
ventricles on C. . scan
Prognosis Good Poor
2.7: Prognostic factors
LEARNING OBJECTIVE: To understand prognostic factors of schizophrenia, and answer
its related MCQs.
Time Needed
1 reading
st
15 mins
2 look
nd
10 mins
Features Weighting Toward Good to Poor Prognosis in Schizophrenia

Good Prognosis Poor Prognosis
Late onset Young onset
Obvious precipitating factors No precipitating factors
Acute onset nsidious onset
Good premorbid social, sexual, and work histories Poor premorbid social, sexual, and work histories
Mood disorder symptoms (especially depressive Withdrawn, autistic behavior
disorders)
Married Single, divorced, or widowed
Family history of mood disorders Family history of schizophrenia
Good support systems Poor support systems
Positive symptoms Negative symptoms
Neurological signs and symptoms
History of perinatal trauma
No remissions in 3 years
Many relapses
Psychiatry
2.8: Treatment of Schizophrenia:
LEARNING OBJECTIVE: To understand various management options in schizophrenia,
Time Needed
1 reading
st
15 mins
2nd look 10 mins
Pharmacological treatment: Antipsychotics (1st generation and 2nd generation)

(Details in last chapter of this book)
Psychosocial Treatment in schizophrenia: Apart from medications, psychological
and social interventions have been found to be effective in treatment of schizophrenia,
especially after the acute phase is treated with medications. The following psychosocial
treatments can be used:
a. Family interventions: The family of patient is involved with focus on illness
education, coping with the illness and providing emotional support to the entire
family.
b. Supported employment: An attempt is made to provide employment to patient
while giving ongoing support.
c. Assertive community treatment: It involves reaching out to the patient in
community and providing necessary support.
d. Skills training: The focus is on improving skills, especially social skills of the patient
e. Token economy: Mostly used in inpatient settings, it involves use of tokens, which
are given to patients, when they indulge in desirable behaviors (like remaining calm,
taking medicines regularly, etc.). Patients can redeem the tokens to get material
items or privileges.
Attenuated psychosis syndrome: (NIMHANS 2018) Attenuated Psychosis Syndrome
has been included in DSM-5 as a condition that needs further study before it can be
included as an official diagnosis. The proposed criterion for this condition include, the
following:
1. At least one of the following symptoms is present in attenuated (less severe and
transient) form, with relatively intact insight,-
a. delusions
b. hallucinations,
c. Disorganized speech
[Here attenuated means that, for example, if delusions are present patient may appear
suspicious at times (transient) but not always and he may be made to question his
beliefs (less severe, not fixed) .
2. Symptom(s) must have been present at least once per week for the past month.
3. Symptom(s) must have begun or worsened in the past year.
4. Symptom(s) is sufficiently distressing and disabling to the individual to warrant
clinical attention.
2.9: Delusional Disorders
LEARNING OBJECTIVE: To understand various types of delusional disorders clinically,
Time Needed
1 reading
st
20 mins
2nd look 10 mins
Delusion A false belief based on incorrect inference about external reality that is firmly
sustained despite what almost everyone else believes and despite what constitutes
incontrovertible and obvious proof of evidence to the contrary. The belief is not one
ordinarily accepted by other members of the person’s culture or subculture (e.g., it is
not an article of religious faith).
Risk factors for development of delusional disorders: (NEET 19)

a. Advanced age
b. Social isolation
c. Sensory impairment or isolation (e.g. auditory or visual disturbances)
d. Family history of delusional disorder
e. Recent immigration
f. Certain personality features, like excessive interpersonal sensitivity (even trivial
interpersonal problems cause lot of negative emotions)
TYPES:
• Erotomanic type: delusions that another person, usually of higher status, is in love
with the individual. (De-clerambaut’s syndrome)
• Grandiose type: delusions of inflated worth, power, knowledge, identity, or special
relationship to a deity or famous person
• Jealous type: delusions that the individual’s sexual partner is unfaithful (Othello
syndrome)
• Persecutory type: delusions that the person (or someone to whom the person is
close) is being malevolently treated in some way.
Induced Delusional Disorder

This is an uncommon delusional disorder characterised by a sharing of delusions between
usually two (folie å deux) or occasionally more per sons (folie å trios, folie å quatre,
folie å famille), who usually have a closely knit emotional bond. Only one person
usually has authentic delusions due to an under lying psychiatric disorder, most often
schizophrenia or delusional disorder.
On separation of the two, the dependent individual may give up his/her delusions and
the patient with the primary delusions should then be treated appropriately
Psychiatry
Somatic type: delusions that the person has some physical defect or general medical
condition
Delusional disorder with somatic delusions has been called monosymptomatic
hypochondriacal psychosis.
The three main types are:
1. delusions of infestation (including parasitosis)
2. delusions of dysmorphophobia, such as of misshapenness, personal ugliness, or
exaggerated size of body parts
3. delusions of foul body odors or halitosis (sometimes referred to as olfactory
reference syndrome)
Delusional Misidentification Syndromes

Capgras Syndrome Fregoli Syndrome
(Delusion of Doubles)
Persecutor (stranger) has replaced my family perosn Family member (Persecutor) Has changed himself to
to harm me. disguise of stranger to harm me.
g ife replaced by nurse g ife in disguise of nurse
Di erential Diagnosis of Delusional Disorders

S.No. Features Paranoid Schizophrenia Delusional Disorder Paranoid
(Paranoid disorder) Personality
Disorder
. General Eccentricities, mannerisms, Eccentricities, decreased Restrained
behaviour stereotypies, decreased social interaction social
self-care, social withdrawal, interaction
guarded and evasive
. Personality Disorganised (although Disturbed in delusional No deterioration
deterioration is much less than area, near normal in
in other type of schizophrenia other areas
. Thought disorder Delusions, Schneiderian FRS, Nonbizarre delusions No thought
loosening of associations, which are well- disorder
formal thought disorder, systematised, no other
delusions may be bizarre thought disorder
. Hallucinations Auditory hallucinations ncommon. f present, Absent
common are not persistent
. Contact with Markedly disturbed Disturbed in area of ntact
reality delusion al belief
. nsight Absent Absent Present
. Affect mood Often inappropriate dually appropriate Usually
in relation to appropriate
thought
2.10: Schi oa ective Disorder
LEARNING OBJECTIVE: To understand clinical presentation of schizoaffective disorder,
Time Needed
1 reading
st
10 mins
2nd look 5 mins
Schizoaffective disorder: Schizoaffective disorder has features of both schizophrenia

and affective disorders (now called mood disorders).
Diagnostic Criteria
A. Schizoaffective disorder is an illness, which meets the criteria for schizophrenia and
concurrently meets the criteria for a major depressive episode, manic episode, or
mixed episode.
B. The illness must also be associated with delusions or hallucinations for two weeks,
without significant mood symptoms.
C. Mood symptoms must be present for a significant portion of the illness.
D. A general medical condition or substance use is not the cause of symptoms.
II. Clinical eatures of Schi oa ective Disorder

A. Symptoms of schizophrenia are present, but the symptoms are also associated with
recurrent or chronic mood disturbances.
B. Psychotic symptoms and mood symptoms may occur independently or together.
C. If manic or mixed symptoms occur, they must be present for one week, and major
depressive symptoms must be present for two weeks.
Treatment of Schi oa ective Disorder

A. Psychotic symptoms are treated with antipsychotic agents.
B. The depressed phase of schizoaffective disorder is treated with antidepressant
medications.
C. For bipolar type, mood stabilizers (eg, lithium, valproate or carbamazepine) are used
alone or in combination with antipsychotics.
D. Electroconvulsive therapy may be necessary for severe depression or mania.
E. Hospitalization and supportive psychotherapy may be required.
Psychiatry
Worksheet
• MCQ OF “SCHI OPHRENIA AND RELATED DISORDERS” FROM DQB

Important Tables (Active recall)
DSM-IV Key Features
Paranoid type
Disorganized type
Catatonic type
Simple Type
Type 1 schizophrenia Type 2 schizophrenia

Symptoms
Type of illness
Response to neuroleptics
Outcome
Intellectual impairment
Etiology
Prognosis
Psychiatry
Features Weighting Toward Good to Poor Prognosis in Schizophrenia
Good Prognosis Poor Prognosis
Di erential Diagnosis of Delusional Disorders
S.No. Features Paranoid Schizophrenia Delusional Disorder Paranoid
(Paranoid disorder) Personality
Disorder
. General
behaviour
. Personality
. Thought disorder
. Hallucinations
. Contact with
reality
. nsight
. Affect mood
in relation to
thought
3 Mood Disorders
CONCEPTS
Â 3.1 Epidemiology and etiology of mood disorders
Â 3.2 Clinical features of depression
Â 3.3 Diagnostic criteria of depression
Â 3.4 DMDD and PMDD
Â 3.5 Dysthymia
Â 3.6 Post-partum psychiatric disorders
Â 3.7 Treatment of depression
Â 3.8 Special types of depression
Â 3.9 Mania
Â 3.10 Bipolar disorders

is r ers
3.1: Epidemiology and Etiology of Mood Disorders
LEARNING OBJECTIVE: To understand the etiological basis of mood disorders and
Time Needed
1 reading
st
30 mins
2 look
nd
15 mins
Epidemiology
1. In the most recent surveys, major depressive disorder has the highest lifetime
prevalence (almost 17 percent) of any psychiatric disorder.Q
2. There is twofold greater prevalence of major depressive disorder in women than in men.
Bipolar I disorder has an equal prevalence among men and women. Manic episodes are
more common in men, and depressive episodes are more common in women.
3. No correlation has been found between socioeconomic status and major depressive
disorder.
4. Major depressive disorder occurs most often in persons without close interpersonal
relationships or in those who are divorced or separated.
5. The mean age of onset of major depressive disorder is 40y.
6. Depression is more common in rural areas than in urban areas.
Etiology of mood disorders: (#extraedge #nimhans)

(Ref : Niraj Ahuja)
Exact aetiology of mood disorders is not known currently, despite several theories having
been propounded.
Genetic Hypothesis
The life-time risk for the first degree relatives of bipolar mood disorder patients is 25 , and
of recurrent depressive disorder patients is 20 . The life-time risk for the children of one
parent with bipolar mood disorder is 27 and of both parents with bipolar mood disorder
is 74 .
The concordance rate in bipolar disorders for mono zygotic twins is 65%Q and
for dizygotic twins is 20 ; the concordance rate in unipolar depression for monozygotic
twins is 46 and for dizygotic twins is 20 .
Therefore, genetic factors are very important in making an individual vulnerable to
mood disorders, particularly so in bipolar mood dis orders. However, environmental
factors are also probably important.
Biochemical Theories
There are several biochemical hypotheses for the causation of mood disorders. The
mono amine hypothesis suggests an abnormality in the monoamine [catecholamine
(norepinephrine and dopamine) and serotonin] system in the central nervous system at
one or more sites. Acetylcholine and GABA are also presumably involved.
Psychiatry
Neurotransmitters in mood disorders: (Ref : Kaplan)

Of the biogenic amines, norepinephrine and serotonin are the two neurotransmitters
most implicated in the pathophysiology of mood disorders.
1. Norepinephrine: Clinical antidepressant responses is probably the single most
compelling piece of data indicating a direct role for the noradrenergic system in
depression.
2. Serotonin: Depletion of serotonin may precipitate depression, and some patients
with suicidal impulses have low cerebrospinal fluid (CSF) concentrations of serotonin
metabolites and low concentrations of serotonin uptake sites on platelets.
3. Dopamine: The data suggest that dopamine activity may be reduced in depression
and increased in mania.
4. Other Neurotransmitter Disturbances: Cholinergic agonist and antagonist drugs
have differential clinical effects on depression and mania. Agonists can produce
lethargy, anergia, and psychomotor retardation in healthy subjects, can exacerbate
symptoms in depression, and can reduce symptoms in mania.
5. Reductions of GABA have been observed in plasma, CSF, and brain GABA levels in
depression.
Patients suffering from severe depression with suicidal intent/attempt appear to have a
marked decrease in the serotonergic function, evidenced by decreased urinary and
plasma 5-HIAA levels and the postmortem studies.
Neuroendocrine Theories
Mood symptoms are prominently present in many endocrine disorders, such as
hypothyroidism, Cushing’s disease, and Addison’s disease. Endocrine function is
often disturbed in depression, with cortisol hypersecretion, non-suppression with
dexamethasone challenge (Dexamethasone suppression test or DST), blunted TSH
response to TRH, and blunted growth hormone (GH) production during sleep.
The neuroendocrine and biochemical mechanisms are closely inter-related.
Sleep Studies
Sleep abnormalities are common in mood disorders (e.g. decreased need for sleep in
mania; insomnia and frequent awakenings in depression). In depression, the commonly
observed abnormalities include decreased REM latency (i.e. the time between falling
asleep and the first REM period is decreased), increased duration of the first REM period,
and delayed sleep onset.
Brain Imaging
In mood disorders, brain imaging studies (CT scan/ MRI scan of brain, PET scan, and
SPECT) have yielded inconsistent, yet suggestive findings. These findings include
ventricular dilatation, white matter hyper-intensities, and changes in the blood flow
and metabolism in several parts of brain (such as prefrontal cortex, anterior cingulate
cortex, and caudate).
is r ers
Psychosocial Theories
Psychoanalytic Theories
In depression, loss of a libidinal object, introjection of the lost objectQ, fixation in the
oral sadistic phase of development, and intense craving for narcissism or self-love are
some of the postulates of different psychodynamic theories. Mania represents a reaction
formation to depression according to the psycho dynamic theory.
Stress
Increased number of stressful life events before the onset or relapse has a formative
rather than a precipitating effect in depression though they can serve a precipitant role
in mania. Increased stressors in the early period of development are probably more
important in depression.
Psychiatry
3.2: Depression: Clinical Features
LEARNING OBJECTIVE: To understand the clinical presentation of depression and
Time Needed
1 reading
st
30 mins
2 look
nd
15 mins
1. Depressed Mood: The most important feature is the sadness of mood or loss
of interest and/or pleasure in almost all activities (pervasive sadness), present
throughout the day (persistent sadness).
2. The loss of interest in daily activities results in social withdrawal, decreased ability
to function in occupational and interpersonal areas and decreased involvement
in previously pleasurable activities. In severe depression, there may be complete
anhedonia (inability to experience pleasure).
3. Depressive Ideation/Cognition: Sadness of mood is usually associated with
pessimism, which can result in three common types of depressive ideas. These are:
a. Hopelessness (there is no hope in the future).
b. Helplessness (no help is possible now).
c. Worthlessness (feeling of inadequacy and inferiority).
Cognitive Theory of Depression (Ref : Kaplan)

Aaron Beck postulated a cognitive triad of depression that consists of (1) views about the
self: a negative self-precept; (2) about the environment: a tendency to experience the
world as hostile and demanding, and (3) about the future: the expectation of suffering
and failure. Therapy consists of modifying these distortions.
Cognitive distortions Definition
Arbitrary inference rawing a specific conclusion without sufficient evidence
Specific abstraction ocus on a single detail while ignoring other, more important aspects
of an experience
Overgenerali ation orming conclusions based on too little and too narrow experience
agnification and minimi ation Over- or undervaluing the significance of a particular event
Personali ation endency to self-reference external events without basis
Absolutist, dichotomous thinking endency to place experience into all-or-none categories
Learned Helplessness
• The learned helplessness theory of depression connects depressive phenomena to the
experience of uncontrollable events.
• For example, when dogs in a laboratory were exposed to electrical shocks from which
they could not escape, they showed behaviors that differentiated them from dogs
that had not been exposed to such uncontrollable events.
• The dogs exposed to the shocks would not cross a barrier to stop the flow of electric
shock when put in a new learning situation. They remained passive and did not move.
is r ers
• According to the learned helplessness theory, the shocked dogs learned that outcomes
were independent of responses, so they had both cognitive motivational deficit
(i.e., they would not attempt to escape the shock) and emotional deficit (indicating
decreased reactivity to the shock).
• In the reformulated view of learned helplessness as applied to human depression,
internal causal explanations are thought to produce a loss of self-esteem after adverse
external events.
The ideas of worthlessness can lead to self reproach and guilt-feelings. The other
features are difficulty in thinking, difficulty in concentration, indecisiveness, slowed
thinking, subjective poor memory, lack of initiative and energy. Often there are
ruminations (repetitive, intrusive thoughts) with pessimistic ideas. Thoughts of death
and preoccupation with death are not uncommon. Suicidal ideas may be present.
In severe cases, delusions of nihilism (e.g. ‘world is coming to an end’, ‘my brain is
completely dead’, ‘my intestines have rotted away’) may occur.
1. Psychomotor Activity
In younger patients (< 40 year old), retardation is more common and is characterised
by slowed thinking and activity, decreased energy and monotonous voice. In a severe
form, the patient can become stuporous (depressive stupor).
In the older patients (e.g. post-menopausal women), agitation is commoner. It often
presents with marked anxiety, restlessness (inability to sit still, hand wriggling,
picking at body parts or other objects) and a subjective feeling of unease.
Anxiety is a frequent accompaniment of depression. Irritability may present as easy
annoyance and frustration in day-to-day activities, e.g. unusual anger at the noise
made by children in the house.
2. Physical Symptoms
Multiple physical symptoms (such as heaviness of head, vague body aches) are
particularly com mon in the elderly depressives and depressed patients from the
developing countries (such as India). These physical symptoms are almost always
present in severe depressive episode.
Another common symptom is the complaints of reduced energy and easy fatigability.
The patients, therefore, not surprisingly attribute their symptoms to physical
cause(s) and consult a physician instead of a psychiatrist.
3. Biological Functions
Disturbance of biological functions is common, with insomnia (or sometimes
increased sleep), loss of appetite and weight (or sometimes hyperphagia and weight
gain), and loss of sexual drive.
4. Suicide
• About 10 to 15 percent of all depressed patients commit suicide, and about two
thirds have suicidal ideation.
• Patients with depressive disorders are at increased risk of suicide as they begin to
improve and regain the energy needed to plan and carry out a suicide (paradoxical
suicide).
Psychiatry
Suicidal risk is much more in the presence of following factors:
a. Presence of marked hopelessness
b. Males; age>40; unmarried, divorced/widowed
c. Written/verbal communication of suicidal intent and/or plan
d. Early stages of depression
e. Recovering from depression (At the peak of depression, the patient is usually either
too depressed or too retarded to commit suicide)
f. Period of 3 months from recovery.
5. Others
• Anxiety, a common symptom of depression, affects as many as 0 percent of
all depressed patients.
• About 50 to 75 percent of all depressed patients have a cognitive impairment,
sometimes referred to as depressive pseudodementia. Such patients commonly
complain of impaired concentration and forgetfulness.
Fig. 3.1: Triangle-shaped fold in the nasal corner of the upper eyelid associated
with depression and referred to as Veraguth’s fold.
Scales Used in Depression:

• Beck Depression Inventory (BDI):
• Hamilton Depression Scale (HAM-D)
• Montgomery-Asberg Depression Rating Scale (MADRS)
is r ers
3.3: Diagnostic Criteria of Major Depressive Episode (DSM-5)
LEARNING OBJECTIVE: To understand the diagnostic criteria of depression and answer
its related MCQs.
Time Needed
1 reading
st
20 mins
2 look
nd
10 mins
A. Five (or more) of the following symptoms have been present during the same
2-week period and represent a change from previous functioning; at least one of the
symptoms is either (1) depressed mood or (2) loss of interest or pleasure.
Note: Do not include symptoms that are clearly due to a general medical condition,
or mood-incongruent delusions or hallucinations.
1. depressed mood most of the day, nearly every day, as indicated by either
subjective report (e.g., feels sad or empty) or observation made by others (e.g.,
appears tearful). Note: In children and adolescents, can be irritable mood
2. markedly diminished interest or pleasure in all, or almost all, activities most of the
day, nearly every day (as indicated by either subjective account or observation
made by others)
3. significant weight loss when not dieting or weight gain (e.g., a change of more
than 5 of body weight in a month), or decrease or increase in appetite nearly
every day. Note: In children, consider failure to make expected weight gains.
4. insomnia or hypersomnia nearly every day
5. psychomotor agitation or retardation nearly every day (observable by others, not
merely subjective feelings of restlessness or being slowed down)
6. fatigue or loss of energy nearly every day
7. feelings of worthlessness or excessive or inappropriate guilt (which may be
delusional) nearly every day (not merely self-reproach or guilt about being sick)
8. diminished ability to think or concentrate, or indecisiveness, nearly every day
(either by subjective account or as observed by others)
9. recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation
without a specific plan, or a suicide attempt or a specific plan for committing suicide
B. The symptoms do not meet criteria for a mixed episode.
C. The symptoms cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
D. The symptoms are not due to the direct physiological effects of a substance (e.g., a
drug of abuse, a medication) or a general medical condition (e.g., hypothyroidism).
E. The symptoms are not better accounted for by bereavement, i.e., after the loss of a
loved one, the symptoms persist for longer than 2 months or are characterized by
marked functional impairment, morbid preoccupation with worthlessness, suicidal
ideation, psychotic symptoms, or psychomotor retardation.
Specifiers (Symptom eatures) (Ref : Kaplan)

With Psychotic Symptoms:
• The presence of psychotic features in major depressive disorder reflects severe
disease and is a poor prognostic indicator.
• The psychotic symptoms themselves are often categorized as either mood
congruent, that is, in harmony with the mood disorder
Psychiatry
• The following factors have been associated with a poor prognosis for patients with
mood disorders: long duration of episodes, temporal dissociation between the mood
disorder and the psychotic symptoms, and a poor premorbid history of social adjustment.
The presence of psychotic features also has significant treatment implications.
• These patients typically require antipsychotic drugs in addition to
antidepressants or mood stabilizers and may need ECT to obtain clinical improvement.
With Melancholic FeaturesQ

• Melancholia is one of the oldest terms used in psychiatry, dating back to Hippocrates
in the 4th century to describe the dark mood of depression.
• It is still used to refer to a depression characterized by severe anhedonia, early
morning awakening, weight loss, and profound feelings of guilt (often over trivial
events).
• It is not uncommon for patients who are melancholic to have suicidal ideation.
• Melancholia is associated with changes in the autonomic nervous system and in
endocrine functions.
• For that reason, melancholia is sometimes referred to as endogenous depression or
depression that arises in the absence of external life stressors or precipitants.
Melancholic Depression: (NIMHANS)
a. Diminished enjoyment in most activities
b. Inability to react to enjoyable stimuli;
c. Feelings of guilt
d. Decreased appetite
e. Psychomotor changes
With Atypical Features (AIIMS May 2018)

• Patients with atypical features have specific, predictable characteristics: overeating
and oversleeping.
• These symptoms have sometimes been referred to as reversed vegetative
symptoms, and the symptom pattern has sometimes been called hysteroid
dysphoria.
• Leyden Paralysis : Heaviness of limbs
• The patients with atypical features are found to have a younger age of onset, more
severe psychomotor slowing, and more frequent coexisting diagnoses of panic
disorder, substance abuse or dependence, and somatization disorder.
• The high incidence and severity of anxiety symptoms in patients with atypical features
have sometimes been correlated with the likelihood of their being misclassified as
having an anxiety disorder rather than a mood disorder.
• Patients with atypical features may also have a long-term course, a diagnosis of
bipolar disorder, or a seasonal pattern to their disorder
Seasonal Pattern
• Patients with a seasonal pattern to their mood disorders tend to experience depressive
episodes during a particular season, most commonly winter.
• The pattern has become known as seasonal affective disorder (SAD)
• These patients are likely to respond to treatment with light therapy.
is r ers
3.4: DMDD and PMDD
LEARNING OBJECTIVE: To understand the clinical presentation of DMDD and PMDD
Time Needed
1 reading
st
20 mins
2 look
nd
10 mins
Disruptive Mood Dysregulation Disorder:

This diagnosis should be made in individuals between the ages of 6 to 18 years.
Individuals should have the following symptoms for at least 12 months and these
symptoms should be present in at least 2 different situational settings:
a. Significant outbursts of temper manifested verbally or physically, not in keeping with
the situational context
b. Temper outbursts not consistent with developmental level
c. These outbursts occur on average at least 3 times per week
d. In between these temper outbursts; the individual’s mood is persistently irritable
Premenstrual Dysphoric Disorder:

Onset of symptoms should be at least in the week prior to the onset of menstruation,
and symptoms should improve within a few days after the onset of menstruation. The
intensity of symptoms should either become minimal or resolve post-menstruation.
An individual needs to have at least 5 of the following signs and symptoms for this
diagnosis to be made:
a. Mood swings
b. Increased interpersonal relationship conflicts
c. Feelings of low mood associated with hopelessness
d. Anxiousness
e. Reduction of interest in usual activities
f. Difficulties with concentration
g. Marked reduction in energy levels
h. Changes in appetite
i. Sleep difficulties
j. Sense of losing control
k. Physical symptoms such as breast tenderness/swelling, muscular pain, bloating
sensation, weight gain
Psychiatry
3.5: Neurotic Depression / Dysthymia
LEARNING OBJECTIVE: To understand the clinical presentation of Dysthymia and
Time Needed
1 reading
st
10 mins
2 look
nd
5 mins
Neurotic depression is usually characterised by the following clinical

features:
1. Presence of mild to moderate depression.
2. Depressive symptoms usually occur in response to a stressful situation but are often
quite disproportionate to the severity of stress.
3. Other ‘neurotic’ symptoms such as anxiety, obsessive symptoms, phobic symptoms,
and multiple somatic symptoms, are often present.
4. Preoccupation with the stressful condition is common. The typical course of neurotic
depression is chronic, with fluctuations. Delusions, hallucinations and other psychotic
features are characteristically absent.
The other common features include:

1. The reactivity of mood is preserved, i.e. the patient is able to emotionally react to
the events occur ring in his surroundings.
2. There may be insomnia or hypersomnia. There is usually difficulty in initiating sleep
and some times difficulty in awakening in the morning.
3. The mood may be worse in the evening, at the end of the day. The mood may also
become better in social gatherings and whilst engaged in recreational activities.
4. Suicidal threats and gestures are more common than completed suicide. However,
as suicide may be completed accidentally, all such threats should be taken seriously.
An episode of major depression may become super imposed on an underlying neurotic
depression. This is then known as double depression.
Neurotic depression has been renamed as dysthymia or dysthymic disorder in DSM-IV-
TR and ICD-10. This category does not require the presence of stress as a precipitating
factor, and does not put emphasis on the presence of other neurotic symptoms or traits.
Dysthymia is defined as any mild depression which is not severe enough to be called a
depressive episode, and lasts for two years or more. This is more common in females,
with an average age of onset in late third decade.
is r ers
3.6: Postpartum Disorders
LEARNING OBJECTIVE: To be able to differentiate clinically different types of post
partum psychiatric disorders and answer its related MCQs.
Time Needed
1 reading
st
20 mins
2 look
nd
10 mins
Disorder Onset Symptoms Mother’s feelings Treatment

toward baby
Postpartum blues Immediately after Sadness, mood o negative Supportive, usually
or baby blues birth up to weeks lability, tearfulness feelings self-limited
Postpartum ithin - months epressed mood, ay have negative Antidepressant
depression after birth weight changes, feelings toward medications
sleep disturbances, baby
and excessive
anxiety
Postpartum ithin - weeks epression, ay have thoughts Antipsychotic
psychosis after birth delusions, and of harming baby medication,
thoughts of harm lithium, and
possibly
antidepressants
Psychiatry
3.7: Treatment of Depression: (Ref : Kaplan)
LEARNING OBJECTIVE: To be able to understand different treatment modalities in
depression and their utility in management
Time Needed
1 reading
st
20 mins
2 look
nd
10 mins
An untreated depressive episode lasts 6 to 13 months; most treated episodes
last about 3 months. The withdrawal of antidepressants before 3 months has elapsed
almost always results in the return of the symptoms.
Depression:
The range of initial treatment modalities includes psychotherapy, pharmacotherapy, or
a combination of the two.
Electroconvulsive Therapy
• Discovered by Cerletti and Bini 1938
• Modified ECT means during anesthesia (Anesthetic agent MC used is Methohexitol)
(JIPMER)
• Most Common side effect of ECT is Amnesia. Mainly retrograde though some
anterograde also although amnesia is reversible in most cases.
• Pregnancy and old age ECT can be given
Fig. 3.2
is r ers
Indications:-
1. Catatonic Schizophrenia
2. Depression with suicidal tendency
3. Pts who are intolerant to S/E of medication non responder (mania, schizophrenia)
Non Psychiatric Indications for ECT:

1. Parkinson’s Disease, particularly rigidity and bradykinesia
2. Intractable seizure
3. Neuroleptic malignant syndrome
Contraindication:
No absolute contraindications
High Risk Patients Are

1. CNS lesions with increased intracranial pressure
2. Neurosurgical procedures.
3. Recent myocardial infarction or stroke within 4 to 6 weeks of events
4. Uncompensated congestive heart failure
5. High Risk Pregnancy
Side E ects:
• Headache
• Delirium confusion 10
• Memory loss 75
• Mortality 0.01 each patient
Choosing ECT as initial treatment in Depression

• ECT should be considered as a first-line therapy for severe major depressive disorder
when there are debilitating neuro-vegetative symptoms (e.g., significant weight loss
and nutritional compromise from reduced appetite, profound psychomotor retardation,
catatonic stupor, etc).
• Also should be considered when the patient has high potential lethality issues
(e.g., intense suicidality, clear evidence of repeated suicide attempts, significantly
aggressive behavior) or prominent psychotic features.
• ECT should also be considered a treatment choice for severely depressed patients who
are pregnant, who have responded well to prior ECT course(s), who have responded
poorly to adequate trials of antidepressants, or in situations where a particularly rapid
response is needed.
Pharmacotherapy (details in last chapter): Antidepressants, Tricyclic, SSRI’s,
SNRI’s, other atypical antidepressants etc
Psychotherapy (details in 9th chapter of this book) : Most evidence based support
in depression psychotherapy is for “COGNITIVE BEHAVIOURAL THERAPY” (CBT). Other
approach is interpersonal therapy or psychodynamic psychotherapy.
Psychiatry
Other Therapies
rTMS Repeated Transcranial Magnetic Stimulation
• Non-invasive technique for stimulating cerebral cortical cells by depolarization with
handheld high power magnets.
• Magnetic field generated: 1.5-2 T.
• Depolarization up to depth of 2 cm from the skull.
• Interneurons (placed horizontally) are depolarized more than others.
• Mechanism of action: Therapeutic mechanism is unknown, studies suggest that
rTMS may downregulate -adrenergic receptor, increases dopamine and serotonin
levels in striatum, frontal cortex seen in patients responding to high frequency rTMS.
• Low frequency current have Inhibitory’ effect on the cortical cells; while high
frequency currents have Excitatory’ effect.
• Labor-intensive procedure, as treatment is administered 5 days/week and a course
has 20-3-sessions.
• Depressive symptoms continue to decrease following cessation of a course of rTMS
treatment.
• Uses
Map motor cortex
Helps to determine hemisphere dominance
Probe short-term memory
Treatment of bradykinesia in parkinson’s disease
Psychiatric indications: Depressive Disorder (most researched), OCD, PTSD,
Schizophrenia, mania.
• Complications: Risk of seizure.
Fig. 3.3
is r ers
Transcranial Magnetic Stimulation
Fig. 3.4:
Fig. 3.5:
Psychiatry
Vagal Nerve Stimulation (VNS)
Fig. 3.6: Fig. 3.7:
• Vagal nerve is the 10th cranial; parasympathetic effect nerve that relays information
from nucleus tractus solitaries to `Locus Coeruleus ‘ and various other areas in Brain.
• VNS refers to stimulation of left vagal, nerve by using a Bipolar Pulse generator, which
is implanted in left chest wall (as Right cagus has supply to heart so not used).
• Uses:
1. Mood stabilization/Mood Elevation
2. Depressive Disorder-not responsive to multiple therapies
3. Intractable seizure disorder.
• Side effect-Mild transient hoarseness.
Vagal Nerve Stimulation

The use of left vagal nerve stimulation (VNS) using an electronic
device implanted in the skin, similar to a cardiac pacemaker.
is r ers
Deep Brain Stimulation
• Involves creating a small hole in the skull, passing a fine wire in the selected brain
region.
• Wire is subcutaneously connect to a pacemaker device implanted in the chest wall.
• Primarily used in Parkinson’s disease-stimulation of thalamus.
• OCD and Tourette’s disorder-stimulation of internal capsule.
Fig. 3.8:
Sleep Deprivation
Sleep deprivation may precipitate mania in patients who are bipolar I and temporarily
relieve depression in those who are unipolar.
Psychiatry
3.8 Special types of Depression:
LEARNING OBJECTIVE: To be able to differentiate clinically unipolar depression and
bipolar depression and answer its related MCQs.
Time Needed
1 reading
st
15 mins
2 look
nd
10 mins
Bipolar depression:
A depression with a previous history of mania/hypomania.
Treatment of Acute Bipolar Depression (Ref : Kaplan)

A fixed combination of olanzapine and fluoxetine has been shown to be effective in
treating acute bipolar depression. Amongst mood stabilizers, for this case, best results
in this case is with LAMOTRIGINE.
Clinical Features Predictive of Bipolar Disorder (JIPMER)
Early age at onset
Psychotic depression before years of age
Postpartum depression, especially one with psychotic features
Rapid onset and offset of depressive episodes of short duration months
Recurrent depression more than five episodes
epression with marked psychomotor retardation
Atypical features reverse vegetative signs
Seasonality
ipolar family history
igh-density, three-generation pedigrees
rait mood lability cyclothymia
yperthymic temperament
ypomania associated with antidepressants
Repeated at least three times loss of efficacy of antidepressants after initial response
epressive mixed state with psychomotor excitement, irritable hostility, racing thoughts, and sexual arousal
during ma or depression
Recurrent Depressive Disorder

This disorder is characterised by recurrent (at least two) depressive episodes minimum
2 weeks apart. (unipolar depression).
is r ers
3.9: Mania
LEARNING OBJECTIVE: To be able to understand the clinical presentation and
diagnosis of mania and hypomania and their management and answer its related MCQs.
Time Needed
1 reading
st
30 mins
2 look
nd
15 mins
Clinical Features:
1. Elevated, Expansive or Irritable Mood
The elevated mood can pass through following four stages, depending on the severity
of manic episode:
a. Euphoria (mild elevation of mood): An increased sense of psychological well-being
and happiness, not in keeping with ongoing events. This is usually seen in hypomania
(Stage I).
b. Elation (moderate elevation of mood): A feeling of confidence and enjoyment, along
with an increased psychomotor activity. Elation is classically seen in mania (Stage
II).
c. Exaltation (severe elevation of mood): Intense elation with delusions of grandeur;
seen in severe mania (Stage III).
d. Ecstasy (very severe elevation of mood): Intense sense of rapture or blissfulness;
typically seen in delirious or stuporous mania (Stage IV).
2. Psychomotor Activity
There is an increased psychomotor activity, ranging from overactiveness and
restlessness, to manic excitement where the person is ‘on-the-toe-on-the-go’, (i.e.
involved in ceaseless activity). The activity is usually goal-oriented and is based on
external environmental cues.
3. Speech and Thought
The person is more talkative than usual; describes thoughts racing in his mind; develops
pressure of speech; uses playful language with punning, rhyming, joking and teasing;
and speaks loudly.
Later, there is ‘flight of ideas’ (rapidly produced speech with abrupt shifts from topic to
topic, using external environmental cues. Typically the connections between the shifts
are apparent). When the ‘flight’ becomes severe, incoherence may occur. A less severe
and a more ordered ‘flight’, in the absence of pressure of speech, is called ‘prolixity’.
There can be delusions (or ideas) of grandeur (grandiosity), with markedly inflated self-
esteem. Delusions of persecution may sometimes develop secondary to the delusions of
grandeur (e.g. I am so great that people are against me). Hallucinations (both auditory
and visual), often with religious content, can occur (e.g. God appeared before me and
spoke to me). Since these psychotic symptoms are in keeping with the elevated mood
state, these are called mood congruent psychotic features.
Distractibility is a common feature and results in rapid changes in speech and activity,
in response to even irrelevant external stimuli.
Psychiatry
4. Goal-directed Activity
The person is unusually alert, trying to do many things at one time. In hypomania, the
ability to function becomes much better and there is a marked increase in productivity
and creativity. Many artists and writers have contributed significantly in such periods. As
past history of hypomania and mild forms of mania is often difficult to elicit, it is really
important to take additional historical information from reliable informants (e.g. family
members). In mania, there is marked increase in activity with excessive planning and,
at times, execution of multiple activities. Due to being involved in so many activities and
distractibility, there is often a decrease in the functioning ability in later stages. There
is marked increase in sociability even with previously unknown people. Gradually this
sociability leads to an interfering behaviour though the person does not recognise it
as abnormal at that time. The person becomes impulsive and disinhibited, with sexual
indiscretions, and can later become hypersexual and promiscuous.
Due to grandiose ideation, increased sociability, overactivity and poor judgement, the
manic person is often involved in the high-risk activities such as buying sprees, reckless
driving, foolish business investments, and distributing money and/or personal articles to
unknown persons. He is usually dressed up in gaudy and flamboyant clothes, although
in severe mania there may be poor self-care.
5. Other Features
Sleep is usually reduced with a decreased need for sleep. Appetite may be increased but
later there is usually decreased food intake, due to marked overactivity. Insight into the
illness is absent, especially in severe mania.
DSM-5 diagnostic Criteria for Manic Episode

A. A distinct period of abnormally and persistently elevated, expansive, or irritable
mood, lasting at least 1 week (or any duration if hospitalization is necessary).
B. During the period of mood disturbance, three (or more) of the following symptoms
have persisted (four if the mood is only irritable) and have been present to a significant
degree:
1. inflated self-esteem or grandiosity
2. decreased need for sleep (e.g., feels rested after only 3 hours of sleep)
3. more talkative than usual or pressure to keep talking
4. flight of ideas or subjective experience that thoughts are racing
5. distractibility (i.e., attention too easily drawn to unimportant or irrelevant external
stimuli)
6. increase in goal-directed activity (either socially, at work or school, or sexually)
or psychomotor agitation
7. excessive involvement in pleasurable activities that have a high potential for
painful consequences (e.g., engaging in unrestrained buying sprees, sexual
indiscretions, or foolish business investments)
C. The symptoms do not meet criteria for a mixed episode.
D. The mood disturbance is sufficiently severe to cause marked impairment in
occupational functioning or in usual social activities or relationships with others, or to
necessitate hospitalization to prevent harm to self or others, or there are psychotic
features.
is r ers
E. The symptoms are not due to the direct physiological effects of a substance (e.g.,
a drug of abuse, a medication, or other treatment) or a general medical condition
(e.g., hyperthyroidism).
Note: Manic-like episodes that are clearly caused by somatic antidepressant treatment
(e.g., medication, electroconvulsive therapy, light therapy) should not count toward a
diagnosis of bipolar I disorder.
Features of hypomania Features of mania
Present for at least 4 days Present for at least 7 days
Core features mild or moderate Core features marked
ild or moderate dysfunction Substantial dysfunction
Partial insight preserved inimal or absent insight
o psychotic features Psychotic symptoms may occur
Treatment of Acute Mania (Details of drugs in last chapter)

1. Lithium Carbonate
2. Valproate
3. “Valproate has surpassed lithium in use for acute mania” (Ref : Kaplan)
4. Carbamazepine and Oxcarbazepine
5. Clonazepam and Lorazepam
6. Atypical and Typical Antipsychotics
Psychiatry
3.10: Bipolar Disorders
LEARNING OBJECTIVE: To be able to understand the clinical presentation and diagnosis
of bipolar disorders and and answer its related MCQs.
Time Needed
1 reading
st
20 mins
2 look
nd
10 mins
Bipolar Mood (or A ective) Disorder

This disorder, earlier known as manic depressive psychosis (MDP), is characterised by
recurrent episodes of mania and depression in the same patient at different times.
These episodes can occur in any sequence.
Bipolar mood disorder is further classified in to bipolar I and bipolar II disorders
• Bipolar Affective Disorder‑1 : Mania and Depression
• Bipolar Affective Disorder‑2: Hypomania and depression
• Cyclothymia is characterized by at least 2 years of frequently occurring hypomanic
symptoms that cannot fit the diagnosis of manic episode and of depressive symptoms
that cannot fit the diagnosis of major depressive episode.
• Rapid Cycling: Patients with rapid cycling bipolar I disorder are likely to be female
and to have had depressive and hypomanic episodes. The DSM-5 criteria specify that
the patient must have at least four episodes within a 12-month period.
Prognostic Factors in Mood Disorders (Ref : Niraj Ahuja)

Good Prognostic Factors
1. Acute or abrupt onset
2. Typical clinical features
3. Severe depression
4. Well-adjusted premorbid personality
5. Good response to treatment.
Poor Prognostic Factors

1. Co-morbid medical disorder, personality disorder or alcohol dependence
2. Double depression (acute depressive episode superimposed on chronic depression
or dysthymia)
3. Catastrophic stress or chronic ongoing stress
4. Unfavourable early environment
5. Marked hypochondriacal features, or mood-incongruent psychotic features
6. Poor drug compliance.
Treatment of Bipolar disorders: Mood stabilizers
is r ers
Worksheet
• MCQ OF “MOOD DISORDERS” FROM DQB

Psychiatry
Elements of Cognitive Theory
Cognitive distortions Definition ample
Arbitrary inference
Specific abstraction
Overgenerali ation
agnification and minimi ation
Personali ation
Absolutist, dichotomous thinking
Disorder Onset Symptoms Mother’s feelings Treatment

toward baby
Postpartum blues or
“baby blues”
Postpartum depression
Postpartum psychosis
Clinical Features Predictive of Bipolar Disorder (JIPMER)

is r ers
Features of hypomania Features of mania
Fill In The Blanks: (Revision)

1. A major depressive episode must last at least ______, and typically a person
with a diagnosis of a major depressive episode also experiences at least four
symptoms from a list that includes changes in appetite and weight, changes in
sleep and activity, lack of energy, feelings of guilt, problems thinking and making
decisions, and recurring thoughts of death or suicide.
2. A manic episode is a distinct period of an abnormally and persistently elevated,
expansive, or irritable mood lasting for at least ______, or less if a patient must
be hospitalized.
3. A hypomanic episode lasts at least ______and is similar to a manic episode
except that it is not sufficiently severe to cause impairment in social or occupational
functioning, and no psychotic features are present.
4. ________ disorder is characterized by at least _____ of depressed mood that
is not sufficiently severe to fit the diagnosis of major depressive episode.
5. _________ disorder is characterized by at least _______of frequently
occurring hypomanic symptoms that cannot fit the diagnosis of manic episode and
of depressive symptoms that cannot fit the diagnosis of major depressive episode.
4 Neurotic Disorders
CONCEPTS
Â Concept 4.1 Anxiety Disorders types
Â Concept 4.2 Phobia types
Â Concept 4.3 Obsessive compulsive disorder (OCD)
Â Concept 4.4 Obsessive – compulsive related disorders
Â Concept 4.5 Trauma and Stress - related disorders
Â Concept 4.6 Disruptive, Impulse control and conduct

disorder
Â Concept 4.7 Somatic Symptom & Related disorders
Â Concept 4.8 Factitious disorder & Conversion disorder
Â Concept 4.9 Dissociative disorders

e r tic is r ers
Concept 4.1: Anxiety Disorders Types
LEARNING OBJECTIVE: To identify different types of anxiety disorders clinically and
understand their management principles.
Time needed
1 reading
st
20 mins
2 look
nd
10 mins
Generalised Anxiety Disorder

• This is characterised by an insidious onset in the third decade and a stable, usually
chronic course (free floating anxiety) which may or may not be punctuated by
repeated panic attacks (episodes of acute anxiety).
• The symptoms of anxiety should last for at least a period of 6 months
Panic Disorder
• This is characterised by discrete episodes of acute anxiety with a feeling of
impending doom (catastrophe). The onset is usually in early third decade with
often a chronic course.
• The episode is usually sudden in onset, lasts for a few minutes and is characterised
by very severe anxiety.
• Classically the symptoms begin unexpectedly or ‘out-of-the-blue’. Usually there is no
apparent precipitating factor, though some patients report exposure to phobic stimuli
as a precipitant. Panic disorder is usually seen about 2-3 times more often in females.
Panic disorder can present either alone or with agoraphobia.
Phobic Disorder
Phobia is defined as an irrational fear of a specific object, situation or activity, often
leading to persistent avoidance of the feared object, situation or activity.
Neurotransmitters INVOLVED: norepinephrine (NE), serotonin, and GABA.
TREATMENT ANXIETY DISORDERS:

1. Psychotherapy is very effective (behavioral therapy used)
2. Pharmacotherapy: SSRI most preferred
3. For Panic Attack: Benzodiazepines and for panic disorder: SSRI
Phobic anxiety Panic disorder Generalized anxiety
Occurrence of anxiety Situational Paroxysmal Persistent
Associated behaviour Avoidance Escape Agitation
Associated cognitions Fear of situation Fear of symptoms Worry
Somatic symptoms With exposure Episodic Persistent
Psychiatry
Concept 4.2: Types of Phobia
LEARNING OBJECTIVE: To identify different types of anxiety PHOBIA clinically and
understand their management principles.
Time needed
1 reading
st
20 mins
2 look
nd
10 mins
Agoraphobia
• Agoraphobia is an example of irrational fear of situations.
• It is characterised by an irrational fear of being in places away from the familiar
setting of home.
• Although it was earlier thought to be a fear of open spaces only, now it includes fear
of open spaces, public places, crowded places, and any other place from where there
is no easy escape to a safe place.
• In fact, the patient is afraid of all the places or situations from where escape may
be perceived to be difficult or help may not be available, if he suddenly develops
embarrassing or incapacitating symptoms.
• These embarrassing or incapacitating symptoms are the classical symptoms of panic.
• A full-blown panic attack may occur (agoraphobia with panic disorder) or only a
few symptoms (such as dizziness or tachycardia) may occur (agoraphobia without
panic disorder).
• As the agoraphobia increases in severity, there is a gradual restriction in the normal
day-to-day activities.
• The activities may become so severely restricted that the person becomes self-
imprisoned at his home.
Social Phobia
• This is an example of irrational fear of activities or social interaction, characterised by
an irrational fear of performing activities in the presence of other people or interacting
with others. The patient is afraid of his own actions being viewed by others critically,
resulting in embarrassment or humiliation.
• examples include fear of blushing (erythrophobia), eating in company of others,
public speaking, public performance (e.g. on stage), participating in groups, writing
in public (e.g. signing a check), speaking to strangers (e.g. for asking for directions),
dating, speaking to authority figures, and urinating in a public lavatory (shy bladder).
Specific (Simple) Phobia

• Specific phobia is characterised by an irrational fear of a specified object or situation.
Anticipatory anxiety leads to persistent avoidant behaviour, while confrontation with
the avoided object or situation leads to panic attacks.
• The disorder is diagnosed only if there is marked distress and/or disturbance in daily
functioning, in addition to fear and avoidance of the specified object or situation.
e r tic is r ers
Phobias
Acrophobia Fear of heights
Agoraphobia Fear of open places
Ailurophobia Fear of cats
Hydrophobia Fear of water
Claustrophobia Fear of closed spaces
Cynophobia Fear of dogs
Mysophobia Fear of dirt and germs
Pyrophobia ear of fire
Xenophobia Fear of strangers
Zoophobia Fear of animals
TREATMENT PHOBIAS:
Behavior therapy :-Systemic de-sensitization (Graded exposure technique)
(treatment of choice); Flooding (sudden exposure) also used
Common Symptoms of anxiety

Component Prominent features
Emotion/mood Anxiety, irritability
Cognitions Exaggerated worries and fears
Behaviour Avoidance of feared situations
Checking
Seeking reassurance
Somatic symptoms Tight chest
Short of breath
Palpitations
utter ies
Tremor
ingling of fingers due to hyperventilation
Aches and pains
Poor sleep
Frequent desire to pass urine and defecate
Psychiatry
Concept 4.3: Obsessive compulsive disorder:
LEARNING OBJECTIVE: To identify different types of OCD clinically and understand
their management principles.
Time needed
1 reading
st
20 mins
2 look
nd
10 mins
An obsession is defined as:

1. An idea, impulse or image which intrudes into the conscious awareness repeatedly.
2. It is recognised as one’s own idea, impulse or image but is perceived as ego-alien
(foreign to one’s personality).
3. It is recognised as irrational and absurd (insight is present).
4. Patient tries to resist against it but is unable to.
5. Failure to resist, leads to marked distress.
An obsession is usually associated with compulsion(s).
A compulsion is defined as:

1. A form of behaviour which usually follows obsessions.
2. It is aimed at either preventing or neutralising the distress or fear arising out of
obsession.
3. The behaviour is not realistic and is either irrational or excessive.
4. Insight is present, so the patient realises the irrationality of compulsion.
5. The behaviour is performed with a sense of subjective compulsion (urge or impulse
to act).
Compulsions may diminish the anxiety associated with obsessions
Four clinical syndromes:

1. Washers: Here the obsession is of contamination with dirt, germs, body excretions
and the like. The compulsion is washing of hands or the whole body, repeatedly
many times a day. It usually spreads on to washing of clothes, washing of bathroom,
bedroom, door knobs and personal articles, gradually. The person tries to avoid
contamination but is unable to, so washing becomes a ritual.
2. Checkers: In this type, the person has multiple doubts, e.g. the door has not been
locked, kitchen gas has been left open, counting of money was not exact, etc. The
compulsion, of course, is checking repeatedly to ‘remove’ the doubt. Any attempt
to stop the checking leads to mounting anxiety. Before one doubt has been cleared,
other doubts may creep in.
3. Pure Obsessions: This syndrome is characterised by repetitive intrusive thoughts,
impulses or images which are not associated with compulsive acts. The content is
usually sexual or aggressive in nature. The distress associated with these obsessions
is dealt usually by counter-thoughts (such as counting) and not by behavioural
rituals. A variant is obsessive rumination, which is a preoccupation with thoughts.
Here, the person repetitively ruminates in his mind about the pros and cons of the
thought concerned.
e r tic is r ers
4. Primary Obsessive Slowness: A relatively rare syndrome, it is characterised by
severe obsessive ideas and/or extensive compulsive rituals, in the relative absence
of manifested anxiety. This leads to marked slowness in daily activities.
Sigmund Freud found obsessions and phobias to be psychogenetically related.
• Isolation of Affect: By this defense mechanism, ego removes the affect (isolates
the affect) from the anxiety-causing idea. The idea is thus weakened, but remains still
in the consciousness. The affect however becomes free and attaches itself to other
neutral idea(s) by symbolic associations. Thus, these neutral ideas become anxiety-
provoking and turn into obsessions. This happens only when isolation of affect is not
fully successful (incomplete isolation of affect). When it is fully successful, both the
idea and affect are repressed and there are no obsessions.
• ndoing: This defense mechanism leads to compulsions, which prevent or undo the
feared consequences of obsessions.
• Reaction formation results in the formation of obsessive compulsive personality
traits rather than contributing to obsessive compulsive symptoms, while displacement
leads to formation of phobic symptoms
Fig 4.1: Bilateral Caudate Atrophy is seen in OCD (JIPMER)
TREATMENT OCD:
Behavior Therapy:
• Exposure and response prevention (ERP) is psychotherapy of choice
• Thought stopping
• Modeling
Drug of choice SSRI (fluoxetine, fluvoxamine preferred), clomipramine (most
effective), risperidone (augmenting agent for resistant OCD)
Treatment resistant ECT and psychosurgery (cingulotomy) may be considered
Psychiatry
Concept 4.4: Obsessive compulsive related disorders:
LEARNING OBJECTIVE: To identify different types of OCD related disorders clinically
and understand their management principles.
Time needed
1 reading
st
20 mins
2 look
nd
10 mins
1. Body Dysmorphic Disorder

Preoccupation with an imagined defect in appearance (Hair, Nose, Skin)
If a slight anomaly is present, the person’s concern is markedly excessive
The preoccupation causes clinically significant distress or impairment in functioning
2. Hoarding Disorder:
Individuals a icted with this condition have marked difficulties with disposing of
items, regardless of their actual value.
The difficulty with disposing items has been attributed to a preoccupation with
regards to needing to save the items, and to the distress associated with disposing.
These behavioural difficulties result in the accumulation of items that clutter
personal living spaces.
The disorder must have resulted in significant impairments in terms of functioning,
and must not have been attributed to another medical disorder such as underlying
brain injury, cerebrovascular disease or Prader-Willi syndrome.
In hoarding disorder, ERP has poor prognosis (NEET 1 )
. Trichotillomania (Hair Pulling disorder)
Fig 4.2:
Habit reversal is the treatment of choice in trichotillomania and other impulse

control disorders. (There is nothing called as habit and response prevention)
e r tic is r ers
. Excoriation (Skin Picking) disorder:
Excessive picking leading to excoriation
Fig 4.3:
OCD and Related Disorder, Includes: Treatment

1. OCD SSRI, ERP
2. BDD SSRI
3. HOARDING DISORDER SSR O RP
4. TRICHOTILLOMANIA SSRI, HABIT REVERSAL
5. EXCORIATION DISORDER SSRI
Psychiatry
Concept 4.5: Stress Related Disorders
LEARNING OBJECTIVE: To identify different types of stress related disorders clinically
and understand their management principles.
Time needed
1 reading
st
30 mins
2 look
nd
15 mins
Acute Stress Reaction

In this disorder there is an immediate and clear temporal relationship between an
exceptional stressor (such as death of a loved one, natural catastrophe, accident, rape)
and the onset of symptoms. The symptoms show a mixed and changing picture. This
disorder is more likely to develop in presence of physical exhaustion and in extremes of
age. It is also more commonly seen in female gender and people with poor coping skills.
The symptoms range from a ‘dazed’ condition, anxiety, depression, anger, despair,
overactivity or withdrawal, and constriction of the field of consciousness. The symptoms
resolve rapidly (within few hours usually), if removal from the stressful environment
is possible. If the stress continues or cannot be reversed, the resolution of symptoms
begins after 1-2 days and is usually minimal after about three days.
Treatment
The treatment consists of removal of the patient from the stressful environment and
helping the patient to ‘pass through’ the stressful experience. IV or oral benzodiazepines
(such as diazepam) may be needed in cases with marked agitation.
Post-traumatic Stress Disorder (PTSD)

• This disorder arises as a delayed and/protracted response to an exceptionally stressful
or catastrophic life event or situation, which is likely to cause pervasive distress
in ‘almost any person’ (e.g disasters, war, rape or torture, serious accident). The
symptoms of PTSD may develop, after a period of latency, within six months after the
stress or may be delayed beyond this period.
• PTSD is characterised by recurrent and intrusive recollections of the stressful event,
either in ash ac s (images, thoughts, or perceptions) and/or in dreams. There is an
associated sense of re-experiencing of the stressful event.
• There is marked avoidance of the events or situations that arouse recollections of the
stressful event, along with marked symptoms of anxiety and increased arousal.
• The other important clinical features of PTSD include partial amnesia for some aspects
of the stressful event, feeling of numbness, and anhedonia (inability to experience
pleasure).
Treatment:
1) Pharmacotherapy
Selective serotonin reuptake inhibitors (SSRIs) are considered first-line treatments
for PTSD.
2) Psychotherapy
e r tic is r ers
Psychotherapeutic interventions for PTSD include behavior therapy, cognitive
therapy, and hypnosis. CBT IS MOST PREFERRED
Another psychotherapeutic technique that is relatively novel and somewhat
controversial is eye movement desensitization and reprocessing (EMDR), in
which the patient focuses on the lateral movement of the clinician’s finger while
maintaining a mental image of the trauma experience.
Adjustment Disorders
• Adjustment disorders are one of the commoner psychiatric disorders seen in the
clinical practice. They are most frequently seen in adolescents and women. Although
adjustment disorder is often precipitated by one or more stressors, it usually
represents a maladaptive response to the stressful life event(s).
• In ICD-10, this disorder is characterised by those disorders which occur within 1
month of a significant life change (stressor). This disorder usually occurs in those
individuals who are vulnerable due to poor coping skills or personality factors. It is
assumed that the disorder would not have arisen in the absence of the stressor(s).
The duration of the disorder is usually less than 6 months, except in the case of
prolonged depressive reaction.
• The various subtypes include brief or prolonged depressive reaction, mixed anxiety
and depressive reaction, and adjustment disorder with predominant disturbance of
other emotions and/or predominant disturbance of conduct.
• Most patients recover within a period of three months.
Treatment: Supportive Psychotherapy is treatment of choice
Acute Stress Disorder Post Traumatic Stress Disorder Adjustment Disorder

Onset: With in 3 Days of Stress With in 1 Month of Stress With in 1 Month of Stress
Duration: Upto 1 Month Beyond 1 Month Maximum Upto 6 Months of
Removal of Stress
Psychiatry
Concept 4.6: Disruptive, Impulse control and conduct disorders
LEARNING OBJECTIVE: To be able to name and categorize different types of habit and
impulse control disorders
Time needed
1 reading
st
10 mins
2 look
nd
5 mins
Habit and impulse control disorder, term was used in DSM IV TR, which included
kleptomania, pyromania, intermittent explosive disorder, pathological gambling and
trichotillomania. From this classification, in DSM 5, trichotillomania is now classified
under OCD and related disorders and pathological gambling has been renamed as
gambling disorder and moved to substance use and related disorder. The new category
disruptive, impulse control and conduct disorder includes the 3 disorders (kleptomania,
pyromania and intermittent explosive disorder) and also includes oppositional defiant
disorder and conduct disorder.
Habit and Impulse Disorders Disruptive, Impulse Control and Conduct

(DSM IV) Disorders (DSM 5)
leptomania impulse to steal Kleptomania
Pyromania impulse to set fire Pyromania
ntermittent explosive disorder uncontrolled anger Intermittent explosive disorder
outbursts
Pathological gambling
Trichotillomania
e r tic is r ers
Concept 4.7: Somatic Symptom and Related Disorders (Previously Kno n
as Somatoform Disorders in DSM-IV TR)
LEARNING OBJECTIVE: To identify different types of somatic symptoms and related
disorders clinically and understand their management principles.
Time needed
1st reading 20 mins
2 look
nd
10 mins
1) Somati ation disorder:

Usually female of age less than 30 years, duration usually more than 2 years
Multiple somatic symptoms involving multiple organ system.
Symptoms are recurrent and chronic changing symptoms
Refusal to accept the advice or reassurance of doctors not explained by another
mental illness e.g. Depression.
2) Hypochondriacal disorder:
Persistent pre occupation with fear or belief of having serious disease, based on
their misinterpretation of physical signs and sensations.
The belief must last 6 months
Fear or belief is not a delusion
Belief persists even after showing normal reports
) Persistent somatoform pain disorder:

It was previously called as psychogenic pain disorder. In this disorder, persistent,
severe and distressing pain is the main feature which is, either grossly in excess
of what is expected from the physical findings, or inconsistent with the anatomical
distribution of nervous system.
Preoccupation with pain is common. There is often a precipitating stressful event
and secondary gain may be present. Repeated change of physicians (doctor-
shopping) is common.
The affected person often assumes a ‘sick-role’ or an ‘invalid-role’. Abuse and
dependence of analgesics and minor tranquilisers is common, particularly when
the course is chronic.
This disorder is more common in females, with an onset in the third or fourth
decade of life.
Somatization disorder Somatoform pain disorder Hypochondriasis

Multiple symptoms Only pain symptom Presents with diagnosis
Ask for symptom relief Ask for pain relief Ask for diagnosis confirmation
Psychiatry
Concept 4.8: Conversion disorder and Factitious disorder
LEARNING OBJECTIVE: To identify clinically conversion disorder and factitious disorder
Time needed
1st reading 20 mins
2 look
nd
10 mins
Conversion Disorder
Conversion disorder is characterised by the following clinical features:
1. Presence of symptoms or deficits affecting motor or sensory function, suggesting a
medical or neurological disorder.
2. Sudden onset.
3. Development of symptoms usually in the presence of a significant psychosocial
stressor(s).
4. A clear temporal relationship between stressor and development or exacerbation of
symptoms.
5. Patient does not intentionally produce the symptoms.
6. There is usually a ‘secondary gain’ (to gain attention of attendants, patient increases
symptoms demonstration in their presence)
7. Detailed physical examination and investigations do not reveal any abnormality that
can explain the symptoms adequately.
8. The symptom may have a ‘symbolic’ relationship with the stressor/conflict.
There can be two different types of disturbances in conversion disorder; motor and
sensory. Autonomic nervous system is typically not involved, except when the voluntary
musculature is involved, e.g. vomiting, globus hystericus.
Treatment:
• Psychiatric interviewing
• Drug assisted interviewing or narcoanalysis
• Hypnosis
• Strong suggestion
• Aversion therapy
FACTITIOUS DISORDER:
Diagnostic Criteria for Factitious Disorder:
A. Intentional production or feigning of physical or psychological signs or symptoms.
B. The motivation for the behavior is to assume the sick role.
C. External incentives for the behavior (such as economic gain, avoiding legal
responsibility, or improving physical well-being, as in malingering) are absent.
e r tic is r ers
Concept 4.9: Dissociative Disorders
LEARNING OBJECTIVE: To identify different types of somatic dissociative disorders
clinically and understand their management principles.
Time needed
1 reading
st
20 mins
2 look
nd
10 mins
The essential feature of the dissociative disorders is a disruption in the usually integrated
functions of consciousness, memory, identity, or perception of the environment. The
disturbance may be sudden or gradual, transient or chronic.
1. Disturbance in the normally integrated functions of consciousness, identity and/or
memory.
2. Onset is usually sudden and the disturbance is usually temporary. Recovery is often
abrupt.
3. Often, there is a precipitating stress before the onset. There is a clear temporal
relationship between the stressor and the onset of the illness. A frequent stressful
situation is an ongoing war.
4. A ‘secondary gain’ resulting from the development of symptoms may be found.
5. Detailed physical examination and investigations do not reveal any abnormality that
can explain the symptoms adequately.
Dissociative Amnesia
The predominant disturbance is one or more episodes of inability to recall important
personal information, usually of a traumatic or stressful nature, that is too extensive to
be explained by ordinary forgetfulness.
Ganser’s syndrome ( hysterical pseudodementia) is commonly found in prison inmates.
The characteristic feature is vorbeireden, which is also called as ‘approximate answers’.
The answers are wrong but show that the person understands the nature of question
asked. For example; when asked the colour of a red pen, the patient calls it blue.
Depersonali ation Disorder

A. Persistent or recurrent experiences of feeling detached from, and as if one is an
outside observer of, one’s mental processes or body (e.g., feeling like one is in a
dream).
B. During the depersonalization experience, reality testing remains
C. intact.
Dissociative Fugue
A. The predominant disturbance is sudden, unexpected travel away from home or one’s
customary place of work, with inability to recall one’s past.
B. Confusion about personal identity or assumption of a new identity (partial or
complete).
Psychiatry
Dissociative Identity Disorder
A. The presence of two or more distinct identities or personality states (each with its
own relatively enduring pattern of perceiving, relating to, and thinking about the
environment and self).
B. At least two of these identities or personality states recurrently take control of the
person’s behavior.
C. Inability to recall important personal information that is too extensive to be explained
by ordinary forgetfulness.
Disso Amnesia Disso Fugue Disso Disso Identity disorder

Depersonalisation
Memory loss Memory loss + Travel “As if” detached from Change of identity
self
Patchy loss Assumes a new identity Out of self experience Amnesia of event
e r tic is r ers
Worksheet
• MCQ OF “NEUROTIC DISORDERS” FROM DQB

Psychiatry
Phobic anxiety Panic disorder Generalized anxiety
Occurrence of anxiety
Associated behaviour
Associated cognitions
Somatic symptoms
OCD and Related Disorder, includes: Treatment

OCD
BDD
HOARDING DISORDER
TRICHOTILLOMANIA
EXCORIATION DISORDER
Acute Stress Disorder Post Traumatic Stress Disorder Adjustment Disorder

e r tic is r ers
Habit and Impulse Disorders Disruptive, Impulse Control and Conduct

(DSM IV) Disorders (DSM 5)
Somatization disorder Somatoform pain disorder Hypochondriasis
Disso Amnesia Disso Fugue Disso Depersonalisation Disso Identity disorder

5 Organic Mental Disorders
(Neurocognitive Disorders)
CONCEPTS
Â Concept 5.1 Delirium
Â Concept 5.2 Dementia
Â Concept 5.3 Amnestic Syndrome
In the Diagnostic Statistical Manual of Mental Disorders (DSM-5), neurocognitive disorders

include three groups of disorders delirium, dementia, and the amnestic disorders are
characterized by the primary symptom common to all the disorders, which is an impairment
in cognition (as in memory, language, or attention).
r anic ental is r ers
Concept 5.1: Delirium
LEARNING OBJECTIVE: To understand the etiology and clinical presentation of acute
delirium and answer its related MCQ.
Time Needed
1 reading
st
30 mins
2 look
nd
15 mins
A. Clouding of consciousness, i.e. Reduced clarity of awareness of the environment,

with reduced ability to Focus, sustain, or shift attention.
B. Disturbance of cognition, manifest by both:
(1) Impairment of immediate recall and recent memory, with relatively intact
remote memory;
(2) Disorientation in time, place or person.
C. At least one of the following psychomotor disturbances:
(1) Rapid, unpredictable shifts from hypo-activity to hyper-activity;
(2) Increased reaction time;
(3) Increased or decreased flow of speech;
(4) enhanced startle reaction.
D. Disturbance of sleep or the sleep-wake cycle, manifest by at least one of the following:
(1) insomnia, which in severe cases may involve total sleep loss, with or without
daytime drowsiness, or reversal of the sleep-wake cycle;
(2) nocturnal worsening of symptoms;
(3) disturbing dreams and nightmares which may continue as hallucinations or
illusions after awakening.
E. Rapid onset and fluctuations of the symptoms over the course of the day.
F. Objective evidence from history, physical and neurological examination or laboratory
tests of an underlying cerebral or systemic disease (other than psychoactive substance-
related) that can be presumed to be responsible for the clinical manifestations in A-D.
The motor symptoms in delirium can include:
1. Asterixis (flapping tremor),
2. Multifocal myoclonus,
3. Carphologia or occillation (picking movements at cover-sheets and clothes),
4. Occupational delirium (elaborate pantomimes as if continuing their usual occupation
in the hospital bed)
5. Tone and reflex abnormalities.
Psychiatry
Predisposing Factors in Delirium
1. Pre-existing brain damage or dementia
2. Extremes of age (very old or very young)
3. Previous history of delirium
4. Alcohol or drug dependence
5. Generalised or focal cerebral lesion
6. Chronic medical illness
7. Surgical procedure and postoperative period
8. Severe psychological symptoms (such as fear)
9. Treatment with psychotropic medicines
10. Present or past history of head injury
11. Individual susceptibility to delirium
Delirium: Some Important Causes

Metabolic Causes iv. Anticonvulsants, L-dopa, Opiates
i. Hypoxia, Carbon dioxide narcosis v. Salicylates, Steroids, Penicillin, Insulin
ii. Hypoglycaemia vi. Methyl alcohol, heavy metals, biocides.
iii. Hepatic encephalopathy, Uremic encephalopa thy utritional Deficiencies
iv. Cardiac failure, Cardiac arrhythmias, Cardiac i. Thiamine, Niacin, Pyridoxine, Folic acid, B12
arrest ii. Proteins
v. Water and electrolyte imbalance (Water, Na+, K+, Systemic Infections
Mg++, Ca++) i. Acute and Chronic, e.g. Septicaemia, Pneumonia,
vi. Metabolic acidosis or alkalosis Endocarditis
vii. Fever, Anaemia, Hypovolemic shock Intracranial Causes
viii. Carcinoid syndrome, Porphyria i. Epilepsy (including post-ictal states)
Endocrine Causes ii. Head injury, Subarachnoid haemorrhage, Subdural
i. Hypo- and Hyperpituitarism haematoma
ii. Hypo- and Hyperthyroidism iii. Intracranial infections, e.g. Meningitis,
iii. Hypo- and Hyperparathyroidism Encephalitis, Cerebral malaria
iv. Hypo- and Hyperadrenalism iv. Migraine
Drugs (Both ingestion and withdrawal can cause v. Stroke (acute phase), Hypertensive encephalopathy
delirium) and Poisons vi. Focal lesions, e.g. right parietal lesions (such as
i. Digitahs, Quinidine, Antihypertensives abscess, neoplasm)
ii. Alcohol, Sedatives, Hypnotics (especially bar Miscellaneous
biturates) i. Postoperative states (including ICU delirium)
iii. Tricyclic antidepressants, Antipsychotics, ii. Sleep deprivation
Anticholinergics, isulfiram iii. Heat, Electricity, Radiation
Emotional disturbances such as depression, anxiety or fear, irritability, euphoria, apathy

or wondering perplexity, disturbances of perception (illusions or hallucinations, often
visual) and transient delusions are typical but are not specific indications for the diagnosis
• Delirium is marked by short term clouding of consciousness and changes in cognition.
• Commonest organic disorder seen in clinical practice.
• 5-15% of all medical and surgical inpatients
• Acute onset, fluctuating course, rapid improvement and generally considered to be
reversible disorder
• New memory registration & retention impaired
• Clouding of consciousness is or impaired consciousness or altered sensorium is main
feature
• Attention reduced ability to direct, focus, sustain, and shift attention
• Disorientation (time > place > person)
• Illusions & Hallucinations (most commonly visual)
• Psychomotor disturbance (hypo or hyperactive)
• carphologia /floccillation (picking movement at bed sheets/clothes)
• Disturbed sleep wake cycle, insomnia, daytime drowsiness, nightmares
• Diurnal variations – worsening of symptoms in evening & night (sun downing)
• Emotional disturbance, e.g. Depression, anxiety or fear, irritability, euphoria, apathy,
or wondering perplexity
• It may occur at any age but is most common at age of 60 years, most cases recover
within 4 weeks or less. However can last up to 6 months
• Treatment : Treat the cause.
• For aggression use antipsychotic (haloperidol)
Psychiatry
Concept 5.2: Dementia
LEARNING OBJECTIVE: To understand the etiology, clinical presentation and diagnosis
of Dementia and answer its related MCQ
Time Needed
1 reading
st
30 mins
2 look
nd
15 mins
(1) A decline in memory, which is most evident in the learning of new information,
although in more severe cases, the recall of previously learned information may be
also affected. The impairment applies to both verbal and non-verbal material.
(2) A decline in other cognitive abilities characterized by deterioration in judgement
and thinking, such as planning and organizing, and in the general processing of
information.
2. Preserved awareness of the environment (i.e. Absence of clouding of consciousness)
during a period of time.
3. A decline in emotional control or motivation, or a change in social behaviour, manifest
as atleast one of the Following:
(1) Emotional liability;
(2) Irritability;
(3) Apathy;
(4) Coarsening of social behaviour.
The diagnosis is further supported by evidence of damage to other higher cortical
functions, such as aphasia, agnosia, apraxia. Judgment about independent living or
the development of dependence (upon others) needs to take account of the cultural
expectation and context. Dementia is specified here as having a minimum duration of
six months for making a diagnosis.
Catastrophic Reaction. Patients with dementia also exhibit a reduced ability to apply
what Kurt Goldstein called the “abstract attitude.”
• Patients have difficulty generalizing from a single instance, forming concepts, and
grasping similarities and differences among concepts. Furthermore, the ability to
solve problems, to reason logically, and to make sound judgments is compromised.
• Goldstein also described a catastrophic reaction marked by agitation secondary to the
subjective awareness of intellectual deficits under stressful circumstances.
• Persons usually attempt to compensate for defects by using strategies to avoid
demonstrating failures in intellectual performance; they may change the subject,
make jokes, or otherwise divert the interviewer.
• Lack of judgment and poor impulse control appear commonly, particularly in dementias
that primarily affect the frontal lobes.
• Examples of these impairments include coarse language, inappropriate jokes, neglect
of personal appearance and hygiene, and a general disregard for the conventional
rules of social conduct.
Sundowner Syndrome. Sundowner syndrome is characterized by drowsiness,

confusion, ataxia, and accidental falls. It occurs in older people who are overly sedated
and in patients with dementia who react adversely to even a small dose of a psychoactive
drug. The syndrome also occurs in demented patients when external stimuli, such as
light and interpersonal orienting cues, are diminished.
Some Common Causes of Dementia

A. Parenchymatous brain disease . Deficiency dementias
Alzheimer's disease, Pick's disease, Parkinson's Pernicious anaemia, pellagra, folic acid deficiency,
disease, Huntington's chorea, Lewy body thiamine deficiency
dementia, Steel Richardson syndrome (Progressive G. Dementias due to infections
Supranuclear Palsy) Creutzfeldt-Jacob disease, neurosyphilis, chronic
B. Vascular dementia meningitis, viral encephalitis, AIDS dementia,
Multi-infarct dementia, subcortical vascular other HIY-related disorders, subacute sclerosing
dementia (Binswanger's disease) panencephalitis (SSPE)
C. Toxic dementias H. Neoplastic dementias
Bromide intoxication, drugs, heavy metals, alcohol, Neoplasms and other intracranial space-occupying
D. Metabolic dementias lesions
Chronic hepatic or uraemic encephalopathy, dialysis I.Traumatic dementias
dementia, Wilson's disease carbon monoxide, Chronic subdural haematoma, head injury
analgesics, anticonvulsants, benzodiazepines, J. Hydrocephalic dementia
psychotropic drugs Normal pressure hydrocephalus
E. Endocrine causes
Thyroid, parathyroid, pituitary, adrenal dysfunction
The dementia can be divided into reversible and irreversible dementias. It is extremely
important to do detailed work up of a patient of dementia as around 15% of cases are
reversible. The reversible causes of dementia are:
A. Neurosurgical conditions (subdural hematoma,
normal pressure hydrocephalus, intracranial tumors, intracranial abscess).
B. Infectious causes (meningitis, encephalitis, neurosyphilis, lyme disease).
C. Metabolic causes (vitamin B12 or folate deficiency, niacin deficiency, hypo and
hyperthyroidism, hypo and hyperparathyroidism).
D. Others (drugs and toxins, alcohol abuse, autoimmune encephalitis).
Dementia can also be classified into cortical and subcortical types depending on the area
of brain which is affected first by the dementing process.
Cortical dementias: These disorders are characterized by early involvement of cortical
structures and hence early appearance of cortical dysfunction. These disorders have
early and severe presentation of the As: amnesia, apraxia, aphasia, agnosia and acalculia
(impaired mathematical skills) indicating cortical involvement. Alzheimer’s disease is the
prototype of cortical dementia. Others include Creutzfeldt-Jakob disease, Pick’s disease
and other frontotemporal dementias.
Subcortical dementia: These disorders are characterized by early involvement of
subcortical structures like basal ganglia, brain stem nuclei and cerebellum. These disorders
Psychiatry
are characterized by early presentation of motor symptoms (abnormal movements like

tics, chorea, dysarthria, etc.), significant disturbances of executive functioning and
prominent behavioral and psychological symptoms like apathy, depression, bradyphrenia
(slowness of thinking). The examples include Parkinson’s disease, Wilson’s disease,
Huntington’s disease, multiple sclerosis, progressive supranuclear palsy, normal pressure
hydrocephalus.
Some dementias such as vascular dementia, dementia with lewy body have mixed
presentation.
Cortical Subcortical
Site Cortex Sub cortical grey matter
Memory loss Severe, recall helped very little by clues Mild to moderate, recall helped partially by
clues and recognizable tasks
Motor System Usually normal Dysarthria dystonia, chorea, rigidity,
tremors , ataxia, exed or extended posture
Others Aphasia, apraxia, Executive functionally, Complex delusions, depression, mania
agnosia, acalculia, bradyphrenia, dyslexia
simple delusions
Characteristics Cortical Dementia Subcortical Dementia

Memory Problem in both i.e. Learning Problem in recalling, ratherthan
new info as well as recalling learning new information (thus, able
them to recall, if provided with clues)
Language (Tem Poral Cortex) Early onset of aphasia Noaphasia
Calculation (Parietal Cortex) Early impairment Preserved till late
Executive Functions (Frontal Degree of impairmentis Disproportionate degree of
Lobe) proportional to the severity of impairment
other symptoms
Speech Articulation (Basal Articulation normal till late Dysarthric
Ganglia)
Coordination And Motor Speed Normal Impaired
(Basal Ganglia)
Extrapyramidal Movement Absent Chorea, tremors, tic, dystonia
Disorder
Mood Normal Depressed
Etiology includes/subtypes Alzheimer, vascular, FTD Parkinsonism, huntington's, LBD,
(pick's) Binswanger's, HIV dementia
The most common cause of Dementia is Alzheimer’s dementia (50 to 60%) followed
by Multi infarct Dementia (15 to 30%). The risk factor for Alzheimer’s is female, family
history, head injury and Down Syndrome. It has gradual and downward progression.
Clinical features distinguishing between the dementias.

Prominent symptoms and signs Other clinical features
Alzheimer’s disease Memory loss, especially short term Relentlessly progressive
Dysphasia and dyspraxia.
Sense of smell impaired early
Behavioural changes, e.g. wandering
Psychotic symptoms at some stage
Vascular dementia Personality change Stepwise progression
Labile mood Signs of cerebrovascular disease
Preserved insight History of hypertension
More common in men, smokers
Dementia with Lewy Fluctuating dementia Antipsychotics worsen condition
bodies Delirium-like phases
Parkinsonism
Visual hallucinations
Frontotemporal dementia Stereotyped behaviours Slowly progressive
Personality change Family history common
Early loss of insight More common in women
Expressive dysphasia Onset usually before age 70
Memory relatively preserved
arly primitive re exes
Huntington’s disease Schizophrenia-like psychosis Presents in the 20s-Ws
Choreiform movements Affected parent and other relatives
Depression and irritability
Dementia occurs later
Normal pressure Mental slowing, apathy, inattention Most common in >70 year old
hydrocephalus Urinary incontinence
Problems walking (gait apraxia) REVERSIBLE DEMENTIA
Prion disease Myoclonic jerks Often pre-senile
Seizures Rapid onset and progression
Cerebellar ataxia Death within a year
Psychiatry
Dementia vs Pseudodementia
Dementia Pseudodementia (Depressive)
1. Patient rarely complains of cognitive impairment Patient usually always complains about memory
impairment
2. Patient often emphasises achievements Patient often emphasises disability
3. Patient often appears unconcerned Patient very often communicates distress
. sually labile affect Severe depression on examination
5. Patient makes errors oil cognitive examination 'Do not know' answers are more frequent
6. Recent memory impairment found on examination Recent memory impairment rarely found on
examination
7. Confabulation may be present Confabulation very rare
8. Consistently poor performance on similar tests Marked variability in performance oil similar tests
9. History of depression less common Past history of manic and/or depressive episodes
may be present
A Comparison of Delirium and Dementia

Features Delirium Dementia
1. Onset Usually acute Usually insidious
2. Course Usually recover in 1 week; may Usually protracted, although may be
take up to 1 month reversible in some cases
3. Clinical features
a. Consciousness Grossly disturbed Usually normal; disturbed only in
b. Orientation Immediate retention and recall late stages
c. Memory disturbed Immediate retention and recall
Recent memory disturbed normal
Recent memory disturbed
Remote memory disturbed only in
late stages
d. Comprehension Impaired Impaired only in late stages
e. Sleep-wake cycle Grossly disturbed Usually normal
f. Attention and concentration Grossly disturbed Usually normal
g. Diurnal variation Marked; sundowning may may
h. Perception be present Usually absent
i. Other features Visual illusions and Hallucinations
hallucinations very common Catastrophic reaction; perseveration
Asterixis; multifocal myoclonus
Treatment of dementia : donepezil, rivastigmine, galantamine and tacrine are
cholinesterase inhibiters Memantine (NMDA antagonists), esterogen replacement
therapy
Conceopt 5.3: Organic Amnestic Syndrome
LEARNING OBJECTIVE: To understand the etiology, clinical presentation and diagnosis
of amnestic syndromes and answer its related MCQ
Time Needed
1 reading
st
30 mins
2 look
nd
15 mins
Amnestic disorders are classified in DSM-5 as major neurocognitive disorders caused by

other medical conditions.
They are marked primarily by memory impairment in addition to other cognitive
symptoms. They may be caused by (1) medical conditions (hypoxia), (2) toxins or
medications (e.g., marijuana, diazepam), and (3) unknown causes.
Etiology
• The major neuroanatomical structures involved in memory and in the development of
an amnestic disorder are particular diencephalic structures such as the dorsomedial
and midline nuclei of the thalamus and mid temporal lobe structures such as the
hippocampus, the mamillary bodies, and the amygdala.
• Amnestic disorders have many potential causes.
• Thiamine deficiency, hypoglycemia, hypoxia (including carbon monoxide poisoning),
and herpes simplex encephalitis all have a predilection to damage the temporal lobes,
particularly the hippocampi, and thus can be associated with the development of
amnestic disorders.
• Similarly, when tumors, cerebrovascular diseases, surgical procedures, or multiple
sclerosis plaques involve the diencephalic or temporal regions of the brain, the
symptoms of an amnestic disorder may develop.
• General insults to the brain, such as seizures, ECT, and head trauma, can also result
in memory impairment.
• Transient global amnesia is presumed to be a cerebrovascular disorder involving
transient impairment in blood flow through the vertebrobasilar arteries.
Diagnostic Criteria:
A. Memory impairment, manifest in both:
(1) a defect of recent memory (impaired learning of new material), to a degree
sufficient to interfere with daily living; and
(2) a reduced ability to recall past experiences.
B. Absence of:
(1) a defect in immediate recall (as tested, for example, by the digit span);
(2) clouding of consciousness and disturbance of attention, as defined in FO5,
criterion A;
(3) global intellectual decline (dementia).
C. Objective evidence (physical & neurological examination, laboratory tests) and/or
history of an insult to or a disease of the brain (especially involving bilaterally the
diencephalic and medial temporal structures but other than alcoholic encephalopathy)
that can reasonably be presumed to be responsible for the clinical manifestations
described under A.
Psychiatry
Comments: Associated features, including confabulations, emotional changes (apathy,

lack of initiative), and lack of insight, are useful additional pointers to the diagnosis but
are not invariably present. In this syndrome the immediate memory is normal, recent
memory is disturbed & remote memory is disturbed.
Korsako s Syndrome
Korsakoff’s syndrome is an amnestic syndrome caused by thiamine deficiency,
most commonly associated with the poor nutritional habits of people with chronic
alcohol abuse.
Other causes of poor nutrition (e.g., starvation), gastric carcinoma, hemodialysis,
hyperemesis gravidarum, prolonged IV hyperalimentation, and gastric plication
can also result in thiamine deficiency. Korsakoff’s syndrome is often associated
with Wernicke’s encephalopathy, which is the associated syndrome of confusion,
ataxia, and ophthalmoplegia.
In patients with these thiamine deficiency related symptoms, the neuropathological
findings include hyperplasia of the small blood vessels with occasional hemorrhages,
hypertrophy of astrocytes, and subtle changes in neuronal axons. Although the
delirium clears up within a month or so, the amnestic syndrome either accompanies
or follows untreated Wernicke’s encephalopathy in approximately 85 percent of all
cases.
Patients with Korsakoff’s syndrome typically demonstrate a change in personality
as well, such that they display a lack of initiative, diminished spontaneity, and a
lack of interest or concern. These changes appear frontal lobe–like, similar to the
personality change ascribed to patients with frontal lobe lesions or degeneration.
Indeed, such patients often demonstrate executive function deficits on
neuropsychological tasks involving attention, planning, set shifting, and inferential
reasoning consistent with frontal pattern injuries.
For this reason, Korsakoff’s syndrome is not a pure memory disorder, although it
certainly is a good paradigm of the more common clinical presentations for the
amnestic syndrome.
The onset of Korsakoff’s syndrome can be gradual. Recent memory tends to be
affected more than is remote memory, but this feature is variable.
Confabulation, apathy, and passivity are often prominent symptoms in the
syndrome. With treatment, patients may remain amnestic for up to 3 months and
then gradually improve over the ensuing year.
Administration of thiamine may prevent the development of additional amnestic
symptoms, but the treatment seldom reverses severe amnestic symptoms when
they are present. Approximately one third to one-fourth of all patients recover
completely, and approximately one-fourth of all patients have no improvement of
their symptoms.
Electroconvulsive Therapy
• Electroconvulsive therapy treatments are usually associated with retrograde amnesia
for a period of several minutes before the treatment and anterograde amnesia after
the treatment. The anterograde amnesia usually resolves within 5 hours.
• Mild memory deficits may remain for 1 to 2 months after a course of ECT
treatments, but the symptoms are completely resolved 6 to 9 months after
treatment.
Head Injury
• Head injuries (both closed and penetrating) can result in a wide range of
neuropsychiatric symptoms, including dementia, depression, personality changes,
and amnestic disorders.
• Amnestic disorders caused by head injuries are commonly associated with a period
of retrograde amnesia leading up to the traumatic incident and amnesia for the
traumatic incident itself.
• The severity of the brain injury correlates somewhat with the duration and severity of
the amnestic syndrome, but the best correlate of eventual improvement is the degree
of clinical improvement in the amnesia during the first week after the patient regains
consciousness.
New topics (recent exam)

Porphyria: (Aiims May 2017)
The porphyrias are disorders of heme biosynthesis that result in excessive accumulation
of porphyrins. The triad of symptoms is acute, colicky abdominal pain; motor
polyneuropathy; and psychosis. Acute intermittent porphyria is an autosomal dominant
disorder that affects more women than men and has its onset between ages 20 and 50
years. The psychiatric symptoms include anxiety, insomnia, lability of mood, depression,
and psychosis. Symptoms of this disease also predominately include psychosis, apathy,
or depression, along with intermittent abdominal pain, neuropathy, and autonomic
dysfunction. Elevated levels of porphobilinogen are found in the urine of symptomatic
patients with acute intermittent porphyria.
Organic mental disorder Functional mental disorder

1. Disease/disorder arising due to disease of the brain 1. Disease/disorder with no such basis
2. Onset: Acute 2. Onset: Gradual
3. Age: Seen in old age 3. Age: Seen in young age
4. Consciousness : Impaired 4. Consciousness: Preserved
5. Hallucinations: Prominent visual hallucinations 5. Hallucinations: mainly auditory types
. eurological deficit Present . eurological eficit Absent one
e.g., delirium, dementia, wernicke s, korsakoff e.g., Schizophrenia, bipolar mood disorder, etc.
psychosis.
Psychiatry
Worksheet
• MCQ OF “Organic Mental Disorders” FROM DQB

Delirium Dementia
Dementia Pseudodementia
Psychiatry
Cortical Dementia Sub Cortical Dementia
Prominent symptoms and signs Other clinical features
Alzheimer’s disease
Vascular dementia
Dementia with Lewy bodies
Frontotemporal dementia
Huntington’s disease
Normal pressure
hydrocephalus
Prion disease
6 Substance use Disorders
CONCEPTS
Â Concept 6.1 Basic terminologies
Â Concept 6.2 Alcohol and related disorders
Â Concept .3 Caffeine Related Disorders
Â Concept 6.4 Amphetamine and related disorders
Â Concept 6.5 Cocaine and related disorders
Â Concept 6.6 Opiod and related disorders
Â Concept 6.7 Cannabis and related disorders
Â Concept 6.8 Tobacco and related disorders
Â Concept 6.9 Hallucinogens and related disorders
Â Concept 6.10 Gambling disorder

100 | Psychiatry
Concept 6.1: Basic Terminologies:
LEARNING OB ECTI E: To understand the basic definitions and terminologies related
to substance use and answer its related MCQ.
Time Needed
1 reading
st
15 mins
2 look
nd
10 mins
1 Dependence The repeated use of a drug or chemical substance, with or without

physical dependence. Physical dependence indicates an altered physiologic state
caused by repeated administration of a drug, the cessation of which results in a
specific syndrome.
2 Abuse Use of any drug, usually by self-administration, in a manner that deviates
from approved social or medical patterns.
3 Misuse Similar to abuse, but usually applies to drugs prescribed by physicians that
are not used properly.
4 Addiction The repeated and increased use of a substance, the deprivation of which
gives rise to symptoms of distress and an irresistible urge to use the agent again and
which leads also to physical and mental deterioration. The term is no longer included
in the official nomenclature, having been replaced by the term dependence, but it is
a useful term in common usage.
5 Intoxication A reversible syndrome caused by a specific substance (e.g., alcohol)
that affects one or more of the following mental functions: memory, orientation,
mood, judgment, and behavioral, social, or occupational functioning.
6 Withdrawal A substance-specific syndrome that occurs after stopping or reducing
the amount of the drug or substance that has been used regularly over a prolonged
period of time. The syndrome is characterized by physiologic signs and symptoms
in addition to psychological changes, such as disturbances in thinking, feeling, and
behavior. Also called abstinence syndrome or discontinuation syndrome.
7 Tolerance Phenomenon in which, after repeated administration, a given dose of
drug produces a decreased effect or increasingly larger doses must be administered
to obtain the effect observed with the original dose. Behavioral tolerance reflects the
ability of the person to perform tasks despite the effects of the drug.
8 Cross-tolerance Refers to the ability of one drug to be substituted for another, each
usually producing the same physiologic and psychological effect (e.g., diazepam and
barbiturates). Also known as cross-dependence.
9 Neuroadaptation Neurochemical or neurophysiologic changes in the body that
result from the repeated administration of a drug. Neuroadaptation accounts for the
phenomenon of tolerance. Pharmacokinetic adaptation refers to adaptation of the
metabolizing system in the body. Cellular or pharmacodynamic adaptation refers
to the ability of the nervous system to function despite high blood levels of the
offending substance.
10 Codependence Term used to refer to family members affected by or influencing
the behavior of the substance abuser. Related to the term enabler, which is a person
who facilitates the abuser’s addictive behavior (e.g., providing drugs directly or
stance se is r ers | 101
money to buy drugs). Enabling also includes the unwillingness of a family member to
accept addiction as a medical-psychiatric disorder or to deny that person is abusing
a substance.
11 Two concepts have been used to define aspects of dependence: behavioral and
physical.
12 In behavioral dependence, substance-seeking activities and related evidence of
pathological use patterns are emphasized, whereas physical dependence refers to
the physical (physiological) effects of multiple episodes of substance use.
13 In definitions stressing physical dependence, ideas of tolerance or withdrawal appear
in the classification criteria.
14 The term intoxication is used for a reversible nondependent experience with a
substance that produces impairment.
15 The terms coaddiction, coalcoholism, and more commonly, codependency or
codependence are used to designate the behavioral patterns of family members
who have been significantly affected by another family member’s substance use or
addiction.
16 Enabling was one of the first, and more agreed on, characteristics of codependence
or coaddiction. Sometimes, family members feel that they have little or no control
over the enabling acts. Either because of the social pressures for protecting and
supporting family members or because of pathological interdependencies, or both,
enabling behavior often resists modification. Other characteristics of codependence
include unwillingness to accept the notion of addiction as a disease. The family
members continue to behave as if the substance-using behavior were voluntary and
willful (if not actually spiteful) and the user cares more for alcohol and drugs than for
family members. This results in feelings of anger, rejection, and failure. In addition
to those feelings, family members may feel guilty and depressed because addicts,
in an effort to deny loss of control over drugs and to shift the focus of concern away
from their use, often try to place the responsibility for such use on other family
members, who often seem willing to accept some or all of it. (nimhans)
17 The major neurotransmitters possibly involved in developing substance abuse and
substance dependence are the opioid, catecholamine (particularly dopamine), and
gamma aminobutyric acid (GABA) systems.
18 The dopaminergic neurons in the ventral tegmental area are particularly
important. These neurons project to the cortical and limbic regions, especially the
nucleus accumbens. This pathway is probably involved in the sensation of reward
and may be the major mediator of the effects of such substances as amphetamine
and cocaine. The locus ceruleus, the largest group of adrenergic neurons, probably
mediates the effects of the opiates and the opioids. These pathways have collectively
been called the brain-reward circuitry.
102 | Psychiatry
Concept 6.2: Alcohol and related disorders
LEARNING OB ECTI E: To understand the clinical presentation of alcohol and related
disorders and answer its related MCQ.
Time Needed
1 reading
st
60 mins
2 look
nd
30 mins
Alcohol E ects on sleep: (PGI NIMHANS)

• Although alcohol consumed in the evening usually increases the ease of falling asleep
(decreased sleep latency), alcohol also has adverse effects on sleep architecture.
• Specifically, alcohol use is associated with a decrease in rapid eye movement sleep
(REM or dream sleep) and deep sleep (stage 4) and more sleep fragmentation, with
more and longer episodes of awakening.
• Therefore, the idea that drinking alcohol helps persons fall asleep is a myth.
Subtypes of Alcohol Dependence ( NIMHANS )

• Various researchers have attempted to divide alcohol dependence into subtypes
based primarily on phenomenological characteristics.
• One recent classification notes that type A alcohol dependence is characterized by
late onset, few childhood risk factors, relatively mild dependence, few alcohol-related
problems, and little psychopathology.
• Type B alcohol dependence is characterized by many childhood risk factors, severe
dependence, an early onset of alcohol-related problems, much psychopathology, a
strong family history of alcohol abuse, frequent polysubstance abuse, a long history
of alcohol treatment, and a lot of severe life stresses.
• Some researchers have found that type A persons who are alcohol dependent may
respond to interactional psychotherapies, whereas type B persons who are alcohol
dependent may respond to training in coping skills.
• Another researcher has suggested a type I, mileau‑limited variety of alcohol
dependence, characterized by late onset, more evidence of psychological than of
physical dependence, and the presence of guilt feelings. Type II, male‑limited
alcohol dependence is characterized by onset at an early age, spontaneous seeking of
alcohol for consumption, and a socially disruptive set of behaviors when intoxicated.
Impairment Likely to be Seen at Di erent Blood Alcohol Concentrations

Level Likely Impairment
20-30 mg/dL Slowed motor performance and decreased thinking ability
30-80 mg/dL Increases in motor and cognitive problems
80-200 mg/dL Increases in incoordination and judgment errors
Mood lability
Deterioration in cognition
200-300 mg/dL Nystagmus, marked slurring of speech, and alcoholic blackouts
>300 mg/dL Impaired vital signs and possible death
Screening Tests
CAGE: an acronym for 4 questions used to assess those with alcohol problem (FASTEST
AND EASIEST)
MAST: Michigan Alcohol Screening Test
DAST: Drug Abuse Screening Test
A DIT: Alcohol Use Disorder Identification Test ( IPMER)
Alcohol Withdra al (Imp Topic)

• Alcohol withdrawal, even without delirium, can be serious; it can include seizures and
autonomic hyperactivity.
• Conditions that may predispose to, or aggravate, withdrawal symptoms include
fatigue, malnutrition, physical illness, and depression.
• The DSM criteria for alcohol withdrawal require the cessation or reduction of alcohol
use that was heavy and prolonged as well as the presence of specific physical or
neuropsychiatric symptoms.
• The diagnosis also allows for the specification with perceptual disturbances.
• The classic sign of alcohol withdrawal is tremulousness, although the spectrum
of symptoms can expand to include psychotic and perceptual symptoms (e.g.,
delusions and hallucinations), seizures, and the symptoms of delirium tremens (DTs),
called alcohol withdrawal delirium in DSM.
• Tremulousness (commonly called the shakes or the jitters) develops to
hours after the cessation of drinking, the psychotic and perceptual symptoms
begin in to 12 hours, seizures in 12 to 24 hours, and Delirium Tremens
during 72 hours, although physicians should watch for the development of
DTs for the first week of withdrawal.
• The tremor of alcohol withdrawal can be similar to either physiological tremor, with a
continuous tremor of great amplitude and of more than 8 Hz, or familial tremor, with
bursts of tremor activity slower than 8 Hz.
• Other symptoms of withdrawal include general irritability, gastrointestinal symptoms
(e.g., nausea and vomiting), and sympathetic autonomic hyperactivity, including
anxiety, arousal, sweating, facial flushing, mydriasis, tachycardia, and mild
hypertension.
Withdra al Sei ures:

• Seizures associated with alcohol withdrawal are stereotyped, generalized, and tonic-
clonic in character.
• Patients often have more than one seizure 3 to 6 hours after the first seizure.
• Status epilepticus is relatively rare and occurs in less than 3 percent of patients.
• Although anticonvulsant medications are not required in the management of alcohol
withdrawal seizures, the cause of the seizures is difficult to establish when a patient is
first assessed in the emergency room; thus, many patients with withdrawal seizures
receive anticonvulsant medications, which are then discontinued once the cause of
the seizures is recognized.
• Seizure activity in patients with known alcohol abuse histories should still prompt
clinicians to consider other causative factors, such as head injuries, CNS infections,
CNS neoplasms, and other cerebrovascular diseases; long-term severe alcohol abuse
can result in hypoglycemia, hyponatremia, and hypomagnesaemia all of which can
also be associated with seizures.
104 | Psychiatry
Treatment
• The primary medications to control alcohol withdrawal symptoms are the
benzodiazepines.
• Many studies have found that benzodiazepines help control seizure activity, delirium,
anxiety, tachycardia, hypertension, diaphoresis, and tremor associated with alcohol
withdrawal.
• Benzodiazepines can be given either orally or parenterally; neither diazepam nor
chlordiazepoxide, however, should be given intramuscularly (IM) because of their
erratic absorption by this route.
• Clinicians must titrate the dosage of the benzodiazepine, starting with a high dosage
and lowering the dosage as the patient recovers.
• Although benzodiazepines are the standard treatment for alcohol withdrawal, studies
have shown that carbamazepine (Tegretol) in daily doses of 800 mg is as effective as
benzodiazepines and has the added benefit of minimal abuse liability.
Delirium:
• Patients with recognized alcohol withdrawal symptoms should be carefully monitored
to prevent progression to alcohol withdrawal delirium, the most severe form of the
withdrawal syndrome, also known as DTs.
• Alcohol withdrawal delirium is a medical emergency that can result in significant
morbidity and mortality. Patients with delirium are a danger to themselves and to
others.
• Because of the unpredictability of their behavior, patients with delirium may be
assaultive or suicidal or may act on hallucinations or delusional thoughts as if they
were genuine dangers.
• Untreated, DTs has a mortality rate of 20 percent, usually as a result of an intercurrent
medical illness such as pneumonia, renal disease, hepatic insufficiency, or heart
failure.
• Although withdrawal seizures commonly precede the development of alcohol
withdrawal delirium, delirium can also appear unheralded.
• The essential feature of the syndrome is delirium occurring within 1 week after a
person stops drinking or reduces the intake of alcohol. In addition to the symptoms of
delirium, the features of alcohol intoxication delirium include autonomic hyperactivity
such as tachycardia, diaphoresis, fever, anxiety, insomnia, and hypertension;
perceptual distortions, most frequently visual or tactile hallucinations; and fluctuating
levels of psychomotor activity, ranging from hyperexcitability to lethargy.
• About 5 percent of persons with alcohol-related disorders who are hospitalized have
DTs.
• Because the syndrome usually develops on the third hospital day, a patient admitted
for an unrelated condition may unexpectedly have an episode of delirium, the first
sign of a previously undiagnosed alcohol-related disorder.
• Episodes of DTs usually begin in a patient’s 30s or 40s after 5 to 15 years of heavy
drinking, typically of the binge type. Physical illness (e.g., hepatitis or pancreatitis)
predisposes to the syndrome; a person in good physical health rarely has DTs during
alcohol withdrawal.
Treatment
• The best treatment for DTs is prevention. Patients withdrawing from alcohol who
exhibit withdrawal phenomena should receive a benzodiazepine, such as 25 to 50 mg
of chlordiazepoxide every 2 to 4 hours until they seem to be out of danger.
• Once the delirium appears, lorazepam (Ativan) should be given intravenously (IV)
• Antipsychotic medications that may reduce the seizure threshold in patients should
be avoided.
• A high-calorie, high-carbohydrate diet supplemented by multivitamins is also
important.
• Physically restraining patients with the DTs is risky; they may fight against the
restraints to a dangerous level of exhaustion. When patients are disorderly and
uncontrollable, a seclusion room can be used.
• Dehydration, often exacerbated by diaphoresis and fever, can be corrected with fluids
given by mouth or IV. Anorexia, vomiting, and diarrhea often occur during withdrawal.
Antipsychotic medications should be avoided because they can reduce the seizure
threshold in the patient.
• The emergence of focal neurological symptoms, lateralizing seizures, increased
intracranial pressure, or evidence of skull fractures or other indications of CNS
pathology should prompt clinicians to examine a patient for additional neurological
disease. Nonbenzodiazepine anticonvulsant medication is not useful in preventing
or treating alcohol withdrawal convulsions, although benzodiazepines are generally
effective.
• Warm, supportive psychotherapy in the treatment of DTs is essential. Patients are
often bewildered, frightened, and anxious because of their tumultuous symptoms,
and skillful verbal support is imperative.
Treatment of Withdra al: (Ref : Kaplan)

Advise the patient to drink plenty of non-alcoholic liquids. Prescribe vitamins (thiamine
200-300 mg per day deficiencies are common and withdrawal may precipitate
Wernicke’s syndrome. Consider parenteral thiamine if risk of Wernicke’s syndrome is
judged to be high.
Clinical Problem Drug of choice Route
Tremulousness and mild to moderate agitation Chlordiazepoxide Oral
Diazepam Oral
Hallucinosis Lorazepam Oral
Extreme agitation Chlordiazepoxide Intravenous
Withdrawal seizures Diazepam Intravenous
Delirium tremens Lorazepam Intravenous
Wernicke-Korsako Syndrome
• The classic names for alcohol-induced persisting amnestic disorder are Wernicke’s
encephalopathy (a set of acute symptoms) and Korsakoff’s syndrome (a chronic
condition).
106 | Psychiatry
• Whereas Wernicke’s encephalopathy is completely reversible with treatment, only
about 20 percent of patients with Korsakoff’s syndrome recover.
• The pathophysiological connection between the two syndromes is thiamine deficiency,
caused either by poor nutritional habits or by malabsorption problems. Thiamine is a
cofactor for several important enzymes and may also be involved in conduction of the
axon potential along the axon and in synaptic transmission.
• The neuropathological lesions are symmetrical and paraventricular, involving
the mammillary bodies, the thalamus, the hypothalamus, the midbrain, the
pons, the medulla, the fornix, and the cerebellum.
• Wernicke’s encephalopathy, also called alcoholic encephalopathy, is an acute
neurological disorder characterized by ataxia (affecting primarily the gait), vestibular
dysfunction, confusion, and a variety of ocular motility abnormalities, including
horizontal nystagmus, lateral orbital palsy, and gaze palsy.
• These eye signs are usually bilateral but not necessarily symmetrical. Other eye signs
may include a sluggish reaction to light and anisocoria. Wernicke’s encephalopathy
may clear spontaneously in a few days or weeks or may progress into Korsakoff’s
syndrome.
Treatment
• In the early stages, Wernicke’s encephalopathy responds rapidly to large doses of
parenteral thiamine, which is believed to be effective in preventing the progression
into Korsakoff’s syndrome.
• The dosage of thiamine is usually initiated at 100 mg by mouth two to three times
daily and is continued for 1 to 2 weeks.
• In patients with alcohol-related disorders who are receiving IV administration of
glucose solution, it is good practice to include 100 mg of thiamine in each liter of the
glucose solution.
• Korsakoff’s syndrome is the chronic amnestic syndrome that can follow
Wernicke’s encephalopathy, and the two syndromes are believed to be
pathophysiologically related. The cardinal features of Korsakoff’s syndrome
are impaired mental syndrome (especially recent memory) and anterograde
amnesia in an alert and responsive patient. The patient may or may not have
the symptom of confabulation.
• Treatment of Korsakoff’s syndrome is also thiamine given 100 mg by mouth two to
three times daily; the treatment regimen should continue for 3 to 12 months. Few
patients who progress to Korsakoff’s syndrome ever fully recover, although many have
some improvement in their cognitive abilities with thiamine and nutritional support.
Blackouts (AIIMS)
• Blackouts are similar to episodes of transient global amnesia in that they are discrete
episodes of anterograde amnesia that occur in association with alcohol intoxication.
• The periods of amnesia can be particularly distressing when persons fear that they
have unknowingly harmed someone or behaved imprudently while intoxicated.
• During a blackout, persons have relatively intact remote memory but experience
a specific short-term memory deficit in which they are unable to recall events that
happened in the previous 5 or 10 minutes.
• Because their other intellectual faculties are well preserved, they can perform
complicated tasks and appear normal to casual observers.
Special notes:
In alcoholic hallucinosis, a heavy drinker experiences recurrent auditory hallucinations,
usually of a threatening or derogatory nature. The hallucinations occur in clear
consciousness (cf. withdrawal hallucinations). The syndrome is an example of a drug -
induced psychosis
Medications for Treating Alcohol Dependence
Disulfiram Naltrexone Acamprosate
Action Inhibits intermediate Blocks opioid receptors, Affects glutamate and
metabolism of alcohol, resulting in reduced craving GABA neurotransmitter
causing a build-up of and reduced reward in systems, but its alcohol-
acetaldehyde and a reaction response to drinking related action is unclear
of ushing, sweating, nausea,
and tachycardia if a patient
drinks alcohol
Contraindications Concomitant use of Currently using opioids or Severe renal impairment
alcohol or alcohol- in acute opioid withdrawal;
containing preparations or anticipated need for opioid
metronidazole; coronary analgesics; acute hepatitis or
artery disease; severe liver failure
myocardial disease
Precautions High impulsivity: likely Other hepatic disease; renal Moderate renal impairment
to drink while using it; impairment; history of suicide (dose adjustment needed)
psychoses (current or attempts. If opioid analgesia depression or suicidality
history); diabetes mellitus; is required, larger doses may
epilepsy; hepatic dysfunction; be required, and respiratory
hypothyroidism; renal depression may be deeper and
impairment; rubber contact more prolonged.
dermatitis
Serious Adverse Hepatitis; optic neuritis; Will precipitate severe Anxiety; depression. Rare
Reactions peripheral neuropathy; withdrawal if patient is events include the following:
psychotic reactions. dependent on opioids; suicide attempt, acute
Pregnancy Category C. hepatoxicity (uncommon kidney failure, heart failure,
at usual doses). Pregnancy mesenteric arterial occlusion,
Category C. cardiomyopathy, deep
thrombophlebitits, and shock.
Pregnancy Category C.
Common Side Metallic after-taste; Nausea; abdominal pain; iarrhea atulence nausea
ects dermatitis constipation; dizziness; abdominal pain; headache;
headache; anxiety; fatigue back pain; infection;
u syndrome chillis
somnolence; decreased
libido; amnesia; confusion
Examples of drug Amitryptyline; anticoagulants Opioid analgesics (blocks No clinically relevant
Interactions such as warfarin; diazepam; action); yohimbine (use with interactions known
isoniazid; metronidazole; naltrexone increases negative
phenytoin; theophylline; drug effects
warfarin; any nonprescription
drug containing alcohol
108 | Psychiatry
Stages of Change (Motivation Cycle)
Fig. 1
State Instructional strategies

Precontemplation • Engage the individual with information about need for change
No intention of taking action • Provide personali ed information about risks if no change and benefits
in the next 6 months of change
Contemplation • otivate and encourage the individual to set goals and make specific
Intends to take action in the plans
next 6 months
Preparation • elp the individual create and implement specific action plans and set
Intends to take action in the realistic goals
next month and has taken
some steps to change behavior
Action • Provide problem-based (action-oriented) learning experiences
Has changed behavior for <6 • Provide social support, feedback
months
Maintenance • Continue to provide social support, assist with problem-solving,
Has changed behavior for >6 positively address slips and relapses if necessary
months • Employ reminder systems/performance support tools
Concept . : Ca eine Related Disorders
LEARNING OB ECTI E: To understand the clinical presentation of caffeine related
Time Needed
1 reading
st
10 mins
2 look
nd
5 mins
Ca eine Intoxication
• The common symptoms associated with caffeine intoxication include anxiety,
psychomotor agitation, restlessness, irritability, and psychophysiological complaints
such as muscle twitching, flushed face, nausea, diuresis, gastrointestinal distress,
excessive perspiration, tingling in the fingers and toes, and insomnia.
• Consumption of more than 1 g of caffeine can produce rambling speech, confused
thinking, cardiac arrhythmias, inexhaustibleness, marked agitation, tinnitus, and mild
visual hallucinations (light flashes).
• Consumption of more than 10 g of caffeine can cause generalized tonic-clonic
seizures, respiratory failure, and death.
Ca eine Withdra al
• The appearance of withdrawal symptoms reflects the tolerance and physiological
dependence that develop with continued caffeine use.
• The most common symptoms are headache and fatigue; other symptoms include
anxiety, irritability, mild depressive symptoms, impaired psychomotor performance,
nausea, vomiting, craving for caffeine, and muscle pain and stiffness. The number
and severity of the withdrawal symptoms are correlated with the amount of caffeine
ingested and the abruptness of the withdrawal. Caffeine withdrawal symptoms have
their onset 12 to 24 hours after the last dose; the symptoms peak in 24 to 48 hours
and resolve within 1 week.
110 | Psychiatry
Concept . : Amphetamine and Related Disorders.
LEARNING OB ECTI E: To understand the clinical presentation of amphetamine
related disorders and answer its related MCQ.
Time Needed
1 reading
st
20 mins
2 look
nd
10 mins
Amphetamine Intoxication:
• The intoxication syndromes of cocaine (which blocks dopamine reuptake) and
amphetamines (which cause the release of dopamine) are similar.
• Symptoms include clinically significant maladaptive behavioral or psychological
changes (e.g., euphoria or affective blunting; changes in sociability; hypervigilance;
interpersonal sensitivity; anxiety, tension, or anger; stereotyped behaviors; impaired
judgment; or impaired social or occupational functioning) that developed during, or
shortly after, use of amphetamine or a related substance.
• Two (or more) of the following, developing during, or shortly after, use of amphetamine
or a related substance:
• tachycardia or bradycardia
• pupillary dilation
• elevated or lowered blood pressure
• perspiration or chills
• nausea or vomiting
• evidence of weight loss
• psychomotor agitation or retardation
• muscular weakness, respiratory depression, chest pain, or cardiac arrhythmias
• confusion, seizures, dyskinesias, dystonias, or coma
Amphetamine Withdrawal:
• After amphetamine intoxication, a crash occurs with symptoms of anxiety,
tremulousness, dysphoric mood, lethargy, fatigue, nightmares (accompanied by
rebound rapid eye movement REM sleep), headache, profuse sweating, muscle
cramps, stomach cramps, and insatiable hunger.
• The withdrawal symptoms generally peak in 2 to 4 days and are resolved in 1 week.
The most serious withdrawal symptom is depression, which can be particularly severe
after the sustained use of high doses of amphetamine and which can be associated
with suicidal ideation or behavior.
Amphetamine-Induced Psychotic Disorder:

• The clinical similarity of amphetamine-induced psychosis to paranoid schizophrenia
has prompted extensive study of the neurochemistry of amphetamine-induced
psychosis to elucidate the pathophysiology of paranoid schizophrenia.
• The hallmark of amphetamine‑induced psychotic disorder is the presence of
paranoia.
• Amphetamine-induced psychotic disorder can be distinguished from paranoid
schizophrenia by several differentiating characteristics associated with the former,
including a predominance of visual hallucinations, generally appropriate affects,
hyperactivity, hypersexuality, confusion and incoherence, and little evidence of
disordered thinking (e.g., looseness of associations).
• The treatment of choice for amphetamine-induced psychotic disorder is the short-
term use of an antipsychotic medication such as haloperidol.
Club Drugs: (VIP Topic)

• The use of a certain group of substances popularly called club drugs is often associated
with dance clubs, bars, and all-night dance parties (raves).
• The group includes LSD, Gamma‑hydroxybutyrate (GHB), ketamine,
methamphetamine, MDMA (ecstasy), and Rohypnol or roofies (flunitrazepam).
• GHB, ketamine, and Rohypnol have been called date rape drugs because they
produce disorienting and sedating effects, and often users cannot recall what occurred
during all or part of an episode under the influence of the drug.
112 | Psychiatry
Concept . : Cocaine and Related Disorders.
LEARNING OB ECTI E: To understand the clinical presentation of cocaine related
Time Needed
1 reading
st
20 mins
2 look
nd
10 mins
Neuropharmacology
• Cocaine’s primary pharmacodynamic action related to its behavioral effects is
competitive blockade of dopamine reuptake by the dopamine transporter. This
blockade increases the concentration of dopamine in the synaptic cleft and results in
increased activation of both dopamine type 1 (D1) and type 2 (D2) receptors.
• The D2 receptors in the mesolimbic dopamine system have been held responsible for
the heightened activity during periods of craving.
Cocaine intoxication (similar to amphetamine intoxication)

(Asked in Recent Exam)
A. Clinically significant maladaptive behavioral or psychological changes (e.g., euphoria
or affective blunting; changes in sociability; hypervigilance; interpersonal sensitivity;
anxiety, tension, or anger; stereotyped behaviors; impaired judgment; or impaired
social or occupational functioning) that developed during, or shortly after, use of
cocaine.
B. Two (or more) of the following, developing during, or shortly after, cocaine use:
tachycardia or bradycardia
pupillary dilation
elevated or lowered blood pressure
perspiration or chills
nausea or vomiting
evidence of weight loss
psychomotor agitation or retardation
muscular weakness, respiratory depression, chest pain, or cardiac arrhythmias
confusion, seizures, dyskinesias, dystonias, or coma
Diagnostic Criteria for Cocaine Withdrawal

A. Cessation of (or reduction in) cocaine use that has been heavy and prolonged.
B. Dysphoric mood and two (or more) of the following physiological changes, developing within a few
hours to several days after Criterion A:
• fatigue
• vivid, unpleasant dreams
• insomnia or hypersomnia
• increased appetite
• psychomotor retardation or agitation
Cocaine-Induced Psychotic Disorder:

• Paranoid delusions and hallucinations can occur in up to 50 percent of all persons who
use cocaine. The occurrence of these psychotic symptoms depends on the dose, the
duration of use, and the individual user’s sensitivity to the substance.
• Cocaine-induced psychotic disorders are most common with IV and crack users.
Men are much more likely to have psychotic symptoms than are women. Paranoid
delusions are the most frequent psychotic symptoms.
• Auditory hallucinations are also common, but visual and tactile hallucinations may
be less common than paranoid delusions. The sensation of bugs crawling just
beneath the skin (formication) has been reported to be associated with
cocaine use.
• Psychotic disorders can develop with grossly inappropriate sexual and generally
bizarre behavior and homicidal or other violent actions related to the content of the
paranoid delusions or hallucinations.
Adverse E ects:
• A common adverse effect associated with cocaine use is nasal congestion
serious inflammation, swelling, bleeding, and ulceration of the nasal mucosa can also
occur.
• Long-term use of cocaine can also lead to perforation of the nasal septa.
• The IV use of cocaine can result in infection, embolisms, and the transmission of
human immunodeficiency virus (HIV).
• Minor neurological complications with cocaine use include the development of acute
dystonia, tics, and migraine-like headaches. The major complications of cocaine use,
however, are cerebrovascular, epileptic, and cardiac. .
Death
• High doses of cocaine are associated with seizures, respiratory depression,
cerebrovascular diseases, and myocardial infarctions all of which can lead to death in
persons who use cocaine. Users may experience warning signs of syncope or chest
pain but may ignore these signs because of the irrepressible desire to take more
cocaine. Deaths have also been reported with the ingestion of speedballs, which
are combinations of opioids and cocaine.
114 | Psychiatry
Concept . : Opioids and Related Disorders.
LEARNING OB ECTI E: To understand the clinical presentation of opium related
Time Needed
1 reading
st
20 mins
2 look
nd
10 mins
DSM-5 Diagnostic Criteria for Opioid Intoxication

A. Recent use of an opioid.
. Clinically significant maladaptive behavioral or psychological changes e.g., initial euphoria followed
by apathy, dysphoria, psychomotor agitation or retardation, impaired judgment, or impaired social or
occupational functioning) that developed during, or shortly after, opioid use.
C. Pupillary constriction (or pupillary dilation due to anoxia from severe overdose) and one (or more) of the
following signs, developing during, or shortly after, opioid use:
1. drowsiness or coma
2. slurred speech
3. impairment in attention or memory
D. The symptoms are not due to a general medical condition and are not better accounted for by another
mental disorder.
Opiod withdrawal:
• Opioid withdrawal consists of severe muscle cramps and bone aches, profuse diarrhea, abdominal
cramps, rhinorrhea, lacrimation, piloerection or goose esh from which comes the term cold turkey for
the abstinence syndrome), yawning, fever, pupillary dilation, hypertension, tachycardia, and temperature
dysregulation, including hypothermia and hyperthermia.
• Persons with opioid dependence seldom die from opioid withdrawal, unless they have a severe preexisting
physical illness such as cardiac disease. Residual symptoms such as insomnia, bradycardia, temperature
dysregulation, and a craving for opioids can persist for months after withdrawal.
• Associated features of opioid withdrawal include restlessness, irritability, depression, tremor, weakness,
nausea, and vomiting. At any time during the abstinence syndrome, a single injection of morphine or
heroin eliminates all the symptoms.
Treatment and Rehabilitation

Overdose Treatment
Naloxone is administered IV at a slow rate initially about 0.8 mg per 70 kg of body
weight. Signs of improvement (increased respiratory rate and pupillary dilation) should
occur promptly
Opioid Agents for Treating Opioid Withdra al
1) Methadone
Methadone is a synthetic narcotic (an opioid) that substitutes for heroin and can be
taken orally. When given to addicts to replace their usual substance of abuse, the drug
suppresses withdrawal symptoms.
2) Buprenorphine
As with methadone, buprenorphine is an opioid agonist approved for opioid dependence
Opioid Antagonists
Opioid antagonists include naloxone, which is used in the treatment of opioid overdose
because it reverses the effects of narcotics, and naltrexone, the longest-acting (72
hours) antagonist.
The theory for using an antagonist for opioid-related disorders is that blocking opioid
agonist effects, particularly euphoria, discourages persons with opioid dependence from
substance-seeking behavior and, thus, deconditions this behavior.
Therapeutic Communities ( NIMHANS )

• Therapeutic communities are residences in which all members have a substance
abuse problem.
• Abstinence is the rule; to be admitted to such a community, a person must show a
high level of motivation.
• The goals are to effect a complete change of lifestyle, including abstinence from
substances; to develop personal honesty, responsibility, and useful social skills; and
to eliminate antisocial attitudes and criminal behavior.
116 | Psychiatry
Concept . : Cannabis and Related Disorders.
LEARNING OB ECTI E: To understand the clinical presentation of cannabis and related
Time Needed
1 reading
st
20 mins
2 look
nd
10 mins
Cannabis Preparations
• All parts of Cannabis sativa contain psychoactive cannabinoids, of which Delta
-tetrahydrocannabinol is most abundant.
• The most potent forms of cannabis come from the flowering tops of the plants or
from the dried, black-brown, resinous exudate from the leaves, which is referred to
as hashish or hash. The cannabis plant is usually cut, dried, chopped, and rolled into
cigarettes (commonly called joints), which are then smoked.
• The common names for cannabis are marijuana, grass, pot, weed, tea, and Mary
ane. Other names, which describe cannabis types of various strengths, are hemp,
chasra, bhang, ganja, dagga, and sinsemilla.
Imp. Points:
• Tolerance to cannabis does develop, however, and psychological dependence has
been found, although the evidence for physiological dependence is not strong.
Withdrawal symptoms in humans are limited to modest increases in
irritability, restlessness, insomnia, and anorexia and mild nausea all these
symptoms appear only when a person abruptly stops taking high doses of
cannabis.
• The most common physical effects of cannabis are dilation of the conjunctival blood
vessels (red eye) and mild tachycardia.
• At high doses, orthostatic hypotension may appear. Increased appetite often referred
to as “the munchies” and dry mouth are common effects of cannabis intoxication.
• That no clearly documented case of death caused by cannabis intoxication alone
reflects the substance’s lack of effect on the respiratory rate.
• The most serious potential adverse effects of cannabis use are those caused by
inhaling the same carcinogenic hydrocarbons present in conventional tobacco, and
some data indicate that heavy cannabis users are at risk for chronic respiratory
disease and lung cancer.
• Cannabis intoxication commonly heightens users’ sensitivities to external stimuli,
reveals new details, makes colors seem brighter and richer than in the past, and
subjectively slows the appreciation of time. In high doses, users may experience
depersonalization and derealization. Motor skills are impaired by cannabis use, and
the impairment in motor skills remains after the subjective, euphoriant effects have
resolved. For 8 to 12 hours after using cannabis, users’ impaired motor skills interfere
with the operation of motor vehicles and other heavy machinery. Moreover, these
effects are additive to those of alcohol, which is commonly used in combination with
cannabis.
Cannabis-Induced Psychotic Disorder

• Cannabis-induced psychotic disorder is diagnosed in the presence of a cannabis-
induced psychosis. Cannabis-induced psychotic disorder is rare; transient paranoid
ideation is more common.
• Florid psychosis is somewhat common in countries in which some persons have long-
term access to cannabis of particularly high potency. The psychotic episodes are
sometimes referred to as hemp insanity.
• Cannabis use rarely causes a bad-trip experience, which is often associated with
hallucinogen intoxication. (LSD better answer for bad trip)
Amotivational Syndrome
• A controversial cannabis-related syndrome is amotivational syndrome. Whether the
syndrome is related to cannabis use or reflects characterological traits in a subgroup
of persons regardless of cannabis use is under debate.
• Traditionally, the amotivational syndrome has been associated with long-term heavy
use and has been characterized by a person’s unwillingness to persist in a tasks be
it at school, at work, or in any setting that requires prolonged attention or tenacity.
Persons are described as becoming apathetic and anergic , usually gaining weight,
and appearing slothful.
Cognitive Impairment
• Clinical and experimental evidence indicates that the long-term use of cannabis may
produce subtle forms of cognitive impairment in the higher cognitive functions of
memory, attention, and organization and in the integration of complex information.
• This evidence suggests that the longer the period of heavy cannabis use, the more
pronounced the cognitive impairment.
lashbacks:
Persisting perceptual abnormalities after cannabis use.
Summary of acute e ects of cannabis

ental ehavioural ects hysical ects
Drowsiness Red eyes
(at high closes) Dry mouth
Euphoria Thirst
Anxjiety Increased appetite
Suspiciousness Tachycardia
Expectations of harm (or Bradycardia at high doses)
Sensation of slowed time Light headedness
Social withdrawal (Postural hypotension)
Impaired judgement
Illusions & hallucination
118 | Psychiatry
Concept . : Tobacco and Related Disorders.
LEARNING OB ECTI E: To understand the clinical presentation of nicotone related
Time Needed
1 reading
st
20 mins
2 look
nd
10 mins
(Most common substance of use in india/world)
Neuropharmacology
• The psychoactive component of tobacco is nicotine, which affects the central nervous
system (CNS) by acting as an agonist at the nicotinic subtype of acetylcholine
receptors.
• The half-life of nicotine is about 2 hours. Nicotine is believed to produce its positive
reinforcing and addictive properties by activating the dopaminergic pathway projecting
from the ventral tegmental area to the cerebral cortex and the limbic system.
Tobacco use Disorder

• The fifth edition of the Diagnostic and Statistical Manual of Mental Disorder (DSM-5)
includes a diagnosis for tobacco use disorder characterized by craving, persistent and
recurrent use, tolerance, and withdrawal if tobacco is stopped.
• Dependence on tobacco develops quickly, probably because nicotine activates the
ventral tegmental area dopaminergic system, the same system affected by cocaine
and amphetamine.
• The development of dependence is enhanced by strong social factors that encourage
smoking in some settings and by the powerful effects of tobacco company advertising.
Tobacco Withdra al
• The DSM-5 does not have a diagnostic category for tobacco intoxication, but it does
have a diagnostic category for nicotine withdrawal.
• Withdrawal symptoms can develop within 2 hours of smoking the last
cigarette they generally peak in the first 24 to 4 hours and can last for
weeks or months.
• The common symptoms include an intense craving for tobacco, tension, irritability,
difficulty concentrating, drowsiness and paradoxical trouble sleeping, decreased
heart rate and blood pressure, increased appetite and weight gain, decreased motor
performance, and increased muscle tension.
Psychopharmacological Therapies
Nicotine Replacement Therapies
All nicotine replacement therapies double cessation rates, presumably because they
reduce nicotine withdrawal. These therapies can also be used to reduce withdrawal in
patients on smoke-free wards. Replacement therapies use a short period of maintenance
of 6 to 12 weeks often followed by a gradual reduction period of another 6 to 12 weeks.
a. Nicotine polacrilex gum

b. Nicotine lozenges
c. Nicotine patches
d. Nicotine nasal spray
e. The nicotine inhaler
Non-nicotine Medications
• Non-nicotine therapy may help smokers who object philosophically to the notion of
replacement therapy and smokers who fail replacement therapy.
• Varenicline (alpha 4 beta 2 nicotine partial agonist) is most commonly used agent.
• Bupropion is an antidepressant medication that has both dopaminergic and adrenergic
actions. Adverse effects include insomnia and nausea, but these are rarely significant.
Seizures have not occurred in smoking trials.
• Interestingly, nortriptyline (Pamelor) appears to be effective for smoking cessation
and is recommended as a second-line drug.
• Clonidine decreases sympathetic activity from the locus ceruleus and, thus, is thought
to abate withdrawal symptoms
120 | Psychiatry
Concept . : Hallucinogens and Related Disorders.
LEARNING OB ECTI E: To understand the clinical presentation of hallucinogens and
related disorders and answer its related MCQ.
Time Needed
1 reading
st
20 mins
2 look
nd
10 mins
• Hallucinogens are natural and synthetic substances that are variously called
psychedelics or psychotomimetics because, besides inducing hallucinations, they
produce a loss of contact with reality and an experience of expanded and heightened
consciousness.
• The hallucinogens are classified as Schedule I drugs; the US Food and Drug
Administration (FDA) has decreed that they have no medical use and a high abuse
potential.
• The classic, naturally occurring hallucinogens are psilocybin (from some mushrooms)
and mescaline (from peyote cactus); others are harmine, harmaline, ibogaine, and
dimethyltryptamine (DMT).
• The classic synthetic hallucinogen is LSD, synthesized in 1 38 by Albert Hoffman,
who later accidentally ingested some of the drug and experienced the first LSD-
induced hallucinogenic episode.
• Some researchers classify the substituted or so-called designer amphetamines, such
as 3,4-methylenedioxyamphetamine (MDMA), as hallucinogens.
• The most common adverse effect of LSD and related substances is a bad
trip, an experience resembling the acute panic reaction to cannabis but sometimes
more severe; a bad trip can occasionally produce true psychotic symptoms. The bad
trip generally ends when the immediate effects of the hallucinogen wear off, but its
course is variable.
• According to studies, from 15 to 80 percent of users of hallucinogens report having
experienced flashbacks. The differential diagnosis for flashbacks includes migraine,
seizures, visual system abnormalities, and posttraumatic stress disorder. The following
can trigger a flashback: emotional stress; sensory deprivation, such as monotonous
driving; or use of another psychoactive substance, such as alcohol or marijuana.
• Flashbacks are spontaneous, transitory recurrences of the substance-induced
experience. Most flashbacks are episodes of visual distortion, geometric hallucinations,
hallucinations of sounds or voices, false perceptions of movement in peripheral fields,
flashes of color, trails of images from moving objects, positive afterimages and halos,
macropsia, micropsia, time expansion, physical symptoms, or relived intense emotion.
• The episodes usually last a few seconds to a few minutes, but sometimes last longer.
Most often, even in the presence of distinct perceptual disturbances, the person
has insight into the pathological nature of the disturbance. Suicidal behavior, major
depressive disorder, and panic disorders are potential complications.
Concept .10: (Ne Addition in DSM- ): Gambling Disorder
LEARNING OB ECTI E: To understand the clinical presentation of gambling disorder
and answer its related MCQ.
Time Needed
1 reading
st
10 mins
2 look
nd
5 mins
Gambling disorder is characterized by persistent and recurrent maladaptive gambling

that causes economic problems and significant disturbances in personal, social, or
occupational functioning.
Aspects of the maladaptive behavior include
(1) a preoccupation with gambling;
(2) the need to gamble with increasing amounts of money to achieve the desired
excitement;
(3) repeated unsuccessful efforts to control, cut back, or stop gambling;
(4) gambling as a way to escape from problems;
(5) gambling to recoup losses;
(6) lying to conceal the extent of the involvement with gambling;
(7) the commission of illegal acts to finance gambling;
(8) jeopardizing or losing personal and vocational relationships because of gambling
( ) a reliance on others for money to pay off debts.
122 | Psychiatry
Worksheet
• MCQ OF “Substance use and related disorders” FROM DQB

Substance Intoxication Symptoms Withdrawal Symptoms
1. Alcohol
2. Nicotine
3. Cannabis
. Caffeine
5. Cocaine
6. Amphetamine
Alcohol blood levels related:

Level Likely Impairment
20-30 mg/dL
30-80 mg/dL
80-200 mg/dL
200-300 mg/dL
>300 mg/dL
124 | Psychiatry
Clinical Problem in alcohol withdrawal Drug of choice
Hallucinosis
Extreme agitation
Withdrawal seizures
Delirium tremens
Medications for Treating Alcohol Dependence
Disulfiram Naltrexone Acamprosate
Action
Contraindications
Summary of acute e ects of cannabis

ental ehavioural ects hysical ects
7 Child Psychiatry
CONCEPTS
Â Concept 7.1 Pervasive Developmental Disorders
Â Concept 7.2 Attention‑Deficit Hyperactivity

Disorder
Â Concept 7.3 Tourette’s syndrome
Â Concept 7.4 Disruptive behavioural disorders of

childhood
Â Concept 7.5 Disruptive mood dysregulation

disorder
126 | Psychiatry
Concept 7.1: Pervasive developmental disorders
LEARNING OBJECTIVE: To understand the clinical presentation of different types of
pervasive developmental disorders of childhood and answer its related MCQ.
Time Needed
1 reading
st
30 mins
2 look
nd
15 mins
The characteristic features are:

1. Autism (marked impairment in reciprocal social and interpersonal
interaction):
i. Absent social smile.
ii. Lack of eye-to-eye-contact.
iii. Lack of awareness of others’ existence or feelings; treats people as furniture.
iv. Lack of attachment to parents and absence of separation anxiety.
v. No or abnormal social play; prefers solitary games.
vi. Marked impairment in making friends.
vii. Lack of imitative behaviour.
viii. Absence of fear in presence of danger.
2. Marked impairment in language and non‑verbal communication
i. Lack of verbal or facial response to sounds or voices; might be thought as deaf
initially.
ii. In infancy, absence of communicative sounds like babbling.
iii. Absent or delayed speech (about half of autistic children never develop useful
speech).
iv. Abnormal speech patterns and content. Presence of echolalia, perseveration,
poor articulation and pronominal reversal (I-You) is common.
v. Rote memory is usually good.
vi. Abstract thinking is impaired.
3. Abnormal behavioural characteristics
i. Mannerisms.
ii. Stereotyped behaviours such as head-banging, body-spinning, hand-flicking,
lining-up objects, rocking, clapping, twirling, etc.
iii. Ritualistic and compulsive behaviour.
iv. Resistance to even the slightest change in the environment.
v. Attachment may develop to inanimate objects.
vi. Hyperkinesis is commonly associated.
4. Mental retardation
Only about 25 of all children with autism have an IQ of more than 70. A large
majority (more than 50 ) of these children have moderate to profound mental
retardation. There appears to be a correlation between severity of mental retardation,
absence of speech and epilepsy in autism.
hil Psychiatry | 127
5. Other features
i. Many children with autism particularly enjoy music.
ii. In spite of the pervasive impairment of functions, certain islets of precocity or
splinter functions may remain (called as Idiot savant syndrome). Examples
of such splinter functions are prodigious rote memory or calculating ability, and
musical abilities.
iii. Epilepsy is common in children with an IQ of less than 50.
iv. Abnormal dermatoglyphics (finger prints)
The course of infantile autism is usually chronic and only 1-2 become near normal
in marital, social and occupational functioning. A large majority (about 70 ) lead
dependent lives.
Aetiology
• Presently, the cause of infantile autism seems to be predominantly biological. Earlier
reports of cold, refrigerator’ mothers causing autism in their children have not
been substantiated and have unnecessarily lead to undue distress to parents of
children with autism.
• The evidence for biological causation includes a higher than average history of perinatal
CNS insult, EEG abnormalities, epilepsy, ventricular dilatation on brain imaging,
increased serotonin (5-HT) levels in brain and/or neurophysiological abnormalities in
some patients.
Di erent types of pervasive developmental disorders:

Feature Autistic Disorder Asperger’s Rett’s Childhood
Syndrome Syndrome Disintegrative
Disorder
Age at recognition 0-36 Usually >36 5-30 >24
(months)
Sex ratio Male > Female Male >> Female Females only Male> Female
Loss of skills Variable Usually not Marked Marked
Social skills Very poor Poor Varies with age Very poor
Communication skills Usually poor Fair Very poor Very poor
Circumscribed Variable Marked (facts) NA NA
interests (mechanical)
Family history- similar Sometimes Frequent Not usually No
problems
Seizure disorder Common Uncommon Frequent Common
Head growth No No Yes No
decelerates
IQ range Severe MR to Mild MR to Severe MR Severe MR
normal normal
Outcome Poor to fair Fair to good Very poor Very poor
128 | Psychiatry
Treatment
The treatment consists of three modes of intervention which are often used together.
1. Behaviour Therapy
i. Development of a regular routine with as few changes as possible.
ii. Structured class room training, aiming at learning new material and maintenance
of acquired learning.
iii. Positive reinforcements to teach self-care skills.
iv. Speech therapy and/or sign language teaching.
v. Behavioural techniques to encourage interpersonal interactions.
2. Psychotherapy
Parental counselling and supportive psychotherapy can be very useful in allaying
parental anxiety and guilt, and helping their active involvement in therapy. However,
overstimulation of child should be avoided during treatment.
3. Pharmacotherapy
Drug treatment can be used for treatment of autism as well as for treatment of co-
morbid epilepsy.
i. Haloperidol decreases dopamine levels in brain. It is believed to decrease hyper
activity and behavioural symptoms. Risperidone, an atypical antipsychotic,
is helpful in some patients and is licensed in some countries for treatment of
autism in children aged 5 and above. Both haloperidol and risperidone can cause
extrapyramidal side-effects (EPSE), though usually more with haloperidol. The
starting dose for Risperidone is usually 0.25-0.5 mg (based on body weight), with
a dose range of 0.02-0.06 mg/kg/day.
ii. Other drugs such as SSRIs, chlorpromazine, amphetamines, methysergide,
imipramine, multi-vitamins and triiodothyronine have been tried with limited
success and should be used only by the experts in the field.
iii. Anticonvulsant medication is used for the treatment of generalised or other
seizures, if present.
Concept .2: Attention-Deficit Hyperactivity Disorder
LEARNING OBJECTIVE: To understand the clinical presentation of attention deficit
hyperactivity disorder and answer its related MCQ.
Time Needed
1 reading
st
15 mins
2 look
nd
10 mins
Attention-deficit/hyperactivity disorder (ADHD) is characterized by a pattern of

diminished sustained attention and higher levels of impulsivity in a child or adolescent
than expected for someone of that age and developmental level.
Diagnostic criteria
• Present for at least 6 months
• Evidence for impaired functioning in two or more settings
• Onset by age 12 (DSM‑5)
ADHD : Clinical eatures

• Fidgets with hands or feet
• Leaves seat in classroom
• Runs about or climbs excessively
• Difficulty engaging in leisure activities
• Often talks excessively
• Careless mistakes in school HYPERACTIVITY
• Difficulty sustaining attention
• Does not seem to listen • Blurts out answers
• Fails to finish work • Difficulty awaiting turn
ATTENTION
• Difficulty organizing tasks DEFICIT
IMPULSIVITY
• Intrudes on others
• Easily distracted by external stimuli
ig: .1
Other eatures
• Distractibility
• Poor at planning and organizing tasks
• Learning difficulties
• Clumsiness
• Low self - esteem
• Socially disinhibited
130 | Psychiatry
• Unpopular with other children
• Non - localizing neurological signs
• Conduct disorder coexists in 50
Treatment
• Pharmacologic treatment is considered to be the first line of treatment for ADHD.
Central nervous system stimulants are the first choice of agents in that they have
been shown to have the greatest efficacy with generally mild tolerable side effects.
• The S Food and Drug Administration (FDA) approved the use of
dextroamphetamine in children 3 years of age and older and methylphenidate
in children years of age and older. These are the two most commonly used
pharmacologic agents for the treatment of children with ADHD
• Atomoxetine , a norepinephrine uptake inhibitor, shown to be effective in the
treatment of children with ADHD;
• Antidepressants, such as bupropion , venlafaxine and the adrenergic receptor
agonists clonidine and guanfacine.
• In children with a history of motor tics, some caution must be used; in some cases,
methylphenidate can exacerbate the tic disorder
• Dextroamphetamine and dextroamphetamine amphetamine salt
combinations are usually the second drugs of choice when methylphenidate
is not effective
Concept . : Tourette s syndrome:
LEARNING OBJECTIVE: To understand the clinical presentation of tourette’s syndrome
and answer its related MCQ.
Time Needed
1 reading
st
10 mins
2 look
nd
5 mins
ig: .2
132 | Psychiatry
Concept . : Disruptive Behavioural Disorders of Childhood:
(Recent Exam)
LEARNING OBJECTIVE: To understand the clinical presentation of disruptive
behavioural disorders of childhood and answer its related MCQ.
Time Needed
1st reading 15 mins
2 look
nd
10 mins
• OPPOSITIONAL DEFIANT DISORDER
• COND CT DISORDER
Oppositional defiant disorder

• Oppositional defiant disorder is a persistent pattern (e.g., 6 months or more) of
markedly defiant, disobedient, provocative or spiteful behaviour that occurs
more frequently than is typically observed in individuals of comparable age and
developmental level and that is not restricted to interaction with siblings.
• Oppositional defiant disorder may be manifest in prevailing, persistent angry or
irritable mood, often accompanied by severe temper outbursts or in headstrong,
argumentative and defiant behaviour.
• The behavior pattern is of sufficient severity to result in significant impairment in
personal, family, social, educational, occupational or other important areas of
functioning
Conduct-dissocial disorder
• Conduct-dissocial disorder is characterized by a repetitive and persistent pattern of
behaviour in which the basic rights of others or major age-appropriate societal norms,
rules, or laws are violated such as aggression towards people or animals; destruction
of property; deceitfulness or theft; and serious violations of rules.
• The behaviour pattern is of sufficient severity to result in significant impairment
in personal, family, social, educational, occupational or other important areas of
functioning.
• To be diagnosed, the behaviour pattern must be enduring over a significant period
of time (e.g., 12 months or more). Isolated dissocial or criminal acts are thus not in
themselves grounds for the diagnosis.
Concept . : Disruptive Mood Dysregulation Disorder (DMDD)
LEARNING OBJECTIVE: To understand the clinical presentation of disruptive mood
dysregulation disorder and answer its related MCQ.
Time Needed
1 reading
st
15 mins
2 look
nd
10 mins
• DMDD is a new diagnosis in DSM 5.
• The diagnosis should not be made for the first time before age of years or after
age of 1 years. The age at onset is before 10 years. Symptoms are not better
explained by another mental disorder (e.g. autism spectrum disorder, posttraumatic
stress disorder, separation anxiety disorder, persistent depressive disorder).
• DMDD cannot occur simultaneously with oppositional defiant disorder, intermittent
explosive disorder, or bipolar disorder, but may coexist with major depressive disorder,
attention-deficit/hyperactivity disorder, conduct disorder, and substance use disorder.
• Diagnostic Criteria (DSM 5)
a. Severe recurrent temper outbursts manifested verbally (e.g. verbal rages) and/or
behaviorally (e.g. physical aggression toward people or property) which is out of
proportion to provocation.
b. The temper outbursts are not compatible with developmental level.
c. The temper outbursts occur three or more times in a week.
d. The mood between temper outbursts is persistently irritable or angry most of the
day, nearly everyday, and is observable by other (e.g. parents, teacher, peers).
Above symptoms must be present in at least two of three settings (i.e. at home, at
school, with peers) and are severe in at least one of these for 12 or more months;
during these 12 month period the individual is not free from symptoms for 3 or more
continuous months.
Course and prognosis: Studies have shown that DMDD in childhood may lead to
anxiety disorder, depression or dysthymic disorder in childhood.
Treatment: It is symptomatic because exact aetiology is not understood till date.
If DMDD resemble anxiety disorder or depression SSRIs are 1st choice; or mimic like
ADHD, then CNS stimulants is drug of choice. If pathophysiology mimic bipolar disorder
mood disorder, then atypical anti-psychotic with mood stabilized were used.
CBT (cognitive behavior therapy will be one necessary part of treatment).
Specific Learning Disability:

ea i i t s e ia
riti i t s rap ia
at emati a a atio i t s a ia
Treatment: Special Education
134 | Psychiatry
Worksheet
• MCQ OF “Child Psychiatry” FROM DQB

Di erent types of pervasive developmental disorders:
Feature Autistic Asperger’s Rett’s Childhood
Disorder Syndrome Syndrome Disintegrative Disorder
Age at recognition
(months)
Sex ratio
Loss of skills
Social skills
Communication skills
Circumscribed interests
Family history- similar

problems
Seizure disorder
Head growth decelerates
IQ range
Outcome
136 | Psychiatry
ADHD SYMPTOM CLUSTER INCLUDES
Hyperactivity
Impulsivity
Inattention
8 Sleep, Eating, Sexual and
Personality Disorders
CONCEPTS
Â Concept 8.1 Eating disorders
Â Concept 8.2 Sleep disorders
Â Concept 8.3 Sexual disorders
Â Concept 8.4 Personality disorders

138 | Psychiatry
Concept 8.1: Eating disorders
eating disorders and answer its related MCQ.
Time Needed
1 reading
st
30 mins
2 look
nd
15 mins
Anorexia Nervosa
Epidemiology
• Anorexia mainly affects females (sex ratio 10-20: 1).
• The average age of onset is 15 16 years.
• The prevalence is estimated to be around 0.5-1%
Diagnostic Criteria:
A. Weight loss, or in children a lack of weight gain, leading to a body weight of
at least 15% below the normal or expected weight for age and height. (The
percentage of weight loss is not mentioned in DSM 5)
B. The weight loss is self-induced by avoidance of “fattening foods”.
C. A self-perception of being too fat, with an intrusive dread of fatness, which leads to
a self-imposed low weight threshold.
D. A widespread endocrine disorder involving the hypothalamic-pituitary-gonadal axis,
manifest in the female as amenorrhoea, and in the male as a loss of sexual interest
and potency (Amenorrhoea is removed as an essential criteria in DSM 5)
E. Does not meet criteria A and B of Bulimia nervosa
Comments: The following features support the diagnosis, but are not necessary
elements: self-induced vomiting; self-induced purging; excessive exercise; use
of appetite suppressants and/or diuretics. If onset is pre-pubertal, the sequence of
pubertal events is delayed or even arrested (growth ceases; in girls the breasts do not
develop and there is a primary amenorrhoea; in boys the genitals remain juvenile). With
recovery, puberty is often completed normally, but the menarche is late.
Physical symptoms
• Sensitivity to cold
• Gastrointestinal symptoms constipation, bloating
• Dizziness
• Amenorrhea
• Poor sleep
Physical signs
• Emaciation
• Cold extremities
• Dry skin, sometimes orange (hypercarotenaemia)
• Downy hair (‘lanugo’) on back, forearms and cheeks
• Poorly developed or atrophic secondary sexual characteristics
lee atin e al an Pers nality is r ers | 139
• Bradycardia, postural hypotension, arrythmias
• Peripheral oedema
• Proximal myopathy
Abnormalities on investigation
• Low LH, FSH, estradiol, T3, somatomedin C
• Increased cortisol and CRH, growth hormone
• Hypoglycaemia
• Hypokalaemia, hyponatraemia, metabolic alkalosis
• ECG: prolonged QT interval (serious)
• Hypercholesterolaemia
• Osteopenia and osteoporosis
• Delayed gastric emptying
• Acute gastric dilatation (due to over - rapid refeeding)
Anorexia nervosa has one of the highest mortality rates (~5.6% per decade of
illness) of any psychiatric disorder.Q
Women with anorexia nervosa are 12 times more likely to die and have a suicide rate 57
times higher than women of a similar age group in the general population.
Poor prognostic factors include:

• Late age of onset.
• Chronicity of illness.
• Lower initial minimum weights.
• Bulimic features (vomiting, purgative abuse).
• Obsessive-compulsive personality features.
While Refeeding in Anorexia Patients (AIIMS)

1. Observe the patient for 2 hours after giving meals (as chances of vomiting are there)
2. Increased calories by 500 kcal per day.
Bulimia Nervosa
A. Recurrent episodes of overeating (at least two times per week over a period of three
months) in which large amounts of food are consumed in short periods of time.
B. Persistent preoccupation with eating and a strong desire or a sense of compulsion to
eat (craving).
C. The patient attempts to counteract the fattening effects of food by one or more of
the following:
(1) self-induced vomiting;
(2) self-induced purging;
(3) alternating periods of starvation;
(4) use of drugs such as appetite suppressants, thyroid preparations or diuretics.
When bulimia occurs in diabetic patients they may choose to neglect their insulin
treatment.
D. A self-perception of being too fat, with an intrusive dread of fatness (usually leading
to underweight).
140 | Psychiatry
Patients with eating disorders have in common the core psychopathology of extreme
concerns about body shape and weight.
• Recurrent binge eating
• ‘Loss of control during binges.
• Attempts to counteract the binges by vomiting, or by using other means such as
laxatives, enemas, diuretics or excessive exercise.
• Does not meet diagnostic criteria for anorexia nervosa.
• The combination of dieting and bingeing means body weight is usually unremarkable
the most obvious difference from anorexia nervosa.
• A small proportion of bulimia nervosa occurs in women with borderline personality
disorder who self - harm (often by cutting) and misuse alcohol or drugs.(15 of
bulimic patients)
• If body weight is decreased, some of the physical features and complications of
anorexia nervosa may be present
• Repeated vomiting may produce pitted teeth (eroded by gastric acid), calluses on
the knuckles (Russell’s sign from putting fingers down throat), hoarse voice,
salivary gland enlargement, metabolic disturbances.
Fig: 8.1
Fig: 8.2: CHIP MUNK FACIES (Bilateral parotid enlargement)
Menstrual disturbances can occur in small proportion of bulimia patients too.

Treatment:
Psychotherapy (the cornerstone of treatment): CBT has a strong evidence base and is
effective in addressing the core symptoms of bulimia nervosa.
Pharmacotherapy
Fluoxetine (at doses of 60mg) is the best studied and currently is the only FDA approved
medication for bulimia nervosa.
DSM-5
Changes
DSM-5 criteria reduce the frequency of binge eating and compensatory behaviors that
people with bulimia nervosa must exhibit, to once a week from twice weekly as specified
in DSM-IV.
Binge Eating Disorder

Recurrent episodes of binge eating.
An episode of binge eating is characterized by both of the following:
• eating, in a discrete period of time (e.g., within any 2-hour period), an amount of food
that is definitely larger than what most people would eat in a similar period of time
under similar circumstances
• a sense of lack of control over eating during the episode (e.g., a feeling that one
cannot stop eating or control what or how much one is eating)
The binge-eating episodes are associated with three (or more) of the following:
• eating much more rapidly than normal
• eating until feeling uncomfortably full
• eating large amounts of food when not feeling physically hungry
• eating alone because of being embarrassed by how much one is eating
• feeling disgusted with oneself, depressed, or very guilty after overeating
Binge eating disorder is defined as recurring episodes of eating significantly more food
in a short period of time than most people would eat under similar circumstances, with
episodes marked by feelings of lack of control. Someone with binge eating disorder
may eat too quickly, even when he or she is not hungry. The person may have feelings
of guilt, embarrassment, or disgust and may binge eat alone to hide the behavior. This
disorder is associated with marked distress and occurs, on average, at least once a week
over three months.
142 | Psychiatry
Concept 8.2: Sleep Disorders
sleep disorders and answer its related MCQ.
Time Needed
1 reading
st
20 mins
2 look
nd
10 mins
NREM parasomnias: Somnambulism (walking), somniloquy (talking), night terrors

(pavor nocturnus), bruxism (teeth grinding) and nocturnal enuresis (bed wetting beyond
5 years of age)
REM Parasomnias: Narcolepsy and Nightmares
Narcolepsy
• There are repeated attacks of daytime somnolence usually leading irresistibly to sleep.
• It usually begins in the second decade and is associated with cataplexy (abrupt
loss of muscle tone), hypnagogic hallucinations and sleep paralysis (the patient
wakes but is unable to move).
• An autoimmune origin is suspected as 98% have the DR15 variant of HLA - DR2.
Types of Narcolepsy: (Ref : Harrison Volume 1)

Type 1 narcolepsy (previously termed narcolepsy with cataplexy). This diagnosis is
based on the individual either having low levels of a brain hormone (hypocretin) or
reporting cataplexy and having excessive daytime sleepiness on a special nap test.
Type 2 narcolepsy (previously termed narcolepsy without cataplexy). People
with this condition experience excessive daytime sleepiness but usually do not
have muscle weakness triggered by emotions. They usually also have less severe
symptoms and have normal levels of the brain hormone hypocretin. Traumatic
brain injury can also damage orexin producing neurons inducing type 2 narcolepsy.
• Pathologically, there is a loss of hypothalamic hypocretin -producing neurons.
Stimulants (amphetamines or modafinil) are the main treatment. (Modafinil is DOC)
Fig: 8.3:
Fig: 8.4:
144 | Psychiatry
Concept 8.2: Sexual Disorders
sexual disorders and answer its related MCQ.
Time Needed
1 reading
st
20 mins
2 look
nd
10 mins
The sexual disorders can be classified into four main types:
1. Gender identity disorders (Transexualism and Dual Role Transvestism)
2. Psychological and behavioural disorders associated with sexual development and
maturation.
3. Paraphilias (disorders of sexual preference).
4. Sexual dysfunctions
Transexualism
Transexualism, the severest form of gender identity disorders, is characterised by the
following clinical features:
1. Normal anatomic sex.
2. Persistent and significant sense of discomfort regarding one’s anatomic sex and a
feeling that it is inappropriate to one’s perceived-gender.
3. Marked preoccupation with the wish to get rid of one’s genitals and secondary sex
characteristics, and to adopt sex characteristics of the other sex (perceived-gender).
4. Diagnosis is made after puberty.
Dual-role Transvestism
Dual-role transvestism is characterised by wearing of clothes of the opposite sex in order
to enjoy the temporary experience of member ship of the opposite sex, but without any
desire for a more permanent sex change (unlike transexualism).
Paraphilias
• Paraphilias (sexual deviations; perversions) are disorders of sexual preference in
which sexual arousal occurs persistently and significantly in response to objects
which are not a part of normal sexual arousal (e.g. nonhuman objects; suffering or
humiliation of self and/or sexual partner; children or nonconsenting person).
• These disorders include: Fetishism; fetishistic transvestism; sexual sadism; sexual
masochism; exhibitionism; voyeurism; frotteurism; pedophilia; zoophilia (bestiality);
and others.
Paraphilic Disorders
• Pedophilia: sexual urges toward children; most common paraphilia
• Exhibitionism: recurrent desire to expose genitals to stranger
• Voyeurism: sexual pleasure from watching others who are naked, grooming, or
having sex; begins early in childhood
• Sadism: sexual pleasure derived from others’ pain
• Masochism: sexual pleasure derived from being abused or dominated
• Fetishism: sexual focus on objects, e.g., shoes, stockings; transvestite fetishism
involves fantasies or actual dressing by heterosexual men in female clothes for sexual
arousal
• Frotteurism: male rubbing of genitals against fully clothed woman to achieve
orgasm; subways and buses
• Zoophilia: animals preferred in sexual fantasies or practices
• Coprophilia: combining sex and defecation
• Urophilia: combining sex and urination
• Necrophilia: preferred sex with cadavers
• Hypoxyphilia: altered state of consciousness secondary to hypoxia while experiencing
orgasm; achieved with autoerotic asphyxiation, poppers, amyl nitrate, nitric oxide
Sexual Dysfunctions:
Phases Dysfunction
1. Desire or Appetitive Phase Hypoactive sexual desire disorder; sexual aversion disorder
2. Excitement and Plateau Female sexual arousal disorder; male erectile disorder (may also occur in
Phase stages 3 and 4); male erectile disorder due to a general medical condition;
3. Orgasmic phase Female orgasmic disorder; male orgasmic disorder; premature ejaculation;
4. Resolution Phase Postcoital dysphoria; postcoital headache
Sexual Desire Disorders

In male hypoactive sexual desire disorder, men experience a deficiency or
absence of fantasies or desires. Reasons: low testosterone, CNS depressants, common
postsurgery, depression, marital discord.
Sexual Arousal Disorders
In female sexual interest/arousal disorder, women are unable to achieve adequate
vaginal lubrication. Reasons: possible hormonal connection (many women report peak
sexual desire just prior to menses), antihistamine and anticholinergic medications which
can reduce vaginal lubrication
Male erectile disorder: Half of men treated for sexual disorder complain of impotence.
The disorder is 50 more likely in smokers. Be sure to check alcohol usage, diabetes,
marital conflict, as it must be determined whether the cause is organic or psychological.
Treatment is sildenafil, vardenafil, tadalafil
Orgasm Disorders
Female orgasm disorder is an inability to achieve orgasm. 5 of married women age
>35 have never achieved orgasm. Overall prevalence from all causes is 30%. Treatment
is fantasy, vibrators.
In premature ejaculation, the male ejaculates before or immediately after entering
vagina. It is more common if there is anxiety about sexual act. Treatment is stop-and-go
technique, squeeze technique, SSRIs.
146 | Psychiatry
Concept 8.4: Personality Disorders
personality disorders and answer its related MCQ.
Time Needed
1 reading
st
30 mins
2 look
nd
15 mins
Cluster A- ODD, Eccentric

Paranoid • Suspicion and distrust of others
• Sensitivity to criticism
• Bears grudges
Schizoid • Emotionally cold and detached
• Introspective and prefers solitary activities
• Social isolation and few close friends
• Lack of joie de vivre(pleasure in activities)
• Psychotic features are typically absent
Schizotypal • Suspiciousness
• Magical thinking
• Metaphorical or stereotypical thinking
• Psychotic symptoms (Deln)
• Maybe seen in individuals related to schizophrenics

Cluster B (Dramatic) Emotionally Labile and Intense
Dissocial (= • Low frustration threshold
psychopathic,
• Irritable and impulsive
antisocial)
• Failure to learn from experience
• Failure to accept responsibility
• Lack of guilt/remorse
• Tend to be young men
• History of conduct disorder in childhood
• Extremely manipulative & gives plausible rationalization for irrational behaviors
Borderline • Multiple, turbulent relationships

(= emotionally • Impulsivity
unstable)
• Recurrent emotional crises
• Variable, intense mood
• Stress - related psychotic - like symptoms
• Tend to be young women
• Chronic feeling of emptiness
• Anxiety and unstable mood
• “confused personality”
• Dialectical behavior therapy (DBT) is the treatment of choice
Histrionic • Exaggerated, theatrical displays of emotion
• Attention seeking
• Vain
• Suggestible
• Shallow, labile mood
• Crushes and fads
Narcissistic • Grandiose self – importance
• Exaggerates achievements and abilities
• Exploits others
• Arrogant
• Expects special praise and respect

148 | Psychiatry
Cluster C (Anxious) Timid, Dependent, Low Self-Esteem
Anankastic • Excessive orderliness
(= obsessional) • Preoccupation with detail
• Perfectionist
• Excessively adherent to social customs
• n exible and dogmatic
• Humourless
• Miserly spending style toward both self and others
Anxious • Persistent tense and apprehensive feelings
(= avoidant) • Avoid personal contact
• Hypersensitivity to rejection by others
• Afraid to speak up in public or to make requests of others
Dependent • Encourage others to make decisions.
• Excessive need to be taken care of unrealistically preoccupied with fears of caring
for self.
• More likely to have “foli a deux” i.e. shared delusional disorder.
2 Types of Personality
Type A Type B
(Coronary artery disease prone) (Coronary artery disease not prone)
• Anxious and time bound • Relaxed
• Competitive • Easy going
• Ambitious
• Career Oriented
• Aggressive, Impatient
• Good job Involvement
Type D: Coronary Artery Disease Prone (PGI/AIIMS)

The type D (distressed) personality are particularly vulnerable to the adverse effect
of general distress. They frequently experience negative emotions and are socially
inhibited.
Miscellaneous
New Topics Added in ICD-11:
Disorders of bodily distress or bodily experience:
Disorders of bodily distress and bodily experience are characterized by disturbances in
the person’s experience of his or her body.
• Bodily distress disorder involves bodily symptoms that the individual finds
distressing and to which excessive attention is directed.
• Body integrity dysphoria involves a disturbance in the person’s experience of
the body manifested by the persistent desire to have a specific physical disability
accompanied by persistent discomfort, or intense feelings of inappropriateness
concerning current non-disabled body configuration.
Compulsive sexual behaviour disorder

• Compulsive sexual behaviour disorder is characterized by a persistent pattern of
failure to control intense, repetitive sexual impulses or urges resulting in repetitive
sexual behaviour.
• Symptoms may include repetitive sexual activities becoming a central focus of the
person’s life to the point of neglecting health and personal care or other interests,
activities and responsibilities; numerous unsuccessful efforts to significantly reduce
repetitive sexual behaviour; and continued repetitive sexual behaviour despite
adverse consequences or deriving little or no satisfaction from it.
• The pattern of failure to control intense, sexual impulses or urges and resulting
repetitive sexual behaviour is manifested over an extended period of time (e.g., 6
months or more), and causes marked distress or significant impairment in personal,
family, social, educational, occupational, or other important areas of functioning.
• Distress that is entirely related to moral judgments and disapproval about sexual
impulses, urges, or behaviours is not sufficient to meet this requirement.
Gaming disorder
Gaming disorder is characterized by a pattern of persistent or recurrent gaming behaviour
(‘digital gaming’ or ‘video-gaming’), which may be online (i.e., over the internet) or
o ine, manifested by:
1) impaired control over gaming (e.g., onset, frequency, intensity, duration, termination,
context);
2) increasing priority given to gaming to the extent that gaming takes precedence over
other life interests and daily activities; and
3) continuation or escalation of gaming despite the occurrence of negative consequences.
The behaviour pattern is of sufficient severity to result in significant impairment
in personal, family, social, educational, occupational or other important areas of
functioning.
The pattern of gaming behaviour may be continuous or episodic and recurrent. The
gaming behaviour and other features are normally evident over a period of at least 12
months in order for a diagnosis to be assigned, although the required duration may be
shortened if all diagnostic requirements are met and symptoms are severe.
150 | Psychiatry
Worksheet
• MCQ OF “Sleep, eating, sexual and personality Disorders” FROM DQB

Anorexia Nervosa Bulimia Nervosa Binge eating disorder
Personality Disorder Key Features

1. Schizoid
2. Schizotypal
3. Paranoid
4. Borderline
5. Histrionic
6. Antisocial
7. Narcissistic
8. Avoidant
9. Dependent
10. OCPD
9 Psychology, PsychotheraPy
and community Psychiatry
CONCEPTS
Â 9.1 Piaget’s Theory
Â 9.2 Freud’s psychosexual stages of development
Â 9.3 Freud’s structural and topographical theory
Â 9.4 Defense mechanisms
Â 9.5 Learning theories
Â 9.6 Maslow’s hierarchy of needs
Â 9.7 Psychotherapy
Â 9.8 Community psychiatry (Video available on

e-medicoz app)
Psych l y Psych thera y an nity Psychiatry
Concept 9.1: Piaget’s Theory of Cognitive Development (AIIMS May
2012)
LEARNING OBJECTIVE: To understand the basic concept of piaget’s stages of cognitive
development and answer its related MCQ.
Time Needed
1st reading 15 mins
2 look
nd
10 mins
Piaget's Stages of Cognitive Development

Stage Age Major Characteristics
Range
Sensori-motor 0-2 years • All knowledge is acquired through senses and movement (such
as looking and grasping)
• Thinking is at the same speed as physical movement
• Object permanence develops
Preoperational 2-7 years • Thinking separates from movement and increases greatly in
speed
• Ability to think in symbols develops
• Nonlogical, "magical" thinking
• Animism: all objects have thoughts and feelings
• Egocentric thinking: unable to see world from others' points of
view
Concrete 7-11 years • Logical thinking develops, including classifying objects and
operations mathematical principles, but only as they apply to real, concrete
objects
• Conservation of liquid, area, volume
• Ability to infer what others may be feeling or thinking
Formal operations 11 and up • Logical thinking extends to hypothetical and abstract concepts
• Ability to reason using metaphors and analogies
• Ability to explore values, beliefs, philosophies
• Ability to think about past and future
• Not everyone uses formal operations to the same degree, and
some not at all
Out of sight is out of mind : Sensorimotor Stage

Psychiatry
Concept 9.2: Freud’s Psychosexual Stages of Development (Ref :
Ahuja)
LEARNING OBJECTIVE: To understand the basic concept of Sigmund Freud’s stages of
psychosexual development and answer its related MCQ.
Time Needed
1st reading 25 mins
2 look
nd
15 mins
No. Stage Age Normal Development Psychiatric syndromes

Range (gratification) to result from fi ation (and regression)
to this stage
1. Oral 0-1.5y a or site of gratification is the oral region. 1. Dependent personality
i. Oral erotic phase (sucking) traits and disorder
ii. Oral sadistic phase (biting) 2. Schizophrenia
3. Severe mood disorder
4. Alcohol dependence
syndrome and drug dependence
2. Anal 1.5-3y a or site of gratification is the anal area 1. Obsessive compulsive personality
It consists of 2 phases: traits and disorder
i. Anal erotic phase (excretion) 2. OCD (Anal sadistic phase)
ii. Anal sadistic phase (‘holding’ and ‘letting go’ at
will)
3. Phallic 3-5y a or site of gratification is the genital area 1. Sexual deviations
According to reud, this development is differentin 2. Sexual dysfunctions
both sexes. 3. Hysteria
Male development
The boy develops castration anxiety(fear of castration
at the hand of his father in retaliationfor the boy’s desire
to replace his father in his mother s affections . his
leads to formation ofthe Oedipus complex(aggressive
impulses directed towards the father named after
the Greektragedy Oedipus rex in which Oedipus
unknowingly kills his father and marries his mother,
unaware of their true identities). Oedipus complex
is usually resolves by identification with father,
attempting to adopt his characteristics.
Female development
The girl develops penis envy(discontent with
femalegenitalia following a fantasy that they result
from loss of penis). This is theorised by Freud tolead
to a wish to ‘receive’ the penis and to bear a child.
Resolution occurs by identification with the mother.
This phase has been called as Electracomplex.
4. Latency 5-12y Oedipus (and Electra) complex is usually resolved at Neurotic disorders
the beginning of this stage. This is astage of relative
sexual quiescence. Super-ego isformed at this stage.
Sexual drive is channelized into socially appropriate
goals such as development of interpersonal
relationships, sports, school, work, etc.
5. Genital >12y Adult sexuality develops. Neurotic disorders
True self-identity develops.
Concept 9.3: Freud’s Structural and Topographical Theory
LEARNING OBJECTIVE: To understand the basic concept of freud’s model of mind,
dream analysis,psychoanalysis and answer its related MCQ.
Time Needed
1 reading
st
40 mins
2 look
nd
20 mins
Fig. 9.1: Structural Theory of Mind
Fig. 9.2:
Psychiatry
2 model’s of freud:
1. Topographical model (Preconscious, Unconscious and Conscious)
2. Structural model (Id, Ego And Superego)
Fig. 9.3:
CONTRIBUTIONS OF FREUD:
1. Father of classical psychoanalysis
2. Gave models of mind
3. Dream analysis (He said “dream is a royal road to unconsciousness”)
4. Coined the terms transference, countertransference, neurosis
5. Gave concept of hysteria
Psychoanalysis techniques:
• Hypnosis (Increased Suggestibility)
• Free association: Patient is allowed to speak uninterrupted (parapraxes: slip tongue)
• Abreation: Recollection of repressed memories with approriate affective response
(AIPG 18) (catharsis) by use of doing thiopentone
Psychiatry
Concept 9.4: Defence Mechanisms
LEARNING OBJECTIVE: To understand the basic concept of defense mechanism and
answer its related MCQ.
Time Needed
1 reading
st
30 mins
2 look
nd
15 mins
The ego deals with the demands of reality, the id, and the superego as
best as it can.
But when the anxiety becomes overwhelming, the ego must defend
itself.
It does so by unconsciously blocking the impulses or distorting them

into a more acceptable, less threatening form.
The techniques are called the ego defense mechanisms
TYPES OF DEFENSE MECHANISMS

Pathological
1. Denial.
2. Projection.
Neurotic Defenses
1. Repression
2. Displacement
3. Reaction formation
4. Undoing
5. Rationalization
Mature Defenses
1. Supression
2. Anticipation
3. Humor
4. Asceticism
5. Sublimation
6. Altruism
Defense Mechanism planation ample
Acting out Avoiding personally unacceptable emotions A depressed 14-year-old girl with no history of
by behaving in an attention-getting, often conduct disorder has sexual encounters with
socially inappropriate manner multiple partners after her parents divorce
Altruisma Assisting others to avoid negative personal A man with a poor self-image, who is a social
feelings worker during the week, donates every other
weekend to charity work
Denial Not accepting aspects of reality that the A man who has a problem with alcohol insists
person finds unbearable that he is only a social drinker
Displacement Moving emotions from a personally A surge on with unacknowledged anger toward
intolerable situation to one that is personally his sister is abrasive to the female residents on
tolerable his service
Dissociation Mentally separating part of one's Although he was not injured, a teenager has
consciousness from real-life events or no memory of a car accident in which he was
mentally distancing oneself from others driving and his girlfriend was killed
Humora Expressing personaIly uncomfortable A man who is concerned about his erectile
feelings without causing emotional problems makes okes about iagra sildenafil
discomfort citrate)
Idealization Seeing others as more competent or A patient tells the doctor that he is not worried
powerful than they are because he is sure that the doctor will always
know what to do
dentification Unconsciously patterning one's behavior A man who wa s terrorized by his gym teacher
(introjection) after that of someone more powerful (can as a child becomes a punitive, critical gym
be either positive or negative) teacher identification with the aggressor
Ihtelectualization Using the mind's higher functions to avoid A sailor whose boat is about to sink calmly
experiencing emotion explains the technical aspects of the hull
damage in great detail to the other crew
members
solation of affect Failing to experience the feelings associated Without showing any emotion, a woman tells
with a stressful life event, although logically her family the results of tests that indicate her
understanding the significance of the event lung cancer has metastasized
Projection Attributing one's own personally A man with unconscious homosexual impulses
unacceptable feelings to others Associated begins to believe that a male colleague is
with paranoid symptoms and prejudice attracted to him
Rationalization Distorting one's perception of an event so A man who loses an arm in an accident says the
that its negative outcome seems reasonable loss of his arm was good because it kept hmi
from getting in trouble with the law
Reaction formation Adopting opposite attitudes to avoid A woman who unconsciously is resentful of the
personally unacceptable emotions, i.e., responsibilities of child rearing overspends on
unconscious hypocrisy expensive gifts and clothing for her children
Regression Reverting to behavior patterns like those A woman insists that her husband stay overnight
seen in someone of a younger age in the hospital with her before surgery
Psychiatry
DEFENCE MECHANISM AND RELATED DISORDERS IN

PSYCHIATRY:
• PROJECTION : Psychosis
• REPRESSION : Neurosis
• DISPLACEMENT : Phobia
• INTROJECTION : Depression (DNB 2018)
• UNDOING, REACTION FORMATION : OCD (PGI)
Concept 9.5: Learning Theories
LEARNING OBJECTIVE: To understand the basic concept of learning models and
answer its related MCQ.
Time Needed
1 reading
st
25 mins
2 look
nd
15 mins
Classical Conditioning Operant Conditioning

A signal is placed before a re ex A reinforcing or punishing stimulus is given after a
behavior
Developed in Rissia Developed in U.S.
Known as "Pavlovian" Known as "Skinnerian"
Also called "respondent conditioning" Also called "instrumental conditioning
Works with involuntary behavior Works with voluntary behavior
Behavior is said to be "elicited" Behavior is said to be "emitted"
ypified by Pavlov s dog ypified by Skinner ox
4 types of operant conditioning:

1. Positive reinforcement
2. Negative reinforcement
3. Punishment
4. Extinction
Fig. 9.4:
Psychiatry
Premack’s Principle
(Type of Operant Conditioning Only) (Nov AIIMS)
• It 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. When he made
playing with the pinball machine contingent on eating a certain amount of candy, the
children increased the amount of candy they ate.”
• This principle is also known as Grandma’s rule (If you eat your spinach, you can have
dessert).
Concept 9.6: Maslow’s Hierarchy (AIIMS November 2016)
LEARNING OBJECTIVE: To understand the basic concept of maslow’s hierarchy of
needs and answer its related MCQ.
Time Needed
1 reading
st
15 mins
2 look
nd
10 mins
Maslow’s hierarchy of needs states that individuals’ main needs are satisfied in
the following sequence: physiological, safety, love and belongingness, esteem,
and self-actualization.
Fig. 9.5:
Psychiatry
Concept 9.7: Psychotherapy
LEARNING OBJECTIVE: To understand the basic concept of different types of
psychotherapies, its applications and answer its related MCQ.
Time Needed
1 reading
st
60 mins
2 look
nd
30 mins
Psychotherapy is treatment of psychiatric disorders by using psychological methods.
Psychoanalysis and Psychoanalytical Psychotherapy (reconstructive) (Ref :

Niraj Ahuja)
These psychotherapeutic methods are based primarily on Sigmund Freud’s work
Classical Psychoanalysis
• Freudian psychoanalysis typically needs 2-5 visits/ week by the patient for a period
of 3-5 years (even longer).
• No detailed history taking, mental status examination, or formalised psychiatric
diagnosis is attempted.
• The patient is allowed to communicate unguided, by using ‘free association’. The
therapist remains passive with a non-directive approach; however, the therapist
constantly challenges the existing defenses and interprets resistance
(during the therapy) and transference (patient’s feelings, behaviours and
relationship with the therapist).
• No direct advice is ever given to the patient.
• The crux of the therapy is on interpretation.
• During the therapy, the patient typically lies on the couch, with the therapist sitting
just out of vision.
• No other therapy is usually used as adjunct.
Psychoanalytically-oriented (Psychodynamic) Psychotherapy

• Psychoanalytically-oriented, psychodynamic psychotherapy is a much more direct
form of psychoanalysis.
• The duration of therapy is much briefer and advice is given to the patient occasionally.
• The patient and the therapist may sit face-to-face or else couch is used.
• The rest of technique is nearly the same as psychoanalysis.
• However, additional modes of treatment, including drug therapy can be used.
• The indications for both psychoanalysis and psychoanalytically-oriented psychotherapy
are not usually based on any psychiatric diagnoses.
• The most important indication is the presence of long-standing mental conflicts which,
although are unconscious, produce significant symptomatology.
• The prerequisites of therapy are that the patient should be motivated for therapy,
should have strong ‘ego-structure’ (which can bear frustrations of impulses during the
therapy), should be psychologically- minded and should not have recent significant
life stressors.
• It is usually used for the treatment of neurotic disorders and personality disorders.
Behavior Therapy (Ref : Niraj Ahuja)

• Behaviour therapy is a type of psychotherapy, which is based on theories of learning,
and aims at modifying maladaptive behaviour and substituting it with adaptive
behaviour.
• Although there are many theories of learning, majority of behaviour therapy techniques
are based on operant conditioning model (Skinner) and classical conditioning
model (Pavlov).
• Many of the ideas actually seem like (and are) common sense principles.
• The learning theories assume that all behaviour is learned behaviour.
• The behaviour that is followed by a reward is more likely to occur again (operant
model), and that behaviour is learned more easily if taught in small steps.
• Behaviour therapy is typically a short duration therapy; therapists are easy to train
and it is usually cost-effective.
• The total duration of therapy is usually 6-8 weeks.
• Initial sessions are scheduled daily but the later sessions are more spaced out.
• A behavioural analysis is usually carried out before planning behaviour therapy.
Psychiatry
One of the simplest methods of behaviour analysis is called as ABC charting,

which involves a close look at the:
i. Antecedent (e.g. circumstances under which the behaviour began; who, if any, were
present; other details),
ii. Behaviour (description of the behaviour in detail), and
iii. Consequence (what happened afterwards; what factors helped to maintain
behaviour).
Some of the important behavioural techniques are described briefly.
1. Systematic Desensitisation
Systematic desensitisation (SD) is based on the principle of reciprocal inhibition.
states that if a response incompatible with anxiety is made to occur at the same time as
an anxiety-provoking stimulus, anxiety is reduced by reciprocal inhibition.
This consists of three main steps:
i. Relaxation training (described later).
ii. Hierarchy construction: Here the patient is asked to list all the conditions which
provoke anxiety. Then, he is asked to list them in a descending order of anxiety
provocation. Thus, a hierarchy of anxiety-producing stimuli is prepared.
iii. Systematic desensitisation proper: This can be done either in imagery (SD-I)
or in reality/ in vivo (SD-R). At first, the lowest item in hierarchy is con fronted (in
reality or in imagery). The patient is advised to signal whenever anxiety occurs.
With each signal, he is asked to relax (Step-I). After a few trials, patient is able
to control his anxiety. Thus, gradually the hierarchy is climbed till the maximum
anxiety provoking stimulus can be faced in the absence of anxiety. SD is a treatment
of choice in phobias.
2. Aversion Therapy
• Aversion therapy is used for the treatment of conditions which are pleasant but felt
undesirable by the patient, e.g. alcohol dependence, transvestism, ego dystonic
homosexuality, other sexual deviations.
• The underlying principle is pairing of the pleasant stimulus (such as alcohol)
with an unpleasant response (such as brief electrical stimulus), so that even
in absence of unpleasant response (after the therapy is over), the pleasant
stimulus becomes unpleasant by association. The unpleasant aversion can
be produced by electric stimulus (low voltage), drugs (such as apomorphine and
disulfiram) or even by fantasy (when it is called as covert sensitisation). Typically,
20-40 sessions are needed, with each session lasting about 1 hour.
3. Flooding
• This is usually the method used in the treatment of phobias. Here, the person is
directly exposed to the phobic stimulus, but escape is made impossible.
• By prolonged contact with the phobic stimulus, therapist’s guidance and
encouragement, and therapist’s modelling behaviour, anxiety decreases and the
phobic behaviour diminishes.
4. Modeling (Participant modeling):

Here, therapist him-self makes the contact with phobic stimulus and demonstrates
this to the patient. Patient learns by imitation and observation.
For example, a therapist himself took a dog in his arms while a patient who had
phobia of dogs observed him.
This technique is used in phobias as well as obsessive compulsive disorders.
5. Assertiveness training:
Here a person is taught to be assertive while asking for his rights and while refusing
unjust demands of others.
6. Social skills training:
Usually used in patients with schizophrenia, it involves imparting skills required for
dealing with others and living a social life
Operant Conditioning Procedures for Decreasing Behaviour

These methods include:
i. Time-out: Here, the reinforcement is withdrawn for some time, contingent upon the
undesired response. Time-out is often used in therapy with children.
ii. Punishment: Aversive stimulus is here presented, contingent upon undesired
response (i.e. whenever undesired response occurs, punishment is given).
iii. Satiation: The undesired response is positively reinforced, so that tiring occurs. A
similar technique is negative practice procedure.
Other Behavioural Techniques such as token economy (for hospitalised patients)
BIOFEEDBACK
• It is a treatment technique that uses the principles of operant conditioning.
• The biofeedback is based on the idea that autonomic nervous system (which is
usually involuntary) can be brought under voluntary control with the help of operant
conditioning.
• It is used for treatment of disorders, which are caused by dysfunction in autonomic
control such as asthma, tension headaches, arrhythmias, etc.
• The technique uses a feedback instrument, the choice of which depends on the
patient’s problem.
• This instrument gives patient a feedback about the current status of a specific
autonomic function.
• For example, an electromyogram (EMG) may be used to give patient feedback about
muscle tension in a particular muscle group.
• When the muscle tension is high, the EMG will emit a higher tone and when muscle
tension is low (i.e. when muscle is relaxed), the EMG will emit a lower tone.
• Using feedback, patient learns to control his muscle tone and hence is able to control
symptoms caused by increased muscle tone (e.g. bruxism).
Psychiatry
Cognitive Therapy
• The cognitive theory assumes that the cognitions (thoughts) are at the core of
psychiatric symptoms.
• On the basis of early experiences, an individual may develop wrong patterns of
thinking, known as cognitive distortions (or maladaptive assumptions).
• The cognitive therapy aims to correct these “negative automatic thoughts” and
“cognitive distortions”.
• When along with these, behavioral techniques are also used, the therapy method is
known as “cognitive behavioral therapy”.
Techniques in CBT are:

i. Cognitive techniques such as recognising and correcting negative automatic
thoughts, teaching reattribution techniques, increasing objectivity in perspectives,
identifying and testing maladaptive assumptions, and decentering,
ii. Behavioural techniques such as activity scheduling, homework assignments,
graded task assignment, behavioural rehearsal, role playing, and diversion
techniques, and
iii. Teaching problem-solving skills.
iv. Mindfulness, originally a Buddhist technique, can also be combined with CBT
Cognitive therapy and cognitive behavioral therapy are used in the treatment of
depression, panic disorder, obsessive compulsive disorder, personality disorder and
somatoform disorder.
Fig. 9.6:
“MENTALIZATION-BASED TREATMENT. (NIMHANS)

• Another type of psychotherapy for borderline personality disorder is called
mentalization-based therapy (MBT).
• Mentalization is a social construct that allows a person to be attentive to the mental
states of oneself and of others; it comes from a person’s awareness of mental
processes and subjective states that arise in interpersonal interactions.
• MBT is based on a theory that borderline personality symptoms, such as difficulty
regulating emotions and managing impulsivity, are a result of patients’ reduced
capacities to mentalize.
• Thus, it is believed that recovery of mentalization helps patients build relationship
skills as they learn to better regulate their thoughts and feelings. MBT was found
to be effective for borderline personality disorder in several randomized, controlled
research trials.”
Supportive Psychotherapy
This is a very directive method of psychotherapy, with the focus clearly on existing
symptoms and/or current life situations. The aims of the therapy are:
i. Correction of the situational problem.
ii. Symptom rectification.
iii. Restoring or strengthening defenses.
iv. Prevention of emotional breakdown.
v. Teaching new coping skills.
The aim is achieved by a conglomeration of techniques which include guidance,
suggestion, environmental manipulation, reassurance, persuasion, development of a
doctor-patient relationship, diversion, and even hospitalisation and medication.
This is a highly skilled method of psychotherapy which can provide excellent results
when used judiciously.
Family and Marital Therapy

• In family therapy and marital therapy (also called as couples therapy), the focus
of intervention is not on the individual but is instead on the family as a unit or the
marital unit.
• There are several varieties of family and marital therapies, such as those based on
psychodynamic, behavioural or systemic principles.
• Whenever there are relational problems within a family or marital unit (either primarily
or secondary to a psychiatric disorder), family and/or marital therapy is indicated.
• For example, in a behavioural marital therapy, components of therapy may include
problem solving, training in communication skills, writing a behavioural marital
contract, and home-work assignments.
Group Therapy
• Group therapy (or group psychotherapy) is a less time-consuming procedure, in which
usually 8-10 people can be treated at one time. Now, it is known that group therapy
is not only time-saving but also especially beneficial for certain group of patients.
Psychiatry
• Group therapy offers patients (and their relatives) an opportunity to realise that many
others have and share problems which are very similar to their own problems, and
that they are not alone in their suffering.
• Typically, sessions are held once or twice a week, with each session lasting 1-2 hours
(often 1½ hours).
• The patients usually sit in a circle, with equal opportunities for interaction.
• Group therapy may utilize psychoanalytic, supportive, transactional or behavioural
app roaches.
• Over the years, many types of group therapies have emerged such as self-help groups
(Alcoholics Anonymous for alcoholics)
Abreaction
• Abreaction is an important procedure which brings to conscious awareness, for the
first time, unconscious conflicts and associated emotions. (NEET PG)
• The release of emotions is therapeutic.
• Although abreaction is an integral part of psycho analysis and hypnosis, it can be used
independently also.
• Method is the use of 5% solution of sodium amobarbital (amytal) or thiopentone
sodium (pentothal), infused at a rate no faster than 1 cc/min to prevent sleep as well
as respiratory depression.
• This procedure must always be done very carefully with support from an anaesthetist
who should be physically present.
• The abreactive procedure is begun with neutral topics at first, gradually approaching
area(s) of conflicts.
The indications of amytal interview include:

i. Abreaction (mainly) e.g. in hysteria.
ii. Interview with a mute patient.
iii. Diagnostic test in catatonic syndrome.
iv. Differentiating test in stupor (for differential diagnosis of depression, schizophrenia,
hysteria and organic brain disorder).
There are certain contraindications for the use of amytal interview:
i. Airway disease including upper respiratory tract infection.
ii. Severe renal or hepatic disease.
iii. History of porphyria.
iv. Hypotension.
v. Dependence on barbiturates.
vi. Psychosis (except for catatonia or stupor).
• The other medications which have been used successfully for abreaction include
diazepam and ketamine.
• The use of abreaction has declined considerably in the last three decades and the
current practice and guidelines do not encourage its routine use.
Psychosocial Treatment
• The patients with substance use disorders (and other problematic behaviors) go
through a series of changes before quitting the substance use.
• Various models of these changes have been described, the most acceptable model
is known as transtheoretical model of change. According to this model, the following
are the stages of change:
1. Precontemplation—not yet acknowledging that there is a problem
2. Contemplation—acknowledging that there is a problem, but not yet ready or willing
to make a change
3. Preparation/determination—getting ready to change behaviors
4. Action/willpower—changing behaviors
5. Maintenance—maintaining the behavioural changes
6. Relapse—returning to old behaviors and abandoning new changes. Does not always
happen.
Fig. 9.7:
• Various psychological treatment methods have been devised to help patient quit
substance use and move from stages of precontemplation to maintenance.
• One of the most commonly used technique, which focuses on increasing the motivation
of the patient to quit substance is known as motivation enhancement therapy or
motivational interviewing.
Psychiatry
Concept 9.8: Community Psychiatry
LEARNING OBJECTIVE: To know the developments in field of community psychiatry
and mental health related act, programme and answer its related MCQ.
Time Needed
1 reading
st
45 mins
2 look
nd
20 mins
• National mental health programme 1982

• National Mental health policy 2014
• Mental health care act 2017
• Mental health gap
National mental health programme

AIM:
• 1. Prevention and treatment of mental and neurological disorders and their associated
disabilities.
• 2. Use of mental health technology to improve general health services.
• 3. Application of mental health principles in total national development to improve
quality of life.
Objectives:
1) To ensure availability and accessibility of minimum mental health care for all in
foreseeable future, particularly most vulnerable and underprivileged section of
population
2) Encourage application of mental health knowledge in general health care and social
development
3) Promote community participation in mental health services development and
stimulate efforts towards self-help in community
Strategies:
1. Integration mental health with primary health care through the NMHP
2. Provision of tertiary care institutions for treatment of mental disorders
3 Eradicating stigmatization of mentally ill patients and protecting their rights through
regulatory institutions like the Central Mental Health Authority and State Mental
health Authority.
Specific approaches:
1. Diffusion of mental health skills to the periphery of health services
2. Appropriate appointment of tasks
3. Equitable and balanced distribution of resources
4. Integration of basic mental health care with general health services
5. Linkage with community development
Components of district mental health programme (1996):
1. Training of medical, paramedical personnel and community leaders
2. Community Mental Health care through existing infrastructure of the health
services
3. Information, Education and Communication (IEC) activities
School mental health programme (2010)

• Provide Class Teachers with Knowledge and Skills to Identify Emotional, Conduct
Problems in their students
• Provide Class Teachers with a system of referral for students with psychological
problems to the District Mental Health Team for inputs and treatment.
• Provide Class Teachers with Facilitative Skills to Promote Life Skills among their
Students.
National mental health policy:

• The vision of the NMHP includes the promotion of mental health, desegregation
and de-stigmatization of mental health issues and psychiatric disorders, ensuring
the availability of accessible and affordable mental health care and focusing on the
paradigms of recovery and prevention in mental health care.
• The NMHP aims to integrate mental health care into the primary healthcare system.
• Main objectives of the National Mental Health Policy includes provision of universal
access to mental health care, increasing access to comprehensive mental health
services, such as, prevention, treatment, care and support services among many
others.
Mental Healthcare Act, 2017 (MHCA 2017): A new legislation that deals with
treatment and rights of patients with mental illness came into being in 2017, and is
referred to as Mental Health Care Act, 2017.
The important clauses of this Act are described below:
A. Capacity to make mental healthcare and treatment decisions : According to
MHCA 2017, every person, including those who have a mental iliness, is assumed to
have a capacity to decide about what kind of treatment (including admission) they
want to have for their mental illness, if they have the ability to
a. Understand the information that is given to them and on the basis of which they
have to take the decision (e.g. information about the illness, the symptoms, the
treatment used, etc.)
b. Understand the consequences of their decisions (e.g. a patient who is having
suicidal thoughts and not willing to take treatment, should be able to understand
that not taking treatment can be life-threatening for him)
c. To communicate their decision by using speech or gestures, etc.
B. Advance directive: (AIIMS)Q Every person (who is not a minor), can make an
advance directive in which he can mention-
a. The way he wishes to be treated for a mental illness
b. The way he wishes not to be treated for a mental illness
Psychiatry
The advance directive would be applicable only if a person, loses the capacity to make
mental healthcare or treatment decisions.
It is the duty of psychiatrist (or medical officer) in charge of treatment, to ensure that
treatment is being given according to advance directive made by the patient.
However, it is the duty of patient (or caregiver or nominated representative) to provide
access to the advance directive to the treating doctor.
If due to following of advance directive, there are some unforeseen consequences,
doctor cannot be held liable for the same.
C. Nominated representative: Every person can appoint an nominated representative
(who should not be a minor, and competent in discharging his duties as a nominated
representative) and remove him, if he wishes to.
If a person loses capacity to make mental healthcare or treatment decisions, his
nominated representative will help (or will take) in taking decisions about treatment of
the person.
D. Admission: the MHCA 2017 allows two types of admissions
a. Independent admissions: When the patient himself wants to get admitted
b. Supported admissions: A person who needs admission, however, has lost the
capacity to make mental healthcare or treatment decisions, and hence needs
high level of support from the nominated representative, can be admitted as a
‘supported admission’. The nominated representative gives consent for admission
in this case.
{Section 86: deals with: Independent admission & treatment.
Section 87: deals with: Admission of minor.
Section 89: deals with: Admission & treatment of persons with mental illness, with
high support needs, up to 30 days (supported admission) (NEET)Q
Section 90: deals with: Admission & treatment of persons with mental illness, with
high support needs, beyond 30 days (supported admission beyond 30 days)}
E. Ban on direct electroconvulsive therapy (ECT without use of muscle relaxants and
anesthesia)
F. Ban on ECT for minors (In a rare case, if psychiatrist in charge considers ECT is
required for treatment of minor, he will have to take informed consent of guardian
and prior permission from mental health review board)
G. Ban on psychosurgery (In a rare case, if psychiatrist in charge considers psychosurgery,
he will have to take informed consent of patient and prior permission from mental
health review board)
H. Decriminalization of suicide: Any person who attempts to commit suicide shall
be presumed to be under severe stress and should not be tried or punished (Earlier,
Section 309 of IPC, prescribed punishment for those who attempted suicide)
I. Restraints and seclusion: A patient can be physically restrained only-
a. If it is the only way to prevent harm to self or others
b. If it is authorized by psychiatrist in charge
Mental health gap (by WHO) (AIIMS)Q
• The mhGAP approach consists of interventions for prevention and management of
priority MNS (Mental, neurological and substance use disorders) conditions, identified
on the basis of evidence about the effectiveness and feasibility of scaling up these
interventions in low- and middle-income countries.
• Priority conditions were identified based on the criteria that they represented a high
burden (in terms of mortality, morbidity and disability), resulted in large economic
costs or were associated with violations of human rights.
• These priority conditions include depression, psychoses, self-harm/suicide, epilepsy,
dementia, disorders due to substance use and mental and behavioural disorders in
children and adolescents.
• The mhGAP-Intervention Guide (mhGAP-IG) is a resource to facilitate delivery of the
mhGAP evidence-based guidelines in non-specialized health care settings
Psychiatry
Worksheet
• MCQ OF “Psychotherapy, psychology, community psychiatry” FROM DQB

Piaget’s Stages of Cognitive Development
Stage Age Important features
No. Stage Age Normal Development Psychiatric syndromes

Range (gratification) to result from fi ation (and
regression) to this stage
1. Oral 0-1.5y
2. Anal 1.5-3y
3. Phallic 3-5y
4. Latency 5-12y
5. Genital >12y
Psychiatry
Id ego Superego
Defense mechanism Definition (in your ords) ample

Learning Models
Classical Conditioning Operant Conditioning
Types of Operant Conditioning

Positive
Reinforcement
Negative Reinforcement
Punishment
tinction
10 Psychopharmacology
Drugs USED in Psychiatry
For psychotic For depression For Bipolar For Anxiety

disorders Disorders Disorders
Mood
Antipsychotics Antidepressants Anxiolytics
Stablizers
CONCEPTS
Â 10.1 Antipsychotics
Â 10.2 Antidepressants
Â 10.3 Mood stablizers
Â 10.4 Anxiolytics
Â 10.5 Antidementia drugs

Psych har ac l y
Concept 10.1: Antipsychotics (Neuroleptics)
LEARNING OBJECTIVE: To understand the antipsychotic action, adverse effects and
their clinical utility in psychiatry and answer its related MCQ.
Time Needed
1 reading
st
60 mins
2 look
nd
30 mins
Typical v/s atypical antipsychotics:

Typical antipsychotics Atypical antipsychotics
Primary action D2 receptor blockade Any action other than D2 blockade
Relieve Only positive symptoms of Positive symptoms, negative
schizophrenia symptoms and cognitive
impairment of schizophrenia
Use in resistant schizophrenia Not useful Useful
Use in indications other than Not useful Useful
schizophrenia
Mood stabilizing property Absent Present; hence used in bipolar
disorder
Extrapyramidal reactions and More prominent Less prominent
hyperprolactinemia
Metabolic complication Less prominent More prominent
Examples of typical antipsychotics (neuroleptics):

1. Phenothiazines
Aliphatics • Chlorproma ine ri uoproma ine
Piperidines • Thioridazine • Mesoridazine
Piperazines • ri uopera ine Prochlorpera ine
• Fluphenazine
2. Butyrophenones • Haloperidol • Droperidol
• ri uperidol
3. Diphenylbutylpiperidines • Pen uridol Pimo ide
4. Thioxanthenes • Chlorprothixene
• Thiothixene
• Flupenthixol
• Zuclopenthixol
5. Dihydroindoles • Molindone
6. Dibenzoxapines • Loxapine
Psychiatry
Examples of Atypical Antipsychotics:
D2 + 5-HT2a blocker • Clozapine (no D1/D2: rather D4 blocker)
• Olanzapine
• Zotepine
• Asenapine
• Quetiapine
• Ziprasidone
• Risperidone/Lurasidone
• Iloperdone
• Sertindole
• Paliperidone
D2 partial agonist • Aripiprazole
• Brexipiprazole
• Cariprazine
D2 and D3 antagonist • Sulpiride
• Amisulpiride
• Levosulipiride
5-HT2a inverse agonist • Pimavanserin
OTHER ACTIONS:
• Alpha-adrenergic blockade; therefore, hypotensive effect
• Anticholinergic action by blocking the muscarinic receptors
• Blocks both NE re-uptake and serotonin and histamine receptors
Atypical Anti-Psychotics
Clozapine (Atypical)
DOC for treatment resistant schizophrenia
Weak reaction on D2 receptors high a nity for serotonin receptors. Affects
negative and positive symptoms.
• Does not block D1/D2 receptors: rather D4 receptor
• No EPS and prolactin increase
• Anti-suicidal properties (Also Lithium)
Side effects are agranulocytosis (<1 ) and seizures (14 of doses 00 mg).
Less incidence of EP, TD, prolactin, or sexual effects.
• Metabolic syndrome • Seizures (DOSE DEPENDENT)

• Obesity (max) • Agranulocytosis(dose independent)
• Type 2 DM • Myocarditits
• Hypersalivation
• Sedation
Psych har ac l y
Risperidone (Atypical)
Affects positive and negative symptoms, thought disorders. Side effects are dizziness,
fatigue, dry mouth, tachycardia, hypotension. Raises prolactin levels, EP effects. Highest
risk of movement disorders.
Olanzapine (Atypical)
Affects positive and negative symptoms, thought disorders. Highest incidence of
diabetes. Increased weight, increased cholesterol.
Quetiapine (Atypical)
D2 and 5-HT2 antagonist; also affects H1 and alpha-1 receptors. For schizophrenia and
bipolar. Side effects: somnolence, dizziness, dry mouth, weight gain. Lowest risk of
movement side effects.
Aripiprazole (Atypical)
Partial agonist on D2 and 5-HT1 receptors. Antagonist at 5-HT2 receptor. Side effects:
akathisia, headache, tiredness, nausea. Also used for bipolar and adjunt therapy for
depression. Partial dopamine against at low doses.
Ziprasidone (Atypical)
High affinity for DA, 5-HT, alpha-adrenergic, and histamine receptors; some inhibition of
5-HT reuptake. For acute agitation of psychoses, acute mania. Intramuscular injection;
prolongs QT interval.
Route:
• Oral: all
• IV/IM: haloperidol, S/L: asenapine, Intranasal: Loxapine
Long-acting injectable antipsychotics (Depot anti-psychotics):

Indications :
1. Poor gastric absorption
2. Poor compliance with medications (i.e. who refuse to take medications)
The patients typically receive the intramuscular injections of antipsychotics once a
month or once a fortnight.
Long-acting injectable preparations are available for following

antipsychotics:
Typical Atypical
• Haloperidol Paliperdone
• Fluphenazine Aripiprazole
• Flupenthixol Risperidone
• Zuclopenthixol Olanzapine
• Perphenazine
Psychiatry
Newer atypical antipsychotics:
Brexpiprazole: It is an atypical antipsychotic that acts as a partial agonist at D2 and
5HT1A receptors, and an antagonist at 5HT2A receptor.
Cariprazine: It is an atypical antipsychotics that acts as a partial agonist at D2, D3 and
5HT1A receptors and an antagonist at 5HT2A receptor. However, unlike aripiprazole and
brexpiprazole, cariprazine exhibits higher affinity for the D3 versus the D2 receptor.
Pimavanserin: It is the first FDA approved drug for treatment of delusions and
hallucinations in Parkinson’s disease associated psychosis. Pimavanserin has a
combination of inverse agonist and antagonist activity at 5HT2A receptors (and to a
lesser extent 5HT2C receptors). It does not bind to D2 receptors. It can increase QT
interval.
1 Blonanserin 5-HT2A + D2 1
antagonist
2 Zotepine D1 + D2 + 5-HT2A + 5-HT2C + 5-HT6 + 5-HT7 antagonist
3 Zicronapine D1 + D2 + 5-HT2A antagonist
4 Bitopertin Glycine transporter 1 inhibitor
Adverse e ects of antipsychotics

1. Sedation : Maximum with chlorpromazine
2. Anticholinergic effects : Maximum with thioridazine > chlorpromazine
Dryness of mouth, Blurring of vision, Constipation, Urinary retention, Delirium
Especially frequent in the elderly
3. Cardiac side effects : Postural hypotension (autonomic) : Maximum with
chlorpromazine
4. Sexual side effects : Inhibition of ejaculation (alpha) and decreased libido (dopamine)
5. Prolactin elevation : Causes amenorrhoea, galactorrhoea (due to D2 blockage)
infertility
6. Metabolic side effects : More with atypical (pines > dones)
7. Extrapyramidal side effects:
Typical Antipsychotics: Max: Haloperidol and Least: Chlorpromazine Atypical
antipsychotics causing EPS and elevated Prolactin –
• Risperidone (max Prolactin), Lurasidone (max EPS), Paliperidone, Asenapine,
Amisulpiride
• Not associated with: Clozapine, Aripiprazole, Pimavanserin
Antiemetic causing EPS and prolactin: METOCLOPRMIDE
Psych har ac l y
Extrapyramidal Symptoms: Onset and treatment
Acute Muscular dystonia 1st dose to 1st week Inj: Promethazine
• Torticollis Diphenhydramine
• Oculogyric crisis
• Sudden abnormal posture
Parkinson disease 1st week to 4 week Oral anticholinergics
(And rabbit syndrome) • Resting tremors • Benzhexol
• Rigidity • Biperidine
• Bradykinesia • Benztropine
• Procyclidine
Akathisia 1st week to 8 week Antianxiety
Most common • Anxiety like • Diazepam
Aggravated by smoking • Restlessness • Propranolol (DOC)
Tardive dyskinesia Several months to years • Valbenazine (DOC)
Last to develop • Tetrabenazine
Permanent symptom Abnormal facial movements
Neurolept malignant syndrome Emergency • Dantrolene (DOC)

• Hyperthermia • romocriptine specific drug
• Severe rigidity
Extrapyramidal Reactions to Antipsychotic Medications

Side ects Peak
Dystonic reactions (jerky movements, trouble speaking) 1 week (younger are more at risk)
Akinesia 2 weeks
Rigidity 3 weeks
Tremors 6 weeks
Akathisia 10 weeks
Pisa and Rabbit syndromes 1S+ weeks
Dystonia (uncontrolled Pseudo-parkinsonism Akathisia Tardive dyskinesia
muscular spasm) (tremor, etc.) (restlessness)1 (abnormal movements)
Signs and Muscle spasm in any Symptoms include: A subjectively unpleasant A wide vanety of movements
symptoms2 part of the body, e.g. • tremor and/or rigidity state of inner restlessness can occur such as:
• eyes rolling upwards • bradykinesia (decreased where there is a strong desire • lip smacking or chewing
(oculogyric crisis) facial expression, at or compulsion to move. e.g. • tongue protrusion y
• head and neck twisted monotone voice, slow • foot stamping when seated catching)
Psychiatry
to the side (torticollis) body movements, • constantly crossing/ • choreiform hand

• the patient may be inability to initiate uncrossing legs movements (pill rolling or
unable to swallow or movement) • rocking from foot to foot piano playing)
speak clearly • bradyphrenia slowed • constantly pacing up and • pelvic thrusting Severe
• in extreme cases, the thinking) down orofacial movements can
back may arch or the • salivation Pseudo- Akathisia can be mistaken lead to difficulty speaking,
jaw dislocate parkinsonism can for psychotic agitation and eating or breathing.
Acute dystonia can be be mistaken for has been linked with suicidal Movements are worse
both painful and very depression or the ideation3 and aggression when under stress
frightening negative symptoms of towards others4
schizophrenia
Time taken to Acute dystonia can occur Days to weeks after Acute akathisia occurs within Months to years:
develop within hours of starting antipsychotic drugs are hours to weeks of starting Approximately 50% of cases
antipsychotics (minutes if started or the dose is antipsychotics or increasing are reversible
the IM or IV route is used) increased the dose. Tardive akatthisia
Tardive dystonia occurs takes longer to develop and
after months to years of can persist after antipsychotics
antipsychotictreatment. have been withdrawn
Treatment Anticholinergic drugs Several options are avilable Several options are avilable Several options are avilable
given orally, IM or IV depending on the clinical depending on the clinical depending on the clinical
depending on the severity circumstances: circumstances: circumstances:
of symptoms: • reduce the antipsychotic • reduce the antipsychotic • stop anticholinergic if
• remember the patient dose dose prescribed
may be unable to • change to an • change to an antipsychotic • reduce dose of
swallow antipsychotic with with lower propensity for antipsychotic
• response to IV lower propensity for akathisia (see section on • change to an antipsychotic
administration will be pseudo-parkinsonism 'Akathisia and relative with lower propensity for
seen within 5 minutes (see section on adverse effects of tardive dyskinesia, note
• tardive dystonia may 'Relative adverse antipsychotics') data are con icting
respond to ECT effects of antipsychotic • a reduction in symp- • clozapine is the antipsy-
• where symptoms in this chapter) toms may be seen with: chotic most likely to be
do not respond to (as antipsychotic propranolol 30–80mg/day associated with resolution
simpler measures monotherapy) (evidence poor), clonaz- of symptoms, Quetiapine
including switching to • prescribe an epam (low dose) 5HT2 may also be useful in this
an antipsychotic with anticholinergic. Use antagonists such as: cy- regard
a low peopensity for should be reciewed at proheptadine mirtazapine, • tetrabenazine and Ginkgo
EPS, botulinuim toxin least ever 3 months. Do trazodone, mianserin, and biloba have some efficacy
may be effective not prescribe at night cyproheptadine may help, as add on treatments. For
rTMS may be helpful (symptoms usually as may diphenhydramine other treatments. For other
absent during sleep) All are unlicenced for this treatment options see the
indication Anticholinergics review by the American
are generally unhelpful Academy of Neurology
and the section on 'Tardive
dyskinesia' in this chapter
Psych
Prevalence Approximately 10%, but Approximately 20%. but Approximately 25%. less with 5% of patients per year of
(with older more common. more common in: SGAs; in decreasing order: antipsychotic exposure.13
drugs) • in young males • elderly females aripiprazole, lurasidone. More common in:
• in the neurolepticnaive • those with pre-existing risperidone, olanzapine, • elderly women
• with high potency neurological damage quetiapine and clozapine12 • those with affective illness
har ac l
drugs(e.g. haloperidol) (head injury. stroke, • those who have had acute
etc.)
y
Dystonic reactions are EPS early m treatment

rare in the elderly Taidrve dyskinesia
may be associated with
neurocognitive deficits
Psychiatry
• Tardive dyskinesia (TD) (rarely seen earlier than 3 6 months 1 month if age >60 ),
caused by a supersensitivity of postsynaptic dopamine receptors
Signs are tongue protrusion, tremors and spasms of the neck, body, and limbs;
stress and movements in other body parts will aggravate condition
May persist even after medication terminated (5 10 remit), incapacitating in
5 of cases
Predisposing factors include older age, long treatment, smoking, diabetes mellitus.
Symptoms do not occur during sleep
Suppressed by voluntary movements for short time (versus cerebellar disease
tremor, which worsens with intentional movement)
One Liners
• Antipsychotic used in Gilles de la Tourette syndrome Haloperidol
• Neurolept anesthesia Droperidol + Fentanyl
• Autonomic side effects are maximum with Chlorpromazine (due to maximum
anticholinergic action)
• Autonomic side effects are minimum with Haloperidol (due to minimum anticholinergic
action)
• Most potent D2 blocking antipsychotics are- butryphenones (haloperidol)
• Mydriasis is maximum with Thioridazine
• Impaired ejaculation is seen with Thioridazine
• Thioridazine can cause irreversible retinal pigmentation. Thioridazine can also cause cardiac
arrhythmias (prolongation of QT interval). It is also the drug with least extrapyramidal
side effects amongst typical antipsychotics
• Sedation is maximum with Chlorpromazine
• Seizures is maximum with Chlorpromazine > Clozapine
• Cholestatic jaundice side effect of chlorpromazine
• Blue-gray metallic discolouration of skin is seen with Chlorpromazine
• Atypical antipsychotic causing seizures Clozapine
• Atypical antipsychotic causing sedation Clozapine
• Agranulocytosis is a side effect of Clozapine
• Paradoxical hypersalivation / sialorrhea is seen with Clozapine (though it has
anticholinergic action)
• Antipsychotics causing Metabolic syndrome (weight gain, DM)- Clozapine (max),
Quetiapine, Olanzapine
• Weight gain and metabolic side effects are least with iprasidone and Aripiprazole,
Asenapine
• Molindone causes weight loss
• Overall clozapine is the antipsychotic with least extrapyramidal side effect.
• Chlorpromazine can cause corneal and lenticular deposits
• Penfluridol is the longest acting antipsychotic.
• Aripiprazole is a partial agonist at D2 receptors.
• QTc prolongation: iprasidone is known to cause cardiac arrhythmias (prolongation of QT
interval) Also with quetiapine, aripiprazole.
Psych har ac l y
Concept 10.2: Antidepressants
LEARNING OBJECTIVE: To understand the antidepressant action, adverse effects and
Time Needed
1 reading
st
60 mins
2 look
nd
30 mins
Indications
a. Depression
b. Anxiety
c. Chronic pain, with and without depression
(B): ANTIDEPRESSANTS
Classification of antidepressants:
1 Tricyclic antidepressants • Imipramine (useful in nocturnal enuresis, DOC-
desmopressin)
• Trimipramine
• Clomipramine –approved for OCD
• Desipramine
• Amitriptyline- useful in prophylaxis of chronic
migraine, peripheral neuropathy
• Nortriptyline
• Protriptyline
• Doxepin- has high antihistamine action useful to
control itching in atopic dermatitis, lichen simplex
• Dothiepin
2 Tetracyclic antidepressants • Mianserin
• Maprotiline
• Amoxapine
3 Bicyclic antidepressants • Viloxazine
4 Selective serotonin reuptake inhibitors • Fluoxetine- longest acting
(SSRIs) • Fluvoxamine
• Paroxetine
• Sertraline
• Citalopram
• Escitalopram- highly selective SSRI
• Dapoxetine
Psychiatry
5 Serotonin norepinephrine reuptake • enlafaxine side effect- sustained hypertension

inhibitors (SNRI) • Milnacipran
• Duloxetine( useful in stress incontinence,
fibromyalgia, diabetic neuropathy pain
• Levo-milnacipran, vilazodone
• Vortioxetine
6 Norepinephrine serotonin reuptake • Tianeptine
enhancer (NSRE)
7 Norepinephrine dopamine reuptake • Bupropion (useful in smoking control, causing
inhibitor(NDRI) weight loss- useful in obesity, important adverse
effect- sei ure
8 oradrenergic and specific serotonergic • Mirtazapine
antidepressant (NaSSA) • Mianserin
Serotonin antagonists and reuptake • Trazodone
inhibitor (SARI) • Nafazodone
Serotonin antagonists and reuptake • Tianeptine
enhancer • Amineptine
10 Norepinephrine antagonists and reuptake • Reboxetine
inhibitors (NARI)
11 Monoamine oxidase (MAO- A ) inhibitors • Moclobemide
• Clorgiline
Herbal product (St johns wort) • Inhibits the reuptake of NE. 5HT
Active compound – Hyperphorin
One Liners
• Longest acting SSRI Fluoxetine (due to formation of an active metabolite: NorFluoxetine)
• SSRI having least chance of producing discontinuation symptom on withdrawal- fluoxetine
(due to longer duration of action)
• SSRI least likely to cause withdrawal symptoms Fluoxetine (due to formation of an
active metabolite)
• Drug discontinuation syndrome max seen with paroxetine (SSRI) and Venlafaxine (SNRI)
• Antidepressant with antipsychotic properties and Cause EPS Amoxapine (d2 blocker)
• Antidepressant used for aggression in elderly Trazodone
• DOC for endogenous depression SSRI
• DOC for neurotic disorders SSRI
• SSRI are drug of choice for- OCD, PTSD, anxiety with panic attack
• DOC for acute exacerbations of neurotic diseases Benzodiazepines
• Avoid class Ia anti arrhythmic drug for treating TCA induced cardiotoxicity
• FDA approved TCA for OCD is clomipramine but DOC is SSRI
Psych har ac l y
Drugs that can precipitate serotonin syndrome:
Drugs that increase serotonin synthesis • Tryptophan
Drugs that increase serotonin release • Amphetamines
• Cocaine
• Ecstasy (Methylenedioxy methamphetamic acid)
• Sibutramine
Drugs that inhibit serotonin reuptake • Dextromethorphan
• Pentazocine
• Pethidine
• SSRIs
• SNRIs
• TCAs
• SARIs
• Tramadol
Drugs that inhibit serotonin catabolism • MAO inhibitors
Drugs that act as serotonin agonists • Buspirone
• Triptans
• Ergot alkaloids
• Lithium
• LSD
• Piperazine
Drugs that can precipitate cheese reactions with MAOi:

• Amphetamines
• Ephedrine
• Pseudoephedrine
• Phenylephrine
• Phenylpropanolamine
• Tyramine
• Linezolid
• INH
Tri Cyclic antidepressants

Mechanism of Action: blocking of re-uptake of serotonin and norepinephrine, blocking of
alpha- I adrenergic receptors, and muscarinic receptors.
Adverse e ects
1. Anticholinergic effects
2. CNS effects: Drowsiness
3. Cardiovascular: from antagonism of alpha- 1 adrenoreceptors and inhibition of 5-HT
reuptake
Psychiatry
Most common in elderly

Tachycardia and Orthostatic hypotension
Lethal in overdose due to cardiac complications
4. Sexual
Men: impotence, testicular swelling
Women: anorgasmia
5. Metabolic: changes in blood sugar levels
Selective serotonin re-uptake inhibitors (SSRI)

(Fluoxetine, Sertraline, Paroxetine, Fluvoxamine, Citalopram, Escitalopram)
a. Most widely used antidepressants
b. No effect on NE or dopamine, very selective blockage of re-uptake of serotonin
c. Least adverse effects amongst all antidepressants
d. Adverse effects:
1. Anorgasmia and delayed orgasm in 15 to 20 of patients
2. Serotonin syndrome
Associated with: high doses, MAOI and SSRI combo
Symptoms: general restlessness, sweating, insomnia, nausea, diarrhea, cramps,
delirium
Treatment: remove causative agent, stop SSRis, give cyproheptadine
Monoamine oxidase inhibitors (MAOls)

a. Mechanism of action: Inhibits MAO, an enzyme that metabolizes serotonin,
epinephrine, and NE
b. Adverse effects
(MAOI + Tyramine : Hypertensive Crisis)

• Problem foods: cheese, dried fish, sauerkraut, sausage, chocolate, avocados
• Safe foods: cottage cheese, some wines
• Signs: occipital headache, stiff neck, nausea and vomiting, chest pain, dilated pupils,
nosebleed, elevated blood pressure
• Treatment: stop medication, give phentolamine (alphablockage) or chlorpromazine
(anti psychotic with hypotensive effects)
Other antidepressants
1. Trazodone (SARI)
a. 5-HT receptor antagonist, alpha- I blocker
b. Almost no anticholinergic adverse effects
c. Sedating, but effective at improving sleep quality
d. May lead to priapism; therefore, sometimes used to treat erectile dysfunction
2. Mirtazapine (NaSSa)
Psych har ac l y
a. Stimulates NE and 5- HT release
b. Blocks 5-HT2 and 5-HT3 receptors
c. Side effects: somnolence (60 ), increased appetite, weight gain
3. Bupropion (NDRI)
a. Weak inhibitor of dopamine, modest effect on NE, no effect on 5-HT reuptake
b. No anticholinergic effect
c. Little cardiac depressant effect
d. Increased risk of seizures
e. Less sexual effects or weight gain
f. Side effects: appetite suppressant, agitation, insomnia
g. Approved for smoking cessation
4. Venlafaxine (SNRI), Duloxetine and Desvenlafaxine
a. Inhibits reuptake of NE and 5-HT, mild dopamine effect (SNRI)
b. Side effects: sweating, nausea, constipation, anorexia, vomiting, somnolence,
tremor, impotence
c. Approved for depression and neuropathic pain
5. Tianeptine (SSRE)
Selective serotonin reuptake enhancer
Newer agents:
Vilazodone (SPARI) : serononin partial agonist and reuptake inhibitor.
Agomelatine : Melatonin analogue
Psychiatry
Concept 10.3: Mood Stabilizers
LEARNING OBJECTIVE: To understand the mood stablizers action, adverse effects and
Time Needed
1 reading
st
40 mins
2 look
nd
20 mins
Drugs for Mood Disorders/ Bipolar Disorder

LITHIUM TOPIRAMATE
VALPROATE ANTIPSYCHOTICS
OXCARBAZEPINE, CARBAMAZEPINE GABAPETIN
LAMOTRGINE
• DOC for BPD prophylaxis is Lithium
• DOC for rapid cycler BPD: Valproate
• DOC acute mania: valproate (ref : Kaplan)
• DOC in pregnancy: Antipsychotics
• Lamotrigine is only given in Depressive phase of BPD
(A): LITHIUM
One-liners:
• Lithium is used in Felty syndrome as it – Increases neutrophil count
• Lithium is also given in Hypnic Headache
• Lithium is ANTI-SUICIDAL DRUG
P/K
• Oral: lithium carbonate/citrate (complete oral absorption)
• T1/2: 24 hours (1 day)
• Lithium should be stopped at least 2 days before surgery
• Lithium cannot be given in ICU settings
• Excretion: urine (not metabolized in liver), rest in sweat, saliva, Milk
• C/I: during lactation, children below 12 years
Narrow therapeutic index: monitoring (Therapeutic plasma levels of

lithium):
Maintenance of bipolar disorder 0.5 – 0.8 mEq/L
Acute mania 0.8 – 1.2 mEq/L
Toxicity > 1.5 mEq/L
emodialysis is effective at > 4 mEq/L
Psych har ac l y
• Amiloride is the DOC for treating lithium indued DI/ lithium toxicity
• Lithium contraindicated in pregnancy and in sick sinus syndrome
Incidences of various side e ects of lithium:

1 Overt hypothyroidism 7 – 10%
2 Reversible wave attening ~ 20%
3 Polyuria / Diabetes insipidus ~ 60%
4 Fine tremors 15 – 70%
One-liners:
• Normal dose: Fine tremors by lithium while Toxicity: Coarse tremors
• requency of fine tremors due to lithium -
• eratogenic effect of lithium bstein s anomaly, etal goiter
Drug interactions of lithium:

• Thiazides Cause lithium retention
• Loop diuretics
• Spironolactone
• Tetracyclines
• NSAIDs
• ACE inhibitors
• Succinylcholine Prolonged paralysis in lithium-treated patients
• Pancuronium
Neuroleptics Marked tremors and rigidity with lithium
Lithium Reduces pressor response to noradrenaline
Lithium Enhances insulin / sulfonylurea induced hypoglycaemia
Lithium
• For long-term control and prophylaxis of bipolar disorder
• Hypothesized mechanism: related to ion channels, blocks inositol- I -phosphate
(second messenger)
• Therapeutic blood levels: 0.8-1.2 mEq/L (acute mania) and 0.6-0.8 meq/l (bipolar
maintenance)
above mEq/L toxicity starts; Severe toxicity at 2.0 meq/L ; above 4 Meq/l:
hemodialysis is indicated
• PRE LITHIUM INVESTIGATIONS:
Serum creatinine
TSH
Pregnancy test
ECG
• Side effects: (ref : chart in Kaplan)
Psychiatry
Neurological
enign, nontoxic dysphoria, lack of spontaneity, slowed reaction time, memory difficulties
Tremor: postural, occasional extrapyramidal
Toxic: coarse tremor, dysarthria, ataxia, neuromuscular irritability, seizures, coma, death
Miscellaneous: peripheral neuropathy, benign intracranial hypertension, myasthenia gravis-like syndrome,
altered creativity, lowered seizure threshold Endocrine
Thyroid: goiter, hypothyroidism, exophthalmos,
hyperthyroidism (rare)
Parathyroid: hyperparathyroidism, adenoma Cardiovascular
Benign T-wave changes, sinus node dysfunction
Renal
Concentrating detect, morphologic changes, polyuria (nephrogenic diabetes insipidus), reduced GFR,
nephrotic syndrome, renal tubular acidosis Dermalological
Acne, hair loss, psoriasis, rash Gastrointestinal
Appetite loss, nausea, vomiting, diarrhea Miscellaneous
Altered carbohydrate metabolism, weight gain, uid retention
GFR, glomerular filtration rate.
Tremor, thirst, anorexia, gastrointestinal distress, Polyuria and polydipsia; Benign
leukocytosis, Hypothyroidism commonly occur at therapeutic levels
• Toxicity:
Signs and Symptoms of Lithium Toxicity

1. Mild to moderate intoxication (lithium level, 1.5-2,0 mEq/L)
Gl Vomiting, Abdominal pain, Dryness of mouth
Neurological Ataxia, Dizziness, Slurred speech, Nystagmus, Lethargy or excitement, Muscle
weakness
2. Moderate to severe intoxication (lithium level: 2-0–2,5 mEq/L)
Gl Anorexia, Persistent nausea and vomiting
Neurological Blurred vision, Muscle tasciculattons, Clonic limb movements, Hyperactive deep
tendon re exes, Choreoathetotd movements, Convulsions, elirium, Syncope
Electroencephalographic changes, Stupor, Coma, Circulatory failure ilowered BP,
cardiac arrhythmias, and conduction abnormalities)
3. Severe lithium intoxication < lithium level >2.5 mEq/L)
Generalized convulsions
Oliguria and renal failure
Death
Nephrotoxicity (Diabetes insipidus like), Neurotoxicity (Seizures and coma); IX.

Nephrotoxic
Psych har ac l y
Management of Lithium Toxicity
1. Contact personal physician or go to a hospital emergency department.
2. Litnium should be discontinued
3. Vital signs and a neurological examination with complete formal mental status examination.
4. Lithium level, serum electrolytes, renal function tests, and ECG
5. Emesis, gastric lavage, and absorption with activated charcoal.
6. For any patient with a serum lithium level greater than 4.0 mEq/L, hemodialysis
ECG, electrocardiography.
• Teratogenicity : produces cardiac malformations (Ebstein anomaly: tricuspid valve)
• The acute use of lithium has been limited in recent years by its unpredictable efficacy,
problematic side effects, and the need for frequent laboratory tests.
• The introduction of newer drugs with more favorable side effects, lower toxicity, and
less need for frequent laboratory testing has resulted in a decline in lithium use.
Valproic Acid
• It is the drug of first choice for acute mania, rapid cycling bipolar disorder
• Mechanism of action: inhibits GABA catabolism, augmentation of GABA in CNS
• Typical dose levels of valproic acid are 750 to 2,500 mg per day, achieving blood
levels between 50 and 120 g/mL.
• Rapid oral loading with 15 to 20 mg/kg of divalproex sodium from day 1 of treatment
has been well tolerated and associated with a rapid onset of response.
• Pre Valproate investigations : SGOT, SGPT (If hepatic transaminases are more than 3
times raised, avoid valproate)
• Side effects:
Adverse E ects of Valproate

Common Rare
GE irritation Fatal hepatotoxicity (primarily in pediatric patients)
Nausea Reversible thrombocytopenia
Sodation Platelet dysfunction
Tremor Coagulation disturbances
Weight gain Edema
Hair loss Hemorrhagic pancreatitis
Uncommon Agranulocytosis
Vomiting Encephalopathy and coma
Diarrhea Respiratory muscle weakness and respiratory
Ataxia
Dysarthria
Persistent elevation of hepatic transminases
GL, gastrointestinal
Sedation, weight gain, alopecia, gastrointestinal distress
Psychiatry
ore Serrious Side ect Management Considerations

Hepatotoxicity Rare, idiosyncratic event
Eslimated risk, 1:1 1.8,1X)0 (adults)
reatest risk profile polypharmacy, younger than yr of
age, mental retardation): 1:800
Pancreatitis Rare, similar pattern to hepatotoxicity
Incidence in clinical trial data k 2 in 2, 416 (0.0008 percenti)
Postmariketing surveillance shows no increased incidence
Relapse with rechallenge
Asvmpiomatic arrrylase not predictive
Hyperammonemia Rare; more common in combination with carbarnazepine
(Tegretol)
Associated with coarse tremor and may respond to t-carnitine
administration
Associated with urea cycle disorders Discontinue valprilate and prortein intake Assess underlying
urea cycle disorder
Divalproex is contraindicated in patients with urea cycle
disorders
Teratogenicity Neural tube defect 1-4 percent with valprote
Preconceptual education and folatevitamin B complex
sopplementation for all young women of childbearing
potential
Somnolence in elderly persons Slower titration than conventional doses

Regular monitoring of uid and nutritional intake
Thrombocytopenia Decrease dose it clinically symptomatic (i.e., bruising
bleeding gums).
hrombocytopenia more likely with valproate levels
g ml women and g ml men
• Toxicity: confusion, coma, cardiac arrest
• Teratogenicity: neural tube defect
Carbamazepine
• Uses: For acute mania, rapid cycling bipolar disorder, impulse control
• Mechanism of action: Blocks sodium channels in neurons with action potential
• Side effects: nausea, rash, mild leukopenia
Psych har ac l y
Dosage elated Adverse ects Idiosyncratic Adverse ects

Double or blurred vision Agranulocytosis
Vertigo Stevens-Johnson syndrome
Gastrointestinal disturbances Aplastic anemia
Task performance impairment Hepatic failure
ematologic effects rash
Pancreatitis
• Occasional agranulocytosis Aplastic anemia
• Toxicity: atrioventricular block, respiratory depression, coma
• Typical doses of carbamazepine to treat acute mania range between 600 and 1,800
mg per day associated with blood levels of between 4 and 12 g/mL.
• The keto congener of carbamazepine, oxcarbazepine, may possess similar antimanic
properties. Higher doses than those of carbamazepine are required, because 1,500
mg of oxcarbazepine approximates 1,000 mg of carbamazepine.
Psychiatry
Concept 10.4: Anxiolytics (Antianxiety)
LEARNING OBJECTIVE: To understand the antianxiety drugs action, adverse effects
and their clinical utility in psychiatry and answer its related MCQ.
Time Needed
1 reading
st
20 mins
2 look
nd
10 mins
Antianxiety Drugs Include

1 SSRIs
2 SNRIs
3 Benzodiazepines
4 Azapirones: 5HT1A AGONIST- non sedative, non habit forming
• Buspirone
• Gepirone
• Ipsapirone
5 H1 antihistaminics
• Hydroxyzine (cetirizine is the active metabolite)
6 -blockers
• Propranolol (DOC for performance anxiety)
Benzodiazepines
• Used for anxiety, acute and chronic alcohol withdrawal, convulsions, insomnia,
“restless legs’, akathisia,
• Mechanism of action: depresses CNS at limbic system, RAS, and cortex; Binds to
GABA-chloride receptors; facilitates action of GABA
• Adverse effects: CNS depression (sedative effect); Paradoxical agitation, Confusion
and disorientation, especially in elderly
• Overdose can cause apnoea and respiratory depression
• Withdrawal: insomnia, agitation, anxiety rebound, gastrointestinal distress; abrupt
withdrawal can bring on seizures
• Diminishes effectiveness of ECT
• Lowers tolerance to alcohol
• Crosses placenta and accumulates in fetus, withdrawal symptoms in newborn
• INCLUDES:
• Alprazolam
• Diazepam
• Flurazepam
• Triazolam
• Chlordiazepoxide
Psych har ac l y
• Clonazepam
• Temazepam
• Lorazepam
• Oxazepam
Buspirone
• Mechanism of action: 5-HT1a partial agonist
• Indications : Panic, anxiety
• Some sedation
• Low abuse potential
• No withdrawal effects
• Not potentiated by alcohol
Psychiatry
Concept 10.5: Anti Dementia Drugs
LEARNING OBJECTIVE: To understand the antidementia drugs action, adverse effects
and their clinical utility in psychiatry and answer its related MCQ.
Time Needed
1 reading
st
15 mins
2 look
nd
10 mins
• Donepezil, rivastigmine, galantamine and tacrine are cholinesterase inhibiters
• Memantine a NMDA antagonist is also approved
• Low dose aspirin and Statins have shown neuroprotective effects.
• Piracetam, Pyritinol, Piribidel, Citicholine, Dihydroergotoxine, Gingko biloba are
• Nootrophic drugs that improves memory.
Solanezumab, Bapineuzumab and Crenezumab are anti-Beta1 amyloid antibodies under
trials.
Estrogen replacement therapy, Tarenflurbil, Semagacestat have failed to provide any
beneficial effects.
New drugs for alzheimers in pipeline

Drug Mechanism of action
1 Etazolate Positive allosteric modulator of the GABAA receptor at the barbiturate binding
site; Adenosine receptor antagonist; Selective PDE4 inhibitor.
2 Semagacestat -secretase inhibitor rials have been abandoned due to lack of efficacy .
3 Bapineuzumab Antibody against A inds to A and helps in its clearance rials have been
abandoned again due to lack of efficacy .
4 Gantenerumab Also an antibody against A inds to A and helps in its clearance.
5 Aducanumab Antibody against aggregated forms of -amyloid helps in amyloid clearance
Psych har ac l y
Worksheet
• MCQ OF “Psychopharmacology” FROM DQB

Psychiatry
Typical v/s atypical antipsychotics:
Typical antipsychotics Atypical antipsychotics
Primary action
Relieve
Use in resistant schizophrenia
Use in indications other than

schizophrenia
Mood stabilizing property
Extrapyramidal reactions and

hyperprolactinemia
Metabolic complication
Psych har ac l y
Examples of typical antipsychotics (neuroleptics):
1. Phenothiazines
Aliphatics
Piperidines
Piperazines
2. Butyrophenones
3. Diphenylbutylpiperidines
4. Thioxanthenes
5. Dihydroindoles
6. Dibenzoxapines
Psychiatry
Extrapyramidal Symptoms: Onset and treatment
Acute Muscular dystonia
Parkinson disease
(And rabbit syndrome)
Akathisia
Most common
Aggravated by smoking
Tardive dyskinesia
Last to develop
Permanent symptom
Neurolept malignant syndrome
Classification of antidepressants:
1 Tricyclic antidepressants
2 Tetracyclic antidepressants
Psych har ac l y
3 Bicyclic antidepressants
4 Selective serotonin reuptake

inhibitors (SSRIs)
5 Serotonin norepinephrine
reuptake inhibitors (SNRI)
6 Norepinephrine serotonin
reuptake enhancer (NSRE)
7 Norepinephrine dopamine
reuptake inhibitor(NDRI)
8 oradrenergic and specific

serotonergic antidepressant
(NaSSA)
9 Serotonin antagonists and

reuptake inhibitor (SARI)
Serotonin antagonists and

reuptake enhancer
10 Norepinephrine antagonists and

reuptake inhibitors (NARI)
11 Monoamine oxidase (MAO- A )

inhibitors

Psychi

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Psychi

Uploaded by

Copyright:

Available Formats

Concept Based Learning

Video Companion on Each Chapter

Comprehensive review series

First Published 1999, Delhi Academy of Medical Sciences

© 2021 DAMS Publication

Â Concept 1.2 Epidemiology of psychiatric disorders

Â Concept 1.3 Examination in psychiatry and basic

There are three major purposes of classification of psychiatric

MENTAL HEALTH CENSUS

EXAMINATION IN PSYCHIATRY AND BASIC TERMINOLOGIES TO

Fig. 1.1: Levels or stages of diminished consciousness.

Fig. 1.2: Three dimensions of unconsciousness

The Mini-Mental State Exam

Attention and Calculation

• EXTRA POINTS FROM DQB

Â 2.4 Clinical features

Â 2.5 Diagnostic criteria

Â 2.7 Prognostic factors

Â 2.9 Delusional disorders

Â 2.10 Schizoaffective disorder

 Prefrontal cortex: Anatomical abnormalities have been found.

Fig. 2.1: Neurodevelopmental Theory of Schizophrenia

Prevalence of Schi ophrenia in Specific Populations

Thought and Speech Disorders

Disorders of Motor Behaviour

Post-Schizophrenic Depression (25% cases)

Suicide in Schizophrenia (10% as per DSM IV) (5-6% as per DSM 5)

Van Gogh Syndrome

ICD-11 Criteria of Diagnosis:

(1) At least one of the following:

DSM-IV Key Features

Type 1 schizophrenia Type 2 schizophrenia

Features Weighting Toward Good to Poor Prognosis in Schizophrenia

2nd look 10 mins

Pharmacological treatment: Antipsychotics (1st generation and 2nd generation)

2nd look 10 mins

Risk factors for development of delusional disorders: (NEET 19)

Induced Delusional Disorder

Delusional Misidentification Syndromes

Di erential Diagnosis of Delusional Disorders

2nd look 5 mins

Schizoaffective disorder: Schizoaffective disorder has features of both schizophrenia

II. Clinical eatures of Schi oa ective Disorder

Treatment of Schi oa ective Disorder

• EXTRA POINTS FROM DQB

Type 1 schizophrenia Type 2 schizophrenia

Â 3.2 Clinical features of depression

Â 3.3 Diagnostic criteria of depression

Â 3.4 DMDD and PMDD

Â 3.6 Post-partum psychiatric disorders

Â 3.7 Treatment of depression

Â 3.8 Special types of depression

Â 3.10 Bipolar disorders

Etiology of mood disorders: (#extraedge #nimhans)

Neurotransmitters in mood disorders: (Ref : Kaplan)

Cognitive Theory of Depression (Ref : Kaplan)

Scales Used in Depression:

Specifiers (Symptom eatures) (Ref : Kaplan)

With Melancholic FeaturesQ

With Atypical Features (AIIMS May 2018)

Disruptive Mood Dysregulation Disorder:

Premenstrual Dysphoric Disorder:

Neurotic depression is usually characterised by the following clinical

The other common features include:

Prefrontal cortex: Anatomical abnormalities have been found.