RGHUS-Vol-7

MD Psychiatry Solved past questions -Vol-7

Paper II (MD Psychiatry Past Questions - Nov 2021 to July 2023)

Nov 2021
2021-01: Research Domain Criteria (RDOC).
2021-02: Craving—Neurobiology and Management.
2021-03: Erectile Dysfunction.
2021-04: Major Neuro-Cognitive Disorders.
2021-05: Bipolar II Disorder.
2021-06: Treatment-Resistant Schizophrenia.
2021-07: Functional Magnetic Resonance Imaging.
2021-08: Electrophysiology of Sleep.
2021-09: Eric Kandel and his contributions.
2021-10: Fibromyalgia.

May 2022
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2022-01: Describe the theories of formation of delusions.
2022-02: Evaluation and management of Somatization Disorder.
2022-03: Obsessive-Compulsive Personality Disorder.
2022-04: Evaluation of male sexual dysfunction.
2022-05: Clinical presentation and management of Dysthymia.
2022-06: Early-onset Alcohol Dependence Syndrome.
2022-07: Mental health and pregnancy.
2022-08: Dissociative Disorder—clinical presentation and management.
2022-09: Treatment-resistant Schizophrenia.
2022-10: Non-pharmacological management of Substance Dependence.

Nov 2022
2022-01: Classify Anxiety Disorders. Describe the clinical features and management of
Panic Disorder.
2022-02: Assessment and management of acute suicidal risk in a general hospital
emergency department.
2022-03: Abuse of over-the-counter drugs.
2022-04: Schizotypal Disorder.
2022-05: Non-pharmacological management of Anorexia Nervosa.
2022-06: Cultural aspects in Dissociative Possession Attacks.
2022-07: Elder abuse.
2022-07: Elder abuse.
2022-08: Evaluation and management of Bipolar Depression.
2022-09: Delirium—assessment and management.
2022-10: Erectile Dysfunction.

July 2023
2023-01: Evaluation and management of late-onset psychosis.
2023-02: Classify Bipolar Disorders. Management and long-term course and outcome of
Bipolar Type 1 Disorder.
2023-03: Impulse Control Disorders.
2023-04: Benzodiazepine abuse in general medical practice.
2023-05: Factitious Disorder.
2023-06: Parasomnias.
2023-07: Life events and psychiatric disorders.
2023-08: Sleep hygiene techniques in clinical practice.
2023-09: Neurobiology of stress.
2023-10: SPECT (Single Photon Emission Computed Tomography).

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2021-01: Research Domain Criteria (RDOC).

Research Domain Criteria (RDoC)

• Due to criticisms of DSM-5’s categorical approach, the National Institute of

Mental Health (NIMH) introduced the Research Domain Criteria (RDoC).
• RDoC focuses on neurobiology, genetics, and dimensional traits rather
than symptom-based categories.

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Major Depressive Disorder (MDD) in the RDoC Framework

RDoC Domain MDD-Related Dysfunction Features
Negative Valence Acute Threat (Fear) Some patients experience excessive fear responses.
Potential Threat (Anxiety) Chronic worry, rumination, anticipatory anxiety.
Frustrative Nonreward Anhedonia (loss of pleasure), reduced motivation.
Positive Valence Reward Responsiveness Blunted response to pleasurable stimuli.
Reward Learning Impaired learning from positive reinforcement.
Reward Valuation Loss of goal-directed behavior due to dopaminergic
 Reward Valuation Loss of goal-directed behavior due to dopaminergic
dysfunction.
Arousal/Regulatory Biological Rhythms Sleep disturbances (insomnia/hypersomnia).
Arousal Dysregulation Low energy levels, psychomotor retardation.
Cognitive Systems Working Memory & Cognitive Difficulty concentrating, decision-making impairment.
Control
Attention Deficits Impaired sustained attention.
Social Processes Affiliation and Attachment Deficits Social withdrawal, impaired social cognition.
Dysfunctional Social Interpersonal difficulties, misinterpretation of social cues.
Communication
Sensorimotor Psychomotor Retardation Reduced movement, slowed speech, physical slowness.
Systems
Habit Formation Deficits Rigid, maladaptive behavior patterns.

• Example: Instead of diagnosing MDD, bipolar disorder, or GAD separately,

RDoC examines neural circuits regulating mood and cognition.

Introduction
• Definition: RDoC is an initiative by the NIMH to redefine mental illness
understanding by focusing on biological mechanisms, genetics, and neural
circuitry rather than traditional diagnostic systems (DSM/ICD).
• Emphasizes integration of various domains such as cognition, arousal, and
positive/negative valence systems.

Merits of RDoC
1. Focus on Underlying Mechanisms

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• Biological Integration: Incorporates neurobiological data for a deeper
understanding of mental disorders.
• Dimensional Approach: Allows study along a continuum of behaviors,
facilitating a nuanced understanding of mental health.
• Cross-Diagnostic Relevance: Highlights commonalities across disorders,
promoting the exploration of transdiagnostic factors.

2. Facilitates Precision Psychiatry

• Individualized Treatment: Aims for tailored treatments based on biological and
behavioral profiles.
• Identification of Biomarkers: Encourages the discovery of biomarkers for
early diagnosis and treatment tracking.

3. Encourages Innovative Research

• Expanding Understanding: Promotes investigation into neural circuits and
cognitive processes contributing to mental health.
• Translational Research: Bridges basic neuroscience findings with clinical
applications.

4. Addresses Limitations of Traditional Systems

• Overcoming Heterogeneity: Aims to tackle diagnostic heterogeneity by
focusing on dimensions of functioning.
• Reducing Comorbidity Confusion: Dissolves artificial boundaries between
disorders for a more integrative understanding.

Demerits of RDoC

1. Lack of Clinical Utility

• Not Yet Clinically Applicable: RDoC is primarily a research framework and
is not intended to replace clinical diagnostic systems like DSM or ICD at this
stage. The complexity of integrating biological, psychological, and social data
makes it difficult to use for direct clinical application in routine practice.
 makes it difficult to use for direct clinical application in routine practice.
• Absence of Treatment Guidelines: Because it is not a diagnostic system,
RDoC does not provide treatment algorithms or guidelines that clinicians can
use for making decisions in day-to-day practice, limiting its immediate utility for
psychiatrists and therapists.

2. Overemphasis on Biological Reductionism

• Biological Bias: One criticism of RDoC is its apparent focus on biological
constructs, such as genetics and neuroimaging, which may lead to biological
reductionism. This could potentially overlook the significant contributions of
environmental, social, and psychosocial factors in the development and
maintenance of mental health disorders.
• Complexity of Human Behavior: Mental health conditions are influenced by a
multitude of factors that are not solely biological. RDoC’s heavy reliance on
neuroscientific methods risks simplifying the complexity of human behavior,
reducing a multifaceted issue to brain circuitry alone.

3. Lack of Clear Diagnostic Categories

• Difficulty in Communication: The lack of a clear diagnostic category within
RDoC creates difficulties in communication among healthcare providers,
patients, and families. Diagnostic categories are often helpful for patients to
understand their condition, seek support, and access treatment.
• Insurance and Administrative Issues: Current healthcare systems, including
insurance claims, are based on categorical diagnoses. The absence of a
diagnostic label can complicate the process of treatment authorization,
reimbursement, and administrative formalities, limiting the practicality of the
RDoC approach.

4. Limited Evidence Base for Some Domains

•

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Research Gaps: While RDoC aims to integrate different levels of analysis,
there is still limited evidence regarding how various domains (e.g., cognitive
systems or positive valence systems) interact and contribute to mental
health conditions. The limited empirical validation of some RDoC constructs
makes it challenging to apply universally.
• Challenges in Translational Application: Translating insights from RDoC into
meaningful clinical outcomes is a major challenge. The domains and constructs
used in RDoC, such as loss, reward responsiveness, or social processes,
are theoretically sound but may be difficult to operationalize for clinical utility
without validated tools and measures.

Conclusion
The Research Domain Criteria (RDoC) represents a promising shift in psychiatric
research by emphasizing neurobiological mechanisms, dimensions of behavior,
and transdiagnostic factors. It holds significant potential for precision psychiatry,
identifying biomarkers, and advancing the understanding of mental health disorders.
However, RDoC also has limitations, particularly regarding its lack of clinical utility,
potential for biological reductionism, and the challenges inherent in moving away
from traditional diagnostic categories. While it is not yet ready to replace existing
clinical tools, RDoC contributes a valuable framework for understanding the
complex interplay between biological, psychological, and social factors in mental
health.

References
1. Insel, T., & Cuthbert, B. (2015). Brain disorders? Precisely. Precision medicine comes to
psychiatry. Science, 348(6234), 499-500.
2. Cuthbert, B. N. (2014). The RDoC framework: Facilitating transition from ICD/DSM to
dimensional approaches that integrate neuroscience and psychopathology. World Psychiatry,
13(1), 28-35.
3. Kozak, M. J., & Cuthbert, B. N. (2016). The NIMH Research Domain Criteria Initiative:
Background, issues, and pragmatics. Psychophysiology, 53(3), 286-297.
2021-02: Craving—Neurobiology and Management.

Neurobiology of Craving

Craving is a core feature of substance use disorders (SUDs), mediated by maladaptive neuroplastic changes in
brain circuits involved in reward, motivation, learning, and executive control.

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1. Neuroanatomical Substrates
Craving involves a cortico-striatal-limbic network, with three major systems:
A. Reward and Reinforcement System
• Ventral Tegmental Area (VTA): Dopaminergic neurons project to the nucleus accumbens (NAc), initiating
drug reinforcement and craving.
• Nucleus Accumbens (NAc): Involved in drug-related reinforcement, craving shifts from the ventral striatum
(NAc shell; voluntary drug use) to the dorsal striatum (NAc core; habitual use).
• Amygdala: Modulates conditioned responses to drug-related cues, contributing to cue-induced craving.
B. Executive Control System
• Prefrontal Cortex (PFC):
○ Dorsolateral PFC (dlPFC): Regulates cognitive control over cravings, which is impaired in SUDs.
○ Orbitofrontal Cortex (OFC): Hyperactivation is linked to compulsive drug-seeking.
○ Anterior Cingulate Cortex (ACC): Mediates conflict resolution between craving and abstinence.
C. Learning and Memory System
• Hippocampus: Stores contextual drug-related memories, triggering craving in associated environments.

2. Neurochemical involved
Neurotransmitter System Role in Craving
Dopamine (DA) Reinforcement and salience attribution to drug cues. Chronic drug use
downregulates D2 receptors, reducing natural rewards while enhancing drug-
related craving.
Glutamate (Glu) Hyperactivation of the PFC–NAc pathway leads to compulsive drug-seeking.
GABA Dysfunction in GABAergic inhibition reduces self-regulation, increasing craving
responses.
Endogenous Opioid System Modulates hedonic effects of drugs; dysfunction increases craving.
Corticotropin-Releasing Stress-related craving via amygdala activation; implicated in withdrawal-induced
Factor (CRF) relapse.
3. Cognitive and Behavioral Mechanisms
• Cue-Induced Craving: Activation of conditioned responses through environmental stimuli (e.g., seeing a
syringe triggers dopamine release in the NAc).
• Negative Reinforcement: Craving arises to avoid withdrawal symptoms rather than to achieve euphoria.
• Memory Reconsolidation: Drug-related memories become persistent and resistant to extinction, contributing
to relapse.

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Koob’s Model of Addiction: Neurobiology of Craving
(Based on the Neurocircuitry of Addiction by Koob & Volkow, 2010)
Koob’s model of addiction conceptualizes substance use disorder (SUD) as a chronic, relapsing brain
disorder that progresses through three interconnected stages:

1. Binge/Intoxication Stage
2. Withdrawal/Negative Affect Stage
3. Preoccupation/Anticipation (Craving) Stage

These stages are mediated by distinct neurocircuits, neurotransmitter systems, and neuroadaptive
changes that sustain addictive behaviors.

1. Binge/Intoxication Stage (Positive Reinforcement)

Brain Regions Involved:

• Nucleus Accumbens (NAc) → Dopamine Surge (Reward Pathway)
• Ventral Tegmental Area (VTA) → Dopaminergic Activation
• Dorsal Striatum (DS) → Habit Formation
• Prefrontal Cortex (PFC) → Goal-Directed Use
Neurotransmitters Involved:
• Dopamine (DA) Increase: Mediates pleasure, motivation, and reinforcement.
• Opioid Peptides: Enhance reward (endorphins).
• Glutamate: Strengthens synaptic plasticity, facilitating drug-seeking behavior.
Process:
Initial drug use hijacks the mesolimbic dopamine system, reinforcing positive effects.
 • Initial drug use hijacks the mesolimbic dopamine system, reinforcing positive effects.
• Over time, the habitual activation of the dorsal striatum (DS) results in compulsive drug use.
Neuroadaptation:
• Repeated drug use reduces dopamine receptor sensitivity (D2 downregulation), requiring higher doses for
the same effect (tolerance).

2. Withdrawal/Negative Affect Stage (Negative Reinforcement)

Key Brain Regions Involved:
• Extended Amygdala (AMG) → Stress & Dysphoria
• Bed Nucleus of the Stria Terminalis (BNST) → Anxiety, Withdrawal
• Hypothalamus → Autonomic Symptoms
• Hippocampus → Memory & Stress Response
Neurotransmitters Involved:
• ↓ Dopamine (DA) Deficiency → Anhedonia, Craving
• ↑ Corticotropin-Releasing Factor (CRF) → Stress & Anxiety
• ↑ Norepinephrine (NE) → Autonomic Withdrawal Symptoms
• ↓ Serotonin (5-HT) → Depression & Irritability
Process:
• Withdrawal induces dysphoria, anxiety, and cravings due to hypodopaminergic states.
• The amygdala and hypothalamus activate stress pathways (HPA axis), increasing CRF and NE.
• This leads to negative reinforcement—drug use becomes necessary to avoid withdrawal symptoms rather
than to achieve pleasure.
Neuroadaptation:
• Chronic drug use leads to persistent changes in stress and reward circuitry, maintaining addiction even
after acute withdrawal subsides.

3. Preoccupation/Anticipation (Craving) Stage

Brain Regions Involved:
• Prefrontal Cortex (PFC) → Decision-Making, Inhibitory Control
• Orbitofrontal Cortex (OFC) → Drug Cues & Motivation
• Anterior Cingulate Cortex (ACC) → Compulsive Drug Seeking

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• Insula → Interoceptive Craving Awareness
• Hippocampus → Memory Triggers & Relapse Risks
Neurotransmitters Involved:
• Glutamate (↑) → Drug cue reactivity & relapse triggers.
• Dopamine (DA) Dysregulation → Impaired impulse control, craving.
• GABA Dysregulation → Reduced inhibitory control over compulsive drug-seeking behavior.
Process:
• Craving is driven by drug-related cues (environmental triggers, stress, emotional states).
• Dysfunction in PFC and OFC impairs inhibitory control, making impulsive relapse more likely.
• Activation of the insula heightens subjective craving experiences (e.g., "I need the drug to feel normal").
Neuroadaptation:
• Sensitization of glutamatergic pathways leads to compulsive drug-seeking even after long periods of
abstinence (relapse vulnerability).

4. Management of Craving & Addiction

Management of Craving

A. Pharmacological Interventions
Drug Class Medications Mechanism of Action Indications
Opioid Naltrexone (50 mg/day) Blocks opioid receptors → Reduces craving Alcohol, Opioid
Antagonists Use Disorder
Glutamate Acamprosate (666 mg TID), Restores glutamatergic balance Alcohol Use
Modulators Memantine Disorder
Partial Agonists Buprenorphine (4–24 mg/day) Reduces withdrawal & craving Opioid
Dependence
Dopamine Bupropion (150–300 mg/day), Increases dopamine availability Nicotine,
Modulators Modafinil Stimulant
Dependence
GABA Enhancers Baclofen (10–60 mg/day), Reduces cue-induced craving Alcohol, Cocaine
Gabapentin Addiction
Naltrexone is the most evidence-based anti-craving agent for alcohol and opioid dependence.
Acamprosate is useful in preventing relapse in alcohol use disorder.
B. Psychosocial & Behavioral Interventions
Therapy Mechanism Effectiveness
Cognitive Behavioral Therapy (CBT) Identifies triggers, builds coping First-line psychosocial
strategies intervention
Motivational Enhancement Therapy Strengthens intrinsic motivation Useful in early stages of
(MET) recovery
Contingency Management (CM) Rewards abstinence with incentives Effective in stimulant use
disorder
Mindfulness-Based Relapse Prevention Reduces stress-induced relapse Useful for chronic relapsers
(MBRP)
CBT with cue-exposure therapy is the most effective treatment for reducing craving and relapse risk.
12-step programs (AA, NA) provide long-term support and relapse prevention.

C. Neuromodulation Therapies
Technique Mechanism Indications
Repetitive Transcranial Magnetic Targets dlPFC, improving cognitive Cocaine, Nicotine use
Stimulation (rTMS) control over craving. disorder.
Deep Brain Stimulation (DBS) Stimulates the NAc, reducing reward- Severe Opioid, Alcohol use
related craving. disorder.
Vagus Nerve Stimulation (VNS) Modulates limbic system activation. Experimental for multiple
SUDs.

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5. Summary of the( Koob Model ) craving
Stage Neurobiology Treatment Target
Binge/Intoxication ↑ Dopamine, Habit formation (DS) Naltrexone, CBT
Withdrawal/Negative Affect ↑ CRF, ↓ Dopamine, ↑ NE Acamprosate, Baclofen, Gabapentin
Preoccupation/Anticipation PFC Dysfunction, Cue Reactivity CBT, Mindfulness, Glutamate Modulation
Koob’s model explains addiction as a cycle driven by neuroadaptations in reward, stress, and executive systems.
Craving is sustained by dysregulated dopamine-glutamate interactions, making combined pharmacotherapy and
psychotherapy the most effective approach.

Conclusion
Craving in substance use disorders is driven by dopaminergic hypofunction, glutamatergic hyperactivity, and
impaired executive control. Effective management requires a multimodal approach,
integrating pharmacotherapy, psychotherapy, and neuromodulation to target distinct neurobiological and
cognitive mechanisms.
2021-03: Erectile Dysfunction.
Erectile Dysfunction
Erectile dysfunction is defined as the consistent or recurrent inability to obtain and
maintain an erection sufficient for satisfactory sexual intercourse, lasting for more than
6 months.

1. Sexual Disorders Classification

Sexual disorders are classified in ICD-10, ICD-11, and DSM-5 under sexual dysfunctions, paraphilic disorders, and
gender identity disorders.

1.1. ICD-10

A. Sexual Dysfunctions (F52)

1. Lack or loss of sexual desire (F52.0) – Persistent absence of sexual thoughts and desire.
2. Sexual aversion and lack of sexual enjoyment (F52.1) – Strong aversion to sexual contact.
3. Failure of genital response (F52.2) – Includes male erectile disorder and female sexual arousal disorder.
4. Orgasmic dysfunction (F52.3) – Absence or delay in orgasm.
5. Premature ejaculation (F52.4) – Persistent or recurrent ejaculation with minimal stimulation.
6. Nonorganic vaginismus (F52.5) – Involuntary spasm of vaginal muscles preventing penetration.
7. Nonorganic dyspareunia (F52.6) – Genital pain during intercourse.
8. Excessive sexual drive (F52.7) – Hypersexuality in males and females.
B. Paraphilic Disorders (F65)
1. Exhibitionism (F65.2) – Recurrent urges to expose genitals.
2. Voyeurism (F65.3) – Sexual pleasure from watching unsuspecting persons.

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3. Paedophilia (F65.4) – Sexual preference for prepubescent children.
4. Fetishism (F65.0) – Sexual fixation on objects or body parts.
5. Sadomasochism (F65.5, F65.6) – Sexual arousal from inflicting or receiving pain.
C. Gender Identity Disorders (F64)
1. Transsexualism (F64.0) – Persistent desire to live as the opposite sex.
2. Gender identity disorder of childhood (F64.2) – Gender dysphoria in prepubertal children.

1.2. ICD-11
ICD-11 has reorganized sexual dysfunctions and gender identity disorders into a separate chapter under
“Conditions Related to Sexual Health.”
A. Sexual Dysfunctions
1. Hypoactive sexual desire dysfunction
2. Erectile dysfunction
3. Female orgasmic dysfunction
4. Premature ejaculation
5. Genito-pelvic pain/penetration disorder
B. Compulsive Sexual Behavior Disorder
• Previously categorized under hypersexuality, now reclassified as Impulse Control Disorder.
C. Gender Incongruence
• Replaces Gender Identity Disorder, removed from mental disorders to reduce stigma.

1.3. DSM-5
A. Sexual Dysfunctions (≥6-month duration required)
1. Female Sexual Interest/Arousal Disorder
2. Male Hypoactive Sexual Desire Disorder
3. Erectile Disorder
4. Female Orgasmic Disorder
5. Delayed Ejaculation
 5. Delayed Ejaculation
6. Premature (Early) Ejaculation
7. Genito-Pelvic Pain/Penetration Disorder
B. Paraphilic Disorders
1. Exhibitionistic Disorder
2. Voyeuristic Disorder
3. Frotteuristic Disorder
4. Sexual Masochism Disorder
5. Sexual Sadism Disorder
6. Paedophilic Disorder
7. Fetishistic Disorder
8. Transvestic Disorder
C. Gender Dysphoria
• DSM-5 replaces Gender Identity Disorder with Gender Dysphoria, emphasizing distress rather than identity
as pathological.

2. Evaluation of Erectile Dysfunction (ED)

1. General Approach
Erectile dysfunction is defined as the consistent or recurrent inability to obtain and maintain an erection
sufficient for satisfactory sexual intercourse, lasting for more than 6 months.
2. Steps in the Evaluation of ED
A structured approach is needed to differentiate between psychogenic and organic causes of ED.
A. History Taking
• Sexual history: Onset, duration, severity, situational vs. generalized dysfunction
• Medical history: Diabetes, hypertension, cardiovascular disease, neurological disorders, previous surgeries

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• Psychosocial history: Stress, depression, anxiety, substance abuse, relationship issues
• Medication history: SSRIs, beta-blockers, antihypertensives, antipsychotics
B. Physical Examination
• General Examination: Signs of metabolic syndrome, obesity, gynecomastia, testicular atrophy
• Cardiovascular Examination: Blood pressure, peripheral pulses
• Neurological Examination: Reflexes, perineal sensation
• Genitourinary Examination: Testicular size, penile plaques (Peyronie’s disease)
C. Laboratory Investigations
• Blood Tests:
○ Fasting glucose, HbA1c (diabetes assessment)
○ Lipid profile (atherosclerosis risk)
○ Serum testosterone (hypogonadism assessment)
○ Thyroid function tests
○ Prolactin (if hypogonadism or decreased libido)
D. Specialized Diagnostic Tests
• International Index of Erectile Function (IIEF): Standardized questionnaire for severity assessment
• Nocturnal Penile Tumescence (NPT) Test: Differentiates psychogenic from organic ED
• Penile Doppler Ultrasound: Evaluates vascular supply and venous leakage
• Bulbocavernosus Reflex Test: Assesses nerve function
• Penile Brachial Index (PBI): Assesses arterial sufficiency

3. Management of Erectile Dysfunction

3.1. Psychotherapy (First-Line for Psychogenic ED)

Psychotherapy is essential for psychogenic erectile dysfunction (ED), where psychological factors such as
performance anxiety, stress, depression, and relationship issues play a role.
 A. Cognitive-Behavioral Therapy (CBT)
○ Focuses on performance anxiety reduction.
○ Helps identify and modify negative thoughts related to sexual activity.
○ Uses systematic desensitization and relaxation techniques.

B. Sex Therapy
○ Involves sensate focus exercises that reduce performance pressure.
○ Includes education about normal sexual response cycles.
○ Encourages partner communication and problem-solving.

C. Behavioral Techniques
○ Gradual exposure to sexual situations (reducing performance anxiety).
○ Guided imagery and mindfulness to enhance sexual arousal.
○ Erotic stimulation techniques to restore confidence in sexual function.
3.2. Pharmacotherapy
• Phosphodiesterase-5 Inhibitors (PDE-5i):

○ Sildenafil (Viagra), Tadalafil (Cialis), Vardenafil.

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Sildenafil (Viagra) Tadalafil (Cialis) Vardenafil (Levitra) Avanafil (Stendra)
Onset 30–60 minutes 30–45 minutes 30–60 minutes Quickest; 15–30
(sometimes sooner) minutes
Duration of 4–6 hours Up to 36 hours 4–6 hours 6–12 hours
action
Food High-fat meal can Not significantly impacted High-fat meal can Not significantly
interactions slow absorption. slow absorption. impacted
Contraindications for PDE-5 inhibitors:
• Use with nitrates (e.g., nitroglycerin) → Risk of life-threatening hypotension.
• Severe cardiovascular disease.
• Severe liver impairment.

• Testosterone Replacement Therapy: If low testosterone confirmed.

Benefits of Optimal Testosterone

3.3. Mechanical & Surgical Options
• Vacuum Erection Devices (VEDs).

• Intracavernosal Injections (Alprostadil).

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• Penile Prosthesis Surgery (last-line).

Summary
Sexual disorders are classified under dysfunctions, paraphilic disorders, and gender dysphoria in ICD-10,
ICD-11, and DSM-5. Erectile Dysfunction is diagnosed based on persistent difficulty with erections and
requires clinical, hormonal, and vascular assessment.

• ED evaluation requires history, physical examination, laboratory tests, and specialized investigations.
• Distinguishing between psychogenic and organic causes is essential for effective treatment planning.
• Treatment includes psychotherapy, PDE-5 inhibitors, and lifestyle modifications.
2021-04: Major Neuro-Cognitive Disorders.

Major Neurocognitive Disorder (MNCD)

1. Definition
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Major Neurocognitive Disorder (MNCD) is a syndrome characterized by acquired cognitive decline
affecting one or more cognitive domains. It corresponds to Dementia (ICD-10) and has been redefined
in DSM-5 and ICD-11 to reflect varying severity.

• ICD-10 (F00-F03): Uses the term "Dementia", defining it as a chronic or progressive syndrome
with multiple cognitive impairments, not accompanied by clouding of consciousness.
• DSM-5: Uses "Major Neurocognitive Disorder", requiring significant cognitive decline that
interferes with independence.
• ICD-11: Uses "Neurocognitive Disorder", categorizing it as mild or major based on functional
impairment.

2. Diagnostic Criteria

ICD-10 Criteria for Dementia (F00-F03)

• Memory impairment: A decline in the ability to retain, recall, and process new information.
• Impairment in other cognitive functions: At least one of:
• Reduced abstract thinking
• Language impairment (aphasia)
• Apraxia (impaired motor function)
• Agnosia (failure to recognize objects)
• Interference with daily functioning
• Absence of clouded consciousness

Subtypes:
• F00 Dementia in Alzheimer’s Disease
• F01 Vascular Dementia
• F02 Dementia in Other Diseases (Parkinson’s, Huntington’s, HIV)
• F03 Unspecified Dementia

DSM-5 Criteria for Major Neurocognitive Disorder

 1. Significant cognitive decline from a previous level of performance in one or more cognitive
domains:
○ Complex attention
○ Executive function
○ Learning and memory
○ Language
○ Perceptual-motor function
○ Social cognition
2. Objective evidence of cognitive impairment from clinical assessment and standardized
neuropsychological testing.
3. Interference with independence, meaning the person requires assistance with daily activities.
4. Not exclusively due to delirium and not better explained by another mental disorder (e.g.,
major depressive disorder)

• Severity classification:
○ Mild: Independent but requires compensatory strategies.
○ Moderate: Needs assistance in daily tasks.
○ Severe: Fully dependent.

ICD-11 Neurocognitive Disorder

• Cognitive impairment from previously attained levels.
• Significant impact on daily functioning.
• Categorized into Mild, Major, and Etiology-Specific subtypes.

3. Etiology
Primary Neurodegenerative Diseases:
• Alzheimer’s Disease (Most common)
• Frontotemporal Dementia
• Lewy Body Dementia

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• Parkinson’s Disease Dementia
• Huntington’s Disease

Vascular and Other Causes:

• Vascular Dementia (multi-infarct dementia, strategic infarct dementia)
• Traumatic Brain Injury (TBI)
• Substance/Medication-induced Neurocognitive Disorder
• Infectious (HIV-associated, Prion diseases)
• Nutritional Deficiencies (B12, folate, thiamine)

4. Clinical Features
• Memory Loss: Initially affects short-term, later long-term.
• Executive Dysfunction: Poor judgment, planning difficulties.
• Aphasia, Apraxia, Agnosia: Language, motor, and object-recognition impairment.
• Behavioral Changes: Apathy, agitation, disinhibition, hallucinations (in Lewy Body Dementia).
• Gait Disturbance: Common in vascular and Parkinson’s-related dementia.

5. Investigations
1. Cognitive Screening:
• Mini-Mental State Examination (MMSE)
• Montreal Cognitive Assessment (MoCA)
• Addenbrooke’s Cognitive Examination (ACE-III)

1. Neuroimaging:
• MRI Brain: Hippocampal atrophy in Alzheimer’s
• CT Brain: Vascular infarcts, atrophy patterns
• PET/SPECT: Amyloid deposition in Alzheimer’s

1. Laboratory Workup:
• Metabolic: B12, folate, thyroid function, glucose
• Infectious: HIV, syphilis serology
• Toxicology: Chronic alcohol use, heavy metal exposure
6. Management

Non-Pharmacological Management:
1. Cognitive Stimulation Therapy (CST): Group-based intervention focusing on memory, problem-
solving, and communication.
2. Reminiscence Therapy: Engaging patients in discussing past events using prompts such as
photographs and music.
3. Behavioral Interventions: Addressing agitation, aggression, and wandering through structured
routines and environmental modifications.
4. Physical Activity: Regular exercise to slow cognitive decline and maintain overall well-being.
5. Nutritional Support: Adequate diet, including Mediterranean-style nutrition (rich in antioxidants
and healthy fats).
6. Social Engagement: Encouraging meaningful social interactions to reduce isolation and
depressive symptoms.
7. Caregiver Support and Education: Training caregivers in behavior management techniques and
self-care.

Pharmacological Management:
1. Acetylcholinesterase Inhibitors (for Alzheimer's Disease and Lewy Body Dementia):
○ Donepezil: 5–10 mg/day
○ Rivastigmine: 1.5–6 mg twice daily (oral) or 4.6–13.3 mg/24h (patch)
○ Galantamine: 8–24 mg/day
2. NMDA Receptor Antagonist (for moderate-to-severe Alzheimer's Disease):
○ Memantine: 5–20 mg/day
3. Vascular Dementia Treatment: Control of hypertension, diabetes, and cholesterol to prevent
further decline.
4. Behavioral Symptom Management:
○ Atypical antipsychotics (e.g., risperidone 0.25–1 mg/day) for severe agitation (used
cautiously due to risk of cerebrovascular events).
○ Antidepressants (SSRIs such as sertraline 25–100 mg/day) for depression in MNCD.

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○ Melatonin 2–10 mg at bedtime for sleep disturbances.

Prognosis & Course:

• Progressive decline in cognitive abilities.
• Alzheimer’s Disease: Progressive, median survival 4-8 years post-diagnosis.
• Vascular Dementia: Stepwise decline with stable periods.
• Lewy Body Dementia: Fluctuating cognition, visual hallucinations, Parkinsonism.
• Frontotemporal Dementia: Behavioral and language dysfunction, younger onset (45-65
years).
• Supportive care planning, including palliative approaches, is essential in advanced stages.

Summary
Feature ICD-10 (Dementia DSM-5 (Major NCD) ICD-11
F00-F03) (Neurocognitive
Disorders)
Terminology Dementia Major Neurocognitive Disorder Neurocognitive
Disorder
Cognitive Domains Memory, abstract 6 domains (attention, executive function, Similar to DSM-5
thinking, language, memory, language, perceptual-motor,
judgment social cognition)
Functional Impact Interferes with daily Interferes with independence Interferes with
life independence
Subtypes Alzheimer’s, Etiology-based Mild, Major,
Vascular, Others Etiology-based
Course Progressive Progressive or stable (TBI, vascular) Progressive or
stable

High-Yield Points for Exam:

1. ICD-10: Dementia (F00-F03) → ICD-11: Neurocognitive Disorder
 1. ICD-10: Dementia (F00-F03) → ICD-11: Neurocognitive Disorder
2. DSM-5 renamed Dementia as Major Neurocognitive Disorder
3. Key differentiator: Cognitive impairment that interferes with independence.
4. Alzheimer’s Disease = most common etiology (60-70%)
5. Early vs Late-Onset Dementia → Alzheimer's vs Frontotemporal
6. Cognitive screening: MMSE ≤24, MoCA ≤26 in early stages
7. MRI: Hippocampal atrophy (Alzheimer’s), Cortical atrophy (FTD), Infarcts (Vascular
Dementia)

References::
• The Maudsley Prescribing Guidelines in Psychiatry (2021)
• CPG Guidelines for Psychiatry (Indian Psychiatric Society)
• Advanced Pharmacology for Prescribers
• Kaplan & Sadock’s Comprehensive Textbook of Psychiatry

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2021-05: Bipolar II Disorder.

Bipolar II Disorder: Clinical Practice Guidelines (CPG-Based)

Definition and Diagnostic Criteria (DSM-5)

Bipolar II Disorder is characterized by recurrent episodes of major depression and at least one hypomanic
episode. The absence of manic episodes differentiates it from Bipolar I Disorder.

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• ICD-10: Bipolar II Disorder is not explicitly listed as a separate category. Instead, bipolar affective disorder
(F31) encompasses both Bipolar I and II.

ICD-10 does not distinguish Bipolar I and II. The general criteria for bipolar affective disorder (F31) include:
Two or more episodes of mood disturbance (mania, hypomania, depression).
One episode must be manic, hypomanic, or mixed.

Exclusion: Not due to substance use or medical conditions.

• DSM-5: Recognizes Bipolar II Disorder (296.89) as a distinct diagnosis, separate from Bipolar I.
DSM-5 Criteria for Bipolar II Disorder (296.89)
1. At least one hypomanic episode (≥4 consecutive days).
○ Elevated, expansive, or irritable mood.
○ Increased energy/activity, with ≥3 symptoms (or ≥4 if mood is irritable):
▪ Inflated self-esteem/grandiosity.
▪ Decreased need for sleep.
▪ More talkative/pressured speech.
▪ Flight of ideas or racing thoughts.
▪ Increased goal-directed activity or psychomotor agitation.
▪ Excessive involvement in risky activities.
2. At least one major depressive episode (≥2 weeks).
○ ≥5 symptoms, including either depressed mood or anhedonia:
▪ Depressed mood most of the day.
▪ Loss of interest/pleasure in activities.
▪ Weight/appetite change.
▪ Insomnia/hypersomnia.
▪ Fatigue or loss of energy.
▪ Feelings of worthlessness/guilt.
▪ Impaired concentration/indecisiveness.
▪ Psychomotor agitation/retardation.
▪ Suicidal ideation/attempts.
3. No history of manic episodes.
4. Symptoms cause significant distress or impairment.
5. Not attributable to substance use or medical conditions.

ICD-11: Introduces Bipolar Type II Disorder (6A61) as a distinct category

ICD-11: Introduces Bipolar Type II Disorder (6A61) as a distinct category
○ At least one hypomanic episode and one depressive episode.
○ Hypomanic symptoms are observable but do not cause severe impairment (unlike mania).
○ No history of full manic episodes.
○ Not better explained by another disorder.

Epidemiology
• Lifetime prevalence: 0.4–2% (lower than Bipolar I).
• Onset: Late adolescence to early adulthood (median age ~20s).
• Sex ratio: Equal prevalence in males and females, but women have more depressive episodes.
• Genetic heritability: 60-80% risk if first-degree relative has Bipolar Disorder.

Hypomanic Episode Criteria (DSM-5)

• A distinct period of elevated, expansive, or irritable mood, lasting at least 4 consecutive days.
• Increased energy or activity.
• At least three (or four, if mood is irritable) of the following:
• Inflated self-esteem or grandiosity.
• Decreased need for sleep.
• Increased talkativeness or pressured speech.
• Flight of ideas or racing thoughts.
• Distractibility.
• Increased goal-directed activity or psychomotor agitation.
• Engaging in activities with a high potential for negative consequences (e.g., spending sprees, risky sexual
behavior).
• No significant impairment in social or occupational functioning (contrast with mania).

Major Depressive Episode Criteria

• Duration: At least 2 weeks, with at least five of the following symptoms:
• Depressed mood.
• Anhedonia (loss of interest/pleasure).
• Weight change or appetite disturbance.

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• Sleep disturbances (insomnia or hypersomnia).
• Psychomotor agitation or retardation.
• Fatigue or loss of energy.
• Feelings of worthlessness or excessive guilt.
• Impaired concentration or indecisiveness.
• Suicidal ideation or attempts.

Exclusion Criteria
• No history of manic episodes (would indicate Bipolar I).
• Symptoms not better explained by a substance or another medical condition.

Management
Non-Pharmacological Interventions (First-Line)
• Psychoeducation: Structured patient and caregiver education to enhance treatment adherence and relapse
prevention.
• Cognitive Behavioral Therapy (CBT): Effective in depressive episodes to identify cognitive distortions and
enhance coping strategies.
• Interpersonal and Social Rhythm Therapy (IPSRT): Helps stabilize daily routines and improve circadian
rhythms, reducing mood instability.
• Lifestyle Adjustments:
○ Regular sleep patterns.
○ Avoidance of psychoactive substances (alcohol, stimulants, recreational drugs).
○ Regular physical exercise.
○ Structured daily activities.
○ Stress reduction techniques (mindfulness, relaxation exercises).

• Electroconvulsive Therapy (ECT): Considered in treatment-resistant cases or severe depression with

suicidality.

Pharmacological Management
Mood Stabilizers (First-Line)
Mood Stabilizers (First-Line)

1. Lithium (Gold Standard)

○ Dosage: 600–1800 mg/day.
○ Therapeutic Range: 0.6–1.2 mEq/L.
○ Monitoring:
○ Renal function (risk of nephrotoxicity).
○ Thyroid function (hypothyroidism risk).
○ Serum lithium levels to avoid toxicity.

○ Evidence: Reduces suicidal risk in bipolar patients.

2. Lamotrigine (Preferred for Bipolar Depression)

○ Dosage: Start at 25 mg/day, titrate to 100–200 mg/day.
○ Caution: Risk of Stevens-Johnson Syndrome (SJS) – slow titration necessary.
○ Indication: Preferred in bipolar depression and maintenance therapy.

3. Valproate (Divalproex Sodium)

○ Dosage: 500–2000 mg/day.
○ Therapeutic Range: 50–125 mcg/mL.
○ Monitoring: Liver function, platelet count.
○ Contraindications: Avoid in pregnancy (teratogenicity risk).

Atypical Antipsychotics (For Mood Stabilization and Depression)

• Used in acute mood stabilization and for bipolar depression.

1. Quetiapine
○ Dosage: 50–300 mg/day.
○ Indication: FDA-approved for bipolar depression.

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2. Lurasidone
○ Dosage: 20–120 mg/day.
○ Indication: Bipolar depression with a lower metabolic side-effect profile.

3. Olanzapine + Fluoxetine (Symbyax)

○ Dosage: 6 mg olanzapine + 25 mg fluoxetine.
○ Indication: FDA-approved for bipolar depression.

Adjunctive Treatments for Depressive Episodes

• Selective Serotonin Reuptake Inhibitors (SSRIs):
• Used only with a mood stabilizer to prevent manic switching.
• Examples: Sertraline, Fluoxetine.

• Bupropion:
• Preferred due to lower risk of mood switching compared to SSRIs.

• Psychostimulants (Modafinil, Armodafinil):

• Used cautiously in treatment-resistant bipolar depression.

Special Considerations
• Suicidal Risk: Lithium has the most robust evidence for suicide prevention in Bipolar II Disorder.
• Rapid Cycling Bipolar II: More responsive to combination therapy (mood stabilizers + atypical
antipsychotics).
• Pregnancy: Avoid valproate and carbamazepine due to teratogenic risks. Lamotrigine is safer.
• Elderly: Start low-dose treatment to minimize adverse effects.

Prognosis & Long-Term Management

• Chronic and relapsing illness.
• Higher risk of suicide than Bipolar I Disorder.
• Early diagnosis, consistent medication adherence, and psychosocial support improve outcomes.
Regular monitoring for medication side effects and metabolic complications.
 • Regular monitoring for medication side effects and metabolic complications.

Summary of Treatment
Phase First-Line Alternative/Adjunct
Acute Hypomania Lithium, Valproate, Atypical Antipsychotics Quetiapine, Lurasidone
Bipolar Depression Quetiapine, Lurasidone, Lamotrigine Lithium + Antidepressant (if necessary)
Maintenance Lithium, Lamotrigine Valproate, Quetiapine

References
• The Maudsley Prescribing Guidelines in Psychiatry (2021)
• CPG Guidelines for Psychiatry (Indian Psychiatric Society)
• Advanced Pharmacology for Prescribers
• Kaplan & Sadock’s Comprehensive Textbook of Psychiatry

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 2021-06: Treatment-Resistant Schizophrenia.

The various criterias of treatment resistant schizophrenia

1) KANE’S CRITERIA
Operational criteria most widely used for TRS.
It is three dimensional

A) HISTORICAL
• Atleast three treatments with antipsychotics of

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• Atleast two different chemical classes
• Doses equivalent to 1000mg/day of chlorpromazine
• For a period of 6weeks without significant relief
• No period of good function within the preceeding 5years

B) CROSS SECTIONAL
• A score of atleast 45 in the BPRS with score≥4 on atleast 2 out of 4
positive symptoms
hallucinatory behavior unusual thought content suspiciousness conceptual
disorganization.

C)PROSPECTIVE CLINICAL RESPONSE

• Failure to achieve BPRS ≤35 in BPRS or CGI≥3 with trial of haloperidol
60mg daily for 6weeks.

Kane's Criteria for Treatment-Resistant Schizophrenia (TRS)

Kane's criteria are three-dimensional, involving historical, cross-sectional, and
prospective clinical response dimensions.
Dimension Original Criteria Modified Criteria
Historical - At least three treatments with - At least two treatments with antipsychotics
antipsychotics
- At least two different chemical - At least two different chemical classes
classes
- Doses equivalent to 1000 mg/day - Doses equivalent to 400-600 mg/day of
of chlorpromazine for a period of chlorpromazine for a period of 4-6 weeks without
six weeks without significant relief significant relief
 - No period of good function within - No period of good function within the preceding
the preceding five years five years
Cross-Sectional - A score of at least 45 on the Brief - A score of at least 45 on the Brief Psychiatric
Psychiatric Rating Scale (BPRS) Rating Scale (BPRS)
- Score of ≥4 on at least two out of - Score of ≥4 on at least two out of four positive
four positive symptoms: symptoms:
- Hallucinatory behavior - Hallucinatory behavior
- Unusual thought content - Unusual thought content
- Suspiciousness - Suspiciousness
- Conceptual disorganization - Conceptual disorganization
Prospective - Failure to achieve a BPRS score of - Failure to achieve a BPRS score of ≤35 or a
Clinical ≤35 or a Clinical Global Impression Clinical Global Impression (CGI) score of ≥3 with
Response (CGI) score of ≥3 with a trial of a trial of haloperidol 60 mg daily for six weeks
haloperidol 60 mg daily for six
weeks

•
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BRENNER ET AL, 1990 CRITERIA-They used a psychosocial approach, rather
than solely a pharmacological one. They defended the existence of different
degrees of treatment response, ranging from clinical remission to severe
treatment-refractoriness.

Level Classification Rehabilitation Need Key Characteristics

1 Clinical remission No need for a formal Rapid response to antipsychotics at recommended
rehabilitation program doses. Patient may show anhedonia or another
negative symptom. CGI normal and score < 2 on
BPRS. Good functional level without supervision.
2 Partial remission No need for a formal Rapid reduction of psychotic symptoms. Mild signs of
rehabilitation program residual psychotic symptoms. CGI 2. None of the
BPRS scale items are ≥ 3.
3 Light resistance Need for a rehabilitation Slight or incomplete reduction of symptoms with
program positive and negative residual symptoms. Alteration
of social or personal functioning in at least two
areas and requiring occasional supervision. No
more than one item with a score ≥ 4 on the BPRS.
4 Moderate Need for a rehabilitation Reduction of symptoms but with a clear persistence of
resistance program them, affecting six or more areas of social and personal
functioning and requiring frequent supervision. CGI 4.
A score of 4 or 2 BPRS items. A BPRS score ≥ 45 on
the 18-item version and 60 on the 24-item version.
5 Severe resistance Need for a continuous Reduction of symptoms but with a clear persistence of
strategy, individual and them, affecting six or more areas of social and personal
oriented toward attempts functioning and requiring frequent supervision. CGI 5.
with atypical A score of 5 on 1 BPRS item or 4 on 3 items. A
 with atypical A score of 5 on 1 BPRS item or ≥ 4 on 3 items. A
antipsychotics and total BPRS > 50 on the 18-item version and 67 on the
adjuvant treatment 24-item version.
6 Refractoriness Longer-term Reduction of mild or non-demonstrable symptoms and
hospitalization with persistence of positive and negative symptoms with
pharmacological and marked alteration in all areas of social and personal
psychosocial attempts functioning. CGI 6. A score of 6 on 1 BPRS item or of
≥ 5 on 2 items. Total BPRS score of ≥ 5 per level.
7 Severe Longer-term No reduction of symptoms with many positive and
refractoriness hospitalization with negative symptoms associated with behavioral
pharmacological and alterations. All areas of social and personal functioning
psychosocial attempts have deteriorated, requiring constant supervision. CGI
7. A score of 7 on 1 BPRS item. Total score of > 5 per
level

3.International Study Group Criteria for Treatment-Resistant Schizophrenia

(TRS)
The International Study Group Criteria provide an alternative approach to defining treatment-resistant
schizophrenia, focusing on persistent symptoms, cognitive dysfunction, mood disturbances, and inadequate
response to typical neuroleptics.
Criteria
Persistent Symptoms: Moderate to severe positive, negative, and disorganization symptoms.
Cognitive Dysfunction: Impairments in multiple cognitive domains.
Mood Disturbance: Recurrent mood disturbances and suicidality.
Functional Impairments: Poor work and social function.
Quality of Life: Subjectively poor quality of life.

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Behavior: Bizarre behavior.
Treatment Trial: One adequate trial of a typical neuroleptic:
- Doses of 2-20 mg/day of haloperidol or equivalent
- Duration of 6-12 weeks
Mnemonic for Kane's Criteria: "Three Critical Treatment Phases"
○ Three Treatments (Historical)
○ Critical Symptoms (Cross-Sectional)
○ Treatment Phases (Prospective)

4.IPAP Criteria for Treatment-Resistant Schizophrenia

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IPAP Criteria for Treatment-Resistant

Schizophrenia
Criteria Details
Historical - No period of good functioning in the
previous five years
- Prior nonresponse to at least two
antipsychotic drugs of two different
chemical classes
- Each trial lasted at least 4-6 weeks
- Dosages equivalent to >400 mg/day of
chlorpromazine or 5 mg/day of risperidone
Clinical Features - Moderate to severe psychopathology,
especially positive symptoms: conceptual
disorganization, suspiciousness, delusions,
 disorganization, suspiciousness, delusions,
or hallucinatory behaviors
Persistent Symptoms After Adequate Trials Patients exhibit any of the following after
two trials of 4-6 weeks each with two
different antipsychotics at adequate
dosages: persistent psychotic symptoms,
recurrent mood symptoms, repeated
suicide attempts or suicidal ideation,
uncontrolled aggressive behavior,
moderate to severe negative symptoms, or
moderate to severe cognitive impairment

5.NICE 2002
stated that "TRS is suggested by a Lack of a satisfactory clinical improvement
Despite the sequential use of the recommended doses for 6 to 8 weeks
Of atleast two antipsychotics
Atleast one of which should be an atypical

6.AMERlCAN PSYCHIATRIC ASSOCIATION 2004

A patient who has not responded to
two or three treatments using atypical antipsychotics
for duration of at least 4 to 6 weeks

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can be considered as having TRS
and is eligible for treatment with clozapine.
2021-07: Functional Magnetic Resonance Imaging.

Memorizable Summary: Use of Functional MRI (fMRI) in Psychiatry

Introduction
• fMRI (Functional Magnetic Resonance Imaging) measures brain activity by detecting
changes in blood oxygenation levels (BOLD signal). It is crucial for understanding the neural
underpinnings of psychiatric disorders, assessing brain connectivity, and monitoring treatment
effects.

How fMRI Works

• BOLD Signal: Indicates neural activity based on blood flow; increased activity leads to
increased oxygen consumption.
• Spatial and Temporal Resolution: Good spatial resolution for pinpointing activated brain
regions; adequate temporal resolution for observing dynamic changes.

Applications in Psychiatry
1. Understanding Neural Circuitry
• Depression: Abnormal activity in the prefrontal cortex, amygdala, and anterior cingulate

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cortex. Connectivity issues contribute to emotion regulation difficulties.
• Schizophrenia: Hypoactivity in the prefrontal cortex and hyperactivity in the default mode
network (DMN) linked to cognitive control deficits.

2. Biomarker Development
• fMRI identifies potential biomarkers for predicting treatment responses and diagnosing
conditions, such as activation patterns in the anterior cingulate cortex for depression.

3. Evaluating Functional Connectivity

• Resting-State fMRI (rs-fMRI) assesses connectivity between brain regions during rest,
revealing abnormalities in networks like the DMN in bipolar disorder and ASD.

4. Monitoring Treatment Effects

• Pharmacotherapy: Changes in brain activation post-medication indicate improvements in
emotional regulation.
• Psychotherapy: Changes in prefrontal-limbic connectivity post-therapy provide evidence of
treatment efficacy.

Examples of Disorders Studied Using fMRI

1. Obsessive-Compulsive Disorder (OCD): Hyperactivity in the orbitofrontal cortex, anterior
cingulate cortex, and caudate nucleus.
2. Post-Traumatic Stress Disorder (PTSD): Exaggerated amygdala responses to trauma-
related stimuli; impaired prefrontal activity.
3. Bipolar Disorder: Altered activity in the ventrolateral prefrontal cortex and amygdala
during emotion regulation tasks.

Limitations of fMRI in Psychiatry

• Indirect Measure: BOLD signal is not a direct measure of neuronal activity.
Individual Variability: Differences in brain structure and function complicate universal
 • Individual Variability: Differences in brain structure and function complicate universal
biomarker development.
• Complexity of Analysis: Requires sophisticated statistical techniques; errors can affect
results.
• Cost and Accessibility: Expensive and not always available for routine clinical use.

Future Directions
• Personalized Medicine: Using fMRI data to tailor treatments based on individual brain
activation patterns.
• Machine Learning and AI: Enhancing diagnostic accuracy and biomarker identification
through advanced data analysis techniques.

Summary
fMRI is a vital tool in psychiatric research, helping to elucidate altered neural circuits in disorders
such as depression, schizophrenia, and PTSD. It aids in identifying biomarkers and assessing
treatment effects, despite limitations like indirect measurement and individual variability. As
technology evolves, fMRI has the potential to lead to more personalized approaches in psychiatric
care.

This summary provides a concise overview of fMRI's relevance in psychiatry, making it easy to
memorize and understand for academic or clinical purposes.

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Use of Functional MRI (fMRI) in Psychiatry

Introduction
Functional Magnetic Resonance Imaging (fMRI) is a non-invasive imaging technique that
measures brain activity by detecting changes in blood oxygenation levels (BOLD signal). It has
become an important tool in psychiatric research for understanding the neural underpinnings of
various psychiatric disorders, assessing brain connectivity, and monitoring the effects of therapeutic
interventions.

How fMRI Works

• BOLD Signal: fMRI relies on the Blood Oxygenation Level Dependent (BOLD) contrast.
When a brain region becomes more active, it consumes more oxygen, which leads to
increased blood flow to that region. This change in oxygen levels can be measured and used
as an indirect marker of neural activity.
• Spatial and Temporal Resolution: fMRI has good spatial resolution, allowing researchers
to pinpoint specific brain regions activated during a task. Its temporal resolution is sufficient
to capture dynamic changes in brain activity over time, albeit not as fast as other techniques
like EEG.
 like EEG.

Applications in Psychiatry
1. Understanding Neural Circuitry of Psychiatric Disorders
• Depression: fMRI studies have identified abnormal activity and connectivity in the prefrontal
cortex, amygdala, and anterior cingulate cortex in patients with major depressive
disorder (MDD). Decreased connectivity between the prefrontal cortex and amygdala is often
linked to the inability to regulate negative emotions, a hallmark of depression.
• Schizophrenia: fMRI has been used to identify hypoactivity in the prefrontal cortex during
executive function tasks and hyperactivity in the default mode network (DMN) in patients
with schizophrenia. These findings have helped support theories of disrupted connectivity and
impaired cognitive control in schizophrenia.

2. Biomarker Development
• fMRI is used in the search for biomarkers that can predict treatment response or differentiate
between psychiatric conditions. For example, the degree of activation in the anterior
cingulate cortex during emotional tasks may help predict an individual's response to
antidepressant therapy.
• In anxiety disorders, altered activation in the amygdala in response to threatening stimuli
has been suggested as a potential biomarker for diagnosis and treatment efficacy.

3. Evaluating Functional Connectivity

• Resting-State fMRI (rs-fMRI): This method is used to assess the functional connectivity of
different brain regions while the subject is at rest. Resting-state abnormalities have been found
in networks like the default mode network (DMN), salience network, and executive control
network in disorders such as bipolar disorder and autism spectrum disorder (ASD).
• Network Dysregulation: Understanding connectivity between brain regions helps identify
network-level dysfunction, which provides insights into the complex, interrelated neural

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systems involved in psychiatric disorders.

4. Monitoring Treatment Effects

• Pharmacotherapy: fMRI can be used to assess the effects of medications on brain function.
For instance, changes in the activation of the amygdala and prefrontal cortex following
antidepressant use can indicate improvements in emotional regulation.
• Psychotherapy: Cognitive-behavioral therapy (CBT) has been shown to induce changes in
prefrontal-limbic connectivity, which can be visualized using fMRI, providing evidence for its
efficacy at the neural level.

Examples of Psychiatric Disorders Studied Using fMRI

1. Obsessive-Compulsive Disorder (OCD): fMRI studies have shown hyperactivity in the
orbitofrontal cortex, anterior cingulate cortex, and caudate nucleus. These areas are
associated with the repetitive thoughts and compulsions characteristic of OCD.
2. Post-Traumatic Stress Disorder (PTSD): fMRI research in PTSD patients shows
exaggerated responses in the amygdala to trauma-related stimuli and impaired prefrontal
cortex activity, suggesting a loss of top-down control over emotional reactivity.
3. Bipolar Disorder: Alterations in the ventrolateral prefrontal cortex and amygdala during
emotion regulation tasks have been observed in bipolar disorder, providing insights into the
mood dysregulation seen in this condition.

Limitations of fMRI in Psychiatry

• Indirect Measure of Neural Activity: The BOLD signal is an indirect measure of neuronal
activity, relying on changes in blood flow and oxygenation rather than direct measurement of
electrical activity.
• Individual Variability: Significant variability in brain structure and function between individuals
makes it challenging to develop universal biomarkers for psychiatric conditions.
• Complexity of Analysis: fMRI data are complex and require sophisticated statistical
techniques for interpretation. Errors in preprocessing or analysis can significantly affect
results.
Cost and Accessibility: fMRI is relatively expensive and not widely accessible for routine
 • Cost and Accessibility: fMRI is relatively expensive and not widely accessible for routine
clinical use, limiting its utility in the general psychiatric population.

Future Directions
• Personalized Medicine: fMRI could be used to tailor treatments for individual patients, such
as predicting which antidepressant might be most effective based on brain activation patterns.
• Machine Learning and AI: Integration of machine learning techniques with fMRI data may
improve diagnostic accuracy and facilitate the identification of biomarkers for specific
psychiatric conditions.

Summary
Functional MRI (fMRI) has emerged as an invaluable tool in psychiatric research, providing
insights into the underlying neural circuits involved in various psychiatric disorders, identifying
potential biomarkers, and assessing treatment effects. It has been particularly useful in elucidating
altered brain networks in disorders like depression, schizophrenia, and PTSD. Despite its
limitations, fMRI continues to contribute to a deeper understanding of the neurobiological
underpinnings of mental illnesses and holds promise for more personalized approaches to
psychiatric care.

References
1. Etkin, A., & Wager, T. D. (2007). Functional neuroimaging of anxiety: a meta-analysis of
emotional processing in PTSD, social anxiety disorder, and specific phobia. American Journal
of Psychiatry, 164(10), 1476-1488.
2. Greicius, M. D., Krasnow, B., Reiss, A. L., & Menon, V. (2003). Functional connectivity in the
resting brain: A network analysis of the default mode hypothesis. Proceedings of the National
Academy of Sciences, 100(1), 253-258.
3. Mayberg, H. S. (2003). Modulation of cortical-limbic pathways in major depression: treatments

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and pathways. Biological Psychiatry, 53(8), 619-630.

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2021-08: Electrophysiology of Sleep.

Electrophysiology of Sleep

1. Introduction
Electrophysiology of sleep refers to the study of brain electrical activity during different sleep stages
using electroencephalography (EEG), electromyography (EMG), and electro-oculography (EOG). It
helps in understanding sleep regulation, disorders, and psychiatric implications.
Significance:
• Differentiates NREM and REM sleep.
• Identifies pathological sleep patterns (e.g., sleep fragmentation, REM abnormalities).
• Essential in diagnosing sleep disorders (narcolepsy, insomnia, REM sleep behavior disorder,
etc.).
• Highlights neurobiological dysfunctions in psychiatric illnesses.

2. History
• 1929: Hans Berger discovered EEG and first recorded sleep-related brain waves.

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• 1937: Loomis et al. classified sleep into stages using EEG.

• 1953: Aserinsky and Kleitman discovered REM sleep.

• 1968: Rechtschaffen & Kales published standard sleep staging criteria.

 • 2007: The American Academy of Sleep Medicine (AASM) revised sleep stage classification.

3. Mechanism and Pathophysiology

Sleep is regulated by two-process model:

mediated).
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• Process S (Homeostatic drive): Sleep pressure accumulates with wakefulness (adenosine-

• Process C (Circadian rhythm): Regulated by the suprachiasmatic nucleus (SCN), controls sleep-
wake cycles.
Key neurotransmitters involved:
• GABA → Sleep-promoting (via VLPO).
• Orexin (Hypocretin) → Wakefulness-promoting.
• Acetylcholine (ACh) → High in wakefulness and REM sleep.
• Serotonin (5-HT) → Initiates NREM sleep.
• Norepinephrine (NE) & Dopamine (DA) → Promote arousal and vigilance.
• Histamine → High in wakefulness, suppressed in sleep.

4. Brain Receptors Involved

Neurotransmitter Receptor Type Effect on Sleep
GABA GABA-A, GABA-B Promotes NREM sleep (inhibitory)
Orexin OX1, OX2 Promotes wakefulness (deficiency → narcolepsy)
Acetylcholine Nicotinic & Muscarinic Promotes REM sleep
Serotonin (5-HT) 5-HT1A, 5-HT2A, 5-HT7 Promotes NREM sleep
Dopamine (DA) D1, D2 Wake-promoting
Norepinephrine (NE) Alpha & Beta receptors Suppressed in REM sleep
Histamine H1, H2 Wake-promoting

5. Sleep Stage Classification (AASM, 2007)

Stage EEG Features EOG EMG Function
Wakefulness Beta (14-30 Hz), Alpha (8-13 Rapid eye High tone Consciousness
Hz) movements
N1 (Stage 1) Theta (4-7 Hz) Slow rolling eye Slightly Transition to sleep
N1 (Stage 1) Theta (4-7 Hz) Slow rolling eye Slightly Transition to sleep
movements reduced tone
N2 (Stage 2) Sleep spindles (12-16 Hz), No eye Further muscle Memory consolidation
K-complexes movement relaxation
N3 (Stage 3) Delta (0.5-2 Hz, ≥20%) No eye Lowest muscle Deep sleep, restorative
movement tone functions
REM Sleep Low voltage, mixed Rapid eye Muscle atonia Dreaming, emotional
frequency (similar to movements processing
wakefulness)

6. Enzymes and Factors Impacting Sleep

Factor Role
Adenosine Sleep-promoting, accumulates with wakefulness
Melatonin Regulates circadian rhythm, secreted by pineal gland
Corticotropin-releasing hormone (CRH) Wake-promoting, linked to stress-induced insomnia
GABAergic inhibition Essential for sleep onset
Cholinergic activation Increases cortical arousal in REM

7. Brain Structures and Their Functions

Brain Structure Function in Sleep
Suprachiasmatic nucleus (SCN) Master circadian clock, controls melatonin secretion
Ventral lateral preoptic nucleus (VLPO) GABAergic inhibition of wake-promoting centers
Locus coeruleus (LC) Norepinephrine release, active in wakefulness
Raphe nuclei Serotonin-mediated sleep induction

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Tuberomammillary nucleus (TMN) Histamine-mediated arousal
Pons (REM generator) Activates REM sleep and atonia

8. Psychiatric Relevance
Disorder Sleep Findings
Depression ↓ REM latency, ↑ REM density, ↓ N3 sleep
Bipolar disorder Sleep-wake cycle disruption, hypersomnia in depression, insomnia in mania
Schizophrenia ↓ Sleep spindles (linked to cognitive deficits)
Insomnia Hyperactive arousal systems, ↓ GABA
Narcolepsy Loss of orexin neurons, cataplexy, sleep paralysis
PTSD Nightmare disorder, fragmented REM sleep

9. Neurological Aspects
Disorder Sleep Correlation
Epilepsy Seizures during NREM sleep
Parkinson’s disease REM sleep behavior disorder (RBD) as an early sign
Alzheimer’s disease ↓ NREM slow waves, impaired memory consolidation

10. Sleep Disorders Based on EEG Findings

Disorder EEG Findings
Narcolepsy Shortened REM latency (<15 min)
Insomnia Increased beta activity (hyperarousal)
Sleep apnea Fragmented sleep, microarousals
REM behavior disorder Loss of REM atonia
Restless Leg Syndrome Periodic limb movements during NREM
11. Mnemonics for Sleep Stages
"BATS Drink Blood" (EEG waves "SANDMAN" (Sleep Regulators)
across sleep stages) • Serotonin – Sleep initiation
• Beta (Wake) • Adenosine – Homeostatic sleep pressure
• Alpha (Relaxed wakefulness) • Norepinephrine – Wake-promoting
• Theta (Stage 1) • Dopamine – Arousal
• Sleep spindles & K-complexes • Melatonin – Circadian rhythm
(Stage 2) • Acetylcholine – REM regulation
• Delta (Stage 3) • Nitric oxide – Sleep modulation
• Beta (REM)

Key viva points

• NREM and REM have distinct EEG, EOG, EMG characteristics.
• Circadian rhythm and homeostasis drive sleep regulation.
• Sleep disturbances are linked to psychiatric and neurological disorders.
• EEG helps differentiate sleep disorders (insomnia, narcolepsy, sleep apnea, RBD).
• Understanding sleep neurophysiology aids in psychiatric diagnosis and treatment.

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2021-09: Eric Kandel and his contributions.

Eric Kandel

Nobel Prize

Eric Kandel is a Nobel Prize-winning neuroscientist whose research on memory formation, synaptic plasticity,
and molecular mechanisms of learning revolutionized our understanding of the human brain. He was awarded
the 2000 Nobel Prize in Physiology or Medicine for his discoveries on signal transmission in the nervous

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system.
His work established a biological basis for learning and memory, linking molecular changes at the
synapse to short-term and long-term memory formation. His discoveries have profound implications
for psychiatric disorders such as schizophrenia, depression, and PTSD.

1. Key Contributions
A. Synaptic Plasticity and Memory Storage
• Kandel demonstrated that long-term memory formation requires changes in synaptic strength, a concept
derived from Hebbian learning theory.
• Using Aplysia californica (a sea slug with large neurons), he identified two forms of synaptic plasticity:
• Short-term memory: Involves transient changes in neurotransmitter release.
• Long-term memory: Requires gene expression and structural changes in synapses.

Discovery of Synaptic Plasticity and Memory Formation

Kandel demonstrated that memory formation is dependent on changes in synaptic strength, particularly long-
term potentiation (LTP) and long-term depression (LTD).
• Short-term memory is mediated by temporary changes in neurotransmitter release.
• Long-term memory involves gene expression and protein synthesis, leading to structural changes in
synaptic connections.
• This work linked molecular neuroscience to cognitive functions, shifting psychiatry toward a biological
model of mental disorders.
Implications: His findings helped develop treatments targeting synaptic dysfunction in Alzheimer’s disease,
PTSD, and mood disorders.

B. Role of cAMP and Protein Kinases in Memory

• He discovered that cyclic adenosine monophosphate (cAMP) and protein kinase A (PKA) mediate synaptic
strengthening during memory formation.
• CREB (cAMP Response Element-Binding Protein) activation leads to gene transcription necessary for
synaptic growth and long-term memory storage.
 •
Molecular Basis of Memory Consolidation
Kandel identified the CREB (cAMP response element-binding protein) as a critical molecule for long-term
memory storage.
• CREB triggers gene expression that leads to synaptic growth.
• Blocking CREB function impairs long-term memory while short-term recall remains intact.
Clinical Relevance:
• CREB modulation is now being explored for treating PTSD, major depressive disorder (MDD), and addiction.
• Antidepressants and cognitive therapy may work by strengthening synaptic connections via CREB-
related pathways.

C. Molecular Basis of Psychiatric Disorders

• Kandel’s findings suggested that psychiatric disorders, such as schizophrenia and depression, involve
dysregulation of synaptic plasticity.
• His work inspired research into neuroplasticity-based treatments, including antidepressants and cognitive-
behavioral therapy (CBT).
•
Influence on Modern Psychiatry
A. Shift from Psychoanalysis to Biological Psychiatry
Kandel initially trained in psychoanalysis under the influence of Freudian theories. However, he abandoned
psychoanalysis in favor of biological psychiatry, emphasizing that:
• Mental disorders have neurobiological underpinnings, rather than being purely psychological.
• Schizophrenia, depression, and anxiety involve molecular and synaptic changes in the brain.
Impact: His work paved the way for modern neurobiological approaches to psychiatric disorders, leading
to drug development targeting neurotransmitters and synaptic plasticity.

B. Contributions to Schizophrenia Research

• Kandel’s findings on synaptic dysfunction and neuronal circuits influenced the dopamine and glutamate
hypotheses of schizophrenia.

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• He suggested that defective synaptic plasticity in the prefrontal cortex contributes to cognitive
impairments in schizophrenia.
• His research supports NMDA receptor modulation as a treatment strategy for schizophrenia.
Impact: New drug developments, such as glutamatergic modulators (e.g., Memantine, Ketamine derivatives),
are based on his work.

D. Studies on the Sea Slug (Aplysia Californica)

Kandel used the sea slug (Aplysia) to study neuronal circuits involved in learning.
• Aplysia has large, identifiable neurons, making it ideal for studying synaptic plasticity.
• His research demonstrated that learning and memory depend on neurotransmitter modulation at synapses.
• The habituation and sensitization reflexes of Aplysia served as a model for human memory processes.
Impact on Psychiatry:
• His research provided a neurobiological explanation for habit formation, learning deficits, and compulsive
behaviors seen in OCD and addiction.
It also laid the foundation for understanding synaptic plasticity in neurodevelopmental disorders like
 • It also laid the foundation for understanding synaptic plasticity in neurodevelopmental disorders like
schizophrenia.

2. Impact on Psychiatry and Neuroscience

Field Impact
Cognitive Neuroscience Established the cellular basis of learning and memory.
Molecular Psychiatry Explained synaptic dysfunction in psychiatric disorders.
Neuropharmacology Provided a framework for drug development targeting synaptic plasticity.
Cognitive Therapy Reinforced the idea that psychotherapy induces neuroplastic cha

3. Honors and Recognition

Award Year Significance
Nobel Prize in Physiology or Medicine 2000 For his discoveries on signal transmission in the
nervous system.
Grand Decoration of Honour in Gold with Star (Austria) 2023 Awarded by Austrian President Alexander Van
der Bellen.
Goldene Rathausmann (City of Vienna) 2023 Recognition of his contributions to science and
neurobiology.
Grand Decoration of Honour with Sash (Vienna 2023 Recognition for advancing medical neuroscience.
Medical Association)
Honorary Doctorates (University of Vienna, Medical 1994, Recognition of his impact on neuroscience.
University of Vienna) 2018

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Despite his forced emigration from Austria due to antisemitic persecution in 1939, Kandel later played a role in
renaming the Universitätsring (formerly named after an antisemitic mayor, Karl Lueger).

Conclusion
Eric Kandel’s contributions revolutionized psychiatry by linking molecular biology with memory, learning, and
mental disorders. His work provided the foundation for neuroplasticity-based interventions in psychiatric
illnesses, making him a central figure in modern biological psychiatry.His legacy extends beyond research, as
he continues to shape neuropsychiatric treatment strategies through ongoing work at Columbia University’s
Zuckerman Institute.
2021-10: Fibromyalgia.

Fibromyalgia: Diagnosis and Management

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Areas of Widespread Fibromyalgia Pain

1. Definition and Epidemiology

Fibromyalgia (FM) is a chronic widespread pain syndrome characterized by central sensitization, fatigue,
cognitive dysfunction ("fibro fog"), sleep disturbances, and psychiatric comorbidities. It is the second most
common musculoskeletal disorder after osteoarthritis, with a global prevalence of 2.7%.

• Female-to-male ratio: 2:1, though sex differences have narrowed with updated diagnostic criteria.
• Peak age of onset: Middle-aged and older adults.
• High comorbidity with: Irritable bowel syndrome (IBS), chronic fatigue syndrome (CFS),
temporomandibular disorders, depression, and anxiety.

Etiology and Risk Factors

The exact cause of fibromyalgia remains unknown, but it is believed to be multifactorial.

Factor Proposed Mechanism

Genetic Familial clustering suggests a heritable component. Polymorphisms in genes regulating
Predisposition serotonin, dopamine, and catecholamines are implicated.
Central Sensitization Increased excitability of central pain-processing pathways in the spinal cord and brain.
Neurotransmitter Decreased serotonin and norepinephrine, increased substance P and glutamate.
Dysregulation
HPA Axis Dysfunction Altered cortisol response, contributing to stress-related symptom exacerbation.
Sleep Disturbance Non-restorative sleep worsens pain perception and cognitive dysfunction.
Psychosocial Stress History of trauma, childhood abuse, PTSD, and high stress are risk factors.
Fibromyalgia is NOT an inflammatory or autoimmune disease but shares symptoms with rheumatoid arthritis (RA) and lupus.

2. Pathophysiology
FM is a centralized pain disorder rather than a peripheral musculoskeletal disease.

A. Central Sensitization Hypothesis

• Increased spinal cord and cortical excitability leads to hyperalgesia (increased pain sensitivity) and
allodynia (pain in response to non-painful stimuli).
• Dysfunction in descending pain modulation pathways (reduced inhibition from the periaqueductal gray and
rostral ventromedial medulla) leads to sustained pain perception.

B. Neurotransmitter Imbalances

Neurotransmitter Alteration in FM Effect

Serotonin (5-HT) ↓ Decreased Poor pain inhibition, depression, fatigue
Dopamine (DA) ↓ Decreased Reduced motivation and reward response
Glutamate (Glu) ↑ Increased Heightened pain processing in cortical areas
Substance P ↑ Increased Enhances pain transmission at the spinal level
Cortisol (HPA Axis) Dysregulated Chronic stress response, worsening pain perception

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C. Fear-Avoidance and Maladaptive Cognitions
• Patients develop pain-related fear, leading to physical inactivity, deconditioning, and further pain amplification.
• Catastrophizing and hypervigilance worsen functional disability.

3. Diagnosis

A. Clinical Criteria
The American College of Rheumatology (ACR) 2016 criteria revised the 1990 tender point criteria, shifting to a
symptom-based approach.

B. ACR 2016 Criteria for FM Diagnosis

B. ACR 2016 Criteria for FM Diagnosis
A diagnosis of FM requires:
1. Widespread Pain Index (WPI) ≥7 and Symptom Severity (SS) Scale Score ≥5 OR WPI 4-6 and SS ≥9.
2. Symptoms persisting for ≥3 months.
3. No other condition explaining the pain.

C. Key Clinical Features

A. Core Symptoms
○ Widespread Pain → Present bilaterally and above & below the waist, persisting >3 months.
○ Fatigue → Often severe, unrelated to exertion, and unrelieved by rest.
○ Sleep Disturbances → Non-restorative sleep, frequent awakenings.
○ Cognitive Dysfunction ("Fibro Fog") → Impaired attention, memory, and verbal fluency.
B. Associated Symptoms
○ Headaches/Migraines
○ Irritable Bowel Syndrome (IBS) → Abdominal pain, bloating, constipation/diarrhea.
○ Depression & Anxiety → Present in >50% of cases.
○ Paresthesias → Numbness/tingling sensations.

Tender Points vs. Widespread Pain Index (WPI): The previous tender point criteria (1990 ACR) has
been replaced by the 2010 ACR criteria, which uses the WPI and Symptom Severity Scale (SSS).

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4. Management
A. Non-Pharmacological Approaches (First-Line Treatment)
1. Patient Education
• Reassure patients that FM is real and treatable (not psychosomatic).
• Explain the role of central sensitization and neuroplasticity in pain processing.

2. Exercise Therapy
• Aerobic exercise (e.g., walking, swimming): Reduces pain, improves function.
• Resistance training: Increases muscle strength and pain tolerance.
• Aquatic therapy: Beneficial for patients with severe pain.

3. Cognitive-Behavioral Therapy (CBT)

• Reduces pain catastrophizing, fear-avoidance behaviors.
• Effective in addressing comorbid depression and anxiety.

B. Pharmacological Treatment
Pharmacotherapy is reserved for moderate-to-severe FM or those unresponsive to non-drug therapies.
Drug Class Example Mechanism Effectiveness
Serotonin-Norepinephrine Duloxetine (FDA), Enhances 5-HT/NE-mediated First-line for pain and
Reuptake Inhibitors (SNRIs) Milnacipran pain inhibition mood
Tricyclic Antidepressants Amitriptyline Increases 5-HT, NE, and blocks Effective for pain,
(TCAs) histamine receptors sleep, mood
Gabapentinoids Pregabalin, Modulates Ca²⁺ channels, Reduces neuropathic
Gabapentin reducing neuronal excitability pain, anxiety

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Muscle Relaxants Cyclobenzaprine Structurally similar to TCAs, Improves sleep, mild
promotes sleep pain relief

• Opioids are not recommended due to lack of efficacy and risk of dependence.

C. Stepped-Care Approach (EULAR Guidelines 2017)

1. Step 1: Patient Education & Exercise Therapy
2. Step 2: CBT, Mindfulness-Based Stress Reduction
3. Step 3: Pharmacotherapy (Duloxetine, Amitriptyline, Pregabalin)
 3. Step 3: Pharmacotherapy (Duloxetine, Amitriptyline, Pregabalin)
4. Step 4: Multimodal Rehabilitation (when severe functional impairment is present).

EULAR revised recommendations

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5. Prognosis and Long-Term Outlook
• FM is a chronic condition, but symptoms can be managed effectively with a multimodal approach.
• Poor prognosis factors: High pain severity, significant psychiatric comorbidity, high opioid use, and lack of
physical activity.
• Better outcomes with: Early diagnosis, structured patient education, and active patient engagement.

Conclusion
Fibromyalgia is a chronic centralized pain disorder with a complex interplay of neurobiological, psychological, and
social factors. Diagnosis is clinical, based on widespread pain, fatigue, and cognitive dysfunction. Multimodal
management, emphasizing exercise, CBT, and SNRIs/TCAs, is the cornerstone of treatment. Early intervention
improves long-term outcomes.
(FFIBRO Mnemonic)

Symptom Description
Fatigue
Fog
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Persistent exhaustion
Cognitive dysfunction (memory, concentration)
Insomnia Sleep disturbances
Blues Depression, anxiety
Rigidity Muscle and joint stiffness
Ow! Chronic, widespread pain
2022-01: Describe the theories of formation of delusions.

Theories of Formation of Delusions

The term "delusion" originates from Latin deludere, meaning to mock, cheat, or deceive. Other linguistic roots include:
• German "Wahn" – signifying false opinion or whim.
• French "délire" – metaphorically meaning "ploughshare jumping out of the furrow", implying disconnection from reality.

Theory Category Theory Name Key Hypothesis Supporting Evidence

Theory Category Theory Name Key Hypothesis Supporting Evidence
Neurobiological Dopaminergic Excess dopamine in the mesolimbic PET studies show increased
Dysregulation pathway leads to aberrant salience, dopamine release in psychosis;
Hypothesis causing random stimuli to appear antipsychotics reduce delusions.
significant.
Neurobiological Glutamatergic Hypofunction of NMDA glutamate Ketamine (NMDA antagonist)
Dysfunction receptors impairs cognitive processing, induces transient delusions in
Hypothesis resulting in delusions. healthy subjects.
Neurobiological Neuroimaging Structural and functional abnormalities Right hemisphere dysfunction is
Findings in in the prefrontal cortex, amygdala, and linked to misidentification delusions
Delusions hippocampus contribute to delusions. (e.g., Capgras syndrome).
Cognitive Jump-to- Patients with delusions form Garety et al. (1991) found that 41%
Conclusions Bias conclusions with minimal evidence, of deluded patients made quick

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(JTC) reinforcing false beliefs. conclusions vs. 4% of controls.
Cognitive Attributional Bias Paranoid delusions arise when Kaney & Bentall (1992)
Model patients externalize blame; grandiose demonstrated external attributions
delusions compensate for low self- in persecutory delusions.
esteem.
Cognitive Predictive Coding Brain's predictive errors prevent Delusional individuals fail to modify
Model updating of false beliefs, making beliefs despite contradictory
delusions persist. evidence.
Cognitive Two-Factor Theory Delusions require two cognitive Two-factor model explains Capgras
(Coltheart, 2007) impairments: an abnormal sensory syndrome, where loss of emotional
experience and a failure to evaluate familiarity leads to misidentification.
beliefs rationally.
Cognitive Bayesian Inference Delusions arise from errors in Studies show deluded individuals
Model Bayesian belief updating, where prior rely excessively on prior beliefs
beliefs override contradictory evidence. instead of adapting to new
evidence.
Psychodynamic Freud`s Theory Delusions are ego-defense Psychodynamic literature describes
Delusions as mechanisms (e.g., projection of inner projection and denial in paranoid
Defense fears onto external threats). and grandiose delusions.
Mechanisms
Psychodynamic Kretschmer Delusions arise in emotionally Observed patterns in individuals
Personality Model sensitive individuals as a reaction to with high sensitivity and social
stress and social withdrawal. withdrawal.
Phenomenological Jaspers Primary Primary delusions occur Jaspers work forms the foundation
Delusion Theory spontaneously, altering subjective of modern phenomenological
experience. psychiatry.
Phenomenological Conrad`s Five-Stage Delusion formation progresses through Case studies confirm the stepwise
Model of Delusion five stages: Trema → Apophany → progression of delusional
Formation Anastrophy → Consolidation → development.
Residuum.
Phenomenological Maher`s Anomalous Delusions result from abnormal Patients with hallucinations often
Experience sensory perceptions, and the mind develop secondary delusions as an
Hypothesis forms false beliefs to explain them. explanatory mechanism.
Social & Social Isolation and Prolonged isolation and trauma Studies show higher delusion rates
Environmental Stress Model increase vulnerability to delusions. in individuals with prolonged
isolation and adverse childhood
events.
Social & Cultural & Cultural background influences Technological delusions are more
Environmental Environmental delusional content; shared delusions common in modern societies;
Factors in Delusion (folie à deux) occur in emotionally cultural narratives shape delusional
Formation close individuals. themes.

A delusion is a belief that is firmly held on inadequate grounds, that is not affected by rational argument or
evidence to the contrary, and that is not a conventional belief that the person might be expected to hold given
their educational, cultural, and religious background.
Historically, delusions have been considered the hallmark of madness. Jaspers (1973) emphasized that delusion is not merely a
false belief held with conviction but a basic psychopathological phenomenon embedded in subjective experience .

1. Neurobiological Theories
A. Dopaminergic Dysregulation Hypothesis
• Excessive dopamine transmission in the mesolimbic pathway is implicated in delusion formation, particularly in
schizophrenia.
• Hyperactivity of D2 receptors in the striatum and nucleus accumbens results in aberrant salience
attribution, leading to random stimuli being misinterpreted as significant.
• Kapur’s Aberrant Salience Hypothesis (2003):suggests that excessive dopamine release leads to excessive
salience being attached to stimuli, thereby contributing to the development of delusions.
• This explains persecutory, referential, and grandiose delusions.

• Evidence:
○ PET scans show increased dopamine release in psychotic patients.
○ Antipsychotics (dopamine antagonists) reduce delusions by blocking D2 receptors.
• This hypothesis is supported by the efficacy of dopamine antagonists (antipsychotics) in reducing delusions.

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B. Glutamatergic Dysfunction
• The NMDA receptor hypofunction model suggests that low glutamate activity impairs cognitive flexibility,
leading to delusions.
• Low NMDA receptor function in the prefrontal cortex and hippocampus disrupts reality testing.
• Evidence:
• Ketamine (an NMDA antagonist) induces transient delusions in healthy individuals.

C. Neuroimaging Findings
• Prefrontal Cortex (PFC): Impairment is associated with defective reality testing and reasoning in delusions.
• Amygdala: Overactivation is linked to threat perception, contributing to persecutory delusions.
• Hippocampus: Dysfunction leads to deficits in memory and contextual processing, affecting delusional
content.
• Right Hemisphere Dysfunction: Damage to the right hemisphere, particularly in cases of stroke or
neurodegenerative disorders, has been associated with Capgras syndrome and other delusions of
misidentification.

Brain Region Role in Delusions

Prefrontal Cortex (PFC) Impaired reality testing and reasoning.
Amygdala Overactive threat perception (persecutory delusions).
Hippocampus Dysfunction in memory and contextual processing

2. Cognitive and Reasoning Theories

A. Jump-to-Conclusions Bias (Probabilistic Reasoning Deficit)
• Patients with delusions tend to make decisions based on limited evidence.
• Garety et al. (1991) demonstrated that 41% of deluded patients reached conclusions with minimal evidence,
compared to 4% of controls.
• This reasoning bias contributes to misinterpretation of ambiguous stimuli as confirming delusional beliefs.
• Example: A patient with persecutory delusions interprets one glance from a stranger as proof of
surveillance.

B. Attributional Bias Model (Defensive Function of Delusions)

Kaney and Bentall (1989, 1992) found that patients with persecutory delusions attribute negative events to
 • Kaney and Bentall (1989, 1992) found that patients with persecutory delusions attribute negative events to
external causes and positive events to internal causes.
• This suggests that delusions serve as a defense against low self-esteem by externalizing blame.
• Grandiose delusions may arise as a defense against low self-esteem
• Example: A failing student develops a belief that professors are deliberately conspiring against them
instead of acknowledging personal shortcomings.

C. Predictive Coding Model (Frith, 1992)

• The brain predicts reality and updates beliefs based on new evidence.
• In delusions, prediction errors fail to correct false beliefs, causing persistence of delusional thinking.

Example:
○ A paranoid patient believes a neighbor is spying on them.
○ Despite evidence to the contrary, their brain fails to revise this belief, leading to delusional certainty.

3. Psychodynamic Theories
A. Freud’s Theory (1907) – Delusions arise from ego-defense mechanisms.

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• Freud proposed that delusions result from unconscious conflicts, with mechanisms including:
• Denial – rejecting reality to protect the ego.
• Projection – attributing unacceptable internal thoughts to an external source (e.g., persecutory delusions).
Example: A patient with homosexual impulses develops a persecutory delusion that others are plotting
against them.

B. Kretschmer’s Personality Model (1927)

• Delusions arise in sensitive, emotionally inhibited individuals who struggle with emotional expression.
• A key life event acts as a trigger, leading to the development of ideas of reference that evolve into delusions.
Kretschmer’s "Sensitive Delusion of Reference" (1927):
○ Personality traits + repeated stressors → Suspiciousness → Delusions.
Social Isolation and Trauma:
○ Early life adversity and isolation increase vulnerability to delusions.
c. Self-Esteem Hypothesis
• Delusions serve as a compensatory mechanism for low self-esteem.
• Grandiose delusions may emerge in response to feelings of inferiority.

4. Phenomenological Models
A. Jaspers’ Primary Delusion Theory (1913)
• Jaspers (1997) suggested that delusions arise de novo, not understandable in psychological terms.
• Jaspers described delusions as "un-understandable" phenomena arising from a fundamental transformation
of reality.
• He described delusional atmosphere, where reality feels altered before a delusion emerges.
• He emphasized the "delusional atmosphere," a vague feeling of significance that precedes delusion
formation.
• Karl Jaspers distinguished between primary delusions, which arise de novo without any understandable cause,
and secondary delusions, which develop as a consequence of other psychopathological experiences, such as
hallucinations or mood disturbances.
○ Primary delusions include:
○ Delusional intuition (autocthonous delusion) – a fully formed, sudden belief arising in the patient’s
mind.
○ Delusional perception – a normal perception is assigned a delusional meaning.
○ Delusional atmosphere (delusional mood) – a sense of change in the world without clear
articulation of the delusion.
 articulation of the delusion.
○ Secondary delusions arise in response to abnormal emotions or perceptions and can often be explained
in context.

B. Conrad’s Five-Stage Model of Delusion Formation

Conrad (1958) described five progressive stages of delusion formation:
1. Trema – A vague sense of unease and strangeness. → "Something feels off... I feel watched."
2. Apophany – Sudden insight into a new (delusional) meaning. → "The news anchor just blinked twice—it’s a
signal meant for me!"
3. Anastrophy – Intensification of delusional thought. → "Everything happening around me is part of a secret
conspiracy."
4. Consolidation – Establishment of the delusional system. → "I am being tracked 24/7 by an intelligence agency!"
5. Residuum – Chronic stabilization or withdrawal into an autistic-like state. → "Even after being hospitalized, I still
KNOW the agency is after me."

Stage Description Theoretical Basis

1. Trema (Premonitory Stage) A vague, distressing feeling that something Jaspers' Delusional Atmosphere
is wrong, but no specific delusion is formed (Altered subjective experience)
yet.
2. Apophany (Insight Stage) The patient suddenly "realizes" a hidden Aberrant Salience Hypothesis
meaning behind ordinary events, leading to (Excess dopamine causes random
delusional insight. stimuli to seem meaningful)
3. Anastrophy (Delusion The delusional idea becomes central to the Predictive Coding Model (Brain fails
Intensification) person’s thinking, gaining explanatory to update incorrect beliefs)
power.
4. Consolidation (Fixed The delusion becomes rigid, and alternative Jump-to-Conclusions Bias (Rapid
Delusional Belief) explanations are rejected. decision-making without enough
evidence)
5. Residuum (Chronic Phase) Either stabilization or withdrawal into Two-Factor Model (Cognitive

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psychotic thinking, where delusions persist impairment prevents belief revision)
despite external reality.

5. Social and Environmental Influences

these theories emphasize external influences in delusion formation.

a. Social Isolation and Stress

○ Prolonged isolation, trauma, and high expressed emotion (EE) within families increase vulnerability to
delusions.
b. Cultural and Environmental Influences
○ The content of delusions varies across cultures (e.g., technological delusions involving the internet are
more common today than in the past).
○ In folie à deux, delusions are shared between individuals, often due to close emotional ties.

Combined model -Stages of Delusion Formation

The process of delusion formation progresses through multiple phases, integrating biological, cognitive, and
phenomenological changes. The staged model of delusion formation describes how a combination of
predisposing and precipitating factors leads to delusional elaboration.

1.Phases of Delusion Formation

Phase Stage Description Theoretical Model Association
I. Pre-Psychotic trema 1. Predisposing Underlying vulnerabilities such as genetics, Dopaminergic Dysregulation,
Factors personality traits, or neurobiological Kretschmer’s Personality Model
abnormalities.
2. Precipitating Environmental stressors, trauma, or Social Isolation & Stress Model,
Factors neurocognitive disruptions trigger the onset. Cultural Influences
II. Acute Apophany + 3. Prodrome State Presence of delusional mood and anomalous Jaspers’ Delusional Atmosphere,
Anastrophy experiences where reality feels altered. Conrad’s Trema Stage
4. Attribution of Attempts to assign meaning to anomalous Maher’s Anomalous Experience
Meaning experiences, leading to simple delusions. Hypothesis, Predictive Coding
Model
III. Elaboration Consolidation + 5. Construction of The delusion solidifies into a structured Jump-to-Conclusions Bias, Two-
Residuum Delusional Systems system, making reality testing difficult. Factor Theory

A. Pre-Psychotic Phase (Vulnerability Stage)

• Predisposing Factors:
• Genetic risk (family history of psychosis).
• Neurochemical imbalances (dopamine dysregulation, NMDA receptor hypofunction).
• Personality traits (sensitive, paranoid, or schizotypal tendencies).

• Precipitating Factors:

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• Stressors like trauma, isolation, or substance abuse trigger delusional processes.
• Dopamine surges due to stress lead to increased salience of neutral stimuli , setting the stage for delusion
formation.

Theories Involved: Kretschmer’s Model, Social Isolation Model, Dopaminergic Dysregulation Hypothesis.

B. Acute Phase (Emergence of Delusional Thought)

1. Prodrome State: Delusional Mood & Anomalous Experience
• Feeling of being watched without clear evidence.
• Sensory distortions (auditory hallucinations, altered perception).
• The patient experiences a vague sense that reality has changed, but cannot articulate why.
• Examples:
• Jaspers described this as "Delusional Atmosphere", where reality feels uncertain before the delusion
crystallizes.

1. Attribution of Meaning to Experience (Formation of Simple Delusions)

• "I feel different; maybe I am being controlled."
• "This strange feeling must mean I have a special purpose."
• The brain attempts to rationalize abnormal experiences, forming initial delusions.
• Examples:
• Jump-to-Conclusions Bias and Predictive Coding Errors cause the belief to persist despite contrary
evidence.

Theories Involved: Jaspers’ Primary Delusion Theory, Maher’s Anomalous Experience Hypothesis, Predictive Coding
Model.

C. Elaboration Phase (Solidification of the Delusional System)

• The simple delusion expands into a fully developed belief system that integrates multiple false
interpretations.
• Examples:
• A persecutory delusion ("They are watching me") evolves into an elaborate conspiracy ("The government
is tracking my every move").
A Capgras delusion ("My spouse has been replaced") expands to include multiple people .
 • A Capgras delusion ("My spouse has been replaced") expands to include multiple people .
• The patient rejects contradicting evidence, reinforcing delusional certainty.

Theories Involved: Two-Factor Theory, Jump-to-Conclusions Bias, Bayesian Inference Model.

Integration with Theoretical Models

Delusion Formation Model Corresponding Stage in the Delusion Formation Process
Dopamine Dysregulation Hypothesis Predisposing Phase (Hyperdopaminergic state leads to aberrant
salience)
Glutamate Dysfunction Model Precipitating Phase (NMDA receptor hypofunction reduces cognitive
flexibility)
Jaspers’ Phenomenological Theory Prodrome Phase (Delusional mood emerges before concrete belief)
Maher’s Anomalous Experience Attribution Phase (Delusions arise as explanations for abnormal
Hypothesis perceptions)
Jump-to-Conclusions Bias Elaboration Phase (Rapid belief formation with minimal evidence)
Predictive Coding Model Elaboration Phase (Failure to update beliefs based on new evidence)

Clinical Relevance & Treatment Approaches

Understanding the phased progression of delusions helps in early intervention and targeted therapy.
.
Delusion Stage Treatment Approach
Prodrome (Pre-Psychotic Cognitive Behavioral Therapy (CBT-P) to challenge emerging distorted beliefs.
Phase)
Simple Delusions (Acute Low-dose Antipsychotics (Risperidone, Aripiprazole) to reduce dopamine-driven

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Phase) salience.
Elaborate Delusional Systems Long-term Therapy + Antipsychotics to modify belief structures and prevent
reinforcement.

Early intervention at the prodrome stage can prevent delusions from crystallizing into rigid false beliefs .

Sum-up
Delusions likely emerge from multiple interacting factors—neurobiological vulnerabilities, cognitive biases,
psychodynamic defenses, and environmental influences. Each theory provides insight into different aspects of
delusion formation, emphasizing that delusions are not a unitary phenomenon but a diverse set of abnormal
beliefs.Conrad’s model explains why delusions develop in stages.Early intervention at the Trema or Apophany
stage (CBT, stress reduction, antipsychotics) can prevent full delusional formation.
© jPsychiatrie
2022-02: Evaluation and management of Somatization
Disorder.

Evaluation and Management of Somatization Disorder

Somatization disorder, classified in ICD-10 as F45.0 (Somatization Disorder) and in DSM-5 under Somatic
Symptom Disorder (SSD), is characterized by multiple, recurrent, and clinically significant somatic complaints that are
not fully explained by medical conditions and persist for several years.

1. Evaluation of Somatization Disorder

A. Clinical Features (ICD-10 F45.0 & DSM-5 SSD)

• Multiple somatic symptoms affecting different organ systems (e.g., gastrointestinal, neurological,
cardiopulmonary).
• Symptoms are persistent (≥2 years in ICD-10) and cause significant distress or impairment.
• Preoccupation with symptoms despite negative investigations.
• High healthcare utilization (frequent medical visits, unnecessary tests, doctor-shopping).
• Psychological distress (anxiety, depression).

B. Differential Diagnosis
• General Medical Conditions (e.g., autoimmune diseases, endocrine disorders).
• Other Psychiatric Disorders:
• Illness Anxiety Disorder (excessive worry about having a serious illness, with minimal symptoms).
• Conversion Disorder (neurological symptoms without organic basis).
• Factitious Disorder (intentional symptom fabrication).

C. Diagnostic Criteria (ICD-10 vs DSM-5)

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1. ICD-10: Somatization Disorder (F45.0)
"Multiple, recurrent, and frequently changing physical symptoms present for at least two years. Most patients
have a long history of medical consultations, negative investigations, or unsuccessful exploratory operations.
Symptoms may involve any body system. The disorder has a chronic and fluctuating course, often with social and
interpersonal disruptions."
Diagnostic Criteria (ICD-10)
• ≥2 years of persistent symptoms involving multiple organ systems.
• Multiple medical consultations, negative findings, or unnecessary procedures.
• Significant distress or functional impairment.
• No evidence of malingering or factitious disorder.

DSM-5: Somatic Symptom Disorder (SSD)

"One or more somatic symptoms that are distressing or result in significant disruption of daily life, with excessive
thoughts, feelings, or behaviors related to symptoms. Symptoms persist for more than six months."
Diagnostic Criteria (DSM-5)
• ≥1 distressing somatic symptom disrupting daily life.
• Excessive thoughts/behaviors about symptoms, evidenced by at least one:
○ Persistent, disproportionate thoughts about symptom severity.
○ High health-related anxiety.
○ Excessive time/energy devoted to symptoms.
• Persistent course ≥6 months, even if symptoms fluctuate.

ICD-11: Bodily Distress Disorder (BDD)

"Characterized by bodily symptoms that are distressing and lead to excessive attention toward them, including
repeated health care visits. The level of distress is disproportionate to the medical findings. The symptoms are not
feigned or intentionally produced. The pattern must persist for at least several months."
Diagnostic Criteria (ICD-11)
• Physical symptoms with excessive distress/attention.
• Disproportionate health-seeking behaviors.
• Symptoms persist for at least several months.
• Not explained by another mental disorder.

D. Investigations
• Basic workup: CBC, ESR, thyroid function tests, metabolic panel (to exclude medical illness).
• Neuroimaging/EKG: If neurological or cardiac symptoms are prominent.
Psychiatric assessment: Depression and anxiety screening (PHQ-9, GAD-7).
 • Psychiatric assessment: Depression and anxiety screening (PHQ-9, GAD-7).

2. Management of Somatization Disorder

Clinical Assessment:
1. History Taking
• Detailed symptom history: Multiple, recurrent, and medically unexplained symptoms.
• Onset and course: Chronic (>6 months), often beginning in early adulthood.
• Psychiatric history: Co-occurring anxiety, depression, or trauma.
• Medical history: Rule out organic causes through appropriate investigations.

2. Physical Examination
• Complete systemic examination to exclude medical conditions.

3. Psychiatric Evaluation
• Assess emotional distress, cognitive patterns, and behavioral response to illness.
• Screen for psychiatric comorbidities (e.g., depression, anxiety, personality disorders).

4. Psychometric Tools
• PHQ-15 (Patient Health Questionnaire-15): Screens for somatic symptoms.
• Somatic Symptom Scale-8 (SSS-8): Measures symptom burden.
• Hamilton Anxiety and Depression Scale (HADS): Evaluates coexisting affective symptoms.

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3. Management Approach
A. Non-Pharmacological Management (First-line)
1. Psychoeducation:
• Explain the mind-body connection and reassure patients about the absence of serious illness.
• Encourage self-management strategies to reduce focus on symptoms.

1. Cognitive Behavioral Therapy (CBT):

• Gold standard treatment for SSD.
• Targets maladaptive illness beliefs, reduces symptom amplification, and improves coping mechanisms.

1. Mindfulness-Based Therapy (MBT) & Relaxation Techniques:

• Useful for patients with high health anxiety.

1. Regular Follow-ups (Scheduled Appointments)

• Avoid excessive medical investigations.
• Shift focus from symptom relief to functionality improvement.

B. Pharmacological Management (Adjunctive Therapy)

1. SSRIs (Selective Serotonin Reuptake Inhibitors)
First-line pharmacotherapy (especially if comorbid depression or anxiety is present).
 • First-line pharmacotherapy (especially if comorbid depression or anxiety is present).
• Examples: Fluoxetine 20–40 mg/day, Sertraline 50–100 mg/day.

1. SNRIs (Serotonin-Norepinephrine Reuptake Inhibitors)

• Used for pain-predominant symptoms.
• Examples: Duloxetine 30–60 mg/day, Venlafaxine 75–150 mg/day.

1. TCAs (Tricyclic Antidepressants)

• Low-dose Amitriptyline (10–25 mg at night) for neuropathic pain and sleep disturbances.

1. Buspirone (5-HT1A Partial Agonist)

• May be considered for somatic anxiety symptoms (10–20 mg/day).

1. Avoid Benzodiazepines
• Due to risk of dependence and worsening of health anxiety.

4. Prognosis and Course

• Chronic but manageable with structured treatment.
• Good prognosis with early intervention and long-term therapeutic alliance.
• Poor prognosis in patients with multiple physician visits, excessive medical procedures, and persistent
sick role behaviors.

tips
Practical Approach for MD Psychiatry Exam
• Evaluation must emphasize:
○ Rule-out medical causes (minimal investigations).
○ Use of structured assessments (PHQ-15, SSS-8).
○ Consideration of comorbid psychiatric disorders.

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• Management should prioritize:
○ CBT as first-line therapy.
○ SSRIs/SNRIs for comorbid affective symptoms.
○ Avoidance of unnecessary medical interventions.

(CPG, Maudsley, AIIMS, psychiatric guidelines.)

2022-05: Clinical presentation and management of
Dysthymia.

Dysthymia
Dysthymia, also known as Persistent Depressive Disorder (PDD), is a chronic
depressive condition characterized by milder but long-lasting depressive symptoms. It
differs from major depressive disorder (MDD) in its duration and persistence.

ICD-10 and DSM-5 Criteria

• In ICD-10, dysthymia (F34.1) is described as chronic depression of mood, lasting at

least two years, but not severe enough to meet criteria for MDD.

• In DSM-5, Persistent Depressive Disorder (PDD) requires a depressed mood for

most of the day, more days than not, for at least two years, along with at least two
additional symptoms (e.g., poor appetite, low energy, low self-esteem).

Common Symptoms

Core Symptoms (Present for ≥2 years in adults, ≥1 year in children)

• Chronic low mood (sad, hopeless, pessimistic outlook).
• Fatigue or low energy (persistent exhaustion).
• Low self-esteem (feelings of inadequacy, guilt).
• Poor concentration and decision-making difficulties.
• Appetite changes (increased or decreased).
• Sleep disturbances (hypersomnia or insomnia).

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• Social withdrawal and reduced interest in activities.
• Feelings of worthlessness and helplessness.

Dysthymia VS MDD
Feature Dysthymia (PDD) Major Depressive Disorder (MDD)
Duration ≥2 years (adults), ≥1 year ≥2 weeks
(children)
Severity Mild to moderate Moderate to severe
Course Chronic, persistent symptoms Episodic, with full recovery between
episodes
Suicide Risk Lower than MDD but still High, especially in severe cases
significant
Psychotic Absent May be present
Features

Double Depression: When a person with dysthymia develops a major

depressive episode.

Course of Dysthymia
• Early Onset (Before 21 Years): More common, associated with higher rates of
comorbid personality disorders and substance use.
• Late Onset (After 21 Years): May develop after a major depressive episode or
significant life stress.
• Chronicity: Symptoms persist for many years, though 50% of patients show clinical
recovery over a 5-year follow-up.

• Progression to Major Depressive Disorder (Double Depression):

○ 20% of dysthymic patients develop MDD.
○ 15% progress to Bipolar II Disorder.
 ○ 15% progress to Bipolar II Disorder.
• Relapse and Remission:
○ Only 10-15% achieve remission within one year of diagnosis.
○ 25% never attain full recovery.

Risk Factors for Chronicity

• Family history of mood disorders.
• Early-onset depression.
• Poor social support.
• High levels of neuroticism and maladaptive coping styles.
• Childhood adversity, trauma, or neglect.

Management of Dysthymia
Treatment is multimodal, involving pharmacotherapy, psychotherapy, and lifestyle
modifications.

A. Psychotherapy (First-Line)

• Cognitive Behavioral Therapy (CBT):

○ Targets negative thought patterns and maladaptive behaviors.
○ Effective in reducing symptom severity and relapse rates.
• Interpersonal Therapy (IPT):
○ Addresses relationship conflicts and social dysfunction.
○ Helps in improving self-esteem and social support.
• Behavioral Activation Therapy:
○ Encourages engagement in pleasurable activities to break cycles of inactivity.

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• Mindfulness-Based Cognitive Therapy (MBCT):
○ Reduces rumination and worry.
○ Useful for relapse prevention.

B. Pharmacological Treatment (Moderate to Severe Cases)

Class Drug Starting Dose Target Dose
SSRIs (First-Line) Fluoxetine 10-20 mg/day 20-40 mg/day
Sertraline 25-50 mg/day 100-200 mg/day
Escitalopram 5-10 mg/day 10-20 mg/day
SNRIs (Second-Line, If SSRIs Fail) Venlafaxine 37.5 mg/day 75-225 mg/day
Duloxetine 30 mg/day 60-120 mg/day
Atypical Antidepressants Bupropion 150 mg/day 300-450 mg/day
Mirtazapine 15 mg/day 30-45 mg/day
• SSRIs are the first-line treatment due to better safety and tolerability.
• SNRIs (Venlafaxine, Duloxetine) are used if SSRIs are ineffective.
• Bupropion (NDRI) is useful for low energy and anhedonia.
• Mirtazapine is beneficial for insomnia and weight loss.

C. Augmentation Strategies (For Treatment-Resistant Cases)

Adjunctive Treatment Indication
Lithium Suicide prevention, refractory
dysthymia
Atypical Antipsychotics (Aripiprazole, Severe depression with comorbid
Quetiapine) anxiety
Psychostimulants (Methylphenidate, Modafinil) Low energy, cognitive dysfunction
Thyroid Hormone (T3 Liothyronine) Adjunct in SSRI-resistant cases
Relapse Prevention
Factor Impact on Outcome
Early treatment initiation Better long-term outcomes
Good medication adherence Reduced relapse rates
Continued psychotherapy Prevents recurrence
Strong social support Better functional recovery
• Relapse Prevention Strategies:
○ Maintain treatment for at least 12-24 months to prevent recurrence.
○ Psychoeducation for patients and families to improve adherence.
○ Regular follow-ups to monitor mood fluctuations.

Summary of Management Approach

Severity First-Line Second-Line Adjunctive
Therapy
Mild CBT, IPT, No medication needed None
Psychoeducation
Moderate CBT + SSRI (Fluoxetine, SNRI (Venlafaxine, None
Sertraline, Duloxetine)
Escitalopram)
Severe SSRI/SNRI + Augmentation with Lithium, Stimulants
Psychotherapy Atypical Antipsychotics (Modafinil) for
energy
Treatment- Combination of Augmentation with Thyroid Maintenance

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Resistant Antidepressants Hormone (T3), ECT (if therapy
suicidal)

Lifestyle and Psychosocial Interventions

• Exercise:
• Improves mood, energy, and sleep.
• Aerobic activity 3-5 times a week has antidepressant effects.
• Dietary Modifications:
• Omega-3 fatty acids and a Mediterranean diet may improve mood stability.
• Sleep Hygiene:
• Regular sleep schedule, avoiding caffeine/alcohol before bedtime.

6. Conclusion
• Dysthymia is a chronic, disabling disorder with a high risk of developing major
depression. Early intervention with antidepressants, psychotherapy, and lifestyle
changes improves long-term prognosis. Despite high relapse rates, 50% of
outpatients can achieve significant recovery over 5 years.

• Dysthymia (PDD) is a chronic, often underdiagnosed condition that requires long-

term treatment.
• Psychotherapy (CBT, IPT) is the first-line treatment, with SSRIs as the preferred
pharmacological option.
• Combination therapy (CBT + Antidepressants) provides the best outcomes in
moderate-severe cases.
• Regular follow-ups and psychoeducation are crucial to prevent relapse and
improve prognosis.

References
Clinical Practice Guidelines (CPG) for Depression and Dysthymia.
• Clinical Practice Guidelines (CPG) for Depression and Dysthymia.
• The Maudsley Prescribing Guidelines in Psychiatry (14th Edition).
• DSM-5 introduced dimensional specifiers (e.g., severity scales in depression).
• ICD-11 incorporates dimensional traits for personality disorders.

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2022-06: Early-onset Alcohol Dependence Syndrome.

Early-Onset Alcohol Dependence Syndrome

Early-onset Alcohol Dependence Syndrome refers to alcohol dependence developing before the age of 25,
characterized by rapid progression, severe withdrawal symptoms, and high genetic vulnerability. This subtype
has worse prognosis, higher rates of psychiatric comorbidity, and increased impulsivity and risk-taking
behaviors.

1. Diagnostic Classification

ICD-10: Alcohol Dependence Syndrome (F10.2)

ICD-10 defines Alcohol Dependence Syndrome as:

Diagnostic Criteria (ICD-10 F10.2)

At least three of the following must be present in the past 12 months:
1. Strong desire or compulsion to drink alcohol.

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2. Impaired control over alcohol consumption (onset, termination, or levels of use).
3. Physiological withdrawal symptoms when alcohol use is reduced or stopped.
4. Tolerance (increased amounts needed to achieve the same effect).
5. Neglect of alternative pleasures or interests due to alcohol use.
6. Persistent drinking despite knowledge of harmful consequences.

Early-Onset Alcohol Dependence is a severe subtype within this category, often associated with impulsivity, early
behavioral issues, and family history of alcoholism.

DSM-5: Alcohol Use Disorder (AUD)

DSM-5 replaced Alcohol Dependence with Alcohol Use Disorder (AUD), classified as mild, moderate, or severe
based on symptom count.

Diagnostic Criteria (DSM-5)

At least two or more of the following in 12 months:
1. Alcohol taken in larger amounts or over a longer period than intended.
2. Persistent desire or unsuccessful efforts to cut down or control alcohol use.
3. Significant time spent obtaining, using, or recovering from alcohol.
4. Craving or strong urge to drink alcohol.
5. Recurrent alcohol use leading to failure in obligations (work, school, home).
6. Continued alcohol use despite social or interpersonal problems.
7. Giving up or reducing important activities due to alcohol use.
8. Recurrent alcohol use in physically hazardous situations.
9. Continued alcohol use despite knowledge of physical/psychological problems caused by drinking.
10. Tolerance (increased alcohol amounts needed for the same effect).
11. Withdrawal symptoms (tremors, sweating, anxiety, seizures, hallucinations, etc.).

Severity Classification:
• Mild: 2–3 symptoms.
• Moderate: 4–5 symptoms.
• Severe: 6 or more symptoms.

Early-onset subtype is typically severe, with rapid progression and high impulsivity and risk-taking behavior.
Early-onset subtype is typically severe, with rapid progression and high impulsivity and risk-taking behavior.

Clinical Course of Early-Onset ADS:

• Rapid progression from social drinking to dependence.
• More severe withdrawal symptoms, often requiring medical intervention.
• Higher rates of poly-substance use (nicotine, cannabis, stimulants).
• Greater relapse risk compared to late-onset alcohol dependence.

ICD-11: Alcohol Dependence (6C40.2)

ICD-11 classifies Alcohol Dependence under Alcohol Use Disorders (6C40):

Key ICD-11 Features

• Impaired control over drinking (compulsive use, unsuccessful attempts to stop).
• Increased salience of alcohol use (priority over other activities and responsibilities).
• Physiological dependence (withdrawal, tolerance).
• Continued use despite harm (physical, psychological, social).
• Persistence for ≥12 months (or shorter if severe).

ICD-11 recognizes early-onset alcoholism as a distinct clinical subtype, with greater neurobiological
vulnerability, higher relapse risk, and poor psychosocial outcomes.

2. Characteristics of Early-Onset Alcohol Dependence

Feature Early-Onset Alcohol Dependence Late-Onset Alcohol Dependence
Age of Onset Before 25 years After 25–30 years
Gender Ratio More common in males More balanced
Genetic Vulnerability Strong family history of alcohol dependence Less genetic influence
Psychiatric High (e.g., ADHD, conduct disorder, ASPD, Lower rates of psychiatric
Comorbidity depression, bipolar disorder) comorbidities

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Impulsivity/Risk- High impulsivity, aggression, sensation-seeking Lower impulsivity
Taking
Progression of Rapid progression to severe dependence Gradual progression over years
Disease
Drinking Pattern Binge drinking, high daily intake More controlled consumption
Withdrawal Severity Severe withdrawal symptoms, early medical Milder withdrawal
complications
Response to Poor compliance, frequent relapse Better long-term outcomes
Treatment

Early-onset alcohol dependence is often linked to Type II alcoholism (Cloninger’s Model), which is:

• Highly heritable (strong genetic component).

• Associated with antisocial traits, impulsivity, and early behavioral issues.
• More resistant to treatment, with a higher risk of relapse.
2022-08: Dissociative Disorder—clinical presentation and
management.

Dissociative Disorders –

Dissociative disorders involve disruptions in consciousness, memory, identity, emotion, perception, and motor
control, often occurring in response to trauma or stress.

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The Five Core Components of Dissociative Disorders

1. Diagnostic Classification

ICD-10: Dissociative (Conversion) Disorders (F44)

ICD-10 subtypes include:

• F44.0 – Dissociative Amnesia (inability to recall important personal information).
• F44.1 – Dissociative Fugue (sudden travel away from home with memory loss and identity confusion).
• F44.2 – Dissociative Stupor (unresponsiveness, but intact physiological function).
• F44.3 – Trance and Possession Disorders (altered consciousness with loss of voluntary movement).
• F44.4 – Dissociative Motor Disorders (loss of voluntary motor function without medical cause).
• F44.5 – Dissociative Convulsions (seizure-like episodes without EEG abnormalities).
• F44.6 – Dissociative Anaesthesia and Sensory Loss (loss of sensation without neurological explanation).
• F44.7 – Mixed Dissociative Disorders (multiple dissociative symptoms).

DSM-5: Dissociative Disorders

DSM-5 defines dissociative disorders as:

Includes:
• Dissociative Identity Disorder (DID) – two or more distinct personality states, memory gaps.
• Dissociative Amnesia – inability to recall autobiographical information, often trauma-related.
• Depersonalization/Derealization Disorder – persistent feelings of detachment from self (depersonalization) or
environment (derealization).
 • Toxicology screen – rule out substance-induced dissociation.
• Autoimmune workup (e.g., NMDA receptor encephalitis) in atypical cases.

4. Management

1. General Principles of Management

• Primary goal: Reduce dissociative symptoms, improve functionality, and address underlying trauma.
• Stepwise approach: Start with non-pharmacological interventions as first-line, followed by pharmacotherapy
for comorbid conditions.

2. Non-Pharmacological Management (First-Line)

A. Psychotherapy (Mainstay of Treatment)
1. Cognitive Behavioral Therapy (CBT)
○ Helps patients recognize dissociative triggers and modify dysfunctional thoughts.
○ Trauma-Focused CBT (TF-CBT): For dissociation related to past abuse or PTSD.
2. Dialectical Behavior Therapy (DBT)
○ Effective for emotional dysregulation in DID.
○ Helps in self-awareness and emotion management.
3. Eye Movement Desensitization and Reprocessing (EMDR)
○ Recommended for trauma-related dissociation (e.g., PTSD with dissociation).
○ Uses bilateral sensory stimulation to process traumatic memories.
4. Hypnotherapy
○ Used in dissociative amnesia or fugue.
○ Helps recover lost memories safely.
5. Grounding Techniques (For Acute Episodes)
○ Techniques to increase awareness of the present moment, such as:
▪ Holding an ice cube.
▪ Deep breathing.
▪ Noting 5 things you see, hear, and feel.
6. Reintegration Therapy (For DID)
○ Goal: Encourage communication between alters to promote cohesive identity integration.

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○ Addresses gaps in memory and time loss.
7. Psychoeducation and Supportive Therapy
○ Explain the nature of dissociation and reduce associated fear or stigma.
○ Involve family therapy to improve interpersonal relationships.

3. Pharmacological Management (Adjunctive Therapy)

A. Medications for Comorbid Conditions
Dissociative disorders themselves do not have a specific pharmacological treatment, but medications are used to
manage comorbid conditions like depression, anxiety, PTSD, or mood instability.
1. Antidepressants (For Comorbid Depression, Anxiety, PTSD)
○ Selective Serotonin Reuptake Inhibitors (SSRIs):
▪ Fluoxetine (20–40 mg/day)
▪ Sertraline (50–100 mg/day)
▪ Paroxetine (Avoid in pregnancy, withdrawal effects high)
○ Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs):
▪ Duloxetine (30–60 mg/day)
▪ Venlafaxine (75–150 mg/day)
2. Mood Stabilizers (For Emotional Dysregulation in DID)
○ Lamotrigine (100–200 mg/day) → Useful in mood instability, affect dysregulation.
○ Valproate (500–1000 mg/day) → Used if comorbid bipolar symptoms.
3. Atypical Antipsychotics (For Severe Dissociation with Psychotic Symptoms)
○ Olanzapine (2.5–5 mg/day)
○ Quetiapine (50–200 mg/day)
○ Avoid high doses as these may worsen emotional numbing.
4. Anxiolytics (Short-Term Use for Severe Anxiety)
○ Clonazepam (0.25–0.5 mg PRN)
○ Lorazepam (0.5–1 mg PRN)
○ Avoid long-term use due to the risk of dependence.

4. Specific Management by Type

Dissociative Disorder Primary Treatment Additional Interventions
Dissociative Amnesia CBT, Hypnotherapy Grounding techniques, SSRI if comorbid
depression
Dissociative Fugue Supportive therapy Psychoeducation, stress management
Dissociative Identity Disorder Trauma-focused CBT, DBT Mood stabilizers if severe affect
(DID) dysregulation
Depersonalization-Derealization CBT, Mindfulness therapy SSRI/SNRI for comorbid anxiety
Disorder
Dissociative Motor & Sensory Psychodynamic therapy, stress Physical therapy for functional recovery
Symptoms reduction

MD Exam Key Points

• CBT is first-line therapy for dissociative disorders.
• DID is strongly linked to childhood trauma.
• Pharmacotherapy targets comorbid depression, PTSD, or affect dysregulation.
• EEG/MRI is necessary to rule out epilepsy or neurological disorders.
• Grounding techniques help with acute dissociative symptoms.
• Hypnotherapy may help recover memories in dissociative amnesia.
• Avoid long-term benzodiazepines.

5. Prognosis and Outcomes

• Better prognosis with early intervention, stable support system, and structured therapy.
• Poor prognosis in untreated DID, chronic trauma exposure, or severe dissociative fugue.
• Ongoing therapy is needed to prevent relapse and manage comorbid conditions

Conclusion
Dissociative disorders involve disruptions in consciousness, identity, and memory, often trauma-related. ICD-10,
DSM-5, and ICD-11 categorize them differently, but core features remain the same. Psychotherapy is the primary
treatment, with medications used for comorbid symptoms.

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CPG, AIIMS, Maudsley, and Oxford Handbook Guidelines
 environment (derealization).
• Other Specified Dissociative Disorder (OSDD) – dissociative symptoms that do not meet full criteria for the
above.

ICD-11: Dissociative Disorders (6B60 - 6B6Z)

Includes:
• 6B60 – Dissociative Amnesia
• 6B61 – Dissociative Neurological Symptom Disorder (includes motor, sensory, and convulsions).
• 6B62 – Trance and Possession Disorder
• 6B63 – Dissociative Identity Disorder
• 6B64 – Depersonalization/Derealization Disorder
• 6B6Y – Other Specified Dissociative Disorders

ICD-11 separates neurological symptoms from identity/memory disturbances and includes severity specifiers.

2. Clinical Presentation
Disorder Key Features
Dissociative Amnesia Sudden memory loss, usually trauma-related, intact procedural memory.
Dissociative Fugue Unexpected travel with amnesia, confusion about identity.
Dissociative Identity Disorder (DID) ≥2 personality states, memory gaps, severe childhood trauma history.
Depersonalization/Derealization Persistent feelings of detachment from self (depersonalization) or
Disorder surroundings (derealization), intact reality testing.
Dissociative Stupor Profound unresponsiveness without medical cause.
Dissociative Neurological Symptoms Sudden motor/sensory deficits, no organic cause, psychological stressor
often present.

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Conversion Symptoms: Sudden blindness, paralysis, or seizures without a neurological cause.

Specific Types and Their Features

1. Dissociative Amnesia
○ Inability to recall important personal information, often after trauma.
○ No evidence of organic brain damage.
2. Dissociative Identity Disorder (DID)
○ Two or more distinct identities (alters).
○ Memory gaps between alters.
○ High association with childhood trauma/abuse.
3. Dissociative Fugue
○ Sudden travel or wandering away from home with amnesia for identity.
○ Often seen after severe stress.
4. Dissociative Motor or Sensory Disorders
○ Loss of motor function (paralysis, tremors) or sensory loss (blindness, deafness).
○ No medical explanation; may resemble conversion disorder.
5. Depersonalization-Derealization Disorder
○ Feelings of detachment from self or unreality of surroundings.
○ Insight is preserved (patients know the experience is not real).

3. Evaluation and Diagnostic Workup

A. Clinical Interview
• Detailed history of trauma, stress, or prior dissociative episodes.
• Examine identity confusion, amnesia, depersonalization, or possession-like states.
•
Screening Tools:
Use Dissociative Experience Scale (DES) for screening.
○ Dissociative Experiences Scale (DES-28).
○ Structured Clinical Interview for Dissociative Disorders (SCID-D).

B. Rule Out Medical Conditions

• Neurological examination (EEG, MRI) – rule out epilepsy, brain lesions.
Toxicology screen – rule out substance-induced dissociation.
2022-03: Abuse of over-the-counter drugs.

Abuse of Over-the-Counter Drugs

OTC Drug Common Brand Reason for Abuse Associated Risks

Names
Dextromethorphan (DXM) Robitussin, Dissociative hallucinations, Serotonin syndrome, tachycardia,
NyQuil, Delsym euphoria, sedation cognitive impairment
Pseudoephedrine Sudafed, Stimulant effects; precursor for Hypertension, arrhythmias,
Claritin-D methamphetamine production anxiety, insomnia
Loperamide Imodium Opioid-like effects (crosses blood- Cardiac arrhythmias (QT
brain barrier at high doses) prolongation), respiratory
depression
NSAIDs/Acetaminophen Advil (ibuprofen), Chronic pain self-medication; Hepatotoxicity (Tylenol), gastric
Tylenol intentional overdose for self-harm ulcers, kidney failure
Diphenhydramine Benadryl, Sedation, delirium, hallucinogenic Anticholinergic toxicity (dry
Sominex effects at high doses mouth, delirium), seizures, coma

Introduction
Over-the-counter (OTC) drug abuse involves the misuse of non-prescription medications for recreational purposes,
self-harm, or self-medication. According to ICD-11 (6C4G), it is classified under "Disorders due to use of non-
dependence-producing substances". The DSM-5 categorizes OTC misuse under "Substance-Related and Addictive
Disorders" (Code F55.8 for non-dependent use of non-psychoactive substances). Despite being perceived as safe,
OTC abuse carries significant risks, including organ toxicity, addiction, and psychiatric sequelae.

•
© jPsychiatrie
Commonly Abused OTC Drugs & Associated ICD/DSM Codes
1. Dextromethorphan (DXM):
ICD-10: F55.8 (Abuse of non-dependence-producing substances).
• Effects: Dissociation, hallucinations (mimicking ICD-11 6A61 "Hallucinogen intoxication").
• Risks: Serotonin syndrome (ICD-10 G25.8), especially with concurrent SSRIs.

2. Pseudoephedrine:
• ICD-11: 6C45.2 (Harmful use of stimulants).
• Abuse: Methamphetamine precursor
• Risks: Hypertension , agitation.

3. Loperamide:
• DSM-5: Opioid Use Disorder (F11.1) due to mu-opioid receptor agonism at high doses.
• Risks: Cardiac arrhythmias and QT prolongation.

4. NSAIDs/Acetaminophen:
• ICD-10: F55.8 for abuse; K70.0 (Alcoholic hepatitis) if combined with alcohol.
• Risks: Hepatotoxicity or acute kidney injury

5. Antihistamines (e.g., diphenhydramine):

ICD-11: 6C44 (Anticholinergic syndrome) for overdose.
 • ICD-11: 6C44 (Anticholinergic syndrome) for overdose.
• DSM-5: Substance-Induced Psychotic Disorder (F19.159) in severe cases.

Psychiatric Risk Factors & Comorbidities

• ICD-11 6E20-6E25 (Mood disorders) and 6B40-6B4Z (Anxiety disorders) are common drivers of self-medication.
• DSM-5 Borderline Personality Disorder (F60.3) correlates with impulsive OTC misuse for emotional regulation.
• Substance Use Disorders (SUDs): Polydrug abuse (ICD-11 6C40.6) increases vulnerability.

Clinical Features & Diagnosis

1. Key Signs:
• Physical: Tremors (ICD-10 R25.1), tachycardia (ICD-10 R00.0).
• Psychiatric: Drug-induced psychosis (DSM-5 F19.159), mood lability (ICD-11 6E60).

2. Diagnostic Criteria:
• DSM-5: ≥2 criteria from Substance Use Disorder (e.g., cravings, tolerance, social impairment).
• ICD-11: Requires "persistent substance use despite harm" (6C4G.1).

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3. Tools:
• CAGE-AID Questionnaire: Validated for OTC misuse screening.
• Urine Toxicology: Limited utility for OTCs but detects co-abused substances (e.g., opioids).

Complications
1. Medical:
• Hepatorenal failure (ICD-10 K72.9, N19).
• Cardiac arrest (ICD-11 ME24.1) from loperamide or pseudoephedrine toxicity.

2. Psychiatric:
• ICD-11 6D11.0 (Depressive disorder with substance-induced features).
• DSM-5 F19.939 (Unspecified stimulant use disorder with severe impairment).

3. Social: Legal repercussions (e.g., pseudoephedrine ) "Problems related to legal circumstances").

Management
1. Acute Care:
• N-acetylcysteine for acetaminophen toxicity (ICD-10 T39.1).
• Benzodiazepines for DXM-induced agitation (ICD-11 6C41 "Sedative-hypnotic toxicity").
2. Long-Term Strategies:
• CBT: Targets maladaptive behaviors (DSM-5 Z71.41 "Counseling for substance use").
• Pharmacotherapy: SSRIs for comorbid depression (ICD-10 F32.9).
3. Prevention:
• Regulatory: Enforce ICD-11 QC30 "Problems related to availability of health services" via OTC sale limits.
• Education: Highlight risks of ICD-11 6C4G diagnoses in schools.

Role of Psychiatrists
• Screening: Use DSM-5 criteria for SUDs in high-risk groups (e.g., adolescents).
• Documentation: Apply ICD-10/11 codes for accurate billing and epidemiological tracking.
• Collaboration: Partner with pharmacists to address ICD-11 QC40 "Problems related to medical
devices/medications".
 devices/medications".

Sum-up
OTC drug abuse, classified under ICD-11 6C4G and DSM-5 F55.8, is a multifaceted issue requiring precise diagnostic
coding and multidisciplinary care. Psychiatrists must integrate ICD-10/11 and DSM-5 frameworks to manage
complications like F19.159 (psychosis) and 6E20 (mood disorders). Regulatory reforms and patient education are
critical to mitigating this underrecognized epidemic.

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2022-04: Schizotypal Disorder.

Schizotypal Disorder

The Meehl’s schizotaxia-schizotypy-schizophrenia model provides an etiological framework where

genetic vulnerability (SZ gene) leads to schizotaxia (neurobiological vulnerability), which progresses to
schizotypy (personality traits). Environmental stressors or a "second hit" determine whether the individual
develops schizophrenia, Schizotypal Personality Disorder (SPD), or subclinical lab abnormalities.

Classification
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Schizotypal Disorder is classified differently across diagnostic systems:
• ICD-10: F21 - "A disorder characterized by eccentric behavior and anomalies of thinking and affect which
resemble those seen in schizophrenia, though no definite and characteristic schizophrenic anomalies have
occurred at any stage".
• ICD-11: Retained under Schizophrenia or Other Primary Psychotic Disorders (6A22), but acknowledges a
broader schizophrenia spectrum.
• DSM-5: Classified as a Cluster A personality disorder, but recognized as part of the schizophrenia spectrum.

ICD-10 Diagnostic Criteria (F21)

The disorder is characterized by:
1. Inappropriate or constricted affect (appearing cold and aloof).
2. Odd, eccentric, or peculiar behavior or appearance.
3. Poor rapport with others and a tendency toward social withdrawal.
4. Odd beliefs or magical thinking (influencing behavior and inconsistent with cultural norms).
5. Suspiciousness or paranoid ideation.
6. Obsessive ruminations (often with dysmorphophobic, sexual, or aggressive content).
7. Unusual perceptual experiences (somatosensory illusions, depersonalization, derealization).
8. Vague, circumstantial, metaphorical, or overelaborate thinking, leading to odd speech.
9. Occasional transient quasi-psychotic episodes (intense illusions, auditory or other hallucinations, and
delusion-like ideas).

Diagnostic Guidelines:
• Symptoms should be present continuously or episodically for at least 2 years.
• The individual must never have met criteria for schizophrenia.
• A family history of schizophrenia adds diagnostic weight but is not required.

ICD-11 Diagnostic Criteria (6A22)

ICD-11 Diagnostic Criteria (6A22)
• Persistent, long-term pattern of unusual behavior, cognition, and perception, not meeting criteria for
schizophrenia.
• Symptoms include:
• Constricted affect (cold and aloof appearance).
• Odd beliefs or magical thinking, influencing behavior.
• Unusual perceptual distortions (illusions, depersonalization, derealization).
• Suspiciousness or paranoid ideas.
• Odd speech, including metaphorical or circumstantial thinking.
• Social withdrawal and poor rapport with others.
• Transient delusions or hallucinations, but not meeting schizophrenia criteria.
• Symptoms must be continuous or episodic for at least 2 years.
• The disorder is relatively stable and rarely progresses into schizophrenia.

DSM-5 Diagnostic Criteria

A pervasive pattern of social and interpersonal deficits, including cognitive/perceptual distortions and
eccentric behavior, present in early adulthood and in multiple contexts, as indicated by ≥5 of the following:
1. Ideas of reference (excluding delusions).
2. Odd beliefs or magical thinking (e.g., telepathy, sixth sense).
3. Unusual perceptual experiences (including bodily illusions).
4. Odd thinking and speech (vague, circumstantial, metaphorical).
5. Suspiciousness or paranoid ideation.
6. Inappropriate or constricted affect.
7. Odd or eccentric behavior/appearance.
8. Lack of close friends other than first-degree relatives.

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9. Excessive social anxiety related to paranoid fears.

Exclusions: Symptoms should not be better explained by schizophrenia, bipolar disorder, or autism spectrum
disorder.

Clinical Features
Core Symptoms:
• Social withdrawal and interpersonal deficits (few friends, discomfort in social situations).
• Cognitive-perceptual distortions (illusions, quasi-psychotic episodes).
• Eccentric behavior (odd clothing, mannerisms, speech).
• Paranoid and suspicious thinking.
• Odd speech (overelaborate, circumstantial, metaphorical).

Neuropsychological Profile:
• Impairments in verbal memory, executive function, and attention.
• Cognitive dysfunction resembles schizophrenia but is milder.

Epidemiology
• Prevalence: 3–4% in the general population.
• More common in males.
• Increased prevalence in first-degree relatives of schizophrenia patients, suggesting a shared genetic
basis.

Differential Diagnosis
1. Schizophrenia – Schizotypal Disorder lacks persistent delusions and hallucinations.
 1. Schizophrenia – Schizotypal Disorder lacks persistent delusions and hallucinations.
2. Schizoid Personality Disorder – Schizotypal individuals have cognitive distortions, while schizoid individuals
simply lack interest in relationships.
3. Paranoid Personality Disorder – Paranoid PD has pervasive distrust without cognitive-perceptual
distortions.
4. Autism Spectrum Disorder (ASD) – ASD involves communication deficits and repetitive behaviors, which
are not prominent in Schizotypal Disorder.

The management approach includes non-pharmacological interventions first, followed by pharmacological

treatment if needed.

1. Non-Pharmacological Management
a) Psychoeducation and Support
○ Educate the patient and their family about the disorder, symptomatology, prognosis, and treatment plan.
○ Supportive therapy to enhance coping strategies and social skills.

b) Cognitive-Behavioral Therapy (CBT)

○ Focuses on restructuring distorted beliefs, reducing paranoia, and improving social skills.
○ Helps patients identify and modify maladaptive thought patterns.

c) Social Skills Training

○ Role-playing exercises to improve interpersonal interactions.
○ Encourages participation in social activities to counteract isolation.

d) Family Therapy
○ Reduces high expressed emotions in the family, which can exacerbate symptoms.
○ Provides guidance on managing communication difficulties.

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e) Vocational Rehabilitation
○ Occupational therapy for patients with functional impairment.
○ Supported employment programs to improve work performance.

2. Pharmacological Management
Pharmacotherapy is used only when symptoms are distressing or interfere with daily functioning.

a) Antipsychotics (for psychotic-like symptoms)

○ Low-dose second-generation antipsychotics (SGAs)
○ Risperidone: 1-3 mg/day
○ Olanzapine: 2.5-10 mg/day
○ Aripiprazole: 5-15 mg/day
○ Quetiapine: 25-300 mg/day
○ Clozapine: for treatment-resistant cases (monitor for agranulocytosis)

○ First-generation antipsychotics (FGAs) (limited use due to side effects)

○ Haloperidol: 0.5-2 mg/day (for severe psychotic symptoms)

b) Antidepressants (for comorbid depression or anxiety)

○ SSRIs preferred:
○ Fluoxetine: 10-40 mg/day
○ Sertraline: 50-200 mg/day
○ Escitalopram: 10-20 mg/day

c) Anxiolytics (for severe anxiety)

○ Short-term use only to prevent dependence:
○ Clonazepam: 0.5-2 mg/day
○ Lorazepam: 0.5-2 mg/day

3. Monitoring and Follow-Up

Regular psychiatric follow-up every 4-6 weeks initially, then every 2-3 months.
 • Regular psychiatric follow-up every 4-6 weeks initially, then every 2-3 months.
• Monitor for medication side effects, adherence, and psychosocial functioning.
• Assess for suicidal ideation, as schizotypal disorder increases the risk of suicide.

Prognosis
• Chronic and stable course, with episodic symptom exacerbations.
• Lower risk of schizophrenia conversion compared to other schizophrenia spectrum disorders.
• Functional impairment is common, especially in occupational and social domains.

Sum-up
Schizotypal Disorder is a schizophrenia spectrum disorder characterized by social withdrawal, cognitive-
perceptual distortions, and eccentric behavior. It requires a multimodal treatment approach, including
psychotherapy, pharmacotherapy, and supportive interventions. Early diagnosis and intervention improve
functional outcomes.

References
1. Kaplan & Sadock’s Concise Textbook of Clinical Psychiatry.
2. Shorter Oxford Textbook of Psychiatry.
3. New Oxford Textbook of Psychiatry.

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2022-05: Non-pharmacological management of Anorexia
Nervosa.

Non-Pharmacological Management of Anorexia Nervosa

Anorexia nervosa (AN) is a severe eating disorder that requires a multidisciplinary approach, with non-
pharmacological interventions as the first-line treatment. The primary aim is psychological intervention and
nutritional rehabilitation, ensuring weight restoration and addressing distorted body image and eating behaviors.

nutrition counseling for anorexia, emphasizing the goals of dietary intervention in managing the disorder.

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ICD-10 Diagnostic Criteria (F50.0)
Anorexia Nervosa is characterized by deliberate weight loss, induced and sustained by the patient. It is
most common in adolescents and young women but can also occur in males and older individuals.

Diagnostic Guidelines:
For a definite diagnosis, all the following criteria must be met:
1. Body weight is maintained at least 15% below expected (either lost or never achieved), or BMI is ≤17.5
kg/m².
• In prepubertal patients, failure to achieve expected weight gain is an equivalent criterion.
2. Weight loss is self-induced through avoidance of “fattening foods” and may involve:
• Self-induced vomiting
• Laxative or diuretic misuse
• Excessive exercise
• Use of appetite suppressants
3. Body image distortion, where the patient has an intense fear of weight gain and a distorted perception
of their own body size.
4. Endocrine dysfunction, particularly involving the hypothalamic-pituitary-gonadal axis, leading to:
• Amenorrhea in females (absence of ≥3 menstrual cycles).
• Loss of sexual interest and erectile dysfunction in males.
5. Delayed puberty (if onset is prepubertal), with arrested growth and delayed secondary sexual characteristics.

1. Psychological Interventions (First-Line Therapy)

a) Cognitive-Behavioral Therapy (CBT)
○ CBT-E (Enhanced CBT) is the most effective individual therapy for AN.
○ Focuses on:
○ Identifying and modifying maladaptive thoughts about body weight and food.
○ Challenging cognitive distortions regarding self-worth and eating behavior.
○ Behavioral strategies to restore normal eating patterns.
○ CBT is effective in both inpatient and outpatient settings.

b) Family-Based Therapy (FBT)

Gold-standard treatment for adolescents with AN.
 ○ Gold-standard treatment for adolescents with AN.
○ Involves three phases:
▪ Phase 1: Parents take full control of meal supervision to restore weight.
▪ Phase 2: Gradual transition of eating responsibility to the patient.
▪ Phase 3: Focus on identity development and relapse prevention.
▪ Superior to individual therapy in adolescents, preventing chronicity.

c) Interpersonal Therapy (IPT)

○ Addresses underlying interpersonal conflicts that contribute to AN.
○ Focuses on social anxiety, perfectionism, and self-esteem issues.

d) Psychoeducation
○ Provides education on the medical and psychological risks of AN.
○ Involves psychiatrists, dietitians, and psychologists to provide a holistic understanding of the
disorder.

2. Nutritional Rehabilitation

a) Gradual Refeeding Approach

○ Goal: Restore weight safely and prevent refeeding syndrome.
○ Energy intake:
▪ Start at 1200–1500 kcal/day, increasing to 2500–3000 kcal/day over weeks.
▪ Ensure a balance of carbohydrates and proteins to prevent catabolism.
▪ Supervised meals and nutrition plans are essential to maintain adherence.
▪ Macronutrient balance: Emphasize carbohydrates and proteins to prevent catabolism.

b) Meal Supervision and Behavioral Strategies

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○ Scheduled meals and snacks prevent restrictive eating patterns.
○ Strict monitoring of exercise prevents excessive physical activity.
• Cognitive restructuring to address fear of weight gain.

3. Social and Occupational Therapy

• Social skills training: Helps patients reintegrate into social settings.
• Occupational therapy: Encourages participation in non-food-related activities.

4. Medical Monitoring (Due to High Physical Risk)

• Regular monitoring of BMI and vital signs (e.g., pulse, blood pressure).
• ECG for QT prolongation risk.
• Electrolyte monitoring to prevent refeeding syndrome (hypokalemia, hypophosphatemia).
• Bone health assessment: AN patients are at risk of osteoporosis.

5. When to Consider Inpatient Treatment

Indications for hospitalization:
• Severe weight loss: BMI < 15 kg/m² or rapid weight loss (>1 kg/week).

• Medical instability:
○ Bradycardia (<40 bpm), hypotension (<80/50 mmHg), hypothermia (<35°C).
○ Electrolyte imbalances (hypokalemia, hypophosphatemia).
○ Cardiac arrhythmias, prolonged QT interval on ECG.
○ Persistent refusal to eat despite intensive outpatient therapy.
○ Suicidality or severe psychiatric comorbidities (e.g., depression, OCD).
Conclusion
• CBT and FBT are first-line interventions for AN.
• Nutritional rehabilitation is essential, ensuring slow and safe weight restoration.
• Medical monitoring is critical due to the risk of severe medical complications.
• A multidisciplinary approach involving psychiatrists, dietitians, and psychologists is necessary for effective
treatment.
•

References
1. Kaplan & Sadock’s Concise Textbook of Clinical Psychiatry.
2. Shorter Oxford Textbook of Psychiatry.
3. New Oxford Textbook of Psychiatry.

#Viva Question
ICD-11 Diagnostic Criteria (6B80)
Anorexia Nervosa is defined as a feeding and eating disorder characterized by persistent
restriction of food intake leading to significantly low body weight.

Essential Features:
1. Restriction of energy intake, leading to significantly low body weight for age, sex, and
developmental trajectory.
2. Intense fear of gaining weight or persistent behavior that interferes with weight gain ,

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despite being underweight.
3. Distorted self-perception, including excessive preoccupation with weight and body shape.
4. Behavior aimed at maintaining low body weight, including:
• Severe dietary restriction
• Excessive exercise
• Purging behaviors (self-induced vomiting, laxatives).
5. Medical risk is not solely dependent on weight status but includes rapid weight loss,
electrolyte imbalances, and cardiovascular instability.

Specifiers in ICD-11:
• Restricting type: Weight loss through dieting, fasting, excessive exercise.
• Binge-purge type: Episodes of binge eating or purging (vomiting, laxatives, diuretics) .
• Anorexia Nervosa in recovery: Diagnosis retained for individuals who have achieved normal
weight but continue disordered eating behaviors.
DSM-5 Diagnostic Criteria
According to DSM-5, Anorexia Nervosa is a disorder characterized by energy intake restriction,
intense fear of weight gain, and body image disturbance.

Criteria:
A. Restriction of energy intake relative to requirements, leading to significantly low body weight. B.
Intense fear of gaining weight or persistent behavior interfering with weight gain, even at a low
weight. C. Disturbance in the way body weight or shape is experienced, undue influence on self-
evaluation, or lack of recognition of low body weight.

Specifiers:
• Restricting Type: No regular episodes of binge eating or purging in the last 3 months.
• Binge-Eating/Purging Type: Regular binge eating or purging in the last 3 months.
2022-06: Cultural aspects in Dissociative Possession
Attacks.

Cultural Aspects in Dissociative Possession Attacks

Introduction
Dissociative possession attacks, also referred to as possession trance disorder, are a type
of dissociative disorder characterized by temporary replacement of an individual's sense
of personal identity by an external entity, spirit, or deity. These conditions are highly
influenced by cultural beliefs, spiritual practices, and sociocultural stressors.

• ICD-10: Classifies possession states under Trance and Possession Disorders

(F44.3), provided they cause distress and functional impairment.

• ICD-11: Introduces Possession Trance Disorder (6B63)

as distinct from Trance Disorder (6B62), emphasizing that
cultural context

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• DSM-5: Recognizes Dissociative Trance Disorder under Other Specified

Dissociative Disorders, requiring exclusion of culturally normative experiences.

ICD-10 Diagnostic Criteria (F44.3)

Trance and possession disorders are characterized by a temporary loss of identity
awareness and full environmental perception. A diagnosis requires:
1. Loss of the sense of personal identity and awareness of surroundings.
2. Possession states where an individual believes they are controlled by another
entity.
3. Symptoms must cause distress or functional impairment.
4. The state must not be culturally or religiously accepted.

ICD-11 Diagnostic Criteria (6B63)

Possession Trance Disorder is defined as an involuntary altered state of consciousness
in which a person’s identity is replaced by an external entity. Core Features:
• Involuntary alteration of personal identity attributed to possession by spirits, deities,
or supernatural forces.
• Cultural context matters: If possession states occur within religious practices, they
are not diagnosed as a disorder.
 are not diagnosed as a disorder.
• Motor, sensory, and verbal changes, such as involuntary movements,
glossolalia, auditory hallucinations, or amnesia.
• Significant distress or impairment in personal, social, or occupational functioning.

DSM-5 Diagnostic
DSM-5 includes possession states under Dissociative Trance Disorder, which is classified
within Other Specified Dissociative Disorders.
Criteria:
• Temporary loss of identity awareness, with external control by a possessing entity.
• Episodes include stereotypical and culturally determined behaviors.
• Significant distress or impairment is required.
• Not a culturally accepted religious or spiritual practice.
• Not due to another mental disorder, substance use, or a medical condition.

Cultural Aspects of Dissociative Possession Attacks

1. Cultural Variability in Possession States
• Culturally accepted possession states exist in religious and shamanistic traditions,
such as:
• Zar possession (Ethiopia, Sudan, Egypt).
• Ufufuyane (Southern Africa), linked to spirit attack and emotional distress.
• Amok (Malaysia), involving violent dissociative outbursts.
• Latah (Malaysia, Indonesia), characterized by exaggerated startle responses.
• Pibloktoq (Arctic Hysteria) among Inuit populations.

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2. Cultural and Religious Factors
• Religious Practices: In many cultures, trance states are spiritually meaningful
rather than pathological. Examples:
• Pentecostal Christian services (speaking in tongues, glossolalia).
• Hindu and Vodou rituals (spirit possession, deity invocation).
• Gender Differences: Possession disorders are more common in women, often
linked to cultural roles and expectations.

3. Cultural Triggers and Sociocultural Stressors

• Mass Possession Events: Reports of possession increase during social crises
(e.g., epidemics, war trauma).
• Collective Trance States: Some societies experience group dissociative episodes,
such as schoolgirl possession outbreaks.
• Spiritual Healing Practices: Some cultures normalize trance states through religious
healing ceremonies.

Differential Diagnosis
Disorder Key Differentiating Features
Schizophrenia Persistent delusions,
hallucinations outside trance
states
Dissociative Identity Disorder Internal personality shifts, not
external possession
Epileptic Seizures Abnormal EEG findings,
neurological basis
Post-Traumatic Stress Disorder Flashbacks, avoidance,
hyperarousal
Management of Dissociative Possession Attacks
1. Cultural Sensitivity in Diagnosis
○ Distinguish between pathological vs. culturally sanctioned possession.
○ Involve cultural liaisons, religious leaders in assessment.

2. Psychological Interventions
○ Cognitive Behavioral Therapy (CBT): Targets distressing beliefs about
possession.
○ Trauma-Focused Therapy: Addresses underlying trauma, which is common in
dissociative disorders.
○ Hypnosis and Grounding Techniques: Help reintegrate fragmented identity.

3. Medical and Pharmacological Management

○ Antipsychotics (e.g., risperidone): Used if symptoms overlap with
schizophrenia.
○ Benzodiazepines (e.g., lorazepam): Short-term use for acute dissociative
episodes.
○ SSRIs (e.g., fluoxetine, sertraline): For comorbid depression or anxiety.

Dissociative possession attacks are highly influenced by cultural, religious, and

sociopolitical factors. While ICD-10, ICD-11, and DSM-5 recognize possession states as
dissociative disorders, diagnosis should exclude culturally normative experiences.
Management requires cultural sensitivity, psychotherapy, and in some cases,

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pharmacological intervention.
2022-07: Elder abuse.

Elder Abuse

Introduction
Elder abuse is defined as an act or omission that results in harm or threatened harm to the health or
welfare of an elderly person. It includes physical, psychological, sexual, financial abuse, and neglect.

• ICD-10: Does not have a specific diagnostic category but recognizes elder abuse under "Other
maltreatment syndromes".
• ICD-11: Classifies it under "Maltreatment and Neglect Disorders", defining it as physical, sexual,
psychological abuse, or neglect by a caregiver.

• WHO Definition: Any single or repeated act, or lack of appropriate action, occurring within a
relationship of trust, that causes harm or distress to an older person.

Prevalence:
• Estimated 2–10% of elderly individuals experience abuse, with higher risks in those with dementia or
social isolation.
• WHO estimates that 1 in 6 adults over 60 years experience elder abuse, but cases are underreported.

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Types of Elder Abuse
1. Physical Abuse
• Definition: Use of physical force that results in injury, pain, or distress (e.g., hitting, slapping, restraining).
• Indicators: Bruises, fractures, burns, unexplained injuries.

2.Emotional Abuse
• Definition: Infliction of mental pain, distress, or anguish through verbal or non-verbal acts.
• Examples: Intimidation, humiliation, isolation, or threats.
• Indicators: Withdrawal, anxiety, depression, fearfulness.

3. Sexual Abuse
• Definition: Any non-consensual sexual contact or exposure to inappropriate material.
• Indicators: Genital bruising, sexually transmitted infections (STIs), difficulty walking or sitting.

4. Financial Abuse
• Definition: Unauthorized use of an elderly person’s finances, property, or assets.
• Examples: Fraud, coercion into financial decisions, misuse of bank accounts.
• Indicators: Unexplained financial transactions, missing valuables.

5. Neglect (Passive or Active)

• Definition: Failure to provide basic needs (food, medical care, hygiene, social interaction).
• Indicators: Malnutrition, dehydration, poor hygiene, untreated medical conditions.

Risk Factors for Elder Abuse

1. Risk Factors Related to the Elderly Individual
• Cognitive Impairment (Dementia, Delirium): Patients with dementia are twice as likely to experience
abuse.
• Physical Frailty and Dependence: Increased vulnerability due to mobility issues.
• Social Isolation: Lack of a support system increases the risk.
• Mental Illness (Depression, Anxiety): Those with psychiatric conditions are at higher risk.

2. Risk Factors Related to the Caregiver

2. Risk Factors Related to the Caregiver
• Mental Health Disorders: Caregivers with depression, substance abuse, or personality disorders are at
higher risk of perpetrating abuse.
• Financial Dependence: Caregivers relying on the elder financially may engage in financial exploitation.
• Lack of Caregiving Skills or Burnout: Stressful caregiving roles can lead to neglect or mistreatment.

3. Environmental and Social Risk Factors

• Living Arrangements: Higher risk when caregivers and elders live together.
• Cultural Norms: In some cultures, ageism and lack of elder rights protection increase abuse
prevalence.

Clinical Consequences of Elder Abuse

• Increased Mortality: Abused elders have a threefold higher risk of death compared to non-abused
counterparts.
• Physical Health Decline: Injuries, chronic pain, worsening of medical conditions.
• Psychiatric Disorders: Depression, anxiety, PTSD, and increased suicidality.
• Cognitive Decline: Abuse is linked to faster cognitive deterioration in dementia patients.

Assessment and Screening for Elder Abuse

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1. Clinical Assessment
• History Taking: Direct but sensitive questioning of the elderly individual and caregiver separately.
Physical Examination: Look for unexplained bruises, fractures, pressure ulcers.
 • Physical Examination: Look for unexplained bruises, fractures, pressure ulcers.
• Cognitive and Psychiatric Evaluation: Screen for delirium, dementia, depression.

2. Screening Tools
• Elder Abuse Suspicion Index (EASI) – 5-item screening tool.
• Hwalek-Sengstock Elder Abuse Screening Test (H-S/EAST) – Assesses risk factors.

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Management of Elder Abuse
1. Multidisciplinary Approach
• Medical Treatment: Treat injuries, malnutrition, infections.
• Psychiatric Support: Address depression, PTSD, or anxiety related to abuse.
• Social Work Intervention: Identify safe housing, legal assistance, financial support.

2. Legal and Protective Interventions

• Mandatory Reporting: In many countries, healthcare providers are legally required to report elder
abuse.
• Guardianship and Conservatorship: Courts may appoint legal guardians for protection.
• Restraining Orders: If necessary, legal protection against perpetrators.

3. Preventive Measures
• Caregiver Training Programs: Reduce stress and improve caregiving skills.
• Respite Care and Support Groups: Prevent burnout and emotional distress in caregivers.
• Community Awareness Campaigns: Encourage early detection and reporting.
Conclusion
Elder abuse is a serious public health issue with significant physical and psychological consequences.
Dementia, frailty, and social isolation increase vulnerability. Screening and early intervention through a
multidisciplinary approach are essential to prevent abuse, ensure safety, and provide medical and legal
support.

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2023-01: Evaluation and management of late-onset
psychosis.

Stepwise Evaluation of Late-Onset Psychosis

1. Definition and Diagnostic Considerations

• Late-onset psychosis refers to the first episode of psychotic symptoms occurring after the
age of 40.

• Subtypes:
○ Late-Onset Schizophrenia (LOS): First episode of schizophrenia-like psychosis after age
40.
○ Very Late-Onset Schizophrenia-Like Psychosis (VLOSLP): Onset after age 60, more
common in women.
○ Psychosis due to neurodegenerative disorders: Includes dementia-related psychosis

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(Alzheimer’s, Lewy body dementia).

2. Differential Diagnosis of Late-Onset Psychosis

Category Common Causes Differentiating Features
Primary Psychotic Late-onset schizophrenia, schizoaffective Chronic course,
Disorders disorder delusions/hallucinations
without cognitive decline
Neurodegenerative Alzheimer’s disease, Lewy body dementia, Cognitive decline,
Disorders Parkinson’s disease dementia visuospatial deficits,
fluctuating cognition
Medical Causes Brain tumors, epilepsy, infections (e.g., Neurological signs, altered
neurosyphilis, HIV), metabolic disorders consciousness, systemic
symptoms
Substance-Induced Alcohol withdrawal, stimulant/cannabis- Clear temporal relationship
induced psychosis, medication side effects with substance use
(e.g., steroids, dopamine agonists)
Mood Disorders with Late-onset bipolar disorder, severe Mood symptoms
Psychotic Features depression with psychosis (depression/mania),
episodic course

Management Approach for Late-Onset Psychosis

Step 1: Comprehensive Assessment
1. History and Clinical Interview
• Detailed history of symptom onset and progression.
• Cognitive assessment (MMSE, MoCA) to rule out neurodegenerative causes.
Medication and substance use history to identify drug-induced psychosis.
 • Medication and substance use history to identify drug-induced psychosis.
• Family history of psychiatric disorders.

2. Physical and Neurological Examination

• Assess for neurological deficits (stroke, Parkinsonism).
• Look for systemic signs of medical illnesses.
3.
4. Laboratory and Imaging Investigations
• Basic Metabolic Panel: Blood glucose, electrolytes, renal and liver function tests.
• Thyroid Function Tests: To rule out endocrine causes.
• Vitamin B12 and Folate Levels: Nutritional deficiencies can cause psychosis.
• Syphilis & HIV Testing: Neurosyphilis and HIV encephalopathy should be ruled out.
• Brain Imaging (MRI/CT scan): Detects strokes, tumors, hydrocephalus, or white matter
changes.
• EEG (if seizures suspected): Identifies epilepsy-related psychosis.

Step 2: Non-Pharmacological Management (First-Line Approach)

1. Psychoeducation and Supportive Therapy
• Educate patient and caregivers about the illness and treatment.
• Address concerns regarding stigma and medication adherence.

2. Cognitive-Behavioral Therapy (CBT)

• Helps reduce delusions and improve insight in primary psychotic disorders.
• Used in conjunction with medication in schizophrenia and schizoaffective disorder.

3. Social and Occupational Support

• Ensuring adequate social engagement to prevent isolation.
• Vocational rehabilitation if functional impairment is present.

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4. Environmental Modifications for Dementia-Related Psychosis
• Minimize stressors and sensory overload.
• Improve lighting, structured routines, and family involvement to reduce paranoia.

Step 3: Pharmacological Management

1. Antipsychotics (First-Line for Psychosis)
• Low-dose atypical antipsychotics preferred due to lower risk of extrapyramidal symptoms
(EPS) and cognitive decline.
• Recommended Agents:
• Risperidone: 0.5–2 mg/day (first-line for late-onset schizophrenia)
• Olanzapine: 2.5–5 mg/day (higher metabolic risk, but effective)
• Quetiapine: 12.5–100 mg/day (preferred in Parkinson’s/Lewy body dementia due to lower
EPS risk)
• Aripiprazole: 2–10 mg/day (fewer metabolic side effects, but risk of akathisia)
• Clozapine: 12.5–50 mg/day (for treatment-resistant cases; requires blood monitoring).

2. Antidepressants (For Depressive Psychosis)

• If depression with psychotic features, consider SSRIs:
• Sertraline (50-100 mg/day)
• Escitalopram (5-10 mg/day)
• Avoid tricyclic antidepressants (TCAs) due to anticholinergic burden in elderly.

3. Mood Stabilizers (For Bipolar Disorder)

• Lithium (300-900 mg/day, maintain levels at 0.6-1.0 mEq/L) – Requires renal and thyroid
monitoring.
• Valproate (250-750 mg/day) – Used if lithium is contraindicated.

4. Cholinesterase Inhibitors (For Dementia-Related Psychosis)

• Donepezil (5-10 mg/day), Rivastigmine (1.5-6 mg BID), Galantamine (8-24 mg/day) can help
cognitive symptoms.
 cognitive symptoms.
• Avoid antipsychotics unless necessary due to increased mortality risk in dementia.

Step 4: Monitoring and Follow-Up

1. Monitor Medication Response and Side Effects
• Assess for EPS, sedation, weight gain, metabolic syndrome.
• ECG monitoring for QT prolongation (especially for risperidone, olanzapine).
• Check prolactin levels in long-term risperidone use.

2. Cognitive and Functional Monitoring

• Regular MMSE/MoCA assessments in dementia patients.
• Ensure ongoing social support and caregiver involvement.

3. Long-Term Maintenance
• Gradual dose reduction after 1 year of stability to assess need for ongoing treatment.
• Clozapine for treatment-resistant psychosis after failure of two antipsychotics.

Special Considerations
1. Avoiding Harmful Medications
• Typical antipsychotics (Haloperidol, Chlorpromazine) → High EPS risk, worsens cognition.
• Benzodiazepines (Diazepam, Lorazepam) → Fall risk, paradoxical agitation in elderly.
• High-dose antipsychotics → Increased risk of cerebrovascular events.

2. Management of Delusions and Hallucinations in Dementia

• Non-pharmacological interventions first (orientation cues, environmental modifications).
• Use Quetiapine or Pimavanserin (34 mg/day) if pharmacological treatment is required.

Summary © jPsychiatrie
Late-onset psychosis requires thorough medical workup to rule out secondary causes.
1. Schizophrenia-like psychosis in elderly responds well to low-dose atypical
antipsychotics.
2. Dementia-related psychosis is best managed non-pharmacologically; if needed, use
quetiapine or pimavanserin.
3. Long-term monitoring is crucial for metabolic and cognitive effects of antipsychotics.
4. Avoid benzodiazepines and typical antipsychotics in elderly due to adverse effects.

References
• CPG Guidelines on Schizophrenia and Late-Onset Psychosis.
• The Maudsley Prescribing Guidelines (14th Edition)
• Kaplan & Sadock’s Comprehensive Textbook of Psychiatry.
2023-02: Classify Bipolar Disorders. Management and long-
term course and outcome of Bipolar Type 1 Disorder.

Introduction
Bipolar disorder is a chronic mood disorder characterized by recurring episodes of mania, hypomania, and depression.
Bipolar I disorder (BP-I) is defined by at least one manic episode, with or without depressive episodes.

• ICD-10: Classified under F31 – Bipolar Affective Disorder, requiring at least two episodes of significant mood
disturbance, including mania or hypomania.
• ICD-11: Bipolar disorder is categorized as Bipolar Type I Disorder (6A60) and Bipolar Type II Disorder (6A61). BP-I
requires at least one manic or mixed episode, while BP-II involves hypomanic and depressive episodes.
• DSM-5: Defines Bipolar I Disorder as requiring at least one manic episode lasting ≥1 week, while Bipolar II
Disorder requires at least one hypomanic and one major depressive episode.

Classification of Bipolar Disorders

Classification ICD-10 ICD-11 DSM-5
Bipolar I Disorder F31.1-F31.9 (various episodes) 6A60 Requires ≥1 manic episode
Bipolar II Disorder F31.8 (no distinct II classification) 6A61 Requires ≥1 hypomanic and
depressive episode
Cyclothymia F34.0 6A62 Chronic mild mood fluctuations

ICD-10 Subcategories of Bipolar Disorder (F31)

ICD-10 Code Category Clinical Description
F31.0 Bipolar affective disorder, current episode Mildly elevated mood, increased energy, no psychotic
hypomanic symptoms
F31.1 Bipolar affective disorder, current episode manic Elevated, irritable mood, grandiosity, hyperactivity,
without psychotic symptoms decreased need for sleep

© jPsychiatrie
F31.2 Bipolar affective disorder, current episode manic Mania with delusions, hallucinations (mood-
with psychotic symptoms congruent or incongruent)
F31.3 Bipolar affective disorder, current episode mild or Depressed mood, anhedonia, fatigue, sleep
moderate depression disturbances, no psychotic features
F31.4 Bipolar affective disorder, current episode severe Severe functional impairment, suicidal ideation,
depression without psychotic symptoms marked psychomotor slowing
F31.5 Bipolar affective disorder, current episode severe Severe depression with mood-congruent or
depression with psychotic symptoms incongruent delusions/hallucinations
F31.6 Bipolar affective disorder, current episode mixed Simultaneous presence of manic and depressive
symptoms
F31.7 Bipolar affective disorder, currently in remission Past bipolar episodes, currently asymptomatic
F31.8 Other bipolar affective disorders Includes Bipolar II disorder and recurrent manic
episodes
F31.9 Bipolar affective disorder, unspecified Atypical or unclassified bipolar symptoms

ICD-11 Subtypes of Bipolar I Disorder:

• 6A60.0: Current episode manic, without psychotic symptoms.
• 6A60.1: Current episode manic, with psychotic symptoms.
• 6A60.5: Current episode depressive, severe with psychotic symptoms.
• 6A60.F: Currently in full remission.

The Akiskal classification recognizes subthreshold and atypical presentations that are not fully captured by ICD-11 and
DSM-5.
Akiskal Classification Clinical Characteristics
Bipolar I Full-blown mania.
Bipolar I ½ Depression with protracted hypomania.
Bipolar II Depression with hypomanic episodes.
Bipolar II ½ Depression associated with cyclothymic temperament.
Bipolar III Hypomania induced by antidepressants.
Bipolar III ½ Hypomania/depression associated with substance use.
Bipolar IV Depression with hyperthymic temperament (i.e., baseline elevated mood traits).
Bipolar V Recurrent depressions mixed with dysphoric hypomania.
Bipolar VI Late-onset depression with mixed mood features, progressing to dementia-like
syndrome.

Management of Bipolar I Disorder

1. Acute Phase Treatment

a) Mania
First-Line Treatment:
○ Mood Stabilizers: Lithium (900–1800 mg/day) – Gold standard for manic episodes.
○ Atypical Antipsychotics: Olanzapine, Risperidone, Quetiapine, Aripiprazole – Used for acute control of
mania.
○ Divalproex (750–2000 mg/day): Preferred in rapid cycling or mixed episodes.

Second-Line Treatment:
○ ECT (Electroconvulsive Therapy): Used in severe mania or treatment-resistant cases.
○ Combination Therapy: Lithium + Antipsychotic for refractory mania.

b) Bipolar Depression
First-Line Treatment:
○ Quetiapine, Lurasidone, Olanzapine-Fluoxetine Combination.
○ Lithium (600–1500 mg/day): Reduces suicidal risk.
○ Lamotrigine (50–200 mg/day): Used as a mood stabilizer in bipolar depression.

Avoid Antidepressant Monotherapy:

○ Antidepressants (e.g., SSRIs, SNRIs) should only be used with a mood stabilizer to prevent switching to
mania.

© jPsychiatrie
2. Maintenance Phase Treatment (Prevention of Relapse)
• Lithium (Therapeutic Range: 0.6–1.2 mmol/L): First-line for long-term mood stabilization.
• Valproate: Used if lithium is ineffective or not tolerated.
• Quetiapine, Olanzapine, or Lamotrigine: Adjuncts for long-term mood stabilization.
• Psychoeducation and Psychotherapy: Essential to enhance adherence and prevent relapse.

Long-Term Course and Outcome of Bipolar I Disorder

Onset and Progression

• Mean Age of Onset: 17–30 years, but varies across populations.
• First Episode:
• 85% begin with a depressive episode.
• 10% begin with mania, 3–5% with mixed episodes.
• Typical Duration of Episodes:
• Manic episodes last ~2 months (treated) or 3 months (untreated).
• Depressive episodes last 2–5 months.

Recurrence and Episode Patterns

• 90–100% of patients experience multiple episodes after the first manic episode.
• The risk of recurrence increases with the number of prior episodes.
• Average of 10 mood episodes over 25 years.
• Intervals between episodes shorten over time.
• Rapid cycling (≥4 episodes/year) occurs in 5–15% of cases and is more common in women.

Functional and Cognitive Outcomes

• 40–60% experience persistent cognitive deficits in executive function, verbal memory, and attention, even during
remission.
• Two-thirds of patients never regain premorbid social and occupational functioning.
• Unemployment rates are 4–10 times higher than in the general population.

Prognostic Indicators
Good Prognosis Poor Prognosis
Later age of onset (>30 years) Early onset (<20 years)
Later age of onset (>30 years) Early onset (<20 years)
Shorter duration of manic episodes Frequent episodes (≥10 in lifetime)
Good treatment adherence Comorbid substance use disorder
Strong social support Psychotic symptoms during episodes
Fewer suicidal thoughts Inter-episode depressive symptoms

Mortality and Suicide Risk

• Suicide attempts occur in 25–50% of patients with bipolar I disorder.
• Suicide completion rate: 8% in men, 5% in women over 40 years.
• Cardiovascular disease is a major cause of mortality, with life expectancy reduced by 9–13 years.
• Lithium reduces suicide risk by 60%.

Long-Term Outcome Categories

Outcome Percentage of Patients
No recurrence of symptoms 7%
Multiple relapses with periods of remission 45%
Partial remission with persistent symptoms 30%
Chronic illness with significant social decline 10%

Treatment Implications for Long-Term Management

• Long-term treatment is required for most patients due to the high recurrence rate.
• Lithium is the most effective maintenance treatment, reducing both relapse and suicide risk.
• Combination therapy (Lithium + Antipsychotics or Valproate) may be required for refractory cases.
• Psychoeducation, psychotherapy, and lifestyle modifications are essential for relapse prevention.

© jPsychiatrie
2023-03: Impulse Control Disorders.

Impulse Control Disorders

Impulse Control Disorders (ICDs) are characterized by difficulty in resisting an impulse or temptation to
perform an act that is harmful to self or others. These disorders involve a sense of tension or arousal
before committing the act, followed by relief or gratification afterward, and often guilt or regret.

2.Types © jPsychiatrie
Intermittent Explosive Disorder (IED) Recurrent aggressive outbursts, disproportionate to triggers, often
resulting in physical assault or property destruction.
Kleptomania Recurrent stealing of items without monetary gain or necessity,
often associated with anxiety relief after theft.
Pyromania Compulsive fire setting for pleasure, fascination with fire and
firefighting.
Pathological Gambling (Gambling Disorder) Uncontrollable urge to gamble despite negative personal and
financial consequences.
Trichotillomania (Hair-Pulling Disorder) Recurrent hair pulling, leading to hair loss and distress.
Compulsive Buying (Oniomania) Uncontrollable shopping urges, leading to financial and
psychological distress.

• ICD-10: Classified under “Habit and Impulse Disorders” (F63), including pathological gambling, pyromania,
kleptomania, and trichotillomania.

• ICD-11: Categorized under “Impulse Control Disorders” (6C70-6C7Z), including compulsive sexual behavior
disorder and intermittent explosive disorder.

• DSM-5: Listed under “Disruptive, Impulse-Control, and Conduct Disorders”, which also includes
oppositional defiant disorder (ODD) and conduct disorder (CD).

Classification of Impulse Control Disorders

ICD-10 (F63 – Habit and Impulse Disorders)

ICD-10 Code Disorder Description
F63.0 Pathological Gambling Persistent, maladaptive gambling behavior
F63.1 Pyromania Repeated deliberate fire-setting without external
motivation
 motivation
F63.2 Kleptomania Recurrent stealing without financial necessity
F63.3 Trichotillomania Recurrent hair-pulling leading to hair loss
F63.8 Other Habit and Impulse Disorders Includes compulsive shopping, compulsive sexual
behavior
F63.9 Unspecified Habit and Impulse Disorder Atypical or unclassified cases

ICD-11 (6C70-6C7Z – Impulse Control Disorders)

ICD-11 Code Disorder Description
6C70 Pyromania Recurrent deliberate fire-setting with tension relief
6C71 Kleptomania Repeated failure to resist stealing
6C72 Compulsive Sexual Behavior Disorder Persistent failure to control sexual urges
6C73 Intermittent Explosive Disorder (IED) Recurrent aggressive outbursts
6C7Y Other Specified Impulse Control Disorders Includes compulsive shopping, self-mutilation
6C7Z Unspecified Impulse Control Disorder Cases that do not fit existing categories

DSM-5 Disruptive, Impulse-Control, and Conduct Disorders

1. Intermittent Explosive Disorder (IED) – Impulsive aggression out of proportion to provocation.

2. Kleptomania – Compulsive stealing of objects not needed for personal use.
3. Pyromania – Fire-setting for emotional release, not for revenge or monetary gain.
4. Oppositional Defiant Disorder (ODD) – Persistent defiance, irritability, and argumentative behavior, mainly in
children.
5. Conduct Disorder (CD) – Violation of societal norms, including aggression and destruction of property.

3. Neurobiology and Risk Factors

a) Neurochemical Basis
• Serotonin Dysfunction: Low levels of 5-HIAA (serotonin metabolite) in cerebrospinal fluid (CSF) are linked

© jPsychiatrie
to impulsivity.
• Dopaminergic System Dysregulation: Increased dopamine activity contributes to reward-seeking behavior
(seen in gambling and kleptomania).
• Testosterone and Aggression: Higher testosterone levels may be associated with intermittent explosive
disorder.

b) Genetic and Environmental Factors

• Family History of ICDs, ADHD, or Substance Use Disorders increases risk.
• Childhood Trauma (Abuse, Neglect, Parental Substance Use) is linked to increased aggressive and
impulsive behaviors.

4. Assessment and Diagnosis

Step 1: Clinical Interview and History
• Detailed history of impulse episodes, triggers, and consequences.
• Assess premonitory urges before the act and relief afterward.

Step 2: Use of Structured Screening Tools

• Barratt Impulsiveness Scale (BIS-11): Measures impulsivity.
• Kleptomania Symptom Assessment Scale (K-SAS).
• Pathological Gambling Screening Questionnaire (PGSI).

Step 3: Rule Out Differential Diagnoses

OCD Repetitive behaviors but driven by anxiety rather than impulse gratification.
Substance Use Disorders Impulsivity linked to drug effects rather than an independent disorder.
Antisocial Personality Disorder Repetitive rule-breaking with lack of remorse.

5. Stepwise Management of Impulse Control Disorders

Step 1: Non-Pharmacological Management (First-Line Treatment)
Step 1: Non-Pharmacological Management (First-Line Treatment)
1. Cognitive-Behavioral Therapy (CBT)
• Exposure-Response Prevention (ERP) for trichotillomania and kleptomania.
• Cognitive restructuring to address dysfunctional impulsive thoughts.
2. Habit Reversal Therapy (HRT)
• Most effective for trichotillomania and skin-picking disorder.
3. Motivational Interviewing (MI)
• Used in gambling disorder to enhance motivation to change.
4. Mindfulness-Based Cognitive Therapy (MBCT)
• Helps increase impulse control and reduce stress-related impulsivity.

Step 2: Pharmacological Management (Adjunct to Therapy)

Disorder First-Line Pharmacotherapy Alternative Treatments

Intermittent Explosive Disorder SSRIs (Fluoxetine 20-60 mg/day) Mood Stabilizers (Valproate, Lithium)
(IED)
Kleptomania SSRIs (Fluoxetine, Sertraline) Naltrexone (Opioid Antagonist) 50-100
mg/day
Pyromania No FDA-approved treatment SSRIs and mood stabilizers (limited
evidence)
Pathological Gambling Naltrexone (50-100 mg/day) SSRIs, Topiramate
Trichotillomania NAC (N-Acetylcysteine) 1200-2400 SSRIs, Olanzapine
mg/day
Compulsive Buying SSRIs (Fluvoxamine, Fluoxetine) Mood stabilizers (Lamotrigine).

© jPsychiatrie
6. Long-Term Course and Prognosis
• Intermittent Explosive Disorder: Symptoms may decrease with age, but risk of legal and social
consequences remains.
• Kleptomania and Pathological Gambling: Chronic with high relapse rates.
• Trichotillomania: 50% may remit with treatment, but often chronic without therapy.
• Pyromania: Often associated with antisocial traits, poor prognosis without intervention.

Factors Affecting Prognosis

Good Prognosis Poor Prognosis
Early intervention Delayed diagnosis
Compliance with therapy Substance use comorbidity
Strong family support Legal consequences

Summary = ICDs involve failure to resist an impulse, leading to harm or distress.

1. Common types: IED, Kleptomania, Pyromania, Pathological Gambling, Trichotillomania.
2. Pathophysiology: Serotonin and dopamine dysfunction play key roles.
3. Diagnosis involves: Clinical history + Impulsivity rating scales (BIS-11, PGSI).
4. First-line treatment: CBT, Habit Reversal Therapy, Motivational Interviewing.
5. Pharmacotherapy:
• SSRIs for Kleptomania, Gambling, IED.
• Naltrexone for Gambling, Kleptomania.
• NAC for Trichotillomania.
6. Chronic course with high relapse rates, requiring long-term behavioral therapy.

References
• Kaplan & Sadock’s Study Guide & Self-Examination Review
• The Maudsley Prescribing Guidelines
• CPG Guidelines on Impulse Control Disorders
2023-04: Benzodiazepine abuse in general medical practice.

Benzodiazepine Abuse
1. Introduction to Benzodiazepine Abuse
• Benzodiazepines (BZDs) are commonly prescribed for anxiety, insomnia, and seizures but have high abuse
potential.
• Dependence can be iatrogenic (prescribed long-term use) or non-iatrogenic (illicit use at high doses).
• Long-term use leads to tolerance, dependence, withdrawal symptoms, and cognitive impairment.

2. Patterns of Benzodiazepine Abuse in Medical Practice

a) Iatrogenic Dependence
○ Occurs due to long-term prescription beyond 4 weeks.
○ Common in older adults, chronic anxiety patients, and those with psychiatric comorbidities.
○ High-risk agents: Alprazolam, Lorazepam (short-acting, high potency).

b) Recreational or Polysubstance Abuse

○ BZDs are used with opioids, alcohol, or stimulants for enhanced sedation.
○ Commonly abused forms:
○ Alprazolam, Clonazepam, Diazepam (prescription diversion).
○ Flualprazolam, Etizolam (illicit designer benzodiazepines).

c) Risk Groups for BZD Misuse

○ Elderly: Long-term prescriptions for insomnia, cognitive decline.
○ Patients with anxiety disorders: Chronic use leads to dependence.

© jPsychiatrie
○ Substance abusers: Co-ingestion with opioids, alcohol increases overdose risk.
○ Medical professionals: Easy access increases risk of self-medication and abuse.

3. Clinical Features of Benzodiazepine Dependence and Withdrawal

a) Signs of Chronic BZD Use
• Cognitive deficits (memory impairment, slowed processing).
• Increased sedation, emotional blunting.
• Paradoxical aggression or disinhibition in some patients.

b) Withdrawal Symptoms (Abrupt Discontinuation)

• Mild: Anxiety, insomnia, tremors, sweating.

• Moderate: Irritability, depersonalization, dizziness.
• Severe (life-threatening): Seizures, delirium, psychosis, autonomic instability.

• Onset:
• Short-acting BZDs (Alprazolam, Lorazepam): Symptoms start in 6-12 hours.
• Long-acting BZDs (Diazepam, Clonazepam): Onset in 24-48 hours, lasts longer.

4. Management of Benzodiazepine Abuse

4. Management of Benzodiazepine Abuse
Step 1: Identification and Screening
• Use screening tools:
• Benzodiazepine Dependence Questionnaire (BDEPQ).
• DSM-5 criteria for Sedative-Hypnotic Use Disorder.
• Assess polysubstance use (opioids, alcohol, cannabis).

© jPsychiatrie
Step 2: Gradual Tapering Approach (First-Line)
• Switch to a long-acting BZD (Diazepam or Clonazepam) to reduce withdrawal severity.
• Tapering Protocol (Diazepam Equivalent Dosing):

• Tapering Protocol (Diazepam Equivalent Dosing):

Week Diazepam Dose
Baseline 30 mg/day
Week 2 25 mg/day
Week 4 20 mg/day
Week 6 18 mg/day
Week 8 16 mg/day
Week 10 14 mg/day
Week 12 12 mg/day
Week 14 10 mg/day
Final taper: Reduce by 2 mg every 2 weeks until cessation.

• Faster Taper (for moderate dependence): Reduce 10-25% dose per week.
• Slower Taper (for severe dependence): Reduce 5-10% per week.

Step 3: Pharmacological Management

1. Adjunctive Medications (for Withdrawal Symptoms)
• Carbamazepine (200-600 mg/day): Helps prevent seizures, mood stabilization.
Valproate (750-1200 mg/day): Reduces withdrawal anxiety.
 • Valproate (750-1200 mg/day): Reduces withdrawal anxiety.
• Melatonin (3-6 mg at bedtime): Improves sleep quality.

2. For Severe Withdrawal Symptoms

• Clonidine (0.1-0.2 mg BID) for autonomic hyperactivity.
• Propranolol (20-40 mg BID) for anxiety and tremors.

3. For Anxiety and Relapse Prevention

• SSRIs (Sertraline 50-100 mg, Escitalopram 10-20 mg) – for comorbid anxiety disorders.
• Gabapentin (300-900 mg/day) – Reduces cravings and anxiety.

Step 4: Non-Pharmacological Interventions

1. Cognitive-Behavioral Therapy (CBT)
• Addresses triggers for BZD use and coping mechanisms.
• Useful in patients with anxiety, insomnia, or trauma history.

2. Motivational Enhancement Therapy (MET)

• Increases patient readiness to discontinue BZDs.

3. Sleep Hygiene Therapy

• Regulates circadian rhythm without sedative-hypnotics.

4. Family and Social Support

• Involvement of caregivers improves adherence to tapering schedules.

5. Prevention Strategies in General Medical Practice

• Prescribe BZDs only for short-term use (2-4 weeks max).
• Use non-BZD alternatives for anxiety (SSRIs, CBT).
• Regularly reassess chronic users for tapering.

© jPsychiatrie
• Educate patients about dependence risks before starting treatment.
• Avoid high-risk prescriptions (Alprazolam, Lorazepam) in elderly.

6. Special Considerations
a) Management of Overdose
• Symptoms: Sedation, respiratory depression, coma.
• First-line Treatment:
• Flumazenil (BZD antagonist) 0.2 mg IV over 30 seconds, max dose 2 mg.
• Caution: Avoid in chronic BZD users due to seizure risk.
• Supportive care: IV fluids, airway protection.

b) BZD Use in Pregnancy

• Avoid withdrawal in pregnancy due to risk of seizures.
• Gradual tapering preferred over abrupt cessation.
• If BZD is required, Diazepam (low dose) is preferred.
Summary
BZDs have high abuse potential, leading to dependence and cognitive impairment.
1. Short-acting BZDs (Alprazolam, Lorazepam) have higher withdrawal risks.
2. Tapering strategy: Convert to long-acting BZD (Diazepam), then gradual dose reduction.
3. Adjunctive therapy (Carbamazepine, Valproate, SSRIs) may help withdrawal symptoms.
4. CBT, Motivational Interviewing, and Psychoeducation are essential in relapse prevention.
5. Flumazenil should be used cautiously in overdose cases due to seizure risk.
6. Prescribe BZDs cautiously in general practice, restricting use to ≤4 weeks.

References
© jPsychiatrie
• The Maudsley Prescribing Guidelines (14th Edition)
• AIIMS Substance Use Manual
• CPG Guidelines on Sedative Use Disorders
© jPsychiatrie