VI.

YEAR
English-questions for psychiatry examination
I. 1.) Diagnosis and classification in psychiatry
2.) Schizophrenia-acute and long term treatment, rehabilitation
II. l.) Important laboratory tests (psychological, imaging,etc.)in psychiatry
2.) Anxiety disorders II.: posttraumatic stress disorder, obsessive-compulsive disorder-
etiology, epidemiology, diagnostic criteria, subtypes, course and outcome, differential
diagnosis
III. l.) Basic psychoanalytic concepts
2.) Alcoholism (inc. alcohol withdrawal and alcohol hallucinosis) treatment and rehabilitation
IV. l.) Family therapy. Autogen training. Hypnosis.
2.) Suicide-etiology, epidemiology and prevention

V. l.) Psychopharmacology I.: Antipsychotics and anxiolytics: mechanism of action, indications,

effects and side effects
2.) Eating disorders-diagnostic criteria and clinical management

VI. l.) Delirium-etiology,diagnostic criteria and clinical management

2.) Anxiety disorders II.:posttraumatic stress disorders,obsessivecompulsive disorder-
treatment

VII. l.) Schizophrenia-etiology, diagnostic criteria, subtypes, course and outcome, differential
diagnosis
2.)Sleep disorders-diagnostic criteria and clinical management

VIII. l.) Mood (affective) disorders-etiology,diagnostic criteria, subtypes, course and

outcome, differential diagnosis
2.) Behavior and cognitive therapies

IX. l.) Anxiety disorders I.:panic disorder and agoraphobia, generalized anxiety disorder, phobic
disorders, etiology, epidemiology, diagnostic criteria.subtypes.course and outcome,
differential diagnosis
2.) Psychopharmacology II.:Antidepressant drugs and other biological therapies (ECT, sleep
deprivation, bright light treatment): mechanism of action, indications, effects and side
effects

X. l.) Anxiety disorders I.:panic disorders and agoraphobia, generalized anxiety disorder, phobic
disorders-treatment
2.) Sexual disorders-diagnostic criteria and clinical management

XI. l.) Somatoform,somatization and conversion disorders and hypocchondriasis-

etiology, diagnostic criteria and clinical management
2.) Dementia-etiology, diagnostic criteria and clinical management

XII. l.) Alcoholism-epidemiology,diagnostic criteria(incl.alcohol withdrawal and alcohol

hallucinosis), course and outcome
2.) Mood (affective)disorders-acute and long term treatment
XIII. l.) Psychoactive Substance use disorders-diagnostic criteria and clinical management
2.) Personality disorders-diagnostic criteria (clusters a-b-c) and clinical management
XIV. l.) Disorders of childhood and adolescence-diagnostic criteria of psychiatric disorders usually
first evident in infancy, childhood or adolescence
2.) Interviewing and assesment incl. special assessment of children
1. Diagnosis and classification in psychiatry

Psychiatric assessment

- Patient information: sex, age, marital status etc

o Reliability of the patient: utilize collateral source if patient unable/unwilling to cooperate
- Chief complaint: in patients own words, duration
- History of present illness
o Reason for seeking help (that day), current symptoms (onset, duration, course), stressors,
supports, functional status, relevant associated symptoms
o Safety screen: endangering self or others? Dependents at home (children, pets)?, ability to drive
safely, ability to care for self (e.g. eating, hygiene, taking medications)
- Psychiatric functional inquiry
o Mood: depression, mania
o Anxiety: worries, panic attacks, phobias, history of trauma
o Obsessive-compullsive: obsessions, compulsions
o Psychosis: hallucinations, delusions
o Risk assessment: suicidal ideation, plan, intent, history of attempts
o Organic: alcohol/drugs use or withdrawal, illness, dementia
- Past psychiatric history
o All previous psychiatric diagnoses, psychiatric contacts, treatments (pharmacological and non-
pharmacological), and hospitalizations
o Include past suicide attempts, substance use/abuse, and problems/encounters with the legal
system
- Past medical/surgical history
- Family psychiatric/medical history
- Past personal/developmental history (as relevant)
o Prenatal and perinatal history (domestic violence, maternal substance abuse and exposures,
complications of pregnancy etc.)
o Early childhood to age 3 (developmental milestones, activity/attention level, family stability,
attachment figures)
o Middle school age to age 11 (school performance, peer relationships, fire-setting, stealing,
incontinence)
o Late childhood to adolescence (drugs/alcohol, legal problems, peer and family relationships)
o History of physical or sexual abuse
o Adulthood (education, occupations, relationships)
o Personality before current illness, recent changes in personality
o Psychosexual history (puberty, first sexual encounter, romantic relationships, gender roles, sexual
dysfunction)

Mental status exam

- ASEPTIC
o Appearance and behavior
o Speech
o Emotions and affect
o Perception
o Thought process and content
o Insight to own illness
o Cognition
- General appearance
o Dress, grooming, gait, body habitus, facial expression, distress etc.
- Behavior
o Psychomotor activity – agitation, retardation
o Abnormal movements – tremors, akathisia, tardive dyskinesia, paralysis
o Attention level and eye contact
o Attitude toward examiner – ability to interact, level of cooperation
- Speech
o Rate, rhythm/fluency, volume, tone, articulation, quantity, spontaneity
- (emotion) Mood and affect
o Mood: subjective emotional state (in patients own words)
o Affect: objective emotional state inferred from emotional responses to stimuli; described in terms
of
§ Quality (euthymic, depressed, elevated, anxious, irritable)
§ Range (full, restricted, flat, blunted)
§ Stability (fixed, labile)
§ Mood congruence (inferred by reader by comparing mood and affect descriptions)
§ Appropriateness to thought content
o Some clinicians use 0-10 scales when rating mood to help get a subjective norm for each patient
that can help establish changes over time and with treatment
- Thought process/form
o Coherence (coherence, incoherent)
o Logic (logical, illogical)
o Stream
§ Goal-directed: clearly answers questions in a linear, organized, logical fashion
§ Circumstantial: speech that is indirect and delayed in reaching its goal; eventually comes
back to the point
§ Tangential: speech is oblique or irrelevant; doesn’t come back to original point
§ Loosening of associations/derailment: illogical shifting btw topics
§ Flight of ideas: quickly skipping from one idea to another where the ideas are marginally
connected, usually associated with mania
§ Word salad: jumble of words lacking meaning or logical coherence
o Perseveration: repetition of the same verbal or motor response to stimuli
o Echolalia: repetition of phrases or words spoken by someone else
o Thought blocking: sudden cessation of flow of thoughts and speech
o Clang association: speech based on sound such as rhyming or punning
o Neologism: use of novel words or of existing words in a novel fashion
- Thought content
o Suicidal ideation/homicidal ideation
§ Frequency and pervasiveness of thoughts, formulation of plan, means to plan, intent,
active vs passive, protective factors
o Preoccupations, ruminations: reflections/thoughts at length, not fixed or false
o Obsession: recurrent and persistent thought, impulse, or image which is intrusive or inappropriate
and unwanted
§ Cannot be stopped by logic or reason
§ Causes marked anxiety and distress
§ Common theme: contamination, orderliness, sexual, pathological doubt/worry/guilt
o Magical thinking: belief that thinking something will make it happen; normal in children and
certain cultures
o Ideas of reference: similar to delusions of reference, but less fixed (the reality of the belief is
questioned)
o Overvalued ideas: unusual/odd beliefs that are not of delusional proportions
o First rank symptoms of schizophrenia: thought insertion/withdrawal/broadcasting
o Delusions: a fixed false belief that is out of keeping with a persons cultural or religious background
and is firmly held despite incontrovertible proof to the contrary
- Perception
o Hallucination: Sensory perception in the absence of external stimuli that is similar in quality to a
true perception
§ Auditory (most common), visual, gustatory, olfactory, tactile
o Illusions: misperception of a real external stimulus
§ E.g. mistaking a coat on a rack as a person late at night
o Depersonalization: change in self-awareness such that the person feels unreal, distant, or
detached from his/her body, and/or unable to feel emotion
o Derealization: feeling that the world/outer environment is unreal
- Cognition
o Level of consciousness (alert, reduced, obtunded)
o Orientation: time, place, person
o Memory: immediate, recent, remote
o Global evaluation of intellect
§ Below average, average, above average
§ In keeping with person’s education
o Intellectual functions: attention, concentration, calculation, abstraction (proverb interpretation,
similarities test), language, communication
o MMS/MOCA useful as standard screening assessment of cognition
- Insight
o Patients ability to realize that he or she has a physical or mental illness and to understand its
implications (none, limited, partial, full)
- Judgement
o Patients ability to understand relationships btw facts and draw conclusions that determine one’s
actions

Assessment and plan

- Historical multiaxial model

o Since DSM-5, this model is no longer used. Instead, relevant psychiatric and mental diagnoses are
simply listed.
o Multiaxial assessment:
§ Axis I: differential diagnosis of DSM-5 clinical disorders
§ Axis II: personality disorders, developmental disability
§ Axis III: general medical conditions potentially relevant to understanding/management of
the mental disorder
§ Axis IV: psychosocial and environmental issues
§ Axis V: global assessment of functioning (GAF, 0 to 100) incorporating effects of axes I to
IV
- After history and MSE, the assessment and plan is recorded
- Assessment/problem formulation
o Identify predominant symptom cluster (mood, anxiety, psychosis, organic) causing the most
distress/interference, persist when other symptoms categories not present (e.g. psychosis in the
absence of mood symptoms)
o Dominating symptoms will direct dfferential
o Consider current issues as they relate to an individuals factors in three domains: biological,
psychological, and social
o For each category: predisposing, precipitating, perpetuating, and protecting factors are
considered
- Approach to management
o Consider short-term and long-term, and three types: biological (e.g. pharmacotherapy),
psychological (e.g. CTB), and social (e.g. support group)

The psychiatric examination

- Goals:
o 1. Assess complaints and mental status of the patient
o 2. Identify symptoms of psychiatric disorder or immediately dangerous behaviors
o 3. Make provisional diagnosis and necessary investigation and treatment plan
o 4. Judge whether emergency intervention is necessary

- Includes physical and neurological examination – certain somatic conditions can cause psychiatric
symptoms and vice versa
- Collect information from family, friends or paramedics
Psychiatric status
- Provides description of the most relevant psychological functions, behavioral responses and
psychopathological symptoms. It records both the pathological symptoms and the physiologic functions/
behaviors.
- Depicts the current mental condition and indicates a pattern of affected functions by the time the patient
was examined by the recording psychiatrist.

1. Consciousness-related functions: - the awareness of self and environment

- Consciousness – alertness (vigility) and quality (integrity)
- Orientation – time, space, self, others
- Attention- alertness (vigility) and ability to sustain focus (tenacity)

2. Perceptual functions: - ability to detect and recognize stimuli

- Perception – formal (quantity, quality) and content by sensory modality
o Hallucinations – sensory perception in absence of any external stimulus
o Illusions - false sensory perceptions in the presence of external stimulus / distortion of
sensory experience
o Pseudohallucination – experienced in internal or subjective space (“voices in my head”) and is
regarded as akin to fantasy

3. Cognitive functions: - ability to process, integrate/associate, learn and forget the perceived stimuli
- Thought – formal/procedural (speed, structure) and thought content disorder
o Thought content describe a patients delusions, overvalued ideas, obsessions, phobias and
preoccupations
- Concept formation – abstract thinking
- Memory – encode, store, retrieve
- Intellect – global cognitive ability

4. Emotional (affective) functions: - Archaic, non-analytic information processing, reflects subjective

involvement and disposition
- Mood – the long-lasting emotional tone with no specific object
o Euthymic, dysphoric, euphoric, angry, anxious, apathetic
- Self-feeling – the emotional tone of perceiving oneself, no object
- Emotional reactions – object oriented reaction reflecting one’s involvement
- Impulse- control – strength of affect control
- Anxiety – vegetative, subjective, behavioral signs

5. Volatile or response functions: - ability to initiate or respond actions

- Psychomotorium – planned motor activity
- Volatile functions – motivation, activity, instinct-driven behavior
- Communication – verbal, non-verbal
- Complex behavior – social activity, value orientation, personality functions, attitude towards the examiner

6. Risk factors: - symptoms that correlate with immediately dangerous behavior or efficacy of treatment
- Suicidal behavior – ideation, intention, past attempts
- Violent behavior – verbal, physical hostility, previous actions
- Insight of illness – adequate, partial
- Critical sense / judgement – intact, diminished
- Reality testing – ability to distinguish the objective / real contents from the subjective / fantasy elements
or distortion

7. Additional domains of mental status examination:

- Appearance: - assess physical aspects of the patient
o Colorful or bizarre clothing -> might suggest mania
o Unkempt, dirty clothes -> might suggest schizophrenia or depression
o Looks older than age -> chronic poor self-care or ill-health
o Body modifications, clothing not typical for gender -> personality
 o Features of alcohol or drug abuse
Classification

- Systems:
o ICD-10: international classification of diseases
o DSM: Diagnostic and statistical manual of mental disorders
- Advangates and disadvantages of DSM and ICD
o Advantages:
§ Improve reliability of dx
§ Clarify dx and facilitate history taking
§ Clarify and facilitate process of differential diagnosis
o Disadvantages:
§ False sense of certainty
§ May sacrifice validity for reliability
• Reliability: capacity of individuals to agree
• Validity: capacity to make useful predictions
§ Treat dx like checklist and forget about patient as a person

Diagnostic chapters of DSM5

- Neurodevelopmental disorders
- Schizophrenia spectrum and other psychotic disorders
- Bipolar

DSM5 classification

- Ideally, a classificactionn of disorder is based onn knowledge of etiology and pathophysiology because this
increases likelihood of improving treatment and prevention efforts, this is not yet possible in psychiatry.
- Diagnosis of mental disorders is absed on clinical observation of clusters of signs and symptoms that are
grouped together into disorders or syndromes which are then agreed upon by a consensus of psychiatrists
and other mental health profesionals
- ICD-10:
o Official classification system used in Europe and many other parts of the word
o DSM5 was designed to correspond to ICD-10, this was done to ensure uniform reporting of
national and international health statistics
o All categories used in DSM5 are found in ICD-10, but not all ICD-10 categories are in DSM-5

Basic features
- Descriptive approach
o Atheoretical with regard to causes
o DSM5 attempts to describe the manifestation of the mental disorder and only rarely attempts to
account for how the disturbance com about
o The definitions of the disorders usually consists of descriptions of clinical features
- Diagnostic criteria
o Specified diagnostic criteria are provided for each specific mental disorder
- Systematic description
o DSM5 systematiclly describes each disorder in terms of its associated features: specific age-
culture, and gender-related features; prevalence, incidence, and risk; course; complications;
predisposing factors; familial pattern; and differential diagnosis.
o DSM5 is a diagnostic manual, not textbook
o It doesn’t mention theories of causes, management, or treatment or the controversial issues

Classification
- 22 major categories
- Organization attempts to follow lifespan
o Neurodevelopmental disorders that occur early in life are listed first in the classifications sytem,
and neurocognitive disorders that occur toward end of life are listed last.
1. Neurodevelopmental disorders - Selective mutism
- Intellectual disability or intellectual
developmental disorder (prev MR) 8. Obsessive-compulsive and related disorder
- Communication disorders - OCD
- Autism spectrum disorder - Body dysmorphic disorder
- ADHD - Hoarding disorder
- Specific learning disorders - Trichotillomania or hair-pulling disorder
- Motor disorders - Excoriation or skin-pricking disorder
- Substance/medication-induced obsessive-
2. Schizophrenia spectrum and other psychotic compulsive disorder
disorders - Obsessive-compulsive disorder due to another
- Schizophrenia medical condition
- Delusional disorder - Other specified obsessive-compulsive and
- Brief psychotic disorder related disorder
- Schizophreniform disorder
- Schizoaffective disorder 9. Trauma- or stressor-related disorder
- Substance/medication-induced psychotic - Reactive attachment disorder
disorder - Disinhibited social engagement disorder
- Psychotic disorder due to another medical - PTSD
condition - Acute stress disorder
- Catatonia - Adjustment disorders
- Persistent complex berievement disorder
3. Bipolar and related disorders
- Bipolar I disorder 10. Dissociative disorders
- Bipolar II disorder - Dissociative amnesia
- Cyclothymic disorder - Dissociative fugue
- Bipolar disorder due to another medical - Dissociative identity disorder
condition - Depersonalization/derealization disorder
- Substance/medication induced bipolar
disorder 11. Somatic symptom and related disorders
- Somatic symptom disorder
4. Depressive disorders - Illness anxiety disorder
- Functional neurological symptom disorder
5. Major depressive disorder - Psychological factors affecting other medical
conditions
6. Persistent depressive disorder or dysthymia - Factitious disorder
- Premenstrual dysphoric disorder - Other specified somatic symptom and related
- Substance/medication-induced depressive disorder
disorder
- Depressive disorder due to another medical 12. Feeding and eating disorder
condition - Anorexia nervosa
- Other specified depressive disorder - Bulimia nervosa
- Unspecified depressive disorder - Binge eating disorder
- Disruptive mood dysregulation disorder - Pica
- Rumination disorder
7. Anxiety disorders - Avoidant/restrictive food intake disorder
- Panic disorder
- Agoraphobia 13. Elimination disorders
- Specific phobia
- Social anxiety disorder or social phobia 14. Sleep-wake disorders
- GAD - Insomnia disorder
- Anxiety disorder due to another medical - Hypersomnolence disorder
condition - Parasomnias
- Substance/medication induced anxiety - Narcolepsy
disorder - Breathing-related sleep disorders
- Separation anxiety disorder - Restless elg syndrome
- Substance/medication-induced sleep disorder - Substance use disorders
- Circadian rhythm sleep-wake diosrders - Alcohol-related disorders
- Other alcohol-induced disorders
15. Sexual dysfunctions - Gambling disorder
- Delayed ejaculation
- Erectile disorder 19. Neurocognitive disorders
- Female orgasmic disorder - Delirium
- Female sexual interest/arousal disorder - Milld cognitive disorder
- Genito-pelvic pain/penetration disorder - Major cognitive disorder
- Male hypoactive sexual desire disorder
- Premature or early ejeaculation 20. Personality disorders
- Substance/medication-induced sexual - Paranoid PD
dysfunction - Schizoid PD
- Other unspecified sexual dysfunction - Schizotypal PD
- OC PD
16. Gender dysphoria - Histrionic PD
- Avoidant PD
17. Disruptive, impulse-control, and conduct - Antisocial PD
disorder - Narcissistic PD
- Oppositional defiant disorder - Borderline PD
- Intermittent explosive disorder - Dependent PD
- Conduct disorder - Personality changes due to another medical
- Pyromania condition
- Kleptomania - Unspecified PD

18. Substance-related disorders 21. Paraphilic disorders

- Substance-induced disorders 22. Other mental disorders
2. Schizophrenia – acute and long term treatment, rehabilitation
13. Schizophrenia – etiology, diagnostic criteria, subtypes, course and outcome,
differential diagnosis.

Psychotic disorders

- Characterized by a significant impairment in reality testing (loss of contact with reality)

- Delusions (fixed false beliefs) or hallucinations (perceptual experiences without an external stimulus). With
or without insight into their pathological nature
- Behaving in a disorganized way so that its reasonable o infer that reality testing is disturbed

Differential diagnosis of psychosis

- Primary psychotic disorders: Schizophrenia, schizophreniform, brief psychotic, schizoaffective, delusional

disorder
- Mood disorders: depression with psychotic features, bipolar disorder (manic or depressive episode with
psychotic feature)
- Personality disorders. Schizotypal, schizoid, borderline, paranoid, obsessive-compulsive
- General medical conditions: tumor, head trauma, dementia, delirium, metabolic, infection, stroke,
temporal lobe epilepsy
- Substance-induced psychosis: intoxication or withdrawal, prescribed medications, toxins

Clinical features

- Positive symptoms (“added on”)

o Delusions: beliefs and conclusions held with strong conviction despite superior evidence to the
contrary. Always centered on one’s subjective self
§ E.g. feeling of being watched/followed/monitered, believing that they have special
abilities/powers, believed they are being controlled by forces or other individuals,
believed responsible for a negative event (e.g. earthquake)
§ Examination: Do you have any special abilities? Do you have a special mission in life? Has
anyone being controlling your thoughts? Etc.
§ Adviced behavior: Do not argue, do not confirm delusions
§ Bizarre – no possibility of being true. Non-bizarre – while not true its understandable and
could be true
§ Classification:
• Ideas/delusions of reference: e.g. tv deliver special message to them
• Grandiose: has special powers/significance
• Paranoid
• Nihilistic: believe they are dead/don’t exist
 • Erotomanic: believes he/she has special relationship with someone
o Conceptual disorganization: Disorganized thought process, observe via examining the patient
speech (how they say something, not what)
§ Clang association (ideas related only by similar or rhyming sounds), losing associations
(words not logically connected), neologism (formation of new meaningless words),
tangentially (wander from topic but they are connected), incoherence (extremely
disorganized speech is called word salad), circumstantiality (don’t answer question
directly, excessive details, eventually return to original point), blocking (abrupt
permanent stop in middle of train of thought)
o Perceptual disturbances
§ Hallucinations: perception in absence of external stimulus (most often auditory, can also
be visual, somatic, olfactory and gustatory) Illusions: external stimuli are present but
their sensation is distorted or misinterpreted.
§ Questions: have you ever had any unusual or strange experience? People sometimes tell
that they hear voices or sounds others cannot hear, how about you? Do you ever receive
personal messages from the tv, god, or devil? Do they give you commands, do you
follow?
o Catatonic symptoms: qualitative psychomotor disturbances, which can be associated with
different (psychiatric) disorders
§ Diagnosis require 3 or more of the following:
• Retarded symptoms:
o Stupor: no psychomotor activity, not actively relating to environment
o Catalepsy: mental inhibition of movement of voluntary muscles,
characterized by rigidity and fixity of posture regardless of external
stimuli
o Waxy flexibility: patient withholds passive movement steadily, but
posture can be altered into different, even bizarre positions, which are
held
o Negativism (active or passive): opposition or no response to
instructions or external stimuli
o Mutism: missing or very little verbal response
• Excited symptoms
o Stereotyping: repetitive, purposeless actions
o Agitation, grimacing: psychomotor agitation not influenced by external
stimuli. Jactation or “storm of movement” is an extreme form.
o Echolalia: mimicking anothers speech
o Echopraxia: mimicking anothers movement
• Other:
o Mannerism: odd, distorded use of normal actions, or use of normal
actions in odd context.
§ NB: Only modifier of another illness, mood/bipolar >> schizophrenia.
- Negative symptoms (“taken away”)
o Blunted affect: lack/decreased emotional reactivity to external stimuli
§ Disorder of non-verbal communication channels such as gesterues (reduced intensity),
vocal tone and inflection (monotonic, flat, emotionless speech)
o Restricted affect: lacking/decreased reactions to emotionally saturated topics (deaths, good news
etc), apathy, emotional distance
o Poor rapport: lacking/decreased eye contact, not answering questions, unable to identify others
feelings, not answering questions etc.
o Passive/apathetic social life or social withdrawal:
§ Hypobulia (lack initiative/will power), only involved in passive actions (e.g. tv), decreased
self sufficiency and hygiene, isolated (friends, family), social connections are short and
superficial, decreased sexual interest
o Lack of spontaneity and poverty of speech
§ Thought process characterized by alogia (unproductive, poor in topics), poor
speech/speak little, short and very concrete aswers after long latency (or not arriving at
all)
 o Disturbed abstract thinking (concretization): may be able to think in very simple terms, but will
not be able to solve complex problems, plan ahead, or organize thoughts
o Stereotypic thinking: only talk about a certain topic
o Other definitions
§ Anhedonia: inability to experience pleasure
§ Apathy: no longer care, lack of emotions and interest
§ Avolition: inability to initiate work towards goal-oriented activities

Management of acute psychosis and mania

- Ensure safety of self, patient, and other patients

- Have an exit strategy
- Decrease stimulation
- Assume a non-threatening stance
- IM medications (patient often refuse oral medication)
o Benzodiazepines + antipsychotics
- Physical restraints may be necessary
- Do not use antidepressants or stimulants

Schizophrenia

- Psychiatric disorder involving chronic or recurrent psychosis. Commonly associated with impairments in
social and occupational functioning.
- Clinical manifesteations: positive symptoms, negative symptoms, cognitive impairment, mood and anxiety
disorders

DSM-5 diagnostic criteria

- A: Two (or more) of the following, each present for a significant portion of time during a 1-month period
(or less if successfully treated). At least one of these must be 1-3.
o 1. Delusions
o 2. Hallucinations
o 3. Disorganized speech (e.g. frequent derailment or incoherence)
o 4. Grossly disorganized or catatonic behavior
o 5. Negative symptoms (i.e. diminished emotional expression or avolition)
- B: Decrease level of function:
o Decreased level of function: for a significant portion of time since onset, one or more major areas
affected (e.g. work, interpersonal relations, self-care) is markedly decreased (or if
childhood/adolescent onset, failure to achieve expected level)
- C: at least 6 months of continuous signs of disturbance.
o Must include at least 1 month of symptoms (or less if treated successfully) that meet criterion A
(i.e. active-phase symptoms) and may include periods of prodromal or residual symptoms (during
which, disturbance may manifest by only negative symptoms or by two or more criterion A
symptoms present in an attenuated form (e.g. odd beliefs, unusual perceptual experiences)
- D: rule out schizoaffective disorder and depressive or bipolar disorder with psychotic features because
either:
o 1) no major depressive or manic episodes have occurred concurrently with the active-phase
symptoms, or
o 2) if mood episodes have occurred during active-phase symptoms, they have been present for a
minority of the total duration of the active and residual periods of the illness
- E: rule out other causes:
o GMC, substances (e.g. drug of abuse, medication)
- F: if history of autism spectrum disorder or communication disorder of childhood onset, the additional
diagnosis of schizophrenia is made only if prominent delusions or hallucinations are present for at least 1
month (or less if successfully treated)
- Specifiers:
o Type of episode (e.g. first episode, multiple episodes, continuous)
o With catatonia
o Current severity based on quantitative assessment of primary symptoms of psychosis (in acute
episode, in partial remission, in full remission)
- Disorganized behaviors in schizophrenia:
o Catatonic stupor: fully conscious, but immobile, mute, and unresponsive
o Catatonic excitement: uncontrolled and aimless motor activity, maintaining bizarre positions for
long time
o Stereotypy: repeated but non-goal directed movement (e.g. rocking)
o Mannerism: goal-directed activities that are odd or out of context (e.g. grimacing)
o Echopraxia: imitates movements and gestures of others
o Automatic obedience: carries out simple commands in robot like fashion
o Negativism: refuses to cooperate with simple requests for no apparent reason
o Inappropriate affect, neglect of self-care, other odd behaviors

Malignant catatonia
- Acute onset of excitement, fever, autonomic instability, delirium, may be fatal

Epidemiology

- Prevalence: 0,3-0,7 %, M:F = 1:1

- Mean age of onset: females late 20s, males early-to mid 20s
- Suicide risk: 10% die by suicide, 30% attempt suicide

Etiology

- Multifactorial: disorder is a result of interaction btw both biological and environmental factors

- Genetic:
o 40% concordance in monozygotic (MZ) twins, 46% if both parents have schizophrenia
o 10% of dizygotic (DZ) twins, siblings, children affected
o Vulnerable genes include disrupted-in-schizophrenia 1 (DISC1), neurogulin 1 (NRG1); dystrobrevin
binding protein/dysbindin (DTNBP1); catechol-O-methyltransferease (COMT); d-amino acid
oxidase activator (DAOA); metabotropic glutamate receptor 3 (GRM3); and brain-derived
neurotrophic factor (BDNF)
- Neurochemistry
o Dopamine hypothesis
§ Excess activity in the mesolimbic dopamine pathway may mediate the positive symptoms
of psychosis
• Supported by:
o Most/all antipsychotic drugs block postsynaptic D2-R, esp in
mesolimbic and striatal-frontal system
o Drugs that increase dopaminergic activity (e.g. amphetamine)
aggravate schizophrenia
o Density dopamine receptors have been found to be increased in brain
of schizophrenic patients
o Successful treatment of schizophrenic patients have been reported to
change amount homovanillic acid
§ Decreased dopamine in the prefrontal cortex may mediate negative and cognitive
symptoms
o Serotonin hypothesis:
§ Majority new SGA are inverse agonists on 5-HT2 (mainly 2a and 2c) receptors
§ Different theories involvolving serotonins involvement in depressive mood, DA and 5-HT
balance etc.
o Glutamate hypothesis
 § Suggested that hypofunction of NMDA receptor located at GABAergic interneurons lead
to diminished inhibitory influence on neuronal function and thereby contributing to
schizophrenia
§ NMDA antagonist PCP may provoke psychotic symptoms
§ NMDA receptor require glycine for full function and has been suggested that patients
with schizophrenia has NMDA receptors with not fully saturated glycine sites
o Disturbance in regulation hypothesis
§ GABA system (stimulation – decrease DA release)
§ 5-HT system
§ Glutamate system (enhance DA release)
§ Cholecystokinin
§ ACh
- Neuroanatomy:
o Decreased frontal lobe function, asymmetric temporal/limbic function; decreased basal ganglia
function; subtle changes in thalamus, cortex, corpus callosum, and ventricles; cytoarchitectural
abnormalities
- Neuroendocrinology
o Abnormal GH, prolactin, cortisol, and ACTH
- Neuropsychology
o Global defects in attention, language, and memory suggest disrupted connectivity of neural
networks
- Environmental
o Indirect evidence of cannabis use, geographic variance, winter season of birth (viral exposure?),
obstetrical complications, and prenatal viral exposure
o More common in lower socioeconomic status groups:
§ Downward drift theory: schizophrenics drift down in social groups as disorder develops
§ Social causation theory: being in lower social class can lead to higher stress levels which
can trigger schizophrenia

Pathophysiology

- Neurodegenerative theory: Natural history may be a rapid or gradual decline in function and ability to
communicate
o Glutamate system may mediate progressive degeneration by excitatory mechanism which lead to
production of free radicals
- Neurodevelopmennntal theory: abnormal development of brain from prenatal life
o Neurons fail to migrate correctly, make appropriate connections, and apoptosis in later life
§ Disconnection or abnormal connection btw frontal, temporal and parietal lobe

Comorbidity

- Substance-related disorders
- Anxiety disorders
- Reduced life expectancy secondary to medical comorbidities (e.g. obesity, DM, metabolic syndrome,
CV/pulmonary disease)

Subtypes

- Five subtypes of schizophrenia have been described based predominantly on clinical presentation:
paranoid, disorganized, catatonic, undifferentiated, and residual
- DSM5 no longer uses these subtypes but they are listed in the ICD-10

- Paranoid type:
o Characterized by one or more delusions or frequent auditory hallucinations
o Classically delusions of persecution or grandeur
o Usually have first episode at an older age than catatonic or disorganized schizophrenia
 o Show less regression of mental faculities, emotional responses, and behavior than to patients
with other types of schizophrenia
o Typically tense, suspicious, guarded, reserved, and sometimes hostile or aggressive, but can
occasionally conduct themselves adequately in social situations
- Disorganized type
o Characterized by a marked regression to primitive, disinhibited, and unorganized behavior and by
the absence of symptoms that meet the criteria for the catatonic type
o Generally early onset (<25y)
o Usually active but inn an aimless, non-constructive manner.
o Thought disorder is pronounced and their contact with reality is poor. Personal appearance is
disheveled, and their social behavior and their emotional responses are inappropriate
o They often burst into laughter without any apparent reason. Incongruous grinning and grimacing
are common in these patients, whose behavior is best described as silly or fatuous
- Catatonic type
o Decreasing incidence
o Classic feature is marked disturbance of motor function; this disturbance may involve stupor,
negativism, rigidity, excitement, or posturing.
o Sometimes patients may show rapid alteration btw extremes of excitement and stupor
o Associated features include stereotypies, mannerism, and waxy flexibility.
o Mutism is particularly common
o During catatonic excitement patients need careful supervision to prevent them from hurting
themselves or others,
o Medical care may be needed because of malnutrition, exhaustion, hyperpyrexia, or self-inflicted
injury
- Undifferentiated type
o Patients with schizophrenio who cannot be asily fit into one type or another
- Residual type
o Characterized by continuing evidence of the schizophrenic disturbance in the absence of a
complete set of active symptoms or sufficient symptoms to meet the diagnosis of another type of
schizophrenia
o Emotional blunting, social withdrawal, eccentric behavior, illogical thinking, and mild loosening of
associations commonly appear in the residual type
o When delusions or hallucinations occur, they are neither prominent nor accompanied by strong
affect
- Other subtypes (appear in literature, esp in countries other than US)
o Bouffee delirante (acute delusional psychosis)
o Latent (now called borderline, schizoid, schizotypal personality)
o Oneiroid (dream like state, engaged in hallucinatory experiences to the exclusion of involvement
in the real world)
o Paraphrenia (sometimes used as synonym for paranoid schizophrenia)
o Pseudoneurotic schizophrenia
o Simple schizophrenia
o Postpsychotic depressive disorder of schizophrenaia
o Early onset (childhood)
o Late onset (>45y)
o Deficit schizophrenia

Management of schizophrenia

- Assessment prior to treatment if possible and at regular intervals for

o Signs of movement disorder incl EPS and TD
o Symptoms of metabolic syndrome, incl BMI, waist circumference, HBA1c, serum lipids, and BP
o ECG for pt with history of cardiac disease or when starting an antipsychotic that prolongs QT
interval
- Changing antipsychotic medication
o Cross titatration – simultaneous taper of current medciation with titration of replacement drug
over days-weeks
 o Maintain current medication at full dose as increase new medication, once second drug has
reached target dose, first med may be gradually decreased (if high risk relapse)

- Biological/somatic:
o Acute treatment and maintenance:
§ Antipsychotics (haloperidol, risperidone, olanzapine etc):
• Often IM every 2-4w to ensure compliance
• Choose drug based on clinical factors and SE profiles. With exception of
clozapine for pt with refractory symptoms there is not convincing evidence to
favor one over the other based on efficacy.
• Should be continued indefinitely at lowest effective dose
§ +/- mood stabilizers
• For aggression/impulsiveness – lithium, valproate, carbamazepine
§ +/- anxiolytics
§ +/- ECT
§ Treat for at least 1-2 years after first episode, at least 5y after multiple episodes (relapse
causes severe deterioration)
- Psychosocial
o Psychotherapy (individual, family, group), supportive, CBT
o ACT (assertive community treatment): mobile health teams that provide individualized treatment
in community and help patients with medication adherence, basic living skills, social support, job
placement, resources
o Social skill training, employment programs, disability benefits
o Housing (group home, boarding home, transitional home)

Course and prognosis

- Majority of individuals display some type of prodromal phase

- Course is variable: some individuals have exacerbations and remissions while others remain chronically ill,
accurate prediction of long-term outcome is not possible
- Negative symptoms may be prominent early in the illness and may become more prominent and more
disabling later on; positive symptoms appear and typically diminish with treatment
- Over time: 1/3 improve, 1/3 remain the same, 1/3 worsen

- Good prognostic factors:

o Acute onset
o Shorter duration prodrome
o Female gender
o Good cognitive functioning
o Good premorbid functioning
o No family history
o Presence of affective symptoms
o Absence of structural brain abnormalities
o Good response to drugs
o Good support system

Schizophreniform disorder

Diagnosis

- Criterion A, D, and E of schizophrenia are met. Lasts 1 month-6months (if beyond 6m = schizophrenia)
- Specifiers:
o W./w.o good prognostic features (e.g. acute onset, confusion, good premorbid functioning,
absence of blunt/flat affect), with catatonia, current severity based on quantitative assessment of
primary symptoms of psychosis

Treatment - Similar to acute schizophrenia

Prognosis

- Better than schizophrenia; begins and ends more abruptly; good pre- and post-morbid function

Brief psychotic disorder

- Can occur after a stressful event or postpartum

Diagnosis

- Criterion A1-A4, D, and E of schizophrenia. Last 1d-1month. Eventual return to premorbid level of
functioning
- Specifiers:
o w/w.o marked stressor, with postpartum onset, with catatonia, current severity

Treatment

- secure environment, antipsychotics, anxiolytics

Prognosis

- Good, self-limiting, should return to pre-morbid function within 1 month

Schizoaffective disorder

DSM-5 diagnostic criteria

- A: concurrent psychosis (criterion A schizophrenia) and a major mood episode – uninterrupted period of
illness
- B: delusions or hallucinations for 2 or more weeks in the absence of a major mood episode during the
lifetime duration of the illness
- C: major mood episode symptoms are present for the majority of the total duration of the active and
residual periods of the illness
- D: the disturbance is not attributable to the effects of a substance or another medical condition

- Specifiers:
o Bipolar type, depressive type, with catatonia, type of episode, severity

Epidemiology

- 1/3 as prevalent as schizophrenia

- Schizoaffective disorder bipolar type more common in young adults, schizoaffective disorder depressive
type ore common in older adults
- Depressive symptoms correlated with higher suicide risk

Treatment - Antipsychotics, mood stabilizers, antidepressants

Prognosis - Between that of schizophrenia and of mood disorder

Delusional disorder

DSM-5 diagnostic criteria for delusional disorder

- A: The presence of one (or more) delusions with a duration of 1 month or longer
- B: Criterion A for schizophrenia has never been met
 o NB: hallucinations, if present, are not prominent and are related to the delusional theme
- C: apart from impact of the delusion(s) or its ramifications, functioning is not markedly impaired, and
behavior is not obviously bizarre or odd
- D: If manic or major depressive episode have occurred, these have been brief relative to the duration of
the delusional periods
- E: the disturbance is not attributable to physiological effects of a substance or another medical condition
and is not better explained by another mental disorder

- Subtypes:
o Erotomanic, grandiose, jealous, persecutory, somatic, mixed, unspecified
- Further specifiy:
o Bizarre content, type of episode (e.g. first episode, multiple episode), severity

Treatment

- Psychotherapy
- Antipsychotics
- Antidepressants

Prognosis

- Chronic, unremitting course but high level of functioning

- A portion will progress to schizophrenia
3. Important laboratory tests (pscyhological, imaging etc.) in psychiatry

Lab

Neuroendocrine tests

- Thyroid function test

o Rule out hypothyroidism which can appear with symptoms of depression
o Up to 10% of pt complaining of depression and associated fatigue have incipient hypothyroid
disease
- Dexamethasone suppression test (DST)
o To help confirm diagnostic impression of major depressive disorder. Not routinely used because
unreliable. Abnormal resul may confirm need for somatic treatment
o Some evidence indicates that depressed nonsuppressors are likely to respond positively to
treatment with ECT or TCA
- Catecholamines
o Low CSF 5-HIAA is associated with suicidal depression, vioulence
o Plasma catecholamine levels are markedly elevated in pheochromocytoma, which is associated
with axiety, agitation, and hypertension
o High levels of urinary NE and E have been found in some patients with PTSD
o NE metabolite 3-methoxy-4-hydroxyphenylglycol level is decreased in pt with severe depressive
disorders, esp in those patients who attempt suicide
- Other
o Anterior pituitary hormones
o Melatonin – implicated in seasonal affective disorder

Renal and hepatic tests

- Renal function tests

o Related to lithium
- Liver function tests
o Elevated bilirubin in hepatocellular and intrahepatic bile staiss, which can occur with
phenothiazine or tricyclic medication and with alcohol and other substance abuse
o Abnormal LFTs can be present in disorientation and delirium
o LFTs must be monitored routinely when using certain drugs such as carbamazepine and valproate

STDs

- Test for it

Tests related to psychotropic drugs

- Benzodiazepines
o No special tests needed
- Antipsychotics
o No specific tests needed, although good to obtain baseline for liver function andn a complete
blood cell count
- Lithium
o Baseline thyroid function, electrolyte monitoring, WBC count, renal function tests, and baseline
ECG

Provocation of panic attacks with sodium lactate

- Up to 72% of patietns with panic disorder have a panic attack when administered with IV Na Lactate
- Lactate provocation is used to confirm diagnosis of a panic disorder and trigger flashbacks in pt with PSTD
- Hyperventilation is as sensitive as lactate provocation in inducing panic attacks
Lumbar puncture

- Used in pt who have a sudden manifestation of psychiatric symptoms, esp changes in cognition. Esp
vigilant if fever or neurological symptoms
- Use in diagnosis of CNS infections

Urine testing for substance abuse

Screening test for medical illness

- Rule out organic causes for the psychiatric disorder

- CBC with differential

- Complete blood chemistries (incl measurementns of electrolytes, glucose, calcium, and magnesium and
tests of hepatic and renal function)
- Thyroid function tests
- RPR or VDRL
- Urinalysis
- Urine toxicology screen
- ECG

Biochemical markers

- Many potential biochemical markers, incl neurotransmitters and their metabolites may help in the
diagnosis and treatment of psychiatric disorders

- Monoamines
o Plasma homovanillic acid, a major dopamine metabolite, may have value in identifying
schizophrenic patients who respond to antipsychotics
o 5-hydroxyindoleacetic acid is associated with suicidal behavior, aggression, poor impulse control,
and depression. Elevated levels may be associated with anxious, obsessional, and inhibited
behaviors
o 6-MPHG, a NE metabolite, decreased in depression and anxiety
Alzheimer’s disease

- Apolipoprotein E allele – associated with increased risk for alzheimers disease. Reduced glucose
metabolism noted on PET in some asymptomaic middle-aged persons, similar to findings in Alzheimer’s
patients
- Neutral thread protein – reported to be increased in patients with alzheimer’s diease. CSF neural thread
protein is marketed as a diagnostic test
- Other potential CSF tests include CSF tau (increased), CSF amyloid (decreased), ratio CSF albumin to serum
albumin (normal in alzheimer’s disease, elevated in vascular dementia), and inflammatory markers (e.g.
CSF acute phase reactive proteins). The gene for the amyloid precursor protein is considered to be of
possible etiological significance, but further research is needed

Imaging

Uses of neuroimaging

- Neurological deficits
o In neurological examination, any change that can be localized to the brain or spinal cord requires
neuroimaging
o Consider neuroimaging for patients with new-onset psychosis and acute change in mental status
- Dementia
o Alzheimer – diffuse loss of brain volume
o Normopressure hydrocephalus
- Stroke, vascular dementia
o Strokes are easily seen
o Vascular dementia is characterized on MRI by patches of inncrased signal in the white matter
§ Extensive atherosclerosis in brain capillaries can cause countless tiny infarctions of brain
tissue
- Degenerative disorders
o Huntingtons – atrophy of caudate nucleus
o Space occupying lesions
- Chronic infections
o Neurosyphilis, cryptococcosis, tuberculosis, and lyme disease may produce a characteristic
enhancement of the meninges, esp at the base of the brain
o MS plaques are easily seen on MRI scans as periventricular patches of increased signal intensity

Modalities

- CT
o Indications:
§ Dementia or depression
§ General cognitive and medical workup
§ Routine workup for any first-break psychosis
- MRI
o Ideal for MS and other demyelinating diseases
- PET
- BEAM (brain electrical activity mapping)
o Topographic imaging of EEG and evoked potentials
- Regional cerebral blood flow (rCBF)
o Blood flow is believed to correlate directly with neuronal activity
- fMRI
o schizophrenic patients show less frontal activation and more left temporal activation during word
fluency task in comparison wtith controls
4. Anxiety disorders: Posttraumatic stress disorder. Obsessive compulsive disorder.
Etiology, epidemiology, diagnostic criteria, subtypes, course and outcome, differential
diagnosis
12. Anxiety disorders. PTSD, OCD. Treatment
17. Anxiety disorders. Panic disorder, agoraphophobia, generalized anxiety disorder,
phobic disorders. Etiology, epidemiology, diagnostic criteria, subtypes, course, and
outcome. Ddx.
19. Anxiety disorders. Panic disorder, agoraphobia, GAD. Treatment

Anxiety disorders
- Mental feelings (worry, feel, hypervigilance) + physical symptoms

- Manifestations of anxiety is result of SNS activation, can be described through:

o Physiology:
§ Main brain structure involved is the amygdala (fear conditioning)
§ NT: 5-HT, cholecystokinin, E, NE, DA
o Psychology:
§ Ones perception of a given situation is distorted which causes one to believe its
threatening in some way
o Behavior:
§ Once feeling threatened, one responds by escaping or facing the situation, thereby
causing disruption in daily functioning
- Anxiety becomes pathological when:
o Fear is greatly out of proportion to risk/severity of threat
o Response continues beyond existence of threat or becomes generalized to other similar or
dissimilar situations
o Social or occupational functioning is impaired
o Often comorbid with substance use and depression

Panic disorder

- Characterized by recurrent episodes of brief overwhelming anxiety which often occur without any
triggering factor (“acute, overt (observable), catastrophic, out of the blue)
- Patients often fear having an attack and avoid situations where they might have an attack
- +/- agoraphobia
 o Perceives environment to be unsafe, fear going outside, being in large crowds etc. DSM-5
diagnostic criteria

- STUDENTS FEAR the 3 C’s

- Panic disorder consists of panic attacks + other criteria
- Panic attack ca occur in context of many different disorder

- A) Recurrent unexpected panic attacks – a panic attack is an abrupt surge of intense fear/discomfort that
reaches a peak within minutes, and during which 4 or more of the following symptoms occur
o Sweating
o Trembling, shaking
o Unsteadiness, dizziness, light-headed, or faint
o Depersonalization, Derealization
§ Derealization – feeling of unreality
§ Depersonalization – being detached from oneself
o Execessive heart rate, palpitations
o Nausea or abdominal distress
o Tingling, paresthesias (numbness, tingling sensation)
o SOB
o Fear of dying, losing control, going crazy
o Chest pain/discomfort
o Chills or heat sensation
o Choking (feelings of)
- B) 1 month (or more) of “anxiety about panic attacks” – at least one of the attacks has been followed by
one or both of the following:
o Persistent concern or worry about additional panic attacks or their consequences
o A significant maladaptive change in behavior related to attacks
- C) the disturbance is not attributable to the physiological effects of a substance or another medical
condition
o If not already diagnosed with panic disorder you need to rule out actual organic disease; ACS,
hyperthyroidism, hypoglycemia, pheochromocytoma, asthma, stroke, abuse, intoxication,
withdrawal etc.
- D) the disturbance is not better explained by another mental disorder

Epidemiology
- Prevalence: 2-5%
- M:F = 1:2-3
- Onset: average early-mid 20s
- Familial pattern

Etiology
- Genetics: familial pattern
- Hypothesis
o Increased catecholamine levels in CNS
o Abnormality in the locus coeruleus (alertness)
o CO2 hypersensitivity: produce respiratory distress, hyperventilation, and anxiety
o Disturbance in lactate metabolism
o Abnormalities of GABA neurotransmission
- Physchoanalysts:
o Repression defence mechanism: holds unaccepatable thoughts, impulses, or desires out of
conscious reach. When the psychic energy attached to these unacceptable thoughts, impulses, or
desires becomes too strong to hold back, they find their way into conscious awareness in
disguised form, leading to anxiety and panic
- Behaviorists:
o Conditioned response to a fearful situation; a car accident might paired with the experience of
heart palpitation and anxiety. Log afte r the accident, palpitation alone, whether from vigorous
exercise or emotional upset, might provoke the conditioned response of panic
Treatment
- Starting medications for anxiety: start low, go slow, aim high and explain symptoms to expect prior to
initiation of therapy to prevent non-compliance due to physical side effects

- Psychological:
o CBT:
§ Interoceptive exposure (eliciting symptoms of panic attack and learning to tolerate the
symptoms with coping strategies)
§ Cognitive restructuring (addressing underlying beliefs regarding the panic attacks)
§ Relaxation techniques (visualization, box-breathing)
o Pharmacologica
§ Benzodiazepines
• Short term, low dose, regular schedule
• Alprazolam, clonazepam, diazepam
§ SSRI, SNRI
• Start low, titrate up slowly
• Anxiety disorders often require treatment at higher doses for a longer period of
time than depression (i.e. full response may take up to 12w)
• Treat for up to 1 year after symptoms to avoid relapse
§ Other antidepressants
• Mirtazapine, MAOIs
• Consider avoiding bupropion or TCAs due to simulating effects (exacerbate
anxious symptoms

Prognosis
- 6-10 year post treatment: 30 % well, 40-50% improved, 20-30% no change or worse
- Clinical course: chronic, but episodic with psychosocial stressors

Agoraphobia
- Anxiety disorder characterized by symptoms of anxiety in situations where the person perceives their
environment to be unsafe with no easy way to escape. These situations can include open spaces, public
transit, shopping centers, or simply being outside their home. Being in these situations may result in a panic
attack
- NB: agoraphobia is diagnosed irrespective of the presence of panic disorder. If an individuals presentation
meets criteria for panic disorder and agoraphobia, both dx should be assigned

DSM-5
- A) marked fear or anxiety about 2 or more of the following situations
o Using public transportation
o Being in open spaces
o Being in enclosed spaces
o Standing in line or being in a crowd
o Being outside of the home alone
- B) the individual fears or avoids these situations because of thoughts that escape might be difficult or help
might not be available in the event of developing panic-like symptoms or other incapacitating or
embarrassing symptoms
- C) the agoraphobic situations almost always provoke fear or anxiety
- D) the agoraphobic situations are actively avoided, require the presence of a companion, or are endured
with intense fear or anxiety
- E) the fear or anxiety is out of proportion to the actual danger posed by the agoraphobic situations and to
the sociocultural context
- F) the fear, anxiety, or avoidance is persistent, typically lasting > 6 months
- G) the fear, anxiety, or avoidance causes clinically significant distress or impairment in social, occupational,
or other important areas of functioning
- H) if another medical condition is present, the fear, anxiety, or avoidance is clearly excessive
- I) the fear, anxiety, or avoidance is not better explained by the symptoms of another mental disorder and
are not related exclusively to obsessions, perceived defects or flaws in physical appearance, reminders of
traumatic events, or fear of separation

Etiology
- Often occurs as complication of panic disorder
- Genetic: familial accumulation
- Social: avoidance of negatively reinforced

Treatment
- As per panic disorder

GAD
- Constant state of worry (most things, most days) for at least 6 months accompanied by three somatic
complaints
- In majority of cases its correlated dwith substance abuse, depression, sleeping disorders etc.

DSM-5 Diagnostic criteria

- - C- FIRST

- A) excessive anxiety and worry (apprehensive expectation), occurring more thays than not for at least 6
months, about a nr of events or activities (such as work or school performance)
- B) the individual finds it difficult to control the worry
- C) the anxiety and worry are associated with 3 or more of the following symptoms (with at least some
symptoms having been present for more days than not for the past 6 months)
o Concentration issues or mind going blank
o Fatigue
o Irritability
o Restlessness or feeling keyed up or on edge
o Sleep disturbance – difficulty falling or staying asleep, or restless, unsatisfying sleep
o Tension (muscle)
- D) the anxiety, worry, or physical symptoms cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning
- E) The disturbance is not attributable to the physiological effects of a substance or another medical
condition
- F) the disturbance is not better explained by another mental disorder

Diagnosis
- Clinical
- PE: exclude organic origin, assess comorbidity
- Lab: ddx
- Psychological tests:
o Bekc anxiety inventory
o Hamilton anxiety scale
o Psychological status
- Ddx:
o CVD, endocrine disorders, metabolic disorders, neurological disorders
o Panic disorder, phobias, OCD, PTSD, acute stress reaction
o Anxiety due to psychoactive substances

Etiology
- Dirturbed neurotransmitter regulation: NE, 5HT, GABA
- Activation of vegetative nervous system
Epidemiology
- 1 yr prevalence: 3-8%, M:F = 1:2
o If concentrating only on those receiving inpatient treatment, ratio 1:1
- Most commonly present in early adulthood

Treatment
- Lifestyle:
o Avoid caffeine and alcohol
o Sleep hygiene
- Psychological (better than meds)
o CBT including relaxation techniques, mindfulness
- Biological:
o SSRI, SNRI – 1st line
o Buspirone, bupropion (caution due to stimulating effects) – 2nd line
o Add-on benzo (short term, low dose, regular schedule, long half-life)
o BB not recommended

Prognosis
- Chronically anxious adults become less so with age
- Depends on pre-morbid personality functioning, stability of relationships, work, and severity of
environmental stress
- Difficulty to treat

- Predictive factors for bad prognosis:

o Comorbid psychiatric illness
o Somatical comorbidity
o Personality disorder
o Poor social connections
o Bad relationship with family members

Phobic disorders
- Marked and persistent, irrational fear of specific objects, situations, phenomenas

Classification
- Specific phobia:
o Marked and persistent (>6m) fear that is excessive or unreasonable, cued by presence or
anticipation of a specific object or situation
o Lifetime prevalence: 12-16%, variable M:F ratio
o Types:
§ Animal/insects
§ Environment (heights, storms)
§ Blood/injection/injury
§ Situational (airplane, closed spaces)
§ Other (loud noise, clowns)
- Social phobia (social anxiety disorder)
o Marked and persistent (>6m) fear of social or performance situations in which one is exposed to
unfamiliar people or to possible scrutiny by others; fearing he/she will act in a way that may be
humiliating or embarrassing (e.g. public speaking, initiating or maintaining conversation, dating,
eating in public)
o 12-month prevalence rate may be as high as 7%, M:F ratio approximately equal
o Generalized social phobia occur in young (around 11y) and appears in majority of social situations.
Simple social phobia occur after 20y and affects 1-2 social activities (e.g. public speech or eating)

Diagnostic criteria
- Exposure to stimulus almost invariably provokes an immediate anxiety response, may present as panic
attack
- Person recognizes fear as excessive or unreasonable
- Situations are avoided or endured with anxiety/distress
- Significant interference with daily routine, occupational/social functioning, and/or marked distress

Treatment
- Psychological
o CBT: Focusing on both in vivo and virtual exposure therapy, gradually facing feared situations
§ Flooding: quick but not as effective
§ Desensitization: more long lasting, more effective, but takes longer time
o Behavioral therapy is more efficacious than medication
- Biological:
o SSRIs/SNRIs, MAOIs
o BB or benzos inn acute situations (e.g. public speaking)

Prognosis - Chronic

Obsessive-compulsive disorder

- Internal intrusive needs/thoughts/obsessions (e.g. safety, contamination, symmetry etc) that causes
anxiety/distress à compulsion, repetitive behavior that the person feels driven to perform in response to
an obsession (e.g. cleaing, checking doors/locks, ordering, counting, touching etc)
- Etiology:
o Genetic
o Neurobiological: structures affected include orbitofrontal cortex, cingulum, and caudate nucleus
- Dx:
o Clinic
o Psychological tests
§ Yale-Brown obsessive-compulsive scale (Y-BOCS)
§ Psychiatric anamnesis and status

DSM-5 diagnostic criteria

- A) presence of obsessions, compulsions, or both

o Obsessions are defined by 1) and 2)
§ 1) Recurrent and persistent thoughts, urges, or images that are experienced, at some
time during the disturbance, as intrusive and unwanted, and cause marked anxiety or
distress in most individuals
§ 2) the individual attempts to ignore or suppress such thoughts, urges, or images, or to
neutralize them with some other thought or action (i.e. by performing a compulsion)
o Compulsions are defined by 1) and 2)
§ 1) repetitive behaviours (e.g. hand washing, ordering, checking) or mental acts (e.g.
praying, counting, repeating words silently) that the individual feels driven to perform in
response to an obsession or according to rules that must be applied rigidly
§ 2) behaviours mental acts are aimed at preventing or reducing anxiety or distress, or
preventing some dreaded event or situation; however, these behaviours or mental acts
are not connected in a realistic way with what they are designed to neutralize or prevent,
or are clearly excessive
- B) the obsession or compulsion are time consuming (e.g. take >1h/d) or cause clinically significant distress
or impairment in social, occupational, or other important areas of functioning
- C) the obsessive-compulsive symptoms are not attributable to the physiological effects of a substance or
another medical condition
- D) the disturbance is not better explained by the symptoms of another mental disorder

Epidemiology
- 12 month prevalence: 1,1-1,8%, females slightly > males
- Rate of OCD in first-degree relatives is higher than in the general population
Treatment
- Psychotherapy (better than meds)
o CBT:
§ Exposure with response prevention – involves exposure to feared situations with the
addition or preventing the compulsive behaviors
• Densensitization – control anxiety with meds and give them stimulus
(obsession)
• Redirecting compulsion – e.g. snap fingers instead of washing them 50 times
§ Cognitive strategies include challenging underlying beliefs
o Psychoeducation
o Family therapy
o Relaxation
- Pharmacotherapy
o SSRIs/SNRIs
§ 12-16 week trials, higher doses vs depression
o Clomipramine
o Adjunctive antipsychotics (risperidone)

Prognosis
- Tends to be refractory and chronic

PTSD
- Exposure (self, others) to event (death, rape, neglect) in the past leading to complaints of recurrent and
intrusive distressing recollections of the event, recurrent nightmares of the event and intensive
psychological distress at exposure cues that symbolize an aspect of the event
o The further away from the stressor/event the more severe the event has had to be to cause PTSD
o Its common to avoid stimuli associated with the trauma
- Characterized by:
o Intrusions: memories, flashbacks, nightmares
o Mood change: almost always depression
o Dissociation: depersonalization
o Avoidance: not going to the place where it happened, not talking about the stressor
o Arousal: hypervigilance, irritability
- Stressor à disorder
o Life threatening, severe stressor à PTSD, acute stress disorder
o Non-life threatening à adjustment disorder
o Neglect/abuse in childhood à reactive attachment disorder (care to little), disinhibited social
engagement disorder (care to much)

DSM-5 criteria
- TRAUMA
o Traumatic event
o Re-experience the event
o Avoidance of stimuli associated with the event
o Unable to function
o More than a month
o Arousal increased
o + negative alterations in cognition and mood

- A) Exposure to actual or threatened death, serious injury, or sexual violence in one (or more) of the
following ways
o Directly experiencing the traumatic event(s)
o Witnessing, in person, the event(s) as it occurred to others
o Learing the the traumatic event(s) occurred to a close family member or close friend. Inn case of
actual or threatened death of a family member or friend, the event(s) must have been violent or
accidental
o Experiencing repeated or extreme exposure to aversive details of the traumatic event(s)
 § E.g. first responders collecting human remains, police officers repeatedly exposed to
details of child abuse
- B) presence of one (or more) of the following intrusion symptoms associated with the traumatic event(s),
beginning after the traumatic event(s) occurred
o Recurrent, involuntary, and intrusive distressing memories of the traumatic event(s)
o Recurrent distressing dreams in which the content and/or affect of the dream are related to the
traumatic event(s)
o Dissociative reactions (e.g. flashbacks) in which the individual feels or acts as if the traumatic
event(s) were recurring.
o Intense or prolonged psychological distress at exposure to internal or external cues that
symbolize or resemble an aspect of the traumatic event(s)
o Marked physiological reactions to internal or external cues that sympbolzie or resemble an aspect
of the traumatic event(s)
- C) persistent avoidance of stimuli associated with the traumatic event(s), beginning after the traumatic
event(s) occurred, as evidenced by one or both of the following
o Avoidance of or efforts to avoid distressing memories, thoughts or feelings about or closely
associated with the traumatic event(s)
o Avoidance of or efforts to avoid external reminders (people, places, conversations, activities,
objects, situations) that arouse distressing memories, thoughts or feelings about or closely
associated with the traumatic event(s)
- D) negative alterations in cognitions and mood associated with the traumatic event(s), beginning or
worsening after the traumatic event(s) occurred, as evidenced by two or more of the following
o Inability to remember to remember an important aspect of the traumatic event(s)
o Persistent and exaggerated negative beliefs or expectations about oneself, others, or the world
o Persistent, distorted cognitions about the cause or consequences of the traumatic event(s) that
lead the individual to blame himself/herself or others
o Persistently negative emotional state (e.g. fear, horror, anger, guilt, or shame)
o Markedly diminished interest or participation in significant activities
o Feelings of detachment or estrangement from others
o Persistent inability to experience positive emotions
- E) Marked alterations in arousal and reactivity associated with the traumatic event(s), beginning or
worsening after the traumatic event(s) occurred, as evidenced by two (or more) of the following
o Irritable behavior and angry outbursts (with little or no provocation) typically expressed as verbal
or physical aggression toward people or objects
o Reckless or self-destructive behavior
o Hypervigilance
o Exaggerated startle response
o Problems with concentration
o Sleep disturbance (e.g. difficulty falling or staying asleep or restless sleep)
- F) duration of the disturbance (criteria B, C, D, and E) is more than 1 month
- G) the disturbance causes clinically significant distress or impairment in social, occupational, or other
important areas of functioning
- H) the history is not attributable to the physiological effects of a substance or another medical condition

- Subtypes:
o With dissociative symptoms – PTSD + persistent or recurring symptoms of either
§ Depersonalization: persistent or recurrent experiences of feeling detached from, and as
if one were outside observer of, one’s metnal processes or body (e.g. feeling as though
one were in a dream, feeling a sense of unreality of selv of body or of time moving
slowly)
§ Derealization: persistent or recurrent experiences of unreality of surroundings (e.g. the
world around the individual is experiences as unreal, dreamlike, distant, or distorted)
o With delayed expression – if full diagnostic criteria are not met until at least six months after the
evet (although the onset and expression of some symptoms may be immediate)
Epidemiology
- Prevalence of 7% in general population
- Mens trauma is most commonly combat experience/physical assault; womenns trauma is usually physical
or sexual assault

Clinic
- Intrusion (shouldn’t be there but are, memories, flashback, nightmares etc)
- Mood change (almost always negative, depressed mood)
- Dissociation (depersonalization)
- Avoidance (avoid place where it happened, not talking about it)
- Arousal (hypervigilance, always looking over your shoulder)

Treatment
- The sooner you treat (i.e. debrief after stressoru) the shorter and less severe the PTSD

- Psychotherapy, CBT
o Ensure safety and stabilize: emotional regulation techniques (e.g. breathing, relaxation)
o Once coping mechanisms established, can explore/mourn trauma – challenge dysfunctional
beliefs, etc.
o Reconnect and integrate – exposure therapy etc.
- Biological
o SSRI
o Prazosin (for disturbing dreams and nightmares)
o Benzo (for acute anxiety)
o Adjunctive atypical antipsychotics (risperidone, olanzapine)
- Eye movement desensitization and reprocessing (EMDR)
o Experimental method of reprocessing memories of distressing events by recounting them while
using a form of dual attention stimulation such as eye movements, bilateral sound, or bilateral
tactile stimulation (its use is controversial because of limited evidence)

Complications
- Substance abuse, relationship difficulties, depression, impaired social and occupational functioning
disorders, personality disorders

Acute stress disorder

- May be a precursor to PTSD
- Similar symptoms to PTSD
- Symptoms persist 3d after a trauma until 1 month after the exposure

Adjustment disorder
- A diagnoses encompassing patients who have difficulty coping with a stressful life event or situation and
develop acute, often transient, emotional or behavioral symptoms that resemble less severe versions of
other psychiatric conditions

DSM 5
- A) the development of emotional or behavioral symptoms in response to an identifiable stressor(s)
occurring within 3 months of the onset of the stressor(s)
- B) the symptoms or behaviors are clinically significant as evidenced by either of the following:
o Marked distress that is in excess of what would be expected from exposure to the stressor
o Significant impairment in social or occupational (academic) functioning
- C) the stress-related disturbance doesn’t meet criteria for another mental disorder and is not merely an
exacerbation of a pre-existing mental disorder
- D) the symptoms do not represent normal bereavement
- E) once the stressor (or its consequences) has terminated, the symptms do not persist for more than an
additional 6 months
- Specifiers:
o With depressed mood, with anxiety/depression, with conduct disturbance, with mixed
disturbance of conduct/emotions, unspecified

Classification
- Types of stressors:
o Single (e.g. termination of a romantic relationship)
o Multiple (e.g. marked business difficulties and marital problems)
o Recurrent (e.g. seasonal business crises)
o Continuous (e.g. living in a crime-ridden neighbourhood)
o Developmental events (e.g. going to school, leaving parental home, getting married, becoming a
parent, failing ot attain occupational goals, retirement)

Epidemiology
- F:M = 2:1
- Prevalence: 2-8% of population

Treatment
- Brief psychotherapy:
o Individual or group (particularly useful for patients dealing with unique and specific medical
issues, e.g. colostomy or renal dialysis), crisis intervention
- Biological
o Benzo may be used for those with significant anxiety symptoms (short-term, low-dose, regular
schedule)

Bereavement (grief, mourning)

- Associated with a significant increase in morbidity and mortality acutely following the loss, with effects
seen up to 1 year after
- Loneliness is the most common symptom that continues to persist in normal bereavement and may last
several years

Clinical presentation
- Bereavement is a normal psychological and emotional reaction to a significant loss
- Length and characteristics of “normal” bereavement are variable btw individuals/cultures
- Normal response:
o Protest -> searching and acute anguish -> despair and detachement -> reorganization
- Presence of the following symptoms may indicate abnormal grief/presence of MDD
o Guilt about things other than actions taken or not taken by the survivor at the time of death
o Thoughts of death other than the survivor feeling that they would be better off dead or should
have died with the deceased person; morbid preoccupation with worthlessness
o Marked psychomotor retardation; prolonged and marked functional impairment
o Hallucinatory experiences other than thinking that the survivor hears the voice of or transiently
sees the image of the deceased person
o Dysphoria that is pervasive and independent of thoughts or triggers of the deceased, absence of
mood reactivity
- After 12 months, if patient continues to yearn/long for the deceased, experience intense
sorrow/emotional pain in response to the death, remain preoccupied with the deceased or with their
circumstance of death, then may start to consider a diagnosis of “persistent complex bereavement
disorder”
- If a patient meets criteria for MDD, even in the context of a loss or bereavement scenario, they are still
diagnosed with MDD

Treatment
- Support and watchful waiting should be first line, as well as education and normalization of the grief
process
- Screen for increased alcohol, cigarette and drug use
- Normal grief should not be treated with antidepressants or antianxiety medication, as it is important to
allow the person to experience the whole morning process to achieve resolution
- Psychosocial: for those needing additional support, complex grief/bereavement, or significant MDD, grief
therapy (individual or group) is indicated
- Pharmacotherapy: if MDD is present, past history of mood disorders, severe, or autonomous symptoms

Risk factors for poor bereavement outcome

- Poor social supports
- Unanticipated death or lack of preparation for death
- Highly dependent relationship with deceased
- High initial distress
- Other concurrent stresses and losses
- Death of a child
- Pre-existing psychiatric disorders
5. Basic psychoanalytic concepts

- Founded by Sigmund Freud (1856-1939) which believed that people could be cured by making conscious
their unconscious thoughts and motivations, thus gaining insight, and with this insight gained during
analysis, the patient can work at improving relationships and productivity, interrupt self-defeating or self
destructive pattenrs, and perhaps even unlock creative potential.

- Assumptions
o See psychological problems as rooted in the unconscious mind
o Manifest symptoms are caused by latent disturbances
o Typical causes include unresolved issues during development or repressed trauma
o Treatment focuses on bringing the repressed conflict to consciousness, where the client can deal
with it

- Psychoanalysis is a method of treating emotional difficulties that involves communication btw a

psychoanalysts and an individual, with the goal of gaining insight into the individuals inner world and how
it affects his or her emotions, behavior, and relationships
- Although both method and theory have advanced since Freud’s day, some of his basic ideas continue to
shape our thinking about human behavior and functioning
- One fundamental Freudian concept is the powerfull effect of the unconscious part of the mind on our
feelings, actions, relationships, and edneavors
o Unconscious conflicts can cause anxiety, moodiness, or depressive thoughts; troubling personality
traits; or difficulties at work or in finding or maintaining long-term relationships. Many such
problems have their root in past experiences and relationships

Psychoanalysis
- Phychoanalysts belives that the human personality can be divided into two parts, the conscious and
unconscious minds, which on a daily basis is in a constant conflict, and in the end, human behavior is result
of compromise btw the two

- ID: (jaba the hut)

o Include immediate desires like eating, sex, aggressiveness, shiny things etc.
o Instinctual, impulsive
o No morality, only knows what it wants
- Superego: (captain America)
o Tells you whats right and wrong based on what you have learned is socially acceptable. Always
follow the rules
- Ego: (judge judy)
o Hears both sides, make final decision on how you should behave
- Psychoanalyst theory says that the conflct btw the desire to ravage and social order results in the
development of defence mechanisms to keeping the id from coming out and defence mechanisms keeps
us safe from guilt and anxiety that we would feel if we gave in to our innermost desires
 o Theory for mental illness – when unconscious conflicts become too intense and the defence
mechanisms are too restrictive the individual begins to show mental health symptoms
o In individual with mental illness, the symptoms = defence mechanisms against and partial release
of our unacceptable impulses
- Goal of psychoanalysis is to make you conscious of your unconscious defence mechanisms
o Psychoanalysis attempts to help the person identify and accept their defences and create more
forgiving defences that allow more mature expression of desires
o Rorschach inkblots and word association can help the client with free association

How it works
- Psychoanalyst and patient meet 3-5 times per week
o Patient free-associated (talk about whatever comes to mind, whenever it comes to mind)
o Frequent meetings encourage emergence of the patients full range of personality traits and
behavior patterns, an important step on the path to self-understanding
- Its collaborative effort
o As patient free-associates, the analyst listens carefully and helps grasp the underlying unconscious
sources of her difficulties
o Analyst not only interpret ongoing patterns but also encourage the patient to re-experience them
– referred to as “transference”. The patient relives their lfie story by transferring to the analyst
feelings and attitudes they originally experienced in relationship with other people
§ E.g. patient is consistently late for appointments (analysts, at home, at work). By
examining the feelings the analyst arouses as the patient talks about reasons for being
late – or perhaps realizing their anger with authority figures – the patient can then
become conscious of her motives for wanting others to wait for them
- Usually require several years (5,7 on average) to resolve long-standing difficulties (e.g. self-defeating
behavior, problems forming personal relationships)
o May be many variations to work through.
o The hope is that over time, the individual can recover lost emotional connections, give up
unhealthy ones, and adapt more effectively to her current circumstances
- Pscyhoanalysts may help with problems such as:
o Difficult finding suitable partner
o Never feel excited about friendships
o Keep missing deadlines at work and sabotaging my career
o Sad my child is leaving for college

Terms and concepts

- Confrontation:
o Practice often done prior to an intervention where the patient is encouraged to attend to
experiences that they have been avoiding
- Transference:
o Projection onto another person (e.g. the analyst) of feelings, past associations, or experiences
o This is an important concept in psychoanalysis because it demonstrates that past experiences
impact the present.
o Interpreting transference in the psychoanalytic setting can shed light on unresolved conflicts
- Countertransference
o Refers to the analysts feelings and attitudes toward the patient: his/her reaction to the patient’s
transference, how his/her own experiences impact his/her understanding of the patient, and the
analysts emotional responses to the patient
- Defense mechanism
o Used by the ego as a way to deal with conflict of problems in life. Operating at an unconscious
level, defense mechanisms help to reduce negative feelings (e.g. anxiety and guilt)
o Common defense mechanisms include repression, denial, and projection
- Denial:
o An individuals refusal to accept certain or confront (or all) aspects of a given reality in order to
avoid potential feelings of discomfort. It exists on a continuum as it ca be seen as just a normal
reaction to a stressful event or to severe psychosis. While commonly defined as a subtype of
 defense mechanism, denial plays a role in all defense mechanisms. Freud also referred to it as
disavowal.
- Repression
o Defece process where an individuals impulses and instinctual desires are blocked from entering
one’s conscious
o Regarded by Freud as the cornerstone of defence mechanisms, eh process of repression involves
unconsciously censoring ideas or memories deemed unacceptable
- Dream
o Mental event that consists of hallucinations involving imaginary and emotions. Dreams occur
during REM sleep.
o According to Freud, current concerns and unconscious childhood wishes are present during the
day and require gratification and I is dreams that allows us to respond to this demands while
continuing to sleep (e.g. a person who is thirsty dreams about drinking water which allows him to
continue sleeping rather than having to wake up and satisfy his thirst)
- Electra complex
o A term coined by jung as the female counterpoint to what freud called the Oedipus complex.
- Fantasy
o Loosely refers to an imagined situation that expresses certain desires or aims of the imagining
individual
o It can occur at the conscious level, also known as daydream, or unconsciously, sometimes
referred to as phantasy
- Ego
o Freud theorized that the mind was divided into three parts; id, ego, and superego
o Function of the ego can be described as running interference btw id and superego. It mediates the
drives of the id and the need for self-preservation
o The ego is responsible for the development of the skills needed to function in the world, e.g.
impulse control, perception, evaluation and judgement
- Ego ideal
o Part of the superego that contain standards, values and moral ideas
o Failure to meet these standards can cause feelings of guit or shame, while success can enhance
self esteem
- Id
o Id is part of the mind that contains ones most basic and instinctive drives
o Its governed by sexual and aggressive desires and pleasure seeking
o The contents of the id are entirely unconscious
o Freud stated that the goal of analysis is to uncover what is repressed in the id so that, “where id
was, there ego shall be”
- Pleasure principle
o Driving force of the id, refers to ones desire to obtain immediate gratification of needs by
obtaining pleasure and avoiding pain
o When our basic need is not met, feelings of anxiety may develop
- Superego
o Superego can be thought of as the part of the mind that acts as the conscience.
o Its function is to stop or punish behavior that is unacceptable according to the ego ideal, i.e. the
standards, values, and images of perfection that begin to develop in childhood, and which some
psychoanalysts believe to develop over a lifetime
o Failure to live up to these standards results in feeling of guilt or shame
o Success in living up to the ego ideal results in enhanced self-esteem, i.e. feeling good about onself
- Parapraxis (Freudian slip)
o Revealing an unconscious desire or conflict through mistake, e.g. slip of tongue or forgetting
someones name
- Oedipus complex
o Freud used the Greek myth of Oedipus to illustrate a childhood developmental stage, occurring
btw 3-6y, when a child desires to have the parent of opposite sex all to him/herself, to the
exclusion of the other parent
o In the myth: Oedipus kills Laius, who he does not realize is his father, and hten marries his widow,
Jokasta, who is acutally oedipus’s mother
- Unconscious
o Freud proposed that there are three parts (levels) of the mind, the conscious, preconscious and
the uncious
o The unconscious part of the mind stores feelinngs, thoughts, and urges unaware to the individual
o These mental contents and processes often influence the conscious experience even though we
are unaware of their existence
- Resistance
o Refers to a patients unconscious opposition to the unveiling and exploration of painful memories
during psychoanalysis
o Its often conveyed through mental process, fantasies, memories, character defensives, and
behaviors
o While it initially occurs unconsciously, it may persist long after the patient is made consciously
aware of this behavior
- Libido
o A term generally used to refer to ones sexual desires or more specifically, the mental energy
responsible for ones sex drive
o This concept represents Freud’s notion that sexual interest exists throughout life and that its
responsible for activities that involve sexual desire and/or affection
- Fixation
o Fixation is a state where a person becomes attached to or overly invested in another individual or
object
o It’s the result of conflict occurring durign the psychosexual stages of development
o Due to frustration or overindulgence occurs, the libido becomes focused on that stage leading to
problematic behaviors later o (e.g. an individual with an oral fixation may engage in nail biting)
- Psychodynamic
o Psychodynamic psychotherapy is a form of psychotherapy derived from psychoanalytic theories
and modeled after a psychoanalytic model of mental functioning
o Psychodynamic psychotherapy is primarily for individuals who will benefit from a more focused
method of treatment that is active and focuses on the realities of ones daily life
o Other terms include psychoanalytic psychotherapy, insight oriented psychotherapy, and
expressive psychotherapy
6. Alcoholism (incl alcohol withdrawal and alcohol hallucinosis) treatment and
rehabilitation
23. alcoholism epidemiology, diagnostic criteria (incl alcohol withdrawal and alcohol
hallucinosis), course and outcome
26. Psychoactive substance use disorders: diagnostic criteria and clinical management

Substance-related and addictive disorders

- Neurobiological disorder involving compulsive drug seeking and drug taking, despite adverse
consequences, with loss of control over drug use
- Usually chronic with relapsing and remitting course
- Dependence:
o Behavioral: substance-seeking activities and pathological use patterns
o Physical: physiological withdrawal effects without use
o Psychological: continuous or intermittent crawings for the substance to avoid dysphoria or attain
drug state
- Abuse:
o Drug use that deviates from the approved social or medical pattern, usually causing impairment
or disruption to function in self or others

Epidemiology
- 47% of those with substance abuse have mental health problems
- 29% of those with a mental health disorder have a substance use disorder
- 47% of those with schizophrenia and 25% of those with an anxiety disorder have substance use disorder

Etiology
- Almost all drugs (and activities) of abuse increase DA in the nucleus accumbens, an action that contributes
to their euphoric properties and, with repeated use, to their ability to change signaling pathways in the
brains rewardd system
- Substance use disorders arise from multifactorial interactions btw genes (personality, neurobiology) and
environment (low socioeconomic status, substance-using peers, abuse history, chronic stress)

Common presentation of drug use

- General:
o Weight loss (esp cocaine, heroin), injected conjunctiva (cannabis), pinpoint pupils (opioids), track
marks (injection drugs), trauma
- GI:
o Viral hepatitis (injection drugs), unexplained elevations in ALT (injection drugs)
- Behavioral:
o Missed appointments, non-compliance, drug-seeking (esp benzo, opioids)
- Psychological:
o Insomnia, fatigue, depression, flat affect (benzo, barbds), paranoia (cocaine), psychosis (cocaine,
cannabis, hallucinogens)
- Social
o Marital discord, family violence, work/school, absenteeism and poor performance

Diagnosis
- Substance use disorder is the diagnostic term applied to the specific substance abused (e.g. alcohol use
disorder, opioid use disorder) that results from the prolonged use of the substannce

- Severity based on nr of criteria met within 12 months: mild = 2-3, moderate= 4-5, severe 6 or more
o Maladaptive pattern of substance use leading to clinically significant impairment or distress, as
manifested by 2 or more of the following occurring within a 12 month period
- Each specific substance is addressed as a specific use disorder and utilizing the same overarching criteria
(e.g. a single patient may have moderat alcohol use disorder, and a mild stimulant use disorder)
- Criteria: (“PEC WITH MCAT”)
 o Use despite physical or psychological problem
§ E.g. alcoholic liver disease or cocaine related nasal problems
o Failure in important external roles at work/school/home
§ E.g. repeated absences at work, poor work performance related to substance use,
substance-related absences, suspensions, or expulsion from school, neglect of children or
household
o Craving or a strong desire to use substance
o Withdrawal
o Continued use despite interpersonal problems
§ E.g. arguments with spouse about consequences of intoxication, physical fights
o Tolerance, needing to use more substance to get same effect
o Use in physically hazardous situations
§ E.g. driving car
o More substance used or for longer period than intended
o Unsuccessful attempts to cut down
o Activities given up due to substance (social, occupational, recreational)
o Excessvie time spent on using or finding substance

Classification of substances

General approach to assessment

- Must be appropriate to the patient’s current state of change
o Prochaska’s stages of change:

- Patient will only change when the pain of change

appears less than the pain of staying the same
- Provider can help by providing psychoeducation
(emphaze neurobiological model of addiction),
motivation, and hope
- Principles of motivational interviewing:
o Non-judgemental stance
o Space for patient to talk and reflect
o Offer accurate emphatic reflections back
to patient to help frame issues

General approach to treatment

- Encourage and offer referral to evidence based
services:
o Social:
§ 12 step programs (AA, narcotics
anonymous)
§ Family education and support
o Psychological:
§ Addiction counseling
 § Motivational enhancement therapy (MET)
§ CBT
§ Contingency management
§ Group therapy
§ Family therapy
§ Marital counselling
o Medical management (differs depending on substance)
§ Acute detoxification
§ Pharmacological agents to aid maintenance
- Harm reduction whenever possible
o Safe-sex practices
o Avoid driving while intoxicated
o Avoiding substances with child care
o Safe needle practices/exchange
o Pill testing kits
o Reducing tobacco use
- Comorbid psychiatric conditions
o Many will resolve with successful treatment of the substance use disorder but patients who meet
full criteria for another disorder should be treated for that disorder with psychological and
pharmacological therapies

Opioids

- Types: Heroin, morphine, oxycodone, Tylenol (codeine), hydromorphone, fentanyl

- Major risks associated with the use of contaminated needles: increased risk of hepatitis B and C, bacterial
endocarditis, HIV/AIDS
- Opioids antagonists
o Naltrexone (revia)
§ Can be used for ethanol dependence (not routine)
§ Long half life
o Naloxone (narcan)
§ Used for life-threatening CNS/respiratory depression in opioid overdose
§ Short half life (<1h)
§ Very fast acting (min)
§ High affinity for opioid receptor
§ Induces opioid withdrawal symptoms

Acute intoxication

- Effect:
o Analgesia, sedation, decreased sex drive, n&v, decreased GI motility (constipation and anorexia),
and respiratory depression
- Toxic reaction:
o Shallow respiration, miosis, bradycardia, hypothermia, decreased level of consciousness
- Management:
o ABCs
o IV glucose
o Naloxone hydrochloride
o Intubation and mechanical ventilation +/- naloxone drip until pt alert without naloxone (up to
>48h with long acting opioids)
- NB:
o Caution with longer half-life; may need to observe for toxic reaction for at least 24h

Withdrawal
- Onset: 6-12h
- Duration: 5-10d
- Symptoms:
 o Depression, insomnia, drug-craving, myalgias, nausea, chills, autonomic instability (lacrimation,
rhinorrhea, piloerection)
- Complications
o Loss of tolerance (overdose on relapse)
o Miscarriage, premature labor
- Management
o Long-acting oral opoids (methadone, buprenorphine)
o Alpha adrenergic agonists (clonidine)

Treatment of opioids use disorder

- Long-term treatment may include withdrawal maintenance treatment with methadone (opoid agonist) or
buprenorphine (mixed agonist-antagonist)
- Suboxone formulation includes naloxone in addition to buprenorphine, in an effort to prevent injection of
the drug
o When naloxone is injected it will precipitate opioids withdrawal and block the opiate effect of
buprenorphine
o Will not have this antagonist action when taken sublingually

Cocaine
- Alkaloid extracted from leaves of the coca plant: blocks presynaptic uptake of dopamine (causing
euphoria), NE and E (causing vasospasm, HTN)
- Admin: inhalation, insufflation, iv

Acute intoxication
- Symptoms:
o Elation, euphoria, pressured speech, restlessness, sympathetic stimulation (e.g. tachycardia,
mydriasis, sweating)
o Prolonged use may result in paranoia and psychosis
- Overdose (medical emergency)
o Clinic:
§ Cardiovascular: HTN, tachycardia, dyspnea, and ventricular arrhythmias, MI, ruptured
AAA
§ CNS: tonic-clonic seizures

o Tx:
§ IV diazepam to control seizures
o NB:
§ Labetalol or propranolol not recommended due to risk unopposed alpha-adrenergic
stimulation
Withdrawal
- Clinical features:
o Initial “crash” (1-48h): increased sleep, increased appetite
o Withdrawal (1-10w): dysphoric mood + fatigue, irritability, vivid unpleasant dreams, insomnia or
hypersomnia, psychomotor agitation or retardation
- Complications:
o Relapse, suicide (significant increase in suicide during withdrawal period)
- Management:
o Supportive care

Treatment cocaine use disorder

- No pharmacological agents have widespread evidence or acceptance of use

Complications
- Cardiovascular: arrhythmias, MI, CVA, ruptured AAA
- Neurologic: seizures
- Psychiatric: psychosis, paranoia, delirium, suicidal ideation
- Other: nasal septum deterioration, acute/chronic lung injury “crack lung”, possible increased risk of CT
disease

Amphetamines
- Includes prescription medications for ADHD such as Ritalin and Adderall

Intoxication
- Symptoms:
o Euphoria, improved concentration, sympathetic and behavioral hyperactivity (at high dose can
mimic mania), psychotic mania
o Eventually cause coma

Chronic use
- Can produce paranoid psychosis which can resemble schizophrenia with agitation, paranoia, delusions and
hallucinations
- Treatment amphetamine induced psychosis:
o Antipsychotics for acute presentation
o Benzo for agitation
o BB for tachycardia, HTN

Withdrawal
- Dysphoria, fatigue, and restlessness

Cannabis (marijuana)
- Most commonly used illicit drug
- Psychoactive substance: delta-9-tetrahydrocannabinol (THC)
- Medical uses:
o Anorexia-cachexia (AIDS, cancer)
o Spasticity, muscle spasms (MS, spinal cord injury)
o Levodopa-induced dyskinesia (parkinsons disease)
o Controlling tics and obsessive-compulsive behavior (Tourette’s syndrome)
o Reducing intra-ocular pressure (glaucoma)

Intoxication
- Clinical features
o Tachycardia, conjunctival vascular engorgement, dry mouth, altered sensorium, increased
appetite, increased sense of well-being, euphoria/laughter, muscle relaxation, impaired
performance on psychomotor tasks (incl driving)
o High doses can cause depersonalization, paranoia, anxiety and may trigger psychosis and
schizophrenia if predisposed

Chronic use
- Associated with tolerance andn apathetic, amotivational state, increase risk of later manic episodes

Withdrawal
- Cessation following heavy use produces a significant withdrawal syndrome: irritability, anxiety, insomnia,
decreased food intake

Hallucinogens
- Psychological effects of high doses: depersonalization, derealization, paranoia, and anxiety (panic with
agoraphobia)
- Tolerance develops rapidly (hours-days) to most hallucinogens so physical dependency is virtually
impossible, although psychological dependency and problematic usage patterns can still occur
- No specific withdrawal syndrome characterized
- Management of acute intoxication:
 o Support, reassurance, diminish stimulation: benzodiazepines or high potency antipsychotics
seldom required (if used, use small doses)
o Minimize use of restraints
- Long term adverse effects:
o Controversial role in triggering psychiatric disorders, particularly mood or psychosis, thought to be
chiefly in individuals with genetic or other risk factors
- Hallucinogen persisting perception disorder:
o DSM5 diagnosis characterized by long lasting, spontaneous, intermittent recurrences of visual
perceptual changes reminiscent of those experienced with hallucinogen exposure

5-HT2A agonists
- Most common
- Drugs:
o LSD, Mescaline (peyote) , Psilocybin mushrooms, DMT (ayahuasca)
- Clinical features:
o Intoxication:
§ Symptoms
• Tachycardia, HTN, mydriasis, tremor, hyperpyrexia
• Variety of perceptual, mood, and cognitive changes
• Rarely, if every, deadly
§ Tx:
• Treat vitals symptomatically

NMDA antagonist
- Drugs:
o PCP, Ketamine

K-opioid agonists
- Drugs:
o Salvia divinorum, Ibogaine

“Club drugs”
- Date rape drugs: GHB, flunitrazepam (rohypnol), ketamine
- Formication: tactile hallucination that insects or snakes are crawling over or under the skin (esp associated
with crystal meth use)
Alcoholism
Investigation and diagnosis

- CAGE: (men: 2 or more is positive, women: 1 or more, if positive – further investigation to distinguish btw
problem drinking and alcohol use disorder)
o Ever felt the need to cut down on drinking?
o Every felt annoyed at criticism of your drinking?
o Ever felt guilty about your drinking?
o Ever needed a drink first thing in the morning (eye opener)?

Treatment of alcohol use disorder

- Non-pharmacological
o Psychosocial treatment and rehabilitation
§ Confrontation with reality and motivation according to individual needs and capacity to
change
§ Focusing on treatment of comorbid mood and anxiety disorders (30-40%)
§ Family level intervention
§ Counseling and community-level intervention:
 • Motivation to maintain abstinence and prevent relapse
• Showing the consequences
• Cope with everyday stress
• Stimulus control and craving
• Build-up alternative lifestype
o Self help groups
§ AA
• Sober peer group, 12 step treatment from confrontation to spiritual awakening
• Role modeling of social functioning without drinking
• Peer help available 24h
• Strong group coherence (“we-ness”)
• Religion and spirituality
- Pharmacological
o Naltrexone (revia)
§ Opioid antagonist, shown to be successful in reducing the “high” associated with alcohol
§ Moderately effective in reducing cravings, frequency or intensity of alcohol binges
o Disulfiram (Antabuse):
§ Prevents oxidation of alcohol (blocks acetaldehyde dehydrogenase)
§ With alcohol consumption, acetaldehyde accumulates to cause a toxic reaction
(vomiting, tachycardia, death)
§ If patient relapses, must wait 48h before restarting Antabuse; prescribed only when
treatment goal is abstinence
§ RCT evidence is generally poor or negative
o Acamprosate (campral)
§ NMDA glutamate receptor antagonist; useful in maintaining abstinence and decreasing
cravings

Substance-induced disorders and mental complications

- Amnestic disorder (Korsakoffs) and Wernicke
o Alcohol induced amnestic disorder due to thiamine deficiency
o Pathology:
§ Necrotic lesions in mammary bodies, thalamus, and brainstem
o Classification
§ Wernicke’s encephalopathy (acute and reversible)
• Triad: nystagmus (CN VI palsy), ataxia, and confusion
§ Korsakoffs syndrome (chronic, only 20% reversible with treatment)
• Anterograde amnesia and confabulations (fabrication of imaginary experiences
to compensate for memory loss)
• Cannot occur during an acute delirium or dementia and must persist beyond
usual duration of intoxication/withdrawal
o Management:
§ Wernicke: thiamine 100 mg po OD x 1-2w
§ Korsakoffs: thiamine 100 mg PO bid/tid x 3-12 months
- Alcohol-induced psychotic disorder with hallucinations:
o Sudden onset while the patient is alert and oriented
o Unpleasant complex auditory hallucinations
o Anxiety, depressed mood, sometimes delusions
o Treatment: antipsychotics
- Alcohol induced psychotic disorder with delusions
o Chronic course, often combined with other diseases
o Gradual development of elaborate and complex delusional system usually involving delusional
jealousy, ideas of reference, overvalued ideas
o Violent acts, frequent suicidality
o Treatment: abstinence and antipsychotics
- Alcohol-induced mood disorder:
o “chicken or egg” casuality dilemma
 o Both bioligcal and psychosocial factors play role
o This comorbidity worsen the prognosis of both conditions (esp in case o fnon-treatment)
o Substantial suicidal risk
o Treatment: abstinence, rehabilitation, antidepressants

Physical complications
- Esp common among elderly patients.
- Can be life threatening, therefore the location and interventions of therapy as well as the prognosis are
highly influenced by them
- Their presence must always be considered, therefore the necessary examinations must be performed as
one of the first actions of treatment

- Neurological complications:
o Wernicke’s encephalopathy
o Central pontine myelinolysis
o Marchiafava-Bignami
§ Disease demyelination of corpus callosum
§ Contributed to deficiency of all eight types of Vit B
o Cerebellar degeneration
o Alcoholic neuropathy
- Internal medicine complicatins.
o Liver diseases: hepatic steatosis, alcoholic hepatitis, cirrhosis
o Cardiovascular diseases: cardiomyopathy, HT, ischaemic heart disease
o GI: Pancreatitis, gastritis, ulcers, hemorrhagic complications
o Infections: pneumonia, meningitis, sepsis – common causes of death!
o Traumas: intracranial hemorrhagic complications

Alcohol intoxication
Pathophysiology
- Effect of alcohol:
o Delayed impulse transmission in CNS
o Arterial hypotension
o Hypoglycemia due to inhibited gluconeogenesis
o Increased diuresis
- Most eliminate ethanol from the blood approx. 0,015-0,2 promille per hour (if alcoholics may have twice
that speed)
- Toxicity
o Children <5y: Can develop severe symptoms if ingest >1ml/kg ethanol
o Adults: develop tolerance, usually clinical signs with promille 1,5-3, if reach 4,5 can be fatal in
non-alcoholic
- Special groups
o Lethal dose can be lower in chronic alcoholics due to reduced general condition and
cardiomyopathy
o Elderly can be more sensitive
o Children under 5y and individuals with poor nutritional status can develop hypoglycemia
o Many Asians are more sensitive for ethanol due to lower activity in acetaldehydedehydrogenase-
isoezymes. Causing higher concentration of acetaldehyde in blood after ethanol intake (can result
in flush, vasoldilation, and tachycardia)

Predisposing factors
- Poor nutritional status
- Children
- Women – lower volume of distribution, lower first pass metabolism (less alcohol dehydrogenase)
- Mixed intoxication
Classification
- Severity depend on blood alcohol concentrations (per mille):
o 0,5-1 - common drunkenness
o 1,5- 2,0 - mild euphoria, concentration impairments
o 2,5 – 3,5 – anesthesia, mydriasis (dilation of pupil)
o > 3,5 % - respiratory failure, coma

- Mild: Smell of alcohol, some behavioral change with affected function and reaction level, some
disturbance of coordination
- Medium: Smell of alcohol, moderate behavioral change with affected function and reaction, marked
affected coordination and reduced ability to cooperate
- Marked: Marked change in behavior with affected function and reaction, marked affected coordination
and reduced ability to cooperate
- Severe: Severly reduced function and reaction, severe lack of coordination, lacking ability to cooperate

Complications
- Accidents, traumas, suicides etc.
- Abstinence phenomena
- Hypothermia – ethanol is sedating and can hide feeling of cold, also inhibt central thermoregulation, and
can by itself cause hypothermia via peropheal vasodilation
- Aspiration pneumonia
- Acute toxic hepatitis
- Acute pancreatitis
- Drug interactions

Diagnosis
- Lab:
o High alcohol (blood, urine). Should measure serum methanol and serum ethylenglycol if suspect
intake of other alcohols or mixed intoxication.
o Check for hypoglycemia (may cause seizures)
o Acid/base status – exclude methanol and ethylene glycol, exclude metabolic acidosis in
malnourished and alcoholics
§ Metabolic acidosis due to accumulation of ketones and lactate
- ECG: arrhythmia (Afib)
- CT caput: if history of head trauma, if worsening mental status, or if no change in mental status within 3h
after arriving at hospital

- Ddx:
o Traumas/other CNS pathology (esp epidural or subdural hemorrhage), intoxication other cause or
mixed intoxication with narcotics, drug poisoning (esp benzo and neuroleptica)

Management
- Surveillance and supportive tx until danger passes
o Unconscious should be observed for respiratory arrest, should lie on their side to prevent
aspiration of vomit
- Gastric lavage
o Considered in case of children if arrive within 1h
o Rarely done in adult due to quick alcohol absoption
- Correct fluid balance and hypoglycemia
- Vitamin B1 (thiamine) is given IV before glucose in alcoholics
o Prevent development of Wernickes encephalopathy and Korsakoffs psychosis
- Alcohol intoxication, unease
o Haloperidol can be indictated in addition to benzo if mared unease/aggression
§ Usually don’t given alone because of risk seizures
- Hemodialysis
o Rarely done
Alcohol withdrawal/abstinence
- Occur 12-48 hours after prolonged heavy drinking and can be life-threatening
- Ca be described as having four stages, however not all stages may be experienced
- Almost completely reversible in young, elderly are often left with cognitive deficits
- Mortality rate is 20% if untreated

Clinical features
Stages

- Stage 1 (onset 12-18h after last drink)

o “the shakes” tremor, sweating, agitation, anorexia, cramps, diarrhea, sleep disturbance
- Stage 2 (onset 7-48h)
o Alcohol withdrawal seizures, usually tonic-clonic, non-focal and brief
- Stage 3 (onset 48h):
o Visual, auditory, olfactory, or tactile hallucinations
- Stage 4 (3-5d)
o Delirium tremens, confusion, delusions, hallcuinations, agitation, tremors, autonomic
hyperactivity (fever, tachycardia, HTN)
Severity
- Mild: unease, anxiety, feeling down, lack of sleep
- Moderate: 24-36h, psychic symptoms and increased adrenergic activity (shivering, sweating, headace,
nausea, tachycardia, hyperventilation, systolic HTN)
- Severe: marked unease, passing hallucinations or ilusions, marker autonomic hyperactivity with severe
shivering, nausea and vomiting. Severely affected general condition
- Complicated: delirium tremens or somatic complications of seizures, hyperthermia, or severe tachycardia
and HTN. Only 5% of patients with alcohol abstinence progress to delirium tremens

Delirium tremens (alcohol withdrawal delirium)

- Consists of:
o Autonomic hyperactivity (diaphoresis, tachycardia, increased respiration)
o Hand tremor
o Insomnia
o Psychomotor agitation
o Anxiety
o Nausea or vomiting
o Tonic-clonic seizures
o Visual/tactile/auditory hallucinations
o Persecutory delusions

Management
- Monitor using clinical institute withdrawal assessement for alcohol (CIWA-A) scoring system:
o Areas of assessment include:
§ Physical (5): n&v, tremor, agitation, paroxysmal sweats, headache/fullness in head
§ Psychological/cognitive (2): anxiety, orientation/clouding of sensorium
§ Perceptual (3): tactile disturbances, auditory disturbances, visual disturbances
o all categories are scored from 0-7 (except orientation/sensorium 0-4), maximum score 67
o classification of severity
§ mild: <10
§ moderate: 10-20
§ Severe: > 20
7. Family therapy. Autogen trainingn. Hypnosis

Psychotherapies

Family therapy
- Based on the theory that family is a system that attempts to maintain homeostasis, regardless of how
maladaptive the system may be. The theory has been referred to as a “family system orientation” and the
techniques include focusing on the family rather than on the identified patient. The family, therefore,
becomes the paitent, rather than the individual family member who has been identified as sick.
- Can be defined as any psychothereapeutic endeavor that explisetly focuses on altering the interactions
among family members and seeks to improve the functioning of the family as a unit, or its subsystems, and
the individual members of the family
- Both family therapy and couple therapy aim at some change in relational functioning. In most cases, they
also aim at some other change, typically in the functioning of specific individuals in the family
- In early years of family therapy, change in the family system was seen as being sufficient to produce
individual change. More recent treatments aimed at the change in individuals, as well as in the family
system, tend to supplement the interventions that focus on interpersonal relationships with specific
strategies that focus on individual behavior

Indications
- Relational difficulty
o E.g. parents and adult children
- Component within multimethod treatment of psychiatric disorders
o Family’s coping with schizophrenia

Techniques
- Initial consultation
o Families may request for it specifically.
o When initial complaint is about an individual family member pretreatment work may be needed
- Interviewing technique
o A family comes to treatment with its history and dynamics firmly in place. To a family therapist,
the established nature of the group, more than the symptoms, consititutes the clinical problem.
- Frequency and length of treatment
o Unless emergency arises, sessions are usually only once a week. Each session may require as
much as 2 hours.

Models of intervention
- Psychodynamic-experimental models
o Emphasize individual maturation in the context of the family system and are free from
unconscious patterns of anxiety and projection rooted in the past.
o Therapists seek to establish an intimate bond with each family member, and sessions alternate
btw the therapists exchanges with the members and the members exchanges with one another.
Clarity of communication and honestly admitted feelings are given high priority.
- Bowen model
o Hallmark is persons differentiation from their family of origin, their ability to be their true selves
in the face of familial or other pressures that threaten the loss of love or social position
o Problem families are assessed on two levels; the degree of their enmeshment versus the degree
of their ability to differentiate and the analysis of emotional triangles in the problem for which
they seek help.
o An emotional triange is defined as a three-party system (an many of these can exist within a
family) arranged so that the closeness of two members expressed as either love or repetitive
conflict tends to exclude a third. Then the excluded third person attempts to joint with onne of
the other two or when one of the involved parties shifts the direction of the excluded one,
emotional cross-currents are activated
§ The therapists role is first to stabilize or shift the “hot” triangle – the one producing the
presenting symptoms – and second to work with the most psychologically available
 family members individually if necessary to achive sufficient personal differentiation so
that the hot triangles does nto recur.
- Structural model
o In this model families are viewed as single, interrelated systems assessed in terms of significant
alliances and splits among family members, hierarchy of power (parents over children), clarity and
firmness of boundaries btw the geerations, and family tolerance for one another
- General systems model
o Based on general system theory, a general system model holds that families are systems and that
every action in a family produces a reaction in one or more of its members
o Every member is presumed to play a role (e.g. persecutor, rescuer, victim, nurturer etc), which is
relatively stable, but which member fills each role may change.
o Some families try to scapegoat one member by blaming him or her for the families problems (the
identified paitent). If the identified patient improves, another family member may become the
scapegoat.

Mofication of techniques
- Family group therapy
o E.g. treatment of schizophrenia has been effective in multiple family groups
o Families of disturbed children may also meet together to share situations
- Social network therapy
o The network includes those with whom the patient comes into contact in daily life, not only the
immediate family but also relatives, friends, teachers etc.
- Paradoxical therapy
o A therapists suggests that the patient intentionally engage in the unwanted behavior (called
paradoxical injunction) and, for example, avoid a phobic object or perform a compulsive ritual
o Although paradoxical therapy and the use of paradoxical injucntions seem to be counterintuitive,
the therapy can create new insights for some patients
- Reframing (positive connotation)
o Labeling of all negatively expressed feelings or behavior as positive. When the therapiest
attempts to get family members to view behavior from a new frame of reference, “this child is
impossible” becomes “this child is desperately trying to distract and protect you from what he or
she perceives as an unhappy marriage”
o Reframing is an important process that allows family members to view themselves in new ways
that can produce change

Autogen training
- It’s a technique of self-hypnosis/self-suggestion developed by a german neurologist.
- It’s a technique that teaches your body to respond to verbal commands. These commands “tell” your body
to relax and help control breathing, blood pressure, heartbeat, and body temperature. The goal of AT is to
achieve deep relaxation and reduce stress. After one learn the technique oe can use it whenever one feels
the need or want relief from symptoms of stress, or one can practice it regularly to enoy the benefits of
deep relaxation and prevent the effects of chronic stress
- Consists of six standard exercsies that make the body feel warm, heavy, and relaxed. For each exercise,
one get into a simple posture (sitting in a comfortable chair or reclininc), concentrate without any goal.
And use visual imagination and verbal cues to relax the body in some specific way. It usually takes about 4-
6 months to master all six exercises.
- the way it works is not fully understood, but its effects on the body are measurable. Experts believe that
AT works inn ways that are similar to hypnosis and biofeedback. The exercises allow communication btw
mind and the body, allowing you to influence body reactions that normally cannot be controlled, such as
BP, HR, and body temperature
- use:
o relieve symptoms of stress
o help with GAD, fatigue, and irritability
o manage pain, insomnia, and increase resistance to stress
- Involves patients directing their attention to specific bodily areas and hearing themselves think certain
phrases reflecting a relaxed state
- In the original germal version, patients progressed through six themes over many sessions
 o Heaviness – “my left arm is heavy”
o Warmth – “my left arm is warm”
o Cardiac regulation – “my heartbeat is calm and regular”
o Breathing adjustment – “it breathes me”
o Solar plexus- “my solar plexus is warm”
o Forehead – “my forehead is cool”
- Autogen relaxation is an American modification of autogenic training, in which all six areas are covered in
one session

Hypnosis
- Greek word = sleep
- In reality its more like a complex process that requires alert focused and repetitive attention. It’s a means
of directing innate capabilities of imagination, imagery, and attention.
- Unlike the common belief that it’s the clinician who has the power to influence the patient, it is in reality
the patient who has the hypnotic gift, and it’s the clinicians role to assess the patients capacity to capitalize
on this asset and to help the patient discover and use it effectively. Patient motivation, personality style,
and biological predisposition may contribute to the manifestation of this talent.
- During the hypnotic trance, focal attention and imagination are enhanced and simultaneously peripheral
awareness is decreased. This trance may be induced by a hypnotist through formalized induction
procedures, but it can also occur spontaneously.

Definition
- Hypnosis is currently understood as a normal activity of a normal mind through which attention is more
focused, critical judgment is partially suspended, and peripheral awareness is diminished.
- The trance state, being a function of the subjects mind, cannot be forcibly projected by an outside person.
The hypnotist, however, may aid in the achievement of the state and use its uncritical, intense focus to
facilitate the acceptance of new thoughts and feelings, thereby accelerating therapeutic change.
- For the subject, hypnosis is typified by a feeling of involuntariness and movements seem automatic.

Trait of hypnoizability
- Experiencing the hypnotic concentration state requires a convergence of three essential components
o Absorption
§ Ability to reduce peripheral awareness that results in a greater focal attention
§ Can be metaphorically described as a psychological zoom lens that increases attention to
the given thought or emotion and increasing exclusion of all context, even including
orientation to time and space.
o Dissociation
§ Separating out form consciousness elements of the patient’s identity, perception,
memory, or motor response as the hypnotic experience deepens
§ The result is that components of self-awareness, time, perception, and physical activity
can occur without being known to the patients consciousness and so may seem
involuntary
o Suggestibility
§ The tendency of the hypnotized patient to accept signals and information with a relative
suspension of normal critical judgement; it is controversial whether critical judgment can
be completely suspended
- Hypnosis in psychiatric disorders
o Easily hypnotized: Histrionic PD, dissociative identity disorder
o Hard to hypnotize: paranoid PD, eating disorder
Neurophysiological correlates of hypnosis

- Neurological testing of individuals in the hypnotized state and those with a high degree of hypnotizability
has led to some interesting findings, but no set of change has been shown to be sensitive or specific for the
trance state or hypnotizability trait.

- EEG studies have shown that hypnotized persons exhibit electrical patterns that are similar to those of fully
awake
o Increased alpha activity and theta power in left frontal region has been reported in highly
hypnotizable patients as compared with those who are less hypnotizable; these differences exist
in the trance and nontrance states.
- PET studies comparing regional blood flow
o Hypnotic suggestions to add color to a visual image result in increased blood flow to the lingual
and fusiform gyri, the color vision processing centers of the brain, suggestions to remove color
have the opposite effect
o Similarly, the intensity and noxiousness of pain are believed to be processed by different regions
of the brain, because different areas of reduced blood flow result when each is minimized
through hypnosis
- Role of anterior brain regions, such as the frontal lobes, in hypnosis has been shown physiologically by the
positive correlation btw homovanillic acid concentrations in the CSF and degree of hypnotizability
o Frontal cortex and basal ganglia have a large nr of neurons that use DA
o This may explain why pharmacological enhancement of hypnotizability, although difficult, is
accomplished with DA agonists (e.g. amphetamine)
o Increased activation of the basal ganglia may relate to the increased automaticity of hypnotic
motor behavior
Clinical assessment of hypnotic capacity

- Two major procedures exist to clinically evaluate hypnotic capacity

o Standford hypnotic susceptibility scale
§ Long laboratory-based test that has been modified for clinical evaluation
§ Take approx. 20 min
§ Primarily measures behavioral compliance and suggestibility
o Hypnotic induction profile
§ Shorter test that uses the eye-role sign as biological indicator and measures cognitive
flow, which differentiates those with no hypnotic capacity because of mental pathology
from those mentally normal patients with any hypnotic capacity

Induction

- Many different induction protocols follow the same basic principles and pattern, but may be better suited
to the patients with different levels of hypnotizability

Indications

- Hypnosis’s effectiveness in facilitating acceptance of new thoughts and feelings makes it useful in treating
habitual problems and also with symptom managmenet
o Smoking
o Overeating
o Phobias
o Anxiety
o Conversion symptoms
o Chronic pain
- Can often be treated in a single session, in which a patient is thought to perform self hypnosis
- May also aid in psychotherapy, notably for PTSD, and it has been used for memory retrieval

Contraindications

- No intrinsic dangers to the hypnotic process exist

- Beucase of the increased dependence that the hypnotized patient has toward the therapist, a strong
transference may occur, however, in which the patient exhibits feelings for the therapist that are
inappropriate in regards to their relationship
o Strong attachments may occur, and its important that these are respected and properly
interpreted
- Negative emotions may also be brought out in the patient, esp those who are emotionally fragile or who
have poor reality testing
o To minimize the likelihood of this negative transference, caution should be taken when choosing
patients who have problems with basic trust, such as those who are paranoid or who requires
high levels of control
- The hypnotized patient also has a reduced ability to critically evaluate hypnotic suggestions and, thus, the
hypnotist must have a strong ethical value system
- Controversy exist about whether patients can perform acts during a trance state that they would
otherwise find repugnant or that run contrary to their moral system
8. Suicide-etiology, epidemiology and prevention

- Must be screened for in every encounter; part of risk assessment along with violent/homicidal ideation

Epidemiology

- Attempted: completed = 20:1

- M:F = 1:4 for attempts, 3:1 for completed

Risk factors

- Epidemiologic factors:
o Age: increase after age 14, second most common cause of death for ages 15-24, highest rate of
completion in persons > 65y
o Sex: male
o Race/ethic background: white or native canadians
o Marital status: widowed/divorced
o Living situation: alone, no children <18y old in household
o Other: stressful life events, access to firearms
- Psychiatric disorders:
o Mood disorders (15% of lifetime risk in depression, higher in bipolar)
o Anxiety disorders (esp panic disorder)
o Schizophrenia (10-15% risk)
o Substance abuse (esp alcohol – 15% lifetime risk)
o Eating disorder (5% lifetime risk)
o Adjustment disorder
o Conduct disorder
o Personality disorders (borderline, antisocial)
- Past history
o Prior suicide attempt
o Family history of suicide attempt/completion

Clinical presentation
- Symptoms associated with suicide include:
o Hopelessness
o Anhedonia
o Insomnia
o Severe anxiety
o Impaired concentration
o Psychomotor agitation
o Panic attacks
Approach

- As every patient – e.g. “have you had any thoughts of wanting to harm or kill yourself?”
- Classify ideation
o Passive ideation: would rather not be alive but has no active plan for suicide (e.g. “id rather not
wake up” or “ I would not mind if a car hit me”
o Active ideation: e.g. “I think about killing myself”
- Assess risk:
o Plan: “do you have a plan as to how you would end your life?”
o Intent: “do you think you would actually carry out this plan?”, if not, why not
o Past attempts: highest risk if previous attempts in past year
§ Ask about lethality, outcome, medical intervention
- Assess suicidal ideation
o Onset and frequency of thoughts: “when did this start?” or “how often do you have these
thoughts?”
o Control over suicidal ideation: “how do you cope when you have these thoughts?”, “could you call
someone for help?”
o Intention: “do you want to end your life” or “do you wish to kill yourself?”
o Intended lethality: “what do you think would happen if you actually took those pills?”
o Access to means: “how will you get a gun” or “which bridge to you think you would go to?”
o Time and place: “have you picked a date and place? It its an isolated location?”
o Provocative factors: “what makes you feel worse (e.g. being alone)?”
o Protective factors: “what keeps you alive (e.g. friends, family, pets, faith, therapist)?”
o Final arrangements: “have you written a suicide note? Made a will? Given away your belongints?”
o Practiced suicde or aborted attempts: “have you ever put the gun to your head?”, “held the
medications in your hand?”, “stood at the bridge”
o Ambivalence: “I wonder if there is a part of you that wants to live, given that you came here for
help?”

Assessment of suicide attempt

- Setting (isolated vs others present/chance of discovery)

- Planned vs impulsive attempt, triggers/stressors
- Substance use/intoxication
- Medical attention (brought in by another person vs brought in by self o ED)
- Time lag from suicde attempt to ED arrival
- Expectation of lethality, dying
- Reaction to survival (guilt/remorse vs disappointment/self blame)

Management

- Asking patients about suicide will not give them the idea or the incentive to commit suicide
- The best predictor of completed suicide is a history of attempted suicide
- The most common psychiatric disorders associated with completed suicide are mood disorders and alcohol
abuse

- Proper documentation of the clinical encounter and rationale for management is essential
- Higher risk (hospitalization needs to be strongly considered)
o Patients with a plan and intention to act on the plan, access to lethal means, recent social
stressors, and symptoms suggestive of a psychiatric disorder
o Do not leave patient alone; remove potentially dangerous s objects from room
o If patient refuses to be hospitalized, complete form for involuntary admission
- Lower risk:
o Patients who are not actively suicidal with no plan or access to lethal means
o Discuss protective factors and supports in their life, remind them of what they live for, promote
survival skills that helped them through previous suicide attempts
o Make a safety plan that could include an agreement that they will:
 § Not harm themselves
§ Avoid alcohol, drugs, and situations that may trigger suicidal thoughts
§ Follow-up with you at a designated time
§ Contact a health care worker, call a crisis line, or go to an emergency department if they
feel unsafe or if their suicidal thoughts return or intensify
o Depression: consider hospitalization if symptoms severe or if psychotic features are present;
otherwise outpatient treatment with good supports and SSRIs/SNRIs
o Alcohol-related: usually resolves with abstinence for a few days; if not, suspect depression
o Personality disorders: crisis intervention, may or may not hospitalize
o Schizophrenia/psychosis: hospitalization might be necessary
o Parasuicide/self-mutilation: long-term psychotherapy with brief crisis intervention when
necessary
9. Psychopharmacology I: Antipsychotics and anxiolytics: Mechanism of action, indications,
effects and side effects

Anxiolytics
- Mask or alleviate symptoms, don’t cure them
- Indications:
o Short-term treatment of transient forms of anxiety disorders, insomnia, alcohol withdrawal (esp
delirium tremens), barbiturate withdrawal, organic brain syndrome (acute agitation in delirium),
EPS and akathisia due to antipsychotics, seizure disorders, musculoskeletal disoders
- Relative CI:
o Major depression (except as adjunct to other treatment), history of drug/alcohol abuse, caution in
pregnancy/breastfeeding
- MA:
o Benzodiazepines potentiate binding of GABA to its receptors – decreased neuronal activity
o Buspirone: partial agonist 5-HT1A-receptor

Benzodiazepines
- Should be used for limited periods (weeks-months) to avoid dependence
- All benzodiazepines are sedating (careful in elderly)
- Have similar efficacy, choose according to half-life, metabolites, and route of admin
- Taper slowly over weeks-months because they can cause withdrawal reactions
o Low dose withdrawal: tachycardia, HTN, panic, insomnia, anxiety, impaired memory and
concentration, perceptual disturbances
o High dose withdrawal: hyperpyrexia, seizures, psychosis, death
- NB:
o potentiation of CNS depression if used with alcohol
o LOT (lorazepam, oxazepam, and temazepam) are safe to use in pt with impaired liver function
because not metabolized in liver
- SE:
o CNS: drowsiness, cognitive impairment, reduced motor coordination, memory impairment
o Physical dependence
o Tolerance
- Withdrawal:
o 1-2d (short acting), 2-4d (long acting)
o Similar to but less severe than alcohol withdrawal, can be fatal
o Clinic:
§ Anxiety, insomnia, autonomic hyperactivity (less common)
§ Lasts weeks-months
§ Complications with above 50 mg diazepam/day: seizures, delirium, arrhythmias,
psychosis
o Management:
§ Taper with long acting benzos
- Overdose:
o Rarely fatal
o May cause death when combined with alcohol, other CNS depressants, or TCAs
Antipsychotics (“neuroleptics”)
- Used in agitation, sleep, psychosis, and mania reduction, mood stabilizing – used in schizophrenia and
other psychotic disorders, mood disiorders w/w.o psychosis, violent behavior, autism, tourettes,
somatoform disorders, dementia, OCD

- Rational use
o No reason to combine antipsychotics
o Choosing an antipsychotics
§ All are equally effective (except clozapine which is considered most effective in
treatment-refractory psychosis)
§ SGA are as effective as FGA but are thought to have better SE profile
§ Choose a drug that the patient has responded to in the past or that was used successfully
in a family member
- Mechanism of action:
o Block dopamine activity:
§ Mesolimbic (emotion, reward)
• High dopamine causes positive symptoms of schizophrenia
§ Mesocortical (cognition, executive function)
• Low dopamine cause negative symptoms of schizophrenia
§ Nigrostriatal (movement)
• Low dopamine causes EPS
§ Tuberoinfundibular (prolactin release)
• Low dopamine causes hyperprolactinemia
- Onset:
o Immediate calming effects and decrease in agitation
o Thought disorder responds in 2-4 weeks
§ If no response in 4-6w switch drugs, if response – titrate dose
- Duration:
o Minimum 6 months (usuall for life)
- Administration:
o PO
 o Depot IM injections
o Sublingual

Typical (FGA)
- MA:
o Block postsynaptic D2 receptors (centrally and peripherally)
- Pros:
o Inexpensive
o Plenty of injectable forms available
- Cons:
o More EPS, tardive syndromes in long term (higher potency, higher risk)
o Not mood stabilizing
o No effect on negative symptoms
o High nr of non-responnders

In order of decreasing potency

1. Haloperidol
- Worst in relation to EPS, NMS, and TD
2. Fluphenazine
3. Zuclopenthixol HCI
4. Loxapine HCI
5. Chlorpromazine

Atypical (SGA)
- MA:
o Block postsynaptic D2 receptors (more specific D2C – less EPS)
o Block 5-HT2 receptors on presynaptic dopaminergic terminals – triggering dopamine release and
reversing dopamine blockade in some pathways
- Pros:
o Fewer EPS, low risk of tardive dyskinesia
o Mood stabilizing effects
o Better action against negative symptoms (also block 5-HT)
o Action in non-responders
- Cons:
o Expensive
o Few injectable forms available
o Metabolic SE: weight gain, hyperglycemia, lipid abnormalities, metabolic syndrome
o Exacerbation (or new onset) of obsessive behavior

In order of decreasing potency

1. Risperidone (Risperdal)
- Quick dissolve (M-tabs), and long acting (consta) available
2. Olanzapine (Zyprexa)
- Quick dissolve formulation (zydis) used commonly inn ER setting for better compliance, IM forma available
- Associated with significant weight gain and medatbolic adverse effects – not first line
3. Quetiapinen (Seroquel)
4. Clozapine
- Weekly blood counter for 6 months, then every 2 weeks
- Do not use with drugs which may cause BM suppression due to risk of agranulocytosis
- Not associated with TD (more selective for 2Dc relative to 2Da)
5. Aripiprazole (abilify)
- Dopaminne-serotonin system stabolizers
- In animal experiments it works as:
o Partial agonist DA
o 5-HT1 antagonist
o 5-HT1a partial agonist
Side effects
- Anticholinergic (low potency > high potency)
o Dry mouth, urinary retention, constipation, blurred vision, toxic confusional states
o FGA > SGA
- Alpha-1 adrenergic blockade (low potency > high potency)
o Orthostatic hypotension, impotence, failure to ejaculate
- Dopaminergic blockade
o EPS
o Galactorrhea, amenorrhea, impotence
§ Elevated prolactin – inhibition GnRH release
o weight gain (5-HTc)
- Anti-histamine
o Sedation
- Hematologic
o Agranulocytosis (clozapine)
- Hypersensitivity reactions
o Liver dysfunction, blood dyscrasias, skin rashes, NMS, altered temperature regulation
(hypothermia or hyperthermia)
- Endocrine
o Metabolic syndrome
- Other:
o Dysphoria
§ FGA can worsen negative symptoms due to blockade of D2-R (involved in reward and
pleasure)
o QT prolongation (many FGA)

NMS
- Psychiatric emergency
- Due to massive dopamine blockade – increased incidence with high potency and depot neuroleptics
- Risk factors:
o Medication factors: sudden increase in dosage, starting a new drug
o Patient factors: medical illness, dehydration, exhaustion, poor nutrition, external heat load, male,
young adults
- Clinical presentation
o Develop over 24-72h
o FARM
§ Fever
§ Autonomic changes – increased HR/BP, sweating
§ Rigidity of muscles (severe global, “lead pipe rigidity”)
§ Mental status changes (usually first) – confusion
o Lab:
§ Elevated CK, leukocytosis, myoglobinuria
- Ddx:
o NMS – severe global rigidity, pallor, no GI sx
o SS – twitchy/shiwering/restless, flushed/sweaty, vomiting, diarrhea, abdominal pain
- Tx:
o Supportive – discontinue drug, hydration, cooling blanket, dantrolene (muscle relaxant),
bromocriptine (DA agonist)
- Prognosis:
o Mortality: 5%

Extrapyramidal symptoms
- Incidence related to increase dose and potency
- Acute (early onset, reversible) vs tardive (late onset, often irreversible)
- Arise due to D2 blockade in nigrostriatal tract, leading to unbalanced excess of cholinergic activity (this is
why antipsychotic drugs with strong anticholinergic activity show fewer EPS)
- Dystonia:
o Acute and tardive
o Due to DA block
o Onset: within 5d acute, >90d tardive
o Risk group: young Asians, black males
o Presentation:
§ Sustained abnormal posture; torsion, twisting, contraction of muscle groups, muscle
spasms
§ Oculogyric crisis (forced sustained elevation of eyes), laryngospasms, torticollis
o Tx:
§ Benztropine or diphenhydramine
§ NB: if give levodopa – precipitate psychosis
- Akathisia
o Acute and tardive
o Onset: within 10d actue, >90d tardive
o Risk group: elderly females
o Due to sensitization
§ Block DA-R, the onces that are not block will become sensitized and have increased
affinity for DA – excessive neurotransmission in nigrostriatal tract
o Presentation:
§ Motor restlessness (compelling need to be in constant motion, urge to moove); crawling
sensation in legs relieved by walking, very distressing, increased risk of suicide and poor
adherence
o Tx:
§ Acute: lorazepam, propranolol, or diphenhydramine
§ Reduce or change neuroleptic to lower potency
- Pseudoparkinsonism (dyskinesia)
o Acute
o Due to DA block
o Onset: within 30 d acute
o Risk group: elderly females
o Presentation:
§ Tremor, rigidity (cogwheeling), akinesia, postural instability (decreased/absent armswing,
stooped posture, shuffling gait, difficulty pivoting)
o Treatment
§ Acute: benztropine (or benzodiazepine if side effects)
§ Reduce or change neuroleptic to lower potency
- Dyskinesia
o Tardive > 90 days
o Late, due to increased nr of dopamine receptors and increase DA release as a compensatory
response to long term DA block
o Presentation:
§ Purposeless, constant movements, involving facial and mouth musculature, or less
commonly the limbs
 § Choreoatetoid movements (involuntary repetitive rhythmic movements), orofacial
dyskinesis (lip smacking, tongue pertrusions or grimacing)
o Treatment
§ No good treatment
§ May try clozapine
§ Discontinue drug or reduce dose

Anticholinergics
- Drugs:
o Benztropine
o Amantadine
o Diphenhydraminen
- Indications:
o With antipsychotics if at high risk of acute EPS or if acute EPS develops
- NB: do not give for tardive syndromes because worsen the condition!
10. Eating disorders: Diagnostic criteria and clinical management

- Epidemiology:
o Anorexia nervosa: 1% adolescents and young adult females, onset 13-20y
o Bulimia nervosa: 2-4% adolescents and young adult females, onset 16-18y
o F:M =10:1, mortality 5-10%
- Etiology:
o Multifactorial:
§ Psychological
§ Sociological
§ Biological associations
o Individual:
§ Perfectionism
§ Lack of control in other life areas
§ History of sexual abuse
o Personality
§ Obsessive-compulsive
§ Histrionic
§ Borderline
o Familial
§ Maintenance of weight equilibrium and control in dysfunctional family
o Cultural
§ Prevalent in industrialized societies
§ Idealization of thinness in media
o Genetic factors
§ AN: 6% prevalence in siblings, with one study of twin pairs finding concordance in 9 of 12
monozygotic twin pairs vs concordance of 1 of 14 in dizygotic pairs
§ BN: higher familial incidence of affective disorders than the general population
- Risk factors:
o Physical factors: obesity, chronic medical illness (e.g. DM)
o Psychological factors: individuals who by career choice are expected to be thin, family history
(mood disorders, eating disorders, substance abuse), history of sexual abuse (esp BN),
homosexual males, competitive athletes, concurrent associated mental illness (depression, OCD,
anxiety disorder (esp panic and agoraphobia), substance abuse (esp for BN)
- Differentiating btw eating disorders:
o AN or bing-eating/puring type (significantly low body weight) takes priority over BN diagnosis (BW
not in criteria)
o BN requires compensatory behaviors
o Binge eating disorder doesn’t involve compensatory behaviors
o Avoidant/restricitive food intake disorder doenst involve disturbances in body image
- Physiological complications of eating disorders:
Anorexia nervosa

DSM5 criteria

- A) intake and weight:

o Restriction of intake relative to requirements, leading to a significantly low body weight in the
context of age, sex, developmental trajectory, and physical health. Significantly low weight is
defined as a weight that is less than minimally normal, or, for children and adolescents, less than
minimally expected
- B) fear or behavior
o Intense fear of gaining weight or of becoming fat, or persistent behavior that interferes with
weight gain, even though at a significantly low weight
- C) perception
o Disturbance in the way in which ones body weight or shape is experienced, undue influence of
body weight and shape on self-evaluation, or persistent lack of recognition of seriousness of the
current low body weight
- Specifiers
o Partial remission, full remission
o Severity based on BMI
§ Mild > 17 kg/m2
§ Moderate 16-16,99
§ Severe 15-15,99
§ Extreme < 15
o Type
§ Restricting = during last 3m no episodes of binge-eating of purging
§ Binge-eating/purging type = in last 3 months have participated in recurrent episodes of
binge-eating/purging
Clinic

- Low weight
- Athletic triad: disordered eating, amenorrhea, osteoporosis
- Some patients with insulin-dependent DM may stop taking their medication in order to loose weight

Management

- Psychotherapy
o Individual, group, family (gold standard)
o Address food and body perception, coping mechanisms, health effects
- Medication (little value)
- Outpatient and inpatient programs available
- Inpaitent hospitalization for treatment of eating disorder is rarely on acute basis (unless there is a
concurrent psychiatric reason for emergent admission, e.g. suicide risk)
- Criteria to admit to medical ward for hospitalization:
o < 65% of standard body weight ( <85% of standard BW for adolescents)
o Hypovolemia requiring IV fluids
o Heart rate < 40
o Abnormal serum chemistry
o Actively suicidal
- Agree on target body weight on admission and reassure this weight will not be surpassed
- Monitor for complications of AN
o See above
o Important electrolytes in eating diorders: KPMg (potassium, phosphate, magnesium)
- Monitor for refeeding syndrome
o Potentially life threatening metabolic response to refeeding in severly malnourished patients
resulting in severe shifts in fluid and electrolyte levels
o Complications
§ Hypophosphatemia
§ Congestive heart failure
§ Cardiac arrhythmias
§ Delirium
§ Death
o Prevention
§ Slow refeeding
§ Gradual increase in nutrition
§ Supplemental phosphorus
§ Close monitoring of electrolytes and cardiac status

Prognosis

- Early intervention much more effective (adolescent onset has much better prognosis than adult onset)
- 1 in 10 adolescents continue to have anorexia nervosa as adults
- With treatment: 70% resume a weight of at least 85% of expected elvels and about 50% resume normal
menstrual function
- Eating peculiarities and associated psychiatric symptoms are common and persistent
- Long term mortality: 10-20% of patients hospitalized will die in next 10-30y (secondary to severe and
chronic starvation, metabolic or cardiac catastrophes, with significant proportion committing suicide)
Bulimia nervosa

DSM5 diagnostic criteria

- A) recurrent episodes of binge-eating; an episode of binge-eating is characterized by both the following

o Eating, in a discrete period of time, an amount of food that is definitely larger than what most
individuals would eat during a similar period of time and under similar circumstances
o A sense of lack of control over eating during the episode
- B) recurrent inappropriate compensatory behavior in order to prevent weight gain, such as self-induced
vomiting, misuse of laxatives, diuretics, enemas, or other medications, fasting, or excessive exercise
- C) the binge-eating and inappropriate compensatory behaviors both occur, on average, at least once a
week for 3 months
- D) self-evaluation is unduly influenced by body shape and weight
- E) the disturbance doesn’t occur exclusively during episodes of AN

- Specifiers:
o Partial remission, full remission
o Severity measured in nr inappropriate compensatory behaviors/w
§ Mild 1-3
§ Moderate 4-7
§ Severe 8-13
§ Extreme 14+

Associated features

- Fatigue and muscle weakness due to repetitive vomiting and fluid/electrolyte imbalance
- Tooth decay
- Swollen appearance around angle of jaw and puffiness of eye sockets due to fluid retention
- Reddened knuckles, Russell’s sign (knucle callus from self-induced vomiting)
- Trouble concentrating
- Weight fluctuation over time

Management

- Admission for significant electrolyte abnormalities

- Biological: treatment of starvation effects, SSRIs (fluoxetine most evidence), as adjuncts
- Psychological: develop trusting relationship with therapist to explore personal etiology and triggers, CBT,
family therapy, recognition of health risks
- Social: challenge destructive social views of women, use of hospital environment to provide external
patterning for normative eating behavior

Prognosis

- Relapsing/remitting disease
- Good prognostic factors: onset before age 15, achieving a healthy weight within 2 y of treatment
- Poor prognostic factors: later age of onset, previous hospitalizations, individual and familial disturbance
- 60% good treatment outcome, 30% intermediate outcome, 10% poor outcome

Binge-eating disorder

- Definition:
o Recurrent episodes of binge-eating that are associated with eating much more rapidly than
normal, eating until feeling uncomfortably full, eating large amounts when not physically hungry,
eating alonen because embarrassed by how much one is eating, feeling disgusted with
self/depressed, very guilty afterwards
o At least once per week x 3 months
- Epidemiology
 o F:M = 2:1
o Begins in adolescence or young adulthood
- Treatment
o CBT

Avoidant/restrictive food intake disorder

- Definition:
o Eating/feeding disturbance to the extent of persistent failure to meet appropriate nutritional
and/or energy needs, resulting in significant weight loss/growth failure and nutritional
deficiencies.
o Patients experience disturbances in psychosocial functioning and may become dependent on
enteral feeding/oral nutritional supplementation
o Does not occur during episode of AN or BN
o No evidence of distress in the way in which ones body weight or shape is experienced
- Risk factors
o Temperament (e.g. anxiety disorders), environment (e.g. familial anxiety), genetic (e.g. history of
GI conditions)
o Begins in infancy and can persist into adulthood
- Treatment
o Watchful waiting
o Behavior modification
o Psychotherapy
11. Delirium: etiology, diagnostic criteria, and clinical management

Acute confusional state/delirium

- Medical emergency carrying significant risk of morbidity and mortality; its characterized by acute onset,
disorientation, fluctuating level of consciousness, poor attention, and marked psychomotor changes
- Visual hallucinations more commonly indicate organic disease

DSM5 diagnostic criteria for delirium

- A) Attention and awareness
o Disturbance in attention (i.e. reduced ability to direct, focus, sustain, and shift attention) and
awareness (reduced orientation to the environment)
- B) Acute and fluctuating:
o Disturbance develops over short period of time (usually hours to days), represents a change from
baseline attention and awareness, and tends to fluctuate in severity during the course of a day
- C) cognitive changes
o An additional disturbance in cognition (e.g. memory deficit, disorientation, language, visuospatial
ability, or perception)
- D) not better explained
o Criteria A and C are not better explained by another neurocognitive disorder (pre-existing,
established, or evolving) and do not occur in the context of a severely reduced level of arousal
(e.g. coma)
- E) direct physiological cause:
o Evidence that disturbance is a direct physiological consequence of another medical condition,
substance intoxication or withdrawal (i.e. due to a drug of abuse or medication), toxin, or its due
to multiple etiologies
- Note: Can have hyperactive, hypoactive, or mixed presentation

Diagnosis
- See DSM5
- Confusion assessment method (CAM)
o Highly sensitive and specific method to diagnose delirium
o Part 1: an assessment instrument that screens for overall cognitive impairment
o Part 2: includes four features found best able to distinguish delirium from other cognitive
impairments
o Need 1 + 2 + 3 or 4
§ Acute onset and fluctuating course
§ Inattention
§ Disorganized thinking
§ Altered level of consciousness – hyperactive or hypoactive
- RASS = Richmond agitation-sedation scale

Clinical presentation and assessment

- Common symptoms
o Distractibility, disorientation (time, place, rarely person)
o Misinterpretations, illusions, hallucinations
§ NB: visual hallucinations are organic until proven otherwise
o Speech/language disturbances (dysarthria, dysnomia, dysgraphia)
o Affective symptoms (anxiety, fear, depression, irritability, anger, euphoria, apathy)
o Shifts in psychomotor activity (groping/picking at clothes, attempts to get out of bed when
unsafe, sudden movements, sluggishness, lethargy)
- Folstein mini mental exam or montreal cognitive assessment are helpful to assess baseline of altered
mental state (i.e. score will improve as symptoms resolve)

Etiology

- Infectious; encephalitis, meningitis, UTI, pneumonia

- Withdrawal: alcohol, barbs, benzos
- Acute metabolic disorder: electrolyte imbalance, hepatic or renal failure
- Trauma: head injury, post-operative
- CNS pathology: stroke, hemorrhage, tumor, seizure disorder, Parkinsons
- Hypoxia: anemia, cardiac failure, pulmonary embolus
- Deficiencies: Vit b12, folic acid, thiamine
- Endocrinopathies: thyroid, glucose, parathyroid, adrenal
- Acute vascular: stroke, vasculitis, hypertensive encephalopathy
- Toxins: substance use, sedatives, opioids (esp morphine), anesthetics, anticholinergics, anticonvulsants,
dopaminergic agents, steroids, insulin, glyburide, antibiotics (esp quinolones), NSAIDs
- Heavy metals: arsenic, lead, mercury

Risk factors

- Hospitalization (incidence 10-56%)

- Previous delirium
- Nursing home residents (incidence 60%)
- Polypharmacy (e.g. anticholinergics)
- Old age (esp males)
- Severe illness (e..g cancer, AIDS)
- Recent anesthesia or surgery
- Substance abuse
- Pre-existing cognitive impairment, brain pathology, psychiatric illness

Investigations

- Standard:
o CBC and differential, electrolytes, glucose, ESR, LFTs, Cr, BUN, TSH, vitamin B12, folate, albumin,
urine C&S, R&M
- As indicated
o ECG, CXR, CT head, toxicology/heavy metal screen, VDRL, HIV, LP, blood cultures
o EEG – typically abnormal, generalized slowing or fast activity, can also be used to rule out
underlying seizures or post-ictal states as etiology
- Indications for CT head
o Focal neurological deficits, acute change in status, anticoagulant use, acute incontinence, gait
abnormality, history of cancer

Management

- Identify and manage underlying cause

o Identify and treat underlying cause immediately
o Stop all non-essential medications
o Maintain nutrition, hydration, electrolyte balance and monitor vitals
- Optimize the environment
o Environment: quiet, well-lit, near window for cues regarding time of day
o Optimize hearing and vision
o Room near nursing station for closer observation; constant care if patient is jumping out of bed,
pulling out lines
o Family members present for reassurance and re-orientation
o Frequent orientation – calendar, clock, reminders
- Pharmacotherapy
o Low dose, high potency antipsychotics:
§ Haloperidol (most evidence)
§ Reasonable alternalitves include risperidone, olanzapine (more sedating, less QT
prolongation), quetiapine (If EPS), aripiprazole
o Benzo – only in alcohol withdrawal delirium, otherwise can worsen delirium!
o Try to minimize anticholinergic SE
- Physical restraints to maintain safety only when necessary

Prognosis

- Up to 50% 1 y mortality rate after episode of delirium

14. Sleep disorders. Diagnostic criteria and clinical management

Sleep disorders
- Adequate sleep is essential to normal functioning, deprivation can lead to cognitive impairment and
increased mortality
- Circadian rhythms help regulate mood and cognitive performance
- NT commonly implicated in psychiatric illnesses also regulate sleep
o Ach activity and decreased activity of monoamine NT is associated with greater REM sleep
o Decreased adrenergic and cholinergic activity with NREM sleep
- Depression is associated with decreased delta sleep, decreased REM latency, and increased REM density
- Criteria:
o Must cause significant distress or impairment in normal functioning
o Not due to a GMC or medications/drugs (unless specified)

Major disorders

Management

- Pharmacological treatments are illness-specific

o Non-benzos preferable (e.g. trazodone, zopiclone, quetiapine), but benzos at short term is option
o Medication should not be prescribed without having first made a diagnosis and considering major
psychiatric illnesses (major depression and alcohol use disorders are common etiologies)
- Sleep hygiene is a simple, effective, but often underutilized method for addressing sleep disturbances;
recommendations include
o Waking up and going to bed at the same every day, including on weekends
o Avoiding long periods of wakefulness in bed
o Not using bed for non-sleep activities (reading, TV, work)
o Avoiding napping
o Discontinuing or reducing consumption of alcohol, caffeine, drugs
o Exercising at least 3-4x per week (but not in the evening, if this interferes with sleep)

Sleep physiology

Sleep architecture

- PSG (polysomniogram) measures:

o EEG
o Eye movemennts (electro-oculogram – EOG)
o EMG
o Respiratory effort
o Oxygenation
o ECG
- Stages:
o Waking state:
§ EEG:
• Alpha waves: high frequency (8-12 Hz), low voltage
§ EOG:
• Rapid, blinking
§ Muscle tone:
• High
o Stage N1 (5%)
§ EEG:
• <50% alpha waves, mixed with slow wave activity
§ EOG:
• Slow, roving eye movements
§ Muscle tone:
• High, but gradually dropping
§ Marker for very light quality sleep or sleep disruption
o Stage N2 (50%)
§ EEG:
• K complexes (high voltage negative and positive discharges) with sleep spindles
(11-16 Hz)
§ EOG:
• still
§ Muscle tone:
• High
o Stage N3 (prev 3 and 4)/slow wave/delta sleep (20%)
§ EEG:
• Delta waves: low frequency (<2 Hz), high voltage (>75 uV)
§ EOG:
• Still
§ Muscle tone:
• Low
§ Homeostatic sleep. Reduced BP, HR, CO, RR.
§ GH release
o Rapid eye movement (REM) sleep (25%)
§ EEG:
• Sawtooth waves, mixed frequency, low voltage
 § EOG:
• Rapid eye movements
§ Muscle tone:
• Very low
§ Irregular inspiration. Arrhythmias, heart rate variation.
§ Classical dreaming state

Insomnia
- Difficulty initiating or maintaining sleep, or waking up earlier than desired (leading to sleep that is
chronically non-restorative/poor quality) despite adequate opportunity and circumstances for sleep

Classification

- Acute: <3 m
- Chronic (real insomnia) > 3 months, with sleeping difficulties at least 3 nights per week OR a pattern of
insomnia for weeks repeating itself for several years
o More common in elderly
o Develops through a cycle of increasing disturbances and thoughts around the lack of sleep, which
increase the sleep problem. In this way the insomnia is maintained. Poor psychisocial working
environemntn (high demands, reduced control, mental demanding work, unbalance with sallory,
tension btw demands and reward, bullying, working shifts etc) is correlates with sleeping
difficulties
- Primary causes:
o Sleep state misperception
o Psychophysiologic insomnia (learned sleep-preventing associations – i.e. clock watching)
o Fatal familial insomnia (rare prion protein mutation causing autonomic dysfunction)
o Idiopathic (lifelong difficulty)
o Most cases starts with a reaction towards a physical or psychosocial stressor. The insomnia is
maintained via cycles of increasing disturbing thoughts around the lac of sleep, which then
increase the sleep problem. In case of primary insomnia the lack of sleep remains after the
triggering problem is resolved, partly as a conditional and learned process
- Secondary causes:
o Psychiatric disorders (80% psychiatric patients)
§ Anxiety and depression
§ Depression is most common. Not only a symptom of depression but long term insomnia
increases the risk of developing depression
o Sleep disorders
§ Restless leg syndrome (sleep initiation difficulties)
§ Sleep apnea (sleep maintenance difficulties)
o Medical conditions
§ Pregnancy, cardiorespiratory (HF, COPD), GERD, pain (arthritis, fibromyalgia, cancer)
o Drugs/toxins
§ Caffeine, stimulants
§ Alcohol – may hasten sleep onset but associated with increased arousals
§ Antidepressants – TCA/MAOI/SSRI reduce REM, prolong REM latency
§ Glucocorticoids
§ Sedative withdrawal
Diagnosis
- Defined as lack of sleep
o Because of:
§ Difficulty falling asleep
§ Not relaxed sleep
§ Early awakening
o Or because the patient has subjective feeling of poor sleep quality
- Problems should be present when there is otherwise good conditions for sleep
- Has to cause daytime problems with reduced function (sleepy/tired, fatigue, mood instabiloity, reduced
concentration, worry about sleep etc.)
Treatment
- Sleep log
o For diagnosis and monitoring of treatment
- CBT
o Sleep hygiene
o Consistent circadian rhythm (awake at the same time every day, avoid sleeping during daytime)
o Reduce activation towards evening/night (avoid stimulants, no alcohol/tobacco close to bedtime,
avoid large meals before bedtime, avoid physical work last 3 hours before bed time (but increase
physical activity generally), avoid phone etc in period before sleep, dark and quiet bedroom, avoid
watching the clock at night)
o Sleep restriction (avoid sleeping during daytime, esp in evening, only stay in bed for the hours you
actually steep)
o Stimulus control (strengthen the association btw sleep and bed (only use bed for sleep andn sex),
if one cant sleep go out of the bed, awaken at the same time no matter how many hours of sleep)
- Relaxation response
o Reduce physical and mental activation
o Progressive muscle relaxation, meditation, mindfulness exercises etc.
- Drugs
o Sleep induction
§ Zopiclon (imovane), zolpidem (stilnoct)
• Short acting benzo analogues
§ Melatonin (circadin)
o Early awakening
§ Zopiclone
§ Nitrazepam (mogadon)
§ Diazepam (vival), oxazepam (sobril)
• Anxiolytic
• Vival has longer action and most likely higher risk of hangover and dependence
- NB:
o Avoid sleep medications (esp in elderly patients) due to increased risk of falls, pseudodepression,
and memory loss

Hypersomnolence

- DSM5 criteria
o A) self reported excessive sleepiness despite a main sleep period lasting at least 7 hours, with
aleast one of the following symptoms
§ Recurrent periods of sleep or lapses into sleep within the same day
§ A prolonged main sleep episode of more than 9 hours per day that is nonrestorative (i.e.
unrefreshing)
§ Difficulty being fully awake after abrupt awakening
o B) the hypersomnolence lasts 3 times/week for at least 3 m
o C) the hypersomnolence is accompanied by significant distress or impairment in cognitive, social,
occupational, or other important areas of functioning
o D) the hypersomnolence is not better explained by and doenst occur exclusively during the coruse
of another sleep disorder (e.g. narcolepsy, breathing related sleep disorder etc)
o E) the hypersomnolence is not attributable to the physiological effects of a substance (e.g. a drug
of abuse, a medication)
o F) Coexisting mental and medical disorders do not adequately explain the predominant complain
of hypersomnolence
- Treatment
o Sleep hygiene mmeasures
o Stimulant drugs
o Naps
Sleep apnea
- Disorder of breathing in sleep associated with sleep disruption and consequent excessive somnolence (or
drowsiness)
- >2-4% of the population, correlated with obesity
- Significant morbidity: HTN, stroke, HF, sleepiness, mortality (accidents)

Classification

- OSA
o Etiology: collapse of airway due to low muscle tone in deep and REM sleep
- Central sleep apnea: no effort to breath > 10 sec
o Etiology: HF, opiates, brainstem pathology, myotonic dystrophy
- Mixed apnea: start as central, eventually becomes obstructive

Diagnosis

- Apnea hypopnea index (AHI) or respiratory disturbance index (RDI) should be < 5 in normal state

Treatment

- Conservative measures, dental devices, CPAP (common), surgery (rare), ensure driving safety

Restless leg syndrome (RLS) and periodic limb movement in sleep (PLMS)
- Definition:
o Urge to move accompanied by uncomfortable sensations that begin or worsen with rest, are
partially or totally relieved with movement, and are worse in evening/night. These features
cannot be accounted for by another medical/behavioral condition
o RLS refers to sensation
o PLMS refers to the manifestation
- Epidemiology:
o 10% north americans
o 90% of RLS have PLMS
o 50% of patients with PLMS have RLS
- Etiology:
o Central (spasticity)
o PNS (radiculopathy, neuropathy)
o Pregnancy
o Iron deficiency
o Alcohol use
- Treatment
o Underlying contributors (B12 and iron supplements)
o Dopaminergic agonists (first line)
o Clonazepam (tachyphylaxis)
o Opioids (only exceptional circumstances)
o NOT recommoneded to use levodopa/carbidopa (causes augmentation)

Narcolepsy
- Definition:
o Excessive daytime sleepiness (all narcoplepsy)
o Cataplexy = loss of muscle tone with emotional stimuli (pathognomonic)
o Sleep paralysis (unable to move upon waking)
o Hypnagogic hallucinations (vivid dreams or hallucination at sleep onset)
- Epidemiology:
o Presumed autoimmune attack on orexin/hypocretin system
§ Hypocretin (orexin) is a NT that regulates arousal, wakefulness, and apetite
o Post head injury
o MS
 o Hypothalamic tumors
o Rarely familial
- Diagnosis:
o Based on clinical history + multiple sleep latency test findings of short sleep latency < 8 min and
REM within 15 min of sleep onset on 2/4 naps
o DSM5:
§ A) recurrent periods of an irrepressible need to sleep, lapsing into sleep, or napping
occurring within the same day. These must have been occurring at least 3x per week over
the past 3 months
§ B) presence of at least one of the following:
• Episode of cataplexy, defined as either occurring at least a few times per month
o In individuals with long-standing disease, brief (seconds to minutes)
episodes of sudden bilateral loss of muscle tone with maintained
consciousness that are precipitated by laughing or joking
o In children or in individuals within 6 months of onset, spontaneous
grimaces or jaw-opening episodes with tongue thrusting or a global
hypotonic, without any obvious emotional triggers.
• Hypocretin deficiency (measured in CSF)
• Nocturnal sleep polysomniography showing REM sleep latency less thann or
equal to 15 minutes, or a multiple sleep latency test showing mean sleep
latency less than or equal to 8 minutes and two or more sleep onset REM
peridos
- Treatment:
o Sleep hygiene and scheduled brief naps
o Restricted driving
o Alerting agents:
§ Modafinil (Non-amphetamine stimulant)
§ Methylphenidate (stimulant)
o Anticataplectic: TCA, SSRI, sodium oxybate

Parasomnias

- Definition:
o Unusual behaviors in sleep with clinical features appropriate to stage of sleep
- Etiology:
o In elderly, REM sleep behavior disorder may be associated with PD
o In children, slow wave sleep arousals (sleep walking) may be associated with sleep disordered
breathing
- Diagnosis:
o Clinical history in children
o Polysomniography in adults to exclude nocturnal seizures
- Treatment
o Behavioural management (safety, adequate sleep)
o Clonazepam for REM sleep behavior
o Tonsillectomy if appropriate in children

Circadian rhythm

- Abnormalities based on time of day rather than sleep (i.e. jet lag, shift work)
- Dx: clinical history
15. Mood (affective) disorders-etiology, diagnostic criteria, subtypes, course and outcome,
ddx

Mood episodes

DSM-5 Diagnostic criteria for major depressive episode

- MSIGECAPS
- Lifetime prevalence: 8-12%
- NB: Do not include symptoms that are clearly attributable to another medical condition
- Complications: loosing ability to work, loose friends and social connections, higher mortality (esp if related
to somatic disorder, untreated depression worsen the prognosis of coexistent domatic disorders), suicde
- Main types based on behavioral symptoms:
o Melancholic type
o Agitated type

- A) 5 or more of the following present during the same 2 week period and represent a change from
previous functioning, at least one of the symptoms is either 1) Depressed mood, or 3) loss of interest or
pleasure (anhedonia)
o 1. Mood: Depressed
§ Most of the day, nearly every day, as indicated by either subjective report or observation
made by others
o 2. Sleep: increased/decreased
§ Insomnia or hypersomnia nearly every day
o 3. Interest: Decreased
§ Markedly diminished interest or pleasure in all, or almost all, activities most of the day,
nearly every day
o 4. Guilt
§ Feeling of worthlessness or excessive or inappropriate guilt (which may be delusional)
nearly every day (not merely self-reproach or guilt about being sick)
o 5. Energy: Decreased
§ Fatigue or loss of energy nearly every day
o 6. Concentration: Decreased
§ Diminished ability to think or concentrate, or indecisiveness, nearly every day
o 7. Appetite: increased/decreased
§ Significant and unintentional weight loss/gain, or decrease/increase in appetite nearly
every day
o 8. Psychomotor: agitation/retardation
§ Psychomotor agitation or retardation nearly every day
o 9. Suicidal ideation
§ Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a
specific plan, or a suicide attempt or a specific plan for committing suicide
- B) The symptoms cause clinically significant distress or impairment in social, occupational, or other
important areas of functioning
- C) the episode is not attributable to the direct physiological effects of a substance or a GMC

DSM-5 Criteria for manic episode

- Lifetime prevalence: 1-2%

- GST-PAID
- Note:
o A full manic episode that emerges during antidepressant treatment but persist at a fully
syndromal level beyond the physiological effect of that treatment is sufficient evidence for a manic
episode, and therefore, a bipolar I diagnosis
o Criteria A-D constitute a manic episode. At least one lifetime manic episode is required for the
diagnosis of bipolar I disorder
- A) A distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally
and persistently increased goal-directed activity or energy, lasting > 1 week and present most off the day,
nearly every day (or any duration if hospitalization is necessary).
- B) During the period of mood disturbance and increased energy or activity, 3 or more of the following
symptoms have persisted (4 if the mood is only irritable) and have been present for a significant degree
and represent a noticeable change from usual behavior
o Grandiosity
§ Inflated self esteem or grandiosity
o Sleep (decreased need)
§ Feels rested after only 3 hours of sleep
o Talkative
§ More talkative than usual or pressure to keep talking
o Pleasurable activity, painful consequences
§ Excessive involvement in pleasurable activities that have high potential for painful
consequences (e.g. engaging in unrestrained shopping sprees, sexual indiscretions, or
foolish business investments)
o Activity
§ Increased goal directed activity (either socially, at school or work, or sexually) or
psychomotor agitation
o Ideas (flight off)
§ Flight of ideas or subjective experience that thoughts are racing
o Distractible
§ Attention too easily drawn to unimportant or irrelevant external stimuli
- C) The mood disturbance is sufficiently severe to cause marked impairment in social or occupational
functioning or to necessitate hospitalization to prevent harm to self or others, or there are psychotic
features
- D) The episode is not attributable to the physiological effects of a substance or another medical condition

Hypomanic episode

- Productivity doesn’t worsen but actually becomes better

- Can occur inn healthy people too (e.g. after sleep deprivation)

- Criterion A and B of manic episode is met, but duration is 4 days or longer

- Episode associated with an uncharacteristic change in functioning that is observable by others but not
severe enough to cause marked impairment in social or occupational functioning or to necessitate
hospitalization
- Absence of psychotic features (if these are present the episode is, by definition, manic)

Mixed features

- An episode specifier in bipolar or depression that indicates the presence of both depressive and manic
symptoms concurrently, classified by the disorder and primary mood episode component (e.g. bipolar
disorder, current episode manic, with mixed features)
- Clinical importance due to increased suicide risk
- If found in patient diagnosed with major depression, high index of suspicion for bipolar disorder
- While meeting the full criteria for a major depressive episode, the patient has on most days 3 or more of
criteria B for manic episode
- While meeting the full criteria for a manic/hypomanic episode, the patient has on most days 3 or more of
criteria A for a depressive episode (the following criterion A cannot count: psychomotor agitation,
insomnia, difficulties concentrating, weight changes)
Depressive disorders

Major depressive disorder (MDD)

- DSM-5 diagnostic criteria

o A) Presence of a MDE
o B) the MDE is not better accounted for by schizoaffective disorder and is not superimposed on
schizophrenia, schizophreniform disorder, delusional disorder, or psychotic disorder NOS
o C) there has never been a manic episode or a hypomanic episode
§ NB:
• Exclusion doesn’t apply if all of the manic-like, or hypomanic-like episodes are
substance ro treatment-induced or are due to the direct physiological effects of
another medical condition
o Specifiers:
§ With anxious distressed, mixed features, melancholic features, atypical features, mood-
congruent psychotic features, mood-incongruent psychotic features, catatonia,
peripartum onset, seasonal pattern
o Single vs recurrent is an episode descriptor that carries prognostic significance
§ Recurrent is classified as the patient having two or more distinct MDE episodes; to be
considered as separate the patient must have gone 2 consecutive months without
meeting criteria
- Epidemiology
o Lifetime prevalence: 12%
o Peak prevalence: 15-25 y (M:F = 1:2)
- Etiology:
o Biological
§ Genetic: 65-75% MZ twins, 14-19% DZ twins, 2-4x increased risk first degree relatives
§ Neurotransmitter dysfunction: decreased activity of 5-HT, NE, and DA at neuronal
synapse; changes in GABA and glutamate , various changes detectable by fMRI
• Drugs doesn’t work right away, think its because work via neural plasticity
§ Neuroendocrine dysfunction: excessive HPA axis activity
§ Neuroanatomy and neurophysiology: decreased hippocampal volume, increased size of
ventricles; decreased REM latency and slow wave sleep; increased REM length
§ Immunologic: increased pro-inflammatory cytokines IL-6 and TNF
§ Secondary to medical condition, medication, substance use disorder
o Psychosocial
§ Psychodynamic (e.g. low self-esteem, unconscious aggression towards self or loved ones,
disordered attachment)
§ Cognitive (e.g. distorted schemata, Beck’s cognitive triad: negative views of self, the
world, and the future)
§ Environmental factors (e.g. job loss, bereavement, history of abuse or neglect, early life
adversity)
§ Comorbid psychiatric diagnosis (e.g. anxiety, substance abuse, developmental disability,
dementia, eating disorder)
- Risk factors:
o Sex: F > M, 2:1
o Fam history: depression, alcohol abuse, suicide attempt/completion
o Childhood experiences: loss of parent before age 11, negative home environment (abuse, neglect)
o Personality: neuroticism, dependent, obsessional
o Recent stressors: illness, financial, legal, relational, academic
o Lack of intimate, confiding relationships or social isolation
o Low socioeconomic status
- Depression in the elderly:
o Affects about 15% of comity residents > 65y, up to 50% in nursing homes
o High suicide risk due to social isolation, chronic medical illness, decreased independence
o Suicide peak: male aged 80-90y, females 50-65y
o Dysphoria may not be a reliable indicator of depression in those >85y
 o Often present with somatic complaints (e.g. changes in weight, sleep, energy) or anxiety
symptoms
o May have prominent cognitive changes after onset of mood symptoms (dementia syndrome of
depression)
- Treatment
o Lifestyle:
§ Increased aerobic exercise, mindfulness-based stress reduction, zinc supplementation
o Biological
§ Drugs: SSRI, SNRI, other antidepressants, somatic therapies
§ 1st line pharmacotherapy: sertraline, escitalopram, venlafaxine, mirtazapine
§ For partial or non-response can change class or add augmenting agent: buproprion,
quetiapine-XR, aripiprazole, lithium
§ Typical response to antidepressant treatment: physical symptoms improve over 2w,
mood/cognition by 4w, if no improvement after 4w at a therapeutic dosage – alter
regeimen
• Therapy should be continued for at least 6-12 months after complete recovery.
In case of recurrent depression, prophylactic antidepressant therapy is needed
on the long term.
§ ECT: currently fastest and most effective treatment for MDD. Consider in severe,
psychotic or treatment resistant cases
§ rTMS: early data support efficacy equivalent to ECT with good safety and tolerability
§ phototherapy: esp if seasonal component, shift work, sleep dysregulation
o psychological
§ individual therapy (interpersonal, CBT), family therapy, group therapy
o Social:
§ Vocational rehabilitation, social skills training
o Experimental:
§ Magnetic seizure therapy, deep brain stimulation, vagal nerve stimulation, ketamine
- Prognosis:
o One year after diagnosis of MDD without treatment: 40% of individuals still have symptoms that
are sufficiently severe to meet criteria for MDD, 20% continue to have symptoms that no longer
meet criteria for MDD, 40% have no mood disorder

Persistent depressive disorder

- DSM-IV = Dysthymia
- DSM-5 criteria:
o A) depressed mood for most of the day, for more days than not, as indicated either by subjective
account or observation by others, for >2 years
§ Note: for children/adolescents, mood can be irritable, and duration must be at least 1
year
o B) presence, while depressed, of 2 or more of the following:
§ Appetite: increased/decreased
§ Insomnia/hypersomnia
§ Low energy/fatigue
§ Low self-esteem
§ Poor concentration or difficulty making decisions
§ Feelings of hopelessness
o C) during the 2y period (1y for children/adolescents) of the disturbance, the person has never
been without the symptoms in criteria A and B for more than 2 months at a time
o D) criteria for a MDD may be continuously present for 2 y
o E) there has never been a manic episode or a hypomanic episode, and criteria have never been
met for cyclothymic disorder
o F) the disturbance is not better explained by a persistent schizoaffective disorder, schizophrenia,
delusional disorder, or other specificied or unspecified schizophrenia spectrum and other
psychotic disorder
 o G) the symptoms are not due to the direct physiological effects of a substance or another medical
condition
o H) the symptoms cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning
- Epidemiology
o Lifetime prevalence: 2-3%, M=F
- Treatment
o Psychotherapy + antidepressants

Postpartum mood disorders

Postpartum “blues”

- Transient period of mild depression, mood instability, anxiety, decreased concentration

o Mild/absent: feelings of inadequacy, anhedonia, thoughts of harming baby, suicidal thoughts
- Considered to be normal changes in response to fluctuating hormonal levels, the stress of childbirth, and
the increased responsibilities of motherhood
- Occurs in 50-80% of mothers; begins 2-4d postpartum, usually lasts 48h, can last up to 10d
- Doesn’t require psychotropic medication

MDD with postpartum onset (postpartum depression)

- Clinical presentation:
o MDD with onset during pregnancy or within 4 week following delivery
o Typically lasts 2-6 months, residual symptoms can last for up to 1y
o May present with psychosis (rare, 0,2%), usually associated with mania, but also with MDE
o Severe symptoms include extreme disinterest in baby, suicidal, and infanticidal ideation
- Epidemiology:
o Occurs in 10% of mothers, risk of recurrence 50%
- Risk factors:
o Previous history of a mood disorder (postpartum or otherwise), family history of mood disorder
o Psychosocial features: stressful life events, unemployment, marital conflict, lack of social support,
unwanted pregnancy, colicky or sick infant
- Treatment:
o Psychotherapy (CBT or IPT)
o Short-term safety of maternal SSRI for breastfeeding infants established, long term effects
unknown
o If depression severe or psychotic symptoms present, consider ECT
- Prognosis:
o Impact on child development: increased risk of cognitive delay, insecure attachment, behavioural
disorders
o Treatment of mother improves outcome for child at 8 months through increased mother-child
interaction

Bipolar disorders

Bipolar I/Bipolar II disorders

- Definition:
o Bipolar I disorder:
§ At least one manic episode has occurred
§ If manic symptoms lead to hospitalization, or if there are psychotic symptoms, the
diagnosis is BP I
§ Commonly accompanied by at least 1 MDE but not required for diagnosis
§ Time spent in mood episode:
• 53% asymptomatic
• 32% depressed
• 9% cycling/mixed
 • 6% hypo/manic

o Bipolar II disorder
§ Disorder in which there is at least 1 MDE, 1 hypomanic and no manic episodes
§ While hypomanie is less severe than mania, BP II is not a “milder” form of BP I
§ Time spent in mood episode
• 46% asymptomatic
• 50% depressed
• 1% cycling/mixed
• 2% hypo/manic
§ Often missed due to the severity and chronicity of depressive episodes and low rates of
spontaneous reporting and recognition of hypomanic episodes

- Classification:
o Involves describing the disorder (I or II) and the current or most recent mood episode as either
manic, hypomanic, or depressed
o Specifiers:
§ With anxious distress, depressed with mixed features, hypo/manic with mixed features,
melancholic features, atypical features, mood-congruent or incongruent psychotic
features, catatonia, peripartum onset, seasonal pattern, rapid cycling (4+ mood epsiodes
in 1y)
- Epidemiology
o Lifetime prevalence: 1% BPI, 1,1% BPII, 2,4% subthreshold BPD; M:F 1=1
o Age of onset: teens-20s, usually MDE first, manic episode 6-10y after, average age of first manic
episode 32y
- Risk factors:
o Genetic:
§ 60-65% bipolar patients have family history of major mood disorder, esp bipolar disorders
o Clinical features of MDE history favoring bipolar over unipolar diagnosis:
§ Age of onset <25y, increased nr of MDEs, psychotic symptoms, postpartum onset, anxiety
disorders (esp. separation, panic), antidepressant failure due ot early “poop out” or
hypomanic symptoms, early impulsivity and aggression, substance abuse, cyclothymic
temperament
- Treatment:
o Lifestyle:
§ Psychoeducation regarding cycling nature of illness
§ Ensure regular check ins
§ Develop early warning system
§ “emergency plan” for manic epsiodes
§ Promote stable routine (sleep, meals, exercise)
o Biological:
 § Mood stabilizers vary in their ability to “treat” (reduce symptoms acutely) or “stabilize”
(prevent relapse and recurrence) manic and depressive symptoms. Multi-agent therapy is
common
§ Treating mania:
• Lithium, valproate, carbamazepine (2nd line), SGA (quetiapine), ECT, benzo (acute
agitation)
§ Preventing mania:
• Same as above but usually lower doses
• Not benzo
§ Preventing depression
• As above + aripiprazole
• Quetiapine is first line in BPII depression
§ Mixed episode or rapid cycling
• Multi-agent therapy
• Lithium or valproate + SGA (lurasidone, aripiprazole, olanzapine)
o Psychological
§ Supportive or psychodynamic psychotherapuy
§ CBT, IPT, or interpersonal social rhythm therapy, family therapy
o Social
§ Vocational rehabilitation, consider leave of absence from school/work, assess capacity to
manage finances, abstinence from alcohol, sleep hygiene, social skills training, education
and recruitment of family members
- Course and prognosis
o High suicide rate (15% mortality from suicide), esp mixed states
§ Patients with bipolar disorder are at higher risk for suicide when they switch from mania
to depression, esp as they become aware of consequences of their behavior during the
manic episode
o BPI and II are chronic conditions with a relapsing and remitting course featuring alternating manic
and depressive episodes; depressive symptoms tend to occur more frequently and last longer than
manic episodes
o Can achieve high level of functioning btw episodes
o May switch rapidly btw depression and mania without any period of euthymia in btw
o High recurrence rate for mania – 90% will have subsequent episode in the next 5y
o Long term follow up of BPI
§ 15% well
§ 45% well with relapses
§ 30% partial remission
§ 10% chronically ill
- NB:
o Lithium is among few agents with proven efficacy in preventing suicide attempts and completions
o Monotherapy with antidepressants should be avoided in patients with bipolar depression as
patients can switch from depression into mania
o 4 L’s for bipolar depression:
§ Lithium, lamotrigine, lurasidone, Seroquel

Cyclothymia

- Intensive affective fluctuations and change in activity

- Affective changes doesn’t reach clinical level

- Diagnosis:
o Presence of numerous episodes of hypomanic and depressive symptoms (not meeting criteria for
full hypomanic or MDE) for >2y, never without symptoms for more than 2 months
o Never met criteria for MDE, manic, or hypomanic episodes
o Symptoms are not due to direct physiological effects of a substance or GMC
o Symptoms cause clinically significant distress or impairment in social occupational, or other
important areas of functioning
- Treatment
o Similar to bipolar I:
§ Mood stabilizers +/- psychotherapy
§ Avoid antidepressant monotherapy
§ Treat any comorbid substance use disorder
16. Behavior and cognitive therapies

Cognitive therapy

- Central feature of the cognitive theory of emotional disorders is the cognitive triad; beliefs about
themselves, their personal world (incl people in their lives), and their future
o When people experience excessive, maladaptive emotional distress, its linked to their
problematic, stereotypic, biased interpretations pertinent top this cognitive triad of self, world,
and future.
§ E.g. clinically depressed pt may be prone to believe that they are incapable and helpless
and to view others as being judgmental and critical and the future as being bleak and
unrewarding
o Although the patients viewpoints are flawed and dysfunctional, they nonetheless tend to be
perpetuated by cognitive processes that maintain them
- Cognitive therapy is a short-term, structured therapy that uses active collaboration btw patient and
therapist to achieve its therapeutic goals
o Cognitive therapy assumes that perception and experiences are active processes that involve both
inspective and introspective data. The patients cognitions (thoughs, visual images) represents a
synthesis of internal and external stimuli.
o Alterations in the content of their underlying cognitive structures affect their affective state and
behavioral pattern. Through psychological therapy, patients can become aware of their cognitive
distortions. Correction of faulty dysfunctional constructs can lead to clinical improvement.
o Use: depression, panic disorder, OCD, personality disorders, and somatoform disorders
o Usually individual basis +/- drugs

Cognitive theory of depression

- According this theory cognitive dysfunctions are the core of depression, and physical changes and other
associated features of depression are consequences of cognitive dysfunctions
o e.g. apathy and low energy results from expectations of failure in all areas, paralysis stems from
persons pessimism and feelings of hopelessness
- Goal of therapy is to alleviate depression and to prevent its recurrence by helping patients identify and test
negative cognitions, to develop alternaltive and more flexible schemas, and to rehearse both new
cognitive and behavioral responses
- Changing the way a person thinks can alleviate the psychiatric disorder

Strategies and techniques

- Duration: approx. 25 weeks (relatively short, if no improvement by this period reevaluate dx, maintenance
can be carried out for years)
- Therapist must exude warmth, understanding, and be genuine and honest. Therapists set an agenda at the
beginning of each session, assign homework, and teach new skills. Therapist and patient collaborate
actively.
- Three components of cognitive therapy: didactic aspects, cognitive techniques, and behavioral techniques.

- Didactic (teaching) aspects

o Include explaining to patients the cognitive triad, schemas, and faulty logic. Include full
explanation of the relation btw depression and thinking, affect, and behavior, as well as the
rationale for all aspects of the treatment.
o Contrasts with psychoanalytically oriented therapies which require little explanation
- Cognitive techniques (includes four processes)
o 1. Eliciting automatic thoughts (cognitive distortions, cognitions that intervene btw external
events and persons emotional reaction to the event)
§ E.g. “belief that people will laugh at me when they see how badly I bowl” is an automatic
thought that occurs to someone who has been asked to go bowling and responds
negatively, or “she doenst like me” when someone passes without saying hello
 § Every psychological disorder has its own specific cognitive profile of distorted thought,
which, if known, provides a framework for specific cognitive interventions

o 2. Testing automatic thoughts:

§ Acting as a teacher, help the patient test the validity of automatic thoughts. Goal is to
encourage the patient to reject inaccurate or exaggerated automatic thoughts after
careful examination
§ Patients often blame themselves when things that are outside their control go awry. The
therapist reviews the entire situation with the patient and helps reassign the blame or
cause of the unpleasant events. Generating alternative explanations for events is another
way of undermining inaccurate and distorted automatic thoughts
o 3. Identifying maladaptive assumptions
§ As patient and therapist continue to identify automatic thoughts, patterns usually
become apparent. The patterns represent rules or maladaptive general assumptions that
guide a patients life. Samples of such rules are “inn order to be happoy I must be
perfect” and if anyone doesn’t like me im not lovable”. Such rules inevitably lead to
disappointments and failure, and ultimately to depression.
o 4. Testing the validity of maladaptive assumptions
§ Testing the accuracy of maladaptive assumptions is similar to testing the validity of
automatic thoughts.

- Behavioral techniques
o Go hand in hand with cognitive techniques. Overall goal of such techniques are to help patients
understand the inaccuracy of their cognitive assumptions and learn new strategies and ways of
dealing with issues
o Include: Scheduling activities, mastery and pleasure, graded task assignments, cognitive rehearsal,
self-reliance training, role playing, and diversion techniques.
 o Schedule activities on an hourly basis. Patients keep records of the activities and review them
with the therapist. In addition to scheduling activities, patients are asked to rate the amount of
mastery the pleasure their activities bring them. Patients are often surprised to learn that they
have much more mastery of activities and enjoy them more then they had thought. To simplify
the situation and allow miniaccomplishments, therapists often break tasks into subtasks, as in
graded task assignments, to show patients that they can succeed. In cognitive rehearsal, patients
imagine and rehearse the various steps in meeting and mastering a challenge.
o Self reliance training: Pt (esp inpatients) are encouraged to become self-reliant by doing such
simple things as making their own beds, doing their own shopping, and preparing their own
meals.
o Role playing: elicit automatic thoughs and to learn new behavior.
o Diversion techniques: help patitents getting through difficult times, include physical activity, social
contact, work, play, and visual imagery.
§ Iagery or thought stoppage can treat impulsive or obsessive behavior, e..g by imagining a
stop sign once they recognize an impulse or obsession that is alien to the ego.

Indications for cognitive therapy

Efficacy

- Cognitive therapy can be used alone in treatment of mild-moderate depression, or in conjunction with
antidepressant medication for MDD
o Studies have clearly shown that cognitive therapy is effective and in some cases superior or equal
to medication alone

Behavior therapy

- Involves changing the behavior of patients to reduce dysfunction and to improve QOL
- Behavioral analysis – strategic selection of behaviors to change
- Behavioral views differ from cognitive views in holding that physical, rather than mental, events control
behavior

Systematic desensitization

- Based on the behavioral principle of counterconditioning, whereby a person overcomes maladaptive

anxiety elicited by a situation or an obect by approaching the feared situation gradually
- Patient attain a state of complete relaxation and are then exposed to the stimulus that elicits the anxiety
response. The negative reaction of anxiety is then inhibited by the relaxed state, a process called reciprocal
inhibition.
- Rather than using actual situations or objects that elicit fear, patients and therapists prepare a graded list
or hierarchy of anxiety-provokinng scenes associated with a patients fears.
- Thus systematic desensitization consists of three steps:
o 1. Relaxation training
§ Physiological effects: slow HR, increase peripheral blood flow, and neuromuscular
stability (i.e. opposite of those induced by adrenergic stress responses)
§ Variety of methods
• Yoga and zen
• Progressive relaxation – relax major muscle groups in a fixed order, beginning
small muscle groups in feed and working up (or vica versa)
• Hypnosis
• Mental imagery – go to “happy place”
o 2. Hierarchy construction
§ Determine all conditions eliciting anxiety, and then create hierarchy of 10-12 scenes in
order of increasing anxiety.
§ E.g. if fear water and heights: taking a bath at home – swimming at the shallow end –
diving from top board
o 3. Desensitization of the stimulus
§ In the final step patiennts proceed systematically through the list from the least to the
most anxiety-provoking scene while in a deeply relaxed state
- Adjunctive use of drugs:
o Can be used to hasten relaxation
o E.g. valium (diazepam)
- Indications:
o Phobias, obsessions, compulsions, and certain sexual disorders

Therapeutic-graded exposure

- Similar to systematic desensitization, except that relaxation training is not involved and treatment is
usually carried out in a real-life context
- Meaning that the individual must be brought inn contact with (i.e. exposed to) the warning stimulus to
learn firsthand that no dangerous consequences will ensue
- Exposure is graded according to hierarchy
- E.g. afraid of cats; start with looking at picture – end with holding one
Flooding (implosion)

- Similar to graded exposure in that it involves exposing the patient to the feared object in vivo, however,
there is no hierarchy
- Based on the premise that escaping from an anxiety-provoking experience reinforces the anxiety through
conditioning. Thus, clinicians can extinguish the anxiety and prevent the conditioned avoidance behavior
by not allowing patients to escape the situation.
- Clinicians encourage patients to confront feared situations directly, without gradual buildup, as in
systematic desensitization or graded exposure.
- Patients experience fear, which gradually subsides after a time. The success of the procedure depends on
having pt remain in the fear-generating situation until they are calm and feel a sense of mastery
- Prematurely withdrawing from the situation reinforces both the conditioned anxiety and the avoidance
behavior and produces the opposite of the desired effect.
- CI: intense anxiety would be hazardous to the patient (e..g heart disease, fragile psychological adaption).

Social skills training

- Use:
o Schizophrenia
§ Negative symptoms consititute behavioral deficits that go beyond difficulties with
assertiveness. They have inadequate expressive behaviors and inappropriate stimulus
control of their social behaviors (i.e. they don’t pick up social cues)
§ Cover skills in conversation, conflict management, assertiveness, community lviinng,
friendship and dating, work and vocation, and medication managements
o Depression
§ Often experience lack of social reinforcement because of lack of social skills
o Social phobia
§ Often haven’t acquired adolescents social skills. Their social defensive behavior (e.g.
avoiding eye contact, making brief statements, and minimizing self-disclosure) increase
the probability of the rejection they fear

Aversion therapy

- When a noxious stimulus (punishment) is presented immediately after a specific behavioral response,
theoretically, the response is eventually inhibited and extinguished
- E.g. noxious stimuli; electrical shocks, substances inducing vomiting, corporal punishment, and social
disapproval.
- Use: alcohol abuse, paraphilias, and other bheaviors with ipuslive or compulsive qualities

Positive reinforcement

- When a behavioral response is followed by a generally rewarding event, such as food, avoidance of pain,
or praise, it tends to strengthened and to occur ore frequently than before the reward
- E.g. token economy – paitents with mental disorders recevei a token which they can use to buy certain
privileges or items as reward for performing a desired behavior
Common clinical applications of behavioral therapy
18. Psychopharmacology II: Antidepressants drugs and other biological therapies (ECT,
sleep deprivation, bright light treatment: Mechanism of action, indications, effects and
side effects

Electroconvulsive therapy (ECT)

- Various methodological improvements have been made since the first treatment in 1938 to reduce
adverse effects
- Modern ECT: induction of a generalized seizure using an electrical pulse through scalp electrodes while the
patient is under GA with a muscle relaxant
- Considerations:
o Unilateral vs bilateral electrode placement (unilateral causes less memory loss than bilateral but
may not be as effective)
o Pulse rate, dose
o nr and spacing of treatments
- Usual course: 6-12 treatments, 2-3 times per week
- Indications:
o Depression refractory to adequate pharmacological trial (MDD or bipolar I depression)
o High suicide risk
o Medical risk in addition to depression (dehydration, electrolytes, pregnancy)
o Previous good response to ECT
o Familial response to ECT
o Elderly
o Psychotic depression
o Catatonic features
o Marked vegetative features
o Acute schizophrenia unresponsive to medication
o Mania unresponsive to medications
o OCD refractory to conventional treatment
- CI:
o Increased ICP
o Recent (<2 eeks) MI (not absolute but require special monitoring)
- SE:
o Risk of anesthesia
o Memory loss (may be retrograde and/or anterograde, tends to resolve by 6-9 months, permanent
impairment is controversial)
o Headache
o Myalgias

MST (magnetic seizure therapy)

- Seizure induction by magnetic current induction rather than direct stimulation

- Early studies demonstrate efficacy for depression as well as anxiety, reduced memory SE vs ECT

Repetitive transcranial magnetic stimulation (rTMS)

- Noninvasive production of focal electrical currents in select brain areas using magnetic induction
- Indications
o Treatment-resistant depression
o Pain disorders; possibly efficacious for anxiety disorders, eating disorders, substance use disorders
- SE:
o Common: transient local discomfort, hearing issues, cognitive changes
o Rare: seizure, syncope, mania induction
Neurosurgical treatments

Ablative/lesion procedures

- Used for intractable MDD or OCD, efficacy ranges from 25-75% depending on procedure
- Adverse effects:
o Related to lesion location and size
o High risk of suicide in those who are not helped by surgery

Deep brain stimulation

- Placement of small electrode leads in specific brain areas to alter neuronal signaling, usually for intractable
MDD
- Response rates (>50% symptom reduction) of 40-70%
- Adverse effects related to surgical risks and poor treatment response

Vagus nerve stimulation

- Direct, intermittent electrical stimulation of left cervical vagus nerve via implanted pulse generatior
- Used for chronic, recurrent MDD that has failed previous therapy and ECT; slow onset, approximately 30%
response rate at 1y

Other

Phototherapy (light therapy)

- Bright light source exposure, best in morning, for 30-60 min (usually 10.000 lux)
- Proposed mechanisms: reverses pathological alterations in circadiuan rhythm through action on
suprachiasmatic nucleus
- Indications
o SAD (original indication)
o Non-seasonal depression (as augmentation)
o Sleep disorders
- Method:
o Expose affected patient to bright light (1500-10.000 lux or more) typiocally with a light box that
sits on a table/desk
§ Patient sit in front of the box 1-2 h before dawn each day
§ Do not look directly at the light source
o Alternaltively one can use light visords, light source built into brim of the hat
§ Allow mobility, but recent controlled studies have questioned the use of this type of light
exposure
- SE: Generally well tolerated
o Mania induction (as any other antidepressant therapy )
o Reaction with photosensitizing drug or photosensitive eye or skin condition

Aerobic exercise

- Moderate-intense aerobic exercise is associated with acute increased secretion of serotonin,

phenethylamine, BDNF, endogenous opioids and cannabinoids (likely this combination is what contributes
to “runnners high”)
- Long term incrase in gray matter in multiple areas, as well as improvement in cognition, memory, and
stress tolerance
- Indications
o Ongoing research suggests efficacy as adjunctive treatment for MDD
o May be helpful in PTSD, schizophrenia
Sleep deprivation

- “Fast onset but short lasting”

- Mood disorders are characterized by sleep disturbance. Mania tends to be characterized by a decreased
need for sleep, depression can be associate with either hypersomnia or insomnia
- Sleep deprivation may precipitate mania in pt with bipolar I disorder and temporary relieve depression in
those who have unipolar depression

- Approx. 60% of patients with depressive disorder exhibit signifigant but transient benefits from total sleep
deprivation
o Positive results are typically reversed by the next night of sleep
- Several strategies have been used in attempt to achieve more sustained response to sleep deprivation
o Serial total sleep deprivation with 1-2d normal sleep in btw – didn’t achieve sustained
antidepressant response, depression returned with normal sleep cycles
§ Has been used successfully to treat insomnia associated with depression
o Phase delay in the time pt go to sleep each night, or partial sleep deprivation – patient stayed
awake from 02-22 – 50% get same day antidepressant effect, benefit wear off in time
o Sleep deprivation + pharmacological tx depression – probably most effective
§ Sustains antidepressant effects of sleep deprivation
§ Several reports have suggested that sleep deprivation accelerates the response to
antidepressants
- Sleep deprivation has also been noted to improve premenstrual dysphoria

Antidepressants
- Onset and duration:
o Relief of neurovegetative/physical symptoms: 1-3w
o Relief of emotional/cognitive symptoms: 2-6w
§ Takes time because involve adaptive changes, incl; A2-R desensitization presynaptically,
5-HT2-R desensitization postsynaptically, enhance 5-HT1A-R activity, B-receptor
desensitization and downregulation
o Treat for 6-12 months if first or second episode
o Treat at least two years (or indefinitely) if third episode, elderly, psychotic features, refractory
depression, or more than 2 episodes in 5 years
- Trial and error of drug, but almost always use SSRI or SNRI
o Attempt single dose for 6 weeks
o Treat depression 6 months once you find effective drug and effective drug
o 6 weeks (closer to 3w) washout to avoid serotonin syndrome
o Goal: maximal dose (limited by SE)
o NB: combination of psychotherapy and medication is best option!
- Taper:
o TCA: slowly (weeks-months) due to withdrawal reactions
o Tapering of any antidepressant is usually required and is based on the medications half-life and
the patients individual sensitivity (e.g. fluoxetine doesn’t require a slow taper due to long half life)
- NB:
o Must be vigilant over the first two weeks of therapy; neurovegetative symptoms may start to
resolve while emotional and cognitive symptoms may not (patients may be particularly at risk for
suicidal behavior during this time, in children/adolescents, paroxetine and venlafaxine increase
restlessness and suicide ideation, so are not prescribed)
o Bipolar disorder – should only be treated with an antidepressant if combined with a mood
stabilizer or antipsychotic, monotherapy with antidepressants is not advisable as the depression
can turn into mania
SSRI
- Indications:
o Anxiety states, OCD, eating disorder, seasonal depression, typical and atypical depression
- Psychopharmacology:
o Post-synaptic serotonin receptor stimulated
§ 5HT1A centrally – relief depression, anxiolytic
§ 5HT2A spinal cord – sexual dysfunction, delayed ejaculation, anorgasmia, decreased
interest/libido
§ 5HT2A /5HT2C in brain – activation: anxiety, insomnia, worst with fluoxetine and
paroxetine, arm patients anxiety may worsen in first 1-2w of treatment
§ 5HT3A in gut – GI upset (n&v, bloating), take with food
- Choosing drug:
o All have similar effectiveness
o Different SE and half lives
o Sertraline, citalopram, and escitalopram have fewest drug-interactions and are sleep-wake
neutral
o Fluoxetine and paroxetine are the most activating drugs (recommended taking in the AM)
o Fluoxetine doesn’t require taper due to long-half life and is the most used in children as it has
most evidence
o Fluvoxamine is sedating (should be taken in PM)
- Drugs:
o Fluoxetine (Prozac)
o Fluvoxamine
o Paroxetine
o Sertraline
o Escitalopram (cipralex)
o Citalopram
- SE:
o CNS: restlessness, tremor, insomnia, headache, drowsiness
§ Anxiety and agitation – because increase 5-HT (excitatory substance)
• Can give benzos when starting SSRI, tapered when patient is managed for the
depressive moods
o GI: n&v, diarrhea, abdominal cramps, weight loss
o Sexual dysfunction: impotence, anorgasmia, decreased libido
o CVS: increased HR, conduction delay, SS, EPS, SIADH
- Risk in overdose:
o Relatively safe
- Drug interactions
o Inhibit P450 enzymes – affect levels of drugs metabolized by p450

SNRI (serotonin and NE reuptake inhibitors)

- Indications:
o Depression
o Anxiety disorders
o Chronic pain (neuropathic pain etc.)
- Drugs:
o Venlafaxine
o Duloxetine
- SE: (fewer, more expensive)
o Low dose SE: insomnia (serotonergic)
o High dose: tremors, tachycardia, sweating, insomnia, dose-dependent increase in DBP
(noradrenergic)
- Risk in overdose:
o Tachycardia, n&v
- Drug interactions
o MAOI, SSRI
Others
- NDRI (NE and DA reuptake inhibitors)
o Bupropion
§ Indication:
• Depression, seasonal depression, quit smoking
§ Pros:
• Less sexual dysfunction (may reverse effects of SSRIs/SNRIs), weight gain, and
sedation
§ Cons:
• Increased risk seizures (CI if history seizures, stroke brain tumor, brain injury,
closed head injury)
• Not recommended for anxiety disorders due to stimulating effects
§ SE:
• CNS: dizziness, headache, tremor, insomnia
• CVS: dysrhythmia, HTN
• GI: dry mouth, n&v, constipation, appetite
• Other: anxiety, agitation, anaphylactic reaction
§ Risk in overdose:
• Tremors and seizures in acute overdose
§ Drug interactions
• Drugs that reduce seizure threshold: antipsychotics, systemic steroids,
quinolone, antibiotics, antimalarial drugs
- TCA (amines)
o Use:
§ OCD (clomipramine)
§ Melancholic depression
o Drugs:
§ Amitryptiline
§ Imipramine
o SE:
§ Anticholinergic
§ Noradrenergic
§ Alpha 1 adrenergic: orthostatic hypotension
§ Antihistamine: sedation, weight gain
§ CNS: sedation, stimulation, seizure threshold
§ CVS: HR, conduction delay
o Risk in overdose:
§ 3x therapeutic ddose is lethal
§ Present with anticholinergic effects, CNS stimulation, then depression and seizures
§ ECG: prolonged QT
§ Tx: activated charcoal, catharacts, supportive tx
§ IV diazepam for seiuzure, physostigmine salicylate for coma
o Drug interactions:
§ MAOI, SSRI, alcohol
- MAOI
o use:
§ moderate/severe depression resistant to SSRI
§ atypical depression
o Drugs:
§ Phenelzine
§ Tranylcypromine
o SE:
§ Hypertensive crisis with tyramine rich food (e.g. wine, cheese), headache, palpitations,
n&v, photophobia, dizziness, reflex tachycardia, postural hypotension, sedation,
insomnia, weight gain, sexual dysfunction, energizing
o Risk in overdose:
 § toxic in OD but wider margin of safety than TCA
o Drug interactions
§ Alcohol, hypertensive crisis with noradrenergic drugs (e.g. TCA, decongestants,
amphetamines), SS with serotonergic drugs (e.g. SSRI, tryptophan, dextromethorpha)
- RIMA (reversible inhibitor MAO-A)
o Use:
§ Depression unresponsive to other therapies
o Drugs:
§ Moclopramide
o SE:
§ CNS: dizziness, headache, tremor, insomnia
§ CVS: dysrhythmia, hypotension
§ GI: dry mouth, &v, diarrhea, abdominal pain, dyspepsia
§ GU: delayed ejecaulation
§ Other: diaphoresis
o Risk in overdose:
§ Risk of fatal overdose when combined with citalopram or clomipramine
o Drug interactions
§ MAOI, SSRI, TCA, opioids
- NASSA (noradrenergic and specific serotonin antagonist)
o Not best antidepressant, used more for SE
o MA:
§ Stimulate NE secretion through presynaptic alpha2 autoreceptor inhibition
§ 5-HT antagonist
o Use:
§ Depression with prominent features of insomnia, agitation, or cachexia (stimulate
appetite)
o Drugs:
§ Mirtazapine
o SE:
§ CNS: somnolence, dizziness, seizure (rare)
§ Endocrine: cholesterol, triglycerides
§ GI: constipation, ALT
o Risk in overdose:
§ Mild symptoms
o Drug interactions
§ MAOI, SSRI, SNRI, RIMA
- Trazodone
o SRI + antagonist 5-HT2a/2C
o Beneficial when insomnia, agitation, and anxiety is present
o SE: priapism (strong a1 block – vasodilation), rarely SS
- Agomelatin
o Agonist melatonin receptors and antagonist 5-HT2C
o Can resynchronize circadian rhythm
o Effective when insomnia is main problem

Serotonin syndrome

- Thought to be due to over-stimulation of serotonergic system

- Can result from medication combinnations such as SSRI + MAOI/tryptophan, MAOI +
meperidine/tryptophan
- Clinic:
o Nausea, diarrhea, palpitation, chills, restlessness, confusion, and lethargy, but can progress to
myoclonus, hyperthermia, rigor and hypertonicity
- Tx:
o Discontinue medication and administer emergency medical care as needed
- Ddx: NMS
Discontinuation syndrome

- Caused by abrupt cessation of an antidepressant; most commonly with paroxetine, fluvoxamine, and
venlafaxine (drugs with shortest half-lives)
- Symptoms:
o Usually begin within 1-3 days and include: anxiety, insomnia, irritability, mood liability, n&v,
dizziness, headache, dystonia, tremor, chills, fatigue, lethargy, and myalgia
o FINISH:
§ Flu-like symptoms
§ Insomnia
§ Nausea
§ Imbalance
§ Sensory disturbances
§ Hyperarousal (anxiety/agitation)
- Treatment:
o Symptoms may last 1-3w but can be relieved within 24h by restarting antidepressant therapy at
the same dose the patient was taking and initiating slow taper over several weeks
o Consider using a drug with longer half life (e.g. fluoxetine)

Approach for treatment of depression

Psychotherapy

- Treatment in which a person with a mental or physical difficulty aims to achieve symptomatic relief
through talks with another person (trained social worker, psychologist, psychiatrist, GP, counsellor)
- Effective psychotherapy creates observable changes in brain circuitry and connectivity, similar to those
observed with successful pharmacologic and other treatment modalities

Modalities (next page)

- Other:
o Group psychotherapy:
§ Aim to promote self-understanding, acceptance, social skills
o Family therapy
§ Family system considered more influential than individual, esp for children
§ Focus on here and now, re-establishing parental authority, strengthening normal
boundaries, and rearranging alliances
o Narrative psychotherapy
§ An integrative approach that attempts to understand the patients experience as a whole
o Hypnosis
§ Mixed evidence for treatment of pain, phobias, anxiety, and smoking cessation
o Mindfulness-based cognitive therapy (MBCT)/stress reduction (MBSR)
§ Derived from Buddhist meditative and philosophical practices: aims to help people
attend to thoughts, behaviours, and emotions in the moment and non-judgementally
using guided breathing exercises
§ Emerging evidence for treating adjustment disorder, MDD, anxiety, pain disorders,
insomnia, substance relapse prevention
20. Sexual disorders: diagnostic criteria, clinical management

Sexual dysfunctions

- “persons inability to participate in a sexual relationship as he or she would wiehs”

- Essential features of sexual dysfunctions are an inability to respond to sexual stimulation, or the
experience of pain during sexual act
- All sexual dysfunction disorders have the same B-D criteria in DSM5 (except substance/medication-induced
sexual dysfunction)
o Criterion A: varies
o Criterion B: symptoms of A have persisted for a minimum of 6 months
o Criterion C: symptoms of A cause clinically significant distress in the individual
o Criterion D: the sexual dysfunction is not better explained by a nonsexual mental disorder or as a
consequence of severe relationship distress or other significant stressors and is not attributable to
the effects of a substance/medication or another medical condition
- Specify:
o Lifelong vs acquired (began after period of relatively normal sexual function)
o Generalized vs situational (only occurs with certain types of stimulation, situations, or partners)
o Mild (mild distress over symptoms of criterion A), moderate, or severe

1. Male hypoactive sexual desire disorder

- Criterion A:
o Persistently or recurrently deficient (or absent) sexual/erotic thoughts or fantasies and desire for
sexual activity. The judgment of deficiency is made by the clinician, taking into account factors
that affect sexual functioning, such as age and general and sociocultural contexts of the
individuals life

2. Female sexual interest/arousal disorder

- Criterion A: At
o Lack of, or significantly reduced, sexual interest/arousal, as manifested by at least three of the
following:
§ 1. Absent/reduced interest in sexual activity
§ 2. Absent/reduced sexual/erotic thoughts or fantasies
§ 3. No/reduced initiation of sexual activity, and typically unreceptive to a partners
attempts to initiate
§ 4. Absent/reduced sexual excitement/pleasure suring sexual activity in almost all or all
(75-100%) sexual encounters 8in identified situational contexts, or, if generalized, in all
contexts)
§ 5. Absent/reduced sexual interest/arousal in response to any internal or external
sexual/erotic cues (e.g. written, verbal, visual)
§ 6. Absent/reduced genital or nongenital sensations during sexual activity in almost all or
all (approx. 75-100%) sexual encounteres (in identified contexts or, If generalized, in all
contexts)

3. Male erectile disorder

- Criterion A:
o At least 1/3 following symptoms must be experiences on almost all or all (approx. 75-100%)
occasions of sexual activity
§ 1. Marked difficulty in obtaining an erection during sexual activity
§ 2. Marked difficulty in maintaining an erection until the completion of sexual activity
§ 3. Marked decrease in erectile rigidity

4. Female orgasmic disorder

- Criterion A:
 o Presence of either of the following symptoms and experienced on almost all or all (approx. 75-
100%) occasions of sexual activity (in identified situational contexts, or if generalized, in all
contexts)
§ 1. Marked delay in, marked infrequency of, or absence of orgasm
§ 2. Markedly reduced intensity of orgasmic sensations

5. Delayed ejaculation
- Criterion A:
o Either of the following symptoms must be experienced on almost all or all occasions (approx. 75-
100%) of partnered sexual activity (in identified situational contexts or, if generalized, in all
contexts), and without the individual desiring delay
§ 1. Marked delay in ejaculation
§ 2. Marked infrequency or absence of ejaculation

6. Premature (early ejaculation

- Criterion A:
o A persistent or recurrent pattern of ejaculation occurring during partnered sexual activity within
approximately 1 minute following vaginal penetration and befre the individual wishes it

7. Genito-pelvic pain/penetration disorder

- In DSM5, this disorder refers to one or more of the following complaints, of which any two or mor may
occur together:
o Difficulty having intercourse
o Genito-pelvic pain
o Fear of pain or penetration
o Tension of the pelvic floor muscles
- Previously these pain disorders where diagnosed as dyspareunia or vaginismus. These former diagnoses
could coexist or one could lead to the other and could understandably lead to fear of pain with sex. The
clinical terms of dyspareunia and vaginismus is still used.
o Dyspareunia
§ Recurrent or persistent genital pain occurring before, during, or after intercourse
§ Its related to, and often coincide with vaginismus. Repeated episodes of vaginismus can
lead to dyspareunia and vica versa. In either cases somatic causes must be ruled out.
§ In most cases, dynamic factors are considered causative. Chronic pelvic pain is a common
complaint in women with a history of rape or childhood sexual abuse.
§ Painful coitus can result from tension and anxiety about the sex act that cause women to
involuntarily contract their pelvic floor muscles. The pain is real and maxes intercourse
unpleasant or unbearable, and the anticipation of further pain may cause women to
avoid coitus altogether.
§ Increased reported dyspareunia postmenopausally due to hormonally induced
physiological changes in the vagina, however, specific complaints of difficulty having
intercourse occur more often in premenopausal women.
o Vaginismus
§ Defined as a constriction of the outer 1/3 of the vagina due to involuntary pelvic floor
muscle tightening or spasm
§ The diagnosis is not made when the dysfunction is caused exlusively by organic factors or
when its symptomatic of another mental disorder.

8. Sexual dysfunction due to a general medical condition

- Male erectile disorder due to a general medical condition
o 20-50% of men with erectile disorder have an organic basis for the disorder
o Physiologic etiology is more likely when men are > 50y
o E.g. leriche syndrome, atherosclerosis, malnutrition, DM, acromegaly, perineal prostatectomy,
radiation therapy
- Dyspareunia due to GMC
o 30% of all surgical procedures on the female genital area result in temporary dyspareunia
o 30-40% of women with the complaint who are seen in sex therapy clinics have pelvic pathology
 o E.g. irritant or infected hymenal remnants, episiotomy scars, Bartholin gland infection, various
forms vaginitis and cervicitis, endometriosis and adenomyosis etc.
- …

9. Substance/medication induced sexual dysfunction

- Antipsychotic drugs
o Most are dopamine antagonists that also block adrenergic and cholinergic receptors, thus
accounting for the adverse sexual effects
o Chlorpromazine and trifluoperazine are potent anticholinergics and they impair erection and
ejaculation
o Rare cases of priapism
- Antidepressant drugs
o TCA and tetracyclic AD have anticholinergic effects that interfere with erection and delay
ejaculation
o SSRIs lower sexual drive and cause difficulty reaching orgasm
o Trazodone can cause priapism
o ..

10. Other specified sexual dysfunction

- These unclassified disorders are rare, poorly documented, not easily classified, or not specifically described
in DSM5
- Include:
o Postcoital dysphoria
o Sex additcition and compulsivity
o Etc.

11. Unspecified sexual dysfunction

Paraphilia

- Paraphilias or perversions are sexual stimuli or acts that are deveiations from normal sexual behaviors, but
are necessary for some persons to experience arousal and orgasm. Individuals with paraphilic interests can
experience sexual pleasure, but they are inhibited from responding to stimuli that are normally considered
erotic.
- intense and persistent sexual interest other than sexual interest in genital stimulation or preparatory
fondling with phenotypically normal, physically mature, consenting human partners
- Paraphilic disorder:
o Paraphilia that causes distress or functional impairment to the individual, or a paraphilia whose
realization entails personal harm, or risk of harm to others
- Rarely self-referred, come to medical attention through interpersonal or legal conflict
- Person usually has more than one paraphilia; 5% of paraphilias attributed to women
- Typical presentation
- Begins in childhood or early adolescence; increasing in complexity and stability with age
- Chronic, decreases with advancing age, but may increase with stress

DSM5

- In DSM5, the criteria for paraphilic disorders requires the patient to have experienced intense and
recurrent arousal from their deviant fantasy fro at least 6 months and to have acted on the paraphilic
impulse

Classification

- Voyeuristic
o Preoccupation with fantasies and acts that involve observing unsuspecting persons who are naked
or engaged in grooming or sexual activity
- Exhibitionistic
o Recurrent urge to expose the genitals to a stranger or to an unsuspecting person
o Sexual excitement occurs in anticipation of the exposure, and orgasm is brought about by
masturbation during or after the event
o Nearly all cases are men exposing themselves to woemn
- Frotteuristic
o Usually characterized by a mans rubbing his penis against the buttocks or other body parts of a
fully clothed women to achieve orgasms. At other times, he may use is hands to rub an
unsuspecting victim
- Sexual masochism
o Preoccupation with sexual urges and fantasies involving the act of being humiliated, beaten,
bound, or otherwise made to suffer
o Specifier: asphyxiophilia
- Sexual sadism
o Recurrent and intense sexual arousal from the physical and psychological suffering of another
person
- Pedophilic
o Recurrent intense sexual urges toward, or arousal by, children 13 y of age or younger
o Persons with pedophilia are at least 16 years of age and at least 5 years older than the victims
- Fetishistic
o Sexual focus is on objects (e.g. shoes, gloves, pantyhose, and stockings) that are intimately
associated with the human body, or on nongenital body part
- Transvestic
o Fantasies and sexual urges to dress in opposite gender clothing as a means of arousal and as an
adjunct to masturbation or coitus
- Other specified paraphilic disorder
o Telephone and computer scatologia
o Necrophilia
o Partialism (coencentrate sexual activity on one part of the body to the exclusion of all others)
o Zoophilia
o Coprophilia and klismaphilia
o Urophilia
o Etc.
- Unspecified paraphilic disorder

Treatment

- Anti-androgen drugs
- Behavior modification
- Psychotherapy

Gender dysphoria

- Definition:
o The distress that may coincide with conflict btw ones experienced/expressed gender and one’s
assigned gender

DSM5 diagnostic criteria

- Gender dysphoria in children:

o A) A marked incongruence btw ones experienced/expressed gender and assigned gender, of at
least 6 months duration, as manifestaed by at least 6 of the following (one of which must be
criterion A1)
§ 1. A strong desire to be of the other gender or an incidence that on is the other gender
(or some alternative gender different from one’s assigned gender)
 § 2. In boys (assigned gender), a strong preference for cross-dressing or stimulating female
attire, or in girls (assigned gender), a strong preference for wearing only typical
masculine clothing and a strong resistance to wearing of typical feminine clothing
§ 3. A strong preference for cross-gender roles in make-believe pløay or fantasy play
§ 4. A strong preference for toys, games, or activities stereotypically used or engaged in by
the other gender
§ 5.A strong preference for playmates of the other gender
§ 6. In boys (assigned gender), a strong rejection of typically masculine toys, games, and
activities and a strong avoidance of rough-and-tumble play; or in girls (assigned gender),
a strong rejection of typically female toys, games, and activities
§ 7. A strong dislike of one’s sexual anatomy
§ 8. A strong desire for the primary and/or secondary sex characteristics that match one’s
experienced gender
o B) The condition is associated with clinically significant distress or impairment in social, school, or
other important areas of functioning
o Specify if:
§ Disorder of sex development (e.g. CAH, AIS)
- Gender dysphoria in adolescents and adults
o A) A marked incongruence btw one’s experienced/expressed gender and assigned gender, of at
least 6 months duration, as manifested by at least two of the following
§ 1. A marked incongruence btw one’s experienced/expressed gender and primary and/or
secondary sex characteristics (or in young adolescents, the anticipated secondary sex
characteristics)
§ 2. A strong desire to be rid of ones primary and/or secondary sex characteristics because
of a marked incongruence with one’s experienced/expressed gender (or in young
adolescents, a desire to prevent the development of the anticipated secondary sex
characteristics)
§ 3. A strong desire for the primary and/or secondary sex characteristics of the other
gender
§ 4. A strong desire to be of the other gender (or some alternaltive gender different from
one’s assigned gender)
§ 5. A strong desire to be treated as the other gender (or some alternaltive gender
different from ones assigned gender)
§ 6. A strong conviction that one has the typical feelings and reactions of the other gender
(or some alternaltive gender different from one’s assigned gender)
o B) The condition is associated with clinically significant distress or impairment in social,
occupational, or other important areas of functioning
o Specify if:
§ With a disorder of sex development
§ Posttransition: the individual has transitioned to full-time living in the desired gender
(w/w.o legalization of gender change) and has undergone (or is preparing to have) at
least one cross-sex medication procedure or treatment regimen – namely, regular cross-
sex hormone treatment or gender reassignment surgery confirming the desired gender
(e.g. penectomy, vaginoplasty in natal male, mastectomy or phalloplasty in natal female)

Treatment

- Psychotherapy
- Hormonal therapy
- Sexual reassignment surgery

Paraphilic disorders
22. Dementia: Etiology, diagnostic criteria and clinical management

Major neurocognitive disorder (Dementia)

- “4 A’s: amnesia, aphasia, apraxia, agnosia”

DSM5 criteria major neurocognitive disorder

- A) evidence of 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, or
social cognition) based on
o 1. Concern of the individual, a knowledgeable informant, or the clinician that there has been a
significant decline in cognitive function; and
o 2. Substantial impairment in cognitive performance, preferably documented bby standardized
neuropsychological testing, or, in its absence, another quantified clinical assessment
- B) Cognitive deficits interfere with independence in everyday activities (i.e. at a minimum, requiring
assistance with complex instrumental activities of daily living such as paying bills or managing medications)
o Note: if do not interfere in B, and impairments are mild-moderate in A, considered “mild cognitive
disorder”
- C) cognitive deficits do not occur exclusively in the context of a delirium
- D) cognitive deficits are not better explained by another mental disorder (e.g. MDD, schizophrenia)

- Specify whether due to:

Diagnosis

- See DSM5
- “mini cog” rapid assessment:
o 3 word immediate recall
o Clock drawn to “10 past 11”
o 3 word delayed recall

Epidemiology

- Prevalence increases with age: 10% in patients >65y of age, 25% in pt > 85y of age
- Prevalence is increased in people with Downs syndrome and head trauma
- Alzheimer disease comprises > 50% of cases, vascular cause compromise approx. 15% of cases
- Average duration of illness from onset of sx to death is 8-10y

Etiology

- Alzheimer disease:
o Predominantly memory and learning issues
- Frontotemporal degeneration:
o Language type (early preservation)
o Behavioral type (apathy/disinhibition/self-neglect)
- Lewy body disease
o Recurrent, soft visual hallucinations (e.g. rabbits)
o Autonomic impairment (falls, hypotension)
o EPS
o Doesn’t respond well to pharmacology
o Fluctuating degree of cognitive impairment
- Vascular disease
o Vascular risk factors
o Focal neurological signs
o Abrupt onset, stepwise progression
- Normal pressure hydrocephalus
o Abnormal gait, early incontinence, rapidly progressive

Subtypes

- w/w.o behavioral disturbance (e.g. wandering, agitation)

- early-onset: age of onset < 65y
- late-onset: age of onset >65y

Investigations (rule out reversible causes)

- Standard: see delirium

- As indicated: VDRL, HIV, SPECT, CT head in dementia
- Indications for CT head: same as for delirium, +:age < 60, rapid onset (unexplained decline in cognition or
function over 1-2 months), dementia of relatively short duration (< 2y), recent significant head trauma,
unexplained neurological symptoms (new onset of severe headache/seizures)
22. Somatoform, somatization, conversion disorder, hypochondriasis: etiology, diagnostic
criteria, clinical management

- Physical signs and symptoms lacking objective medical support in the presence of psychological factors
that are judged to be important in the initiation, exacerbation, or maintenance of the disturbance
- Cause significant distress or impairment in functioning
- Symptoms are produced unconsciously and are not the result of malingering or factitous disorder, which
are disorders of voluntary “faking” of symptoms (or intentionally inducing, e.g. injecting feces) for
secondary gain
o Malingering: intentional production of false or grossly exaggerated physical or psychological
symptoms, motivated by external reward (e.g. avoiding work, obtaining financial compensation,
or obtaining drugs)
o Factitious disorder: intentional production or feigning of physical or psychological symptoms
- Primary gain:
o Somatic symptoms represent a symbolic resolution of an unconscious psychological conflict;
serves to reduce anxiety and conflict with no external incentive
- Secondary gain:
o The sick role; external benefits obtained or unpleasant duties avoided (e.g. work)

Management of somatic symptom and related disorders

- Brief, regular scheduled visits with the GP to facilitate therapeutic relationship and help patient feel cared
for
- Limit nr of physicians involved in care, minimize medical investigations, coordinate necessary
investigations
- Emphasis on what the patient can change and control; the psychosocial coping skills, not their physical
symptoms (functional recover > explanation of symptoms)
- Do not tell the patient its “ all in their head”, emphasize these disorders are real entities or functional in
nature
- Psychotherapy:
o CBT
o Mindfulness interventions
o Biofeedback
o Conflict resolution
- Drugs:
o Minimize psychotropic drugs
o Anxiolytics in short-term only
o Antidepressants for comorbid depression and anxiety

Somatic symptom disorder

- patients have physical symptoms and believe these symptoms represent the manifestation of a serious
illness
- persistent belief despite negative medical investigations and may develop different symptoms over time
- lifetime prevalence: 5-7%
- females > males, cultural factors may influence sex ratio
- NB:
o Often a misdiagnosis for an insidious illess so rule out all organic illnesses (e.g. MS)

DSM5 criteria

- A) one or more somatic symptoms that are distressing or result in significant disruption of daily life
- B) excessive thoughts, feelings, or behaviors related to the somatic symptoms or associated health
concerns as manifested by at least one of the following:
o 1. Disproportionate and persistent thoughts about the seriousness of ones symptoms
o 2. Persistently high level of anxiety about health or symptoms
o 3. Excessive time and energy devoted to these symptoms or health concerns
- C) although any one somatic symptom may not be continuously present, the state of being symptomatic is
persistent (typically > 6m)
- Specify:
o With predominant pain (prev. “pain disorder”) for those whose somatic symptom is primarily pain

Complications

- Anxiety and depression (up to 80%)

- Unnecessary medications or surgery

Illness anxiety disorder (formerly hypochondriasis)

- Preoccupation with fear of having, or the idea that one has, a serious disease, to the point of causing
significant impairment
- Convictions persist despite negative investigations and medical reassurance
- Somatic symptoms are mild or not present
- There is a high level of anxiety about health and individual is easily alarmed about personal health status
- Person engages in maladaptive behavior such as excessive physical checking or total healthcare avoidance
- Duration: > 6 months
- Onset: 3rd-4th decade
- New diagnostic entity so epidemiology is not well known; however, its likely less common than SSD
- Tx: possible role for SSRI due to generally high level of anxiety

DSM5 criteria

- The individual is preoccupied with having or acquiring a serious illness

- Somatic symptoms are not present or, if present, are only mild in intensity. If another medical condition is
present or there is a high risk for developing a medical condition (e.g. strong family history is present), the
preoccupation is clearly excessive or disproportionate
- The individual has high level of anxiety about health, and is easily alarmed about personal health satus
- The individual preforms excessive health-related behaviors or exhibits maladaptive avoidance
- The individual has been preoccupied with illness for at least 6 months
- The individuals preoccupation is not better explained b y another mental disorder

Conversion disorder

- One or more symptoms or deficits affecting voluntary motor or sensory function that mimic a neurological
or GMC (e.g. impaired coordination, local paralysis, double vision, seizures, or convulsions)
- Does not have to be preceded by a psychological event as per previous DSM criteria, however, this is still
worth exploring as many patients will present after an event or related to a medical diagnosis inn a first
degree relative
- 2-5/100.000 in general population, 5% of referrals to neurology clinic
- More common in rural populations and in individuals with little medical knowledge
- Spontaneous remission in 95% of acute cases, 50% of chronic cases (>6m)
- Incompatible findings detected from specific neurological testing can help differentiate btw functional and
neurological origin (e.g. Hoovers sign, dermatome testing)

DSM criteria

- One or more symptoms of altered voluntary or sensory function

- Physical findings provide evidence of incompatibility btw the symptom and recognized neurological or
medical conditions
- The symptom or deficit is not better explained by another medical or mental disorder
- The symptom or deficit causes clinically significant distress or impairment in social, occupational, or other
important areas of functioning or warrants medical evaluation
24. Mood (affective) disorders – acute and long term treatment

Mood stabilizers

- Used in conjunction with atypical antipsychotics for managing episodes of bipolar disorder – depression,
mania, stabilization
- Full effects not for 2-4w, thus may need acute coverage with benzodiazepines or antipsychotics

1. Lithium
- Before starting therapy screen for pregnancy, thyroid disease, seizure disorder, neurological, renal, and
cardiovascular diseases
- MA:
o Unknown
o Therapeutic response within 7-14d

- Indications:
o 1st line:
§ Acute mania (monotherapy or with adjunct SGA)
§ Bipolar I depression (monotherapy or inn combinantion with SSRI, divalproex, or
bupropion)
§ Bipolar disorder maintenance (monotherapy or with adjunct SGA)
o Other:
§ Bipolar II depression
§ Augmentation of antidepressants in MDE and OCD
§ Schizoaffective disorder
§ Chronic aggression antisocial behavior
§ Recurrent depression
- Pharmacokinetics:
o Complete absorption from GI
o T ½: 20 hours
o Not metabolized, excreted in urine
§ Any drug affecting GFR can alter lithium level
§ Reduced clearance if on thiazides and/or NSAIDs
- Monitoring:
o Monitor serum levels until therapeutic (always wait 12h after dose)
§ Therapeutic level: adult 0,8-1 mmol/l (1-1,25 for acute mania, 0,5-0,8 in elderly)
o Then monitor biweekly or monthly until a steady state is reached, then every 2nd month
o Every 6m monitor thyroid function and creatinine. Urinalysis 1/y
- Toxicity:
o Clinical diagnosis as toxicity can occur at therapeutic level
o Can separate into acute (early) and chronic lithium toxicity
§ Acute: GI symptoms (n&v, diarrhea)
§ Chronic: neurologic (tremor, confusion, ataxia)
o Common causes: overdose, Na/fluid loss, concurrent medical illness
o Clinical presentation:
§ GI: severe n&v, diarrhea, stomach pain
§ Cerebellar: ataxia, slurred speech, lack of coordination
§ Cerebral: drowsiness/lethargy/fatigue, headache, myoclonus, tremor, upper motor
neuron signs, seizures (can enter cells “as Na” and cause depolarization), delirium, coma
§ GU: polyuria, polydipsia, GN, renal failure, nephrogenic DI (ADH receptor is Gs coupled)
§ Hematologic: reversible leukocytosis
§ Other: teratogenic (Ebstein’s anomaly), weight gain, edema, psoriasis, hypothyroidism
(rarely symptomatic, prevents effects of TSH because decrease IC cAMP (TSH-R is Gs
coupled) and peripheral deiodinase inhibitor), hair thinning, muscle weakness, ECG
changes
o Management:
 § Discontinue lithium for several doses and begin again at a lower dose when lithium level
has fallen to a non-toxic range
§ Serum lithium levels, BUN, electrolytes
§ Saline infusion
§ Hemodialysis if Lithium > 2 mmol/l, coma, shock, severe dehydration, failure to respond
to treatment after 24h, or deterioration
- Drug interactions:
o NSAIDs (decrease clearance)

2. Lamotrigine (lamictal)
- Indications
o 1st line
§ Bipolar I depression (monotherapy)
§ Bipolar disorder maintenance (limited efficacy in preventing mania, more effective when
combined with lithium)
o Other uses:
§ Bipolar II depression
o NB: not recommended for acute mania as monotherapy
- MA:
o May inhibit 5-HT3 receptors
o May potentiate DA activity
o Complex MA as antiepileptic:
§ Increase inactivation of Na+
§ Reduce Glu release via inhibition of presynaptic Na channels
- Monitor:
o Monitor for suicidality, esp when initiating tx
- SE:
o GI: n&v, diarrhea
o CNS: ataxia, dizziness, diplopia, headache, somnolence
o Skin: rash (should discontinue drug due to risk SJS) – increased lamotrigine levels = increased risk
of rash
o Other: anxiety

3. Divalproex (epival, sodium valproate)

- Indications:
o 1st line:
§ Acute mania (monotherapy or with adjunct SGA)
§ Bipolar I depression (combination with SSRI or lithium)
§ Bipolar disorder maintenance (monotherapy or with adjunct SGA)
o Other:
§ Bipolar II depression
§ Rapid cycling bipolar disorder
§ Mixed phase/dysphoric mania
- MA:
o Depresses synaptic transmission
o Raises seizure threshold
o Complex MA as antiepileptic:
§ Extend inactivated phase Na channels
§ May increase GABA levels in CNS (increase production/decrease degradation)
§ Inhibition T type Ca2+ channels
- Monitor:
o LFTs weekly for 1 monht, then montly
o Watch for signs of liver dysfunction (nausea, edema, malaise)
o Monitor levels to confirm adherence
- SE:
o GI: liver dysfunction, n&v, diarrhea
o CNS: ataxia, drowsiness, tremor, sedation, cognitive blurrinng
 o Other: hair loss, weight gain, transient thrombocytopenia, NTD when used in pregnancy,
pancreatitis, hematological abnormal
- Drug interactions:
o OCP

4. Carbamazepine (tegretol)
- Indications:
o 2nd line:
§ Acute mania (monotherapy)
§ Bipolar disorder maintenance (monotherapy or in combination with Li+)
o Other:
§ Rapid cycling bipolar disorder
§ Trigeminal neuralgia
- MA:
o Depresses synaptic transmission (block Na+ channels)
o Raises seizure threshold
- Monitor:
o Weekly blood counts first month, due to risk of agranulocytosis
o Watch for signs of blood dyscrasias (fever, rash, sore throat, easy bruising)
- SE:
o GI: n&v, diarrhea, hepatic toxicity
o CNS: ataxia, dizziness, slurred speech, drowsiness, confusion, nystagmus, diplopia
o Hematologic: transient leukopenia (10%), agranulocytosis, aplastic anemia
o Skin: rash (5% risk; should discontinue due to risk of SJS)
o Other: NTD when used in pregnancy, gin
- Drug interactions:
o OCP
26. Personality disorders: diagnostic criteria (clusters a-b-c) and clinical management

- An enduring pattern of inner experience and behavior that deviates markedly from the expectations of the
individuals culture, manifested in two or more of: cognition, affect, interpersonal functioning, impulse
control
- Rigid, permanent, and maladaptive traits that define the way a person behaves.
- Pt. don’t see the problem.
- Inflexible and pervasive across a range of situations
- Pattern is stable and well established by adolescence or early adulthood (vs a sudden onset). Cant dx
before 18 because can grow out of it.
- Associated with many complications, such as depression, suicide, violence, brief psychotic episodes,
multiple drug use, and treatment resistance
- Relationship building and establishing boundaries are important, focus should be placed on validating,
finding things to be truly empathetic about, and speaking to the patients strengths
- Mainstay of treatment is psychotherapy, add pharmacology to treat associated axis I disorders (e.g.
depression, anxiety, substance abuse)
- NB:
o schizotypal, antisocial, and borderline PD have familial associations
o if sounds like have PD but not affecting lives in any way – said to have “cluster traits” (in order to
be disorder need to interfere with functionality)

Classification

Cluster A (“Mad”/ “wierdos”)

- Patients seem odd, eccentric, withdrawn

- Familial association with psychotic disorders
- Common defense mechanisms: intellectualization, projection, magical thinking

1. Paranoid PD (0.5-3%)
- Pervasive distrust and suspicious of others, interpret motives as malevolent
- Blame problem on others and seem angry and hostile
- Defece mechanism: projection (whatever they are feeling they will think others are feeling)
- Diagnosis requires 4 or more of “SUSPECT”:
o Suspicious that others are exploiting or deceiving them
o Unforgiving (bears grudges)
o Spousal infidelity suspected without justification
o Perceive attacks on character, counterattacks quickly
o Enemies or friends? Preoccupied with acquaintance trustworthiness
o Confiding in others is feared
o Threats interpreted in benign remarks

2. Schizoid PD
- Neither desires nor enjoys close relationships incl being a part of a family; prefers to be alone
- Lifelong pattern of social withdrawal
- Seen as eccentric and reclusive with restricted affect
- Night shift toll booth
- Diagnosis requires 4 of “DISTANT”
o Detached/flat affect, emotionally cold
o Indifferent to praise or criticism
o Sexual experiences of little interest
o Tasks done solitarily
o Absence of close friends (other than first degree relatives)
o Neither desires nor enjoys close relationships (incl family)
o Takes pleasure in few (if any) activities

3. Schizotypal PD (3,5-6%)
- Pattern of eccentric behaviors, peculiar thought patterns
- No hallucinations, don’t respond to internal stimuli, but are bizarre. Fully functional
- Lady gaga
- Diagnosis require 5 or more of “ME PECULIAR”
o Magical thinking
o Experiences unusual perceptions (incl body illusions)
o Paranoid ideation
o Eccentric behavior or appearance
o Constricted or inappropriate affect
o Unusual thinking/speech (e.g. vague, stereotyped)
o Lacks close friends
o Ideas of reference
o Anxiety in social situations
- note: rule out psychotic/pervasive developmental disorders – this is not part of the criteria)

Cluster B (Bad)

- Patients seem dramatic, emotional, inconsistent

- Familial association with mood disorders
- Common defense mechanisms: Denial, acting out, regression (histrionic PD), splitting (borderline PD),
projective identification, idealization/devaluation

1. Borderline PD (2-4%)
- Unstable moods and behavior, feel alone in the world, problems with self-image
- Unstable, impulsive, often promiscuous. F > M.
- History of repeated suicide attempts, self-harm behaviours
- Inpatients commonly report history of sexual abuse
- Tends to fizzle out as patients age
- Splitting: youre either terrible or perfect
- DBT (dialectical behavior therapy) is principal treatment
o A form of CBT
- NB: 10% suicide rate!
- Diagnosis requires 5 or more of “IMPULSIVE”
o Impulsive (min 2 self damaging ways, e.g. sex/drugs/spending)
o Mood/affect instability
o Unstable self image
o Labile intense relationships
o Suicidal gestures/self -harm
o Inappropriate anger
o aVoiding abandomnment (real or imagined, frantic efforts to)
o emptiness (feelings of)

2. Antisocial PD (M 3%, F 1%)

- Lack of remorse for actions, manipulative and deceitful, often violate the law
- May appear charming on first impression.
- Pattern of disregard for others and violation of others rights must be present before age 15; hoever for the
diagnosis of ASPD patients must be at least 18.
- Strong association with conduct disorder, history of trauma/abuse common
- Diagnosis require 3 or more of “CORRUPT”
o Cannot conform to law
o Obligations ignored (irresponsible)
o Reckless disregard for safety
o Remorseless
o Underhanded (deceitful)
o Planning insufficient (impulsive)
o Temper (irritable and aggressive)

3. Narcissistic PD (2%)
- Sense of superiority, needs constant admiration, lacks empathy, but with fragile sense of self
- Consider themselves “special” and will exploit others for personal gain
- Diagnosis requires 5 or more of “GRANDIOSE”
o Grandiose
o Requires excessive admiration
o Arrogant
o Needs to be special (and associate with other specials)
o Dreams of success, power, beuty, lover
o Interpersonally exploitative
o Others (lacks empathy, unable to recognize feeligns/needs of)
o Sense of entitlement
o Envious (or believes others are envious)

4. Histrionic PD (1,3-3%)
- Attention seeking behavior and excessively emotional.
- Dramatic, flamboyant, and extroverted
- Cannot form meaningful relationships
- Often sexually inappropriate
- Marilyn Monroe
- Trouble when getting older (dependent on looks, getting older – clash with their PD
- Diagnosis requires 5 or more of: “ACTRESS”
o Appearance used to attract attention
o Centre of attention (else uncomfortable)
o Theatrical
o Relationships (believed to be more intimate than they are)
o Easily influenced
o Seductive behavior
o Shallow expression of emotions (which rapidly shift)
o Speech (impressionistic and vague)

Cluster C (Sad)

- Patients seem anxious, fearful

- Familial association with anxiety disorder
- Common defense mechanisms: isolation, avoidance, hypochondriasis

1. Avoidant PD (0,5-1,6%)
- Timid and socially awkward with a pervasive sense of inadequacy and fear of criticism
- Fear of embarrassing or humiliating themselves in social situations so remain withdrawn and socially
inhibited
- Shy hot libarian
- Diagnosis requires 4 or more of “CRINGLES”
o Criticism or rejection preoccupies thoughts in social situations
o Restraint in relationships due to fear of being shamed
o Inhibited in new relationships due to fear of inadequacy
o Needs to be sure of being liked before engaging socially
o Gets around occupational activities requiring interpersonal contact
 o Embarrassment prevents new activity or taking risks
o Self-viewed as unappealing or inferior

2. Dependent PD (1,6-6,7%)
- Pervasive and excessive need to be taken care of, excessive fear of separation, clinging and submissive
behaviors
- Difficulty making everyday decisions
- Stay at home in abusive relationship
- Useful to set regulated treatment schedule (regular, brief visits) and being firm about in btw issues.
Encourage pt to do more for themselves, engage in own problem-solving
- Diagnosis require 5 of “RELIANCE”
o Reassurance required for everyday decisions
o Expressing disagreement difficult
o Life responsibilities assumed by others
o Initiating projects difficult (because no confidence)
o Alone (feels helpless and ucomfortable when alone)
o Nurturance (goes to excessive lengths to obtain)
o Companionship sought urgently
o Exaggerated fears of being left to care for self

3. Obsessive-compulsive PD (3-10%)
- Preoccupation with orderliness, perfectionism, and mental and interpersonal control
- Is inflexible, closed off, and inefficient
- Extreme preoccupation with orderliness, control and perferfection, and do so at the expense of efficacy
- Diagnosis requires 4 or more of “SCRIMPER”
o Stubborn
o Cannot discard worthless objects
o Rule/detail obsessed (to point of activity lost)
o Inflexible in matters of morality, ethics, values
o Miserly
o Perfectionistic
o Excludes leisure due to devotion to work
o Reluctant to delegate others
27. Diagnostic criteria dementia
15. (III) Primary degenerative dementia
16. (III) Dementia in cerebrovascular disorders
38. (III) Genetic background of dementia

Mild neurocognitive disorder (mild cognitive impairment)

- Cognitive impairment not meeting criteria for major neurocognitive disorder

- Measurable deficit in at least one cognitive domain by a patient or others without impairment in ADLs
- Amnestic (precursor to AD) vs non-amnestic
- Represent intermediate stage btw major NCD and normal aging

Epidemiology

- Mild NCD: 1-10% at age 65y, and 5-25% by age 85y

Risk factors

- Vascular: HTN, DM, obesity, cardiac disease, apolipoprotein E epsilon 4 genotype

Clinical features

- Cognitive impairment
o Particularly in amnestic subtype
o Important to ascertain that memory complaints represent change from baseline
o Patients with mild NCD are often troubled by memory symptoms in comparison to patients with
dementia
- Neuropsychiatric symptoms
o Depression (50%), irritability, anxiety, aggression, and apathy

Investigations

- Establish a baseline for follow-up

- Clinical interview with patient and his/her caregivers is the cornerstone of mild NCD evaluation
- Neuropsychological testing:
o MMSE or MoCA; should not be used in isolation
o If abnormal, follow-up in one year to monitor cognitive and functional decline
- Neuroimaging:
o Role uncertain
o Most advocate for non-contrast brain CT to evaluate for structural abnormalities (CVD, SDH, NPH,
or mass lesion)
- Other testing:
o Exclude treatable conditions and underlying psychiatric conditions

Treatment

- Watch and wait

- No evidence for cholinesterase inhibitors, anti-inflammatory agents, vascular risk factor modification,
exervise, cognitive interventions

Prognosis

- 10% progress to major NCD per year

- Typically progress to major NCD over a period of 2-3y
Dementia (major neurocognitive disorder)

- Prevalence increases with age: 10% in patients >65y of age, 25% in pt > 85y of age
- Prevalence is increased in people with Downs syndrome and head trauma
- Alzheimer disease comprises > 50% of cases, vascular cause compromise approx. 15% of cases
- Average duration of illness from onset of sx to death is 8-10y
- Can be classified as early (<65y) or late (>65y) onset

Definition

- Progressive deterioration of intellect, behavior and personality as a consequence of diffuse disease of the
cerebral hemispheres, maximally affecting the cerebral cortex and hippocampus
- Distinguish from delirium which is an acute disturbance of cerebral function with impaired conscious level,
hallucinations and autonomic overactivity as a consequence of toxic, metabolic or infectious conditions
- Any age, more common in elderly (1% in 60s, 5% 70s, 15% 80s)
- It’s a symptom of disease rather than a single disease entity
- When occurring before 65y its labelled “presenile” dementia

Risk factors

- Old age
- Genetics (increased incidence in first degree relatives)
- Cerebrovascular disease
- Hyperlipidemia
- Lifestyle factors such as smoking, obesity, high saturated fat diet
- HTN

Clinical course

- Rate of progression depends on underlying cause:

- Dementia due to cerebrovascular disease appears to occur “stroke by stroke”

- All show tendency to be accelerated by change of environment, intercurrent infection, or surgical
procedures

Development of symptoms

- Introspective, unsure of self à difficulty in coping with work and ordinary routine (retained insight) à loss
of insight, behavioral changes, loss of inhibition à long-term care, cannot be left unattended à mutism,
incontinence, death
- NB:
o Initial phase of dementia may be inseparable from pseudodementia of depressive illness

- Early signs:
o Altered intellectual capacity, behavior, and personality
- Memory loss (main symptom)
 o Self reported reduced memory is not a good indicator, self reported loss of function is stronger
indicator
o Forgettinnng names of close relations, increased frequency of forgetting, repeating
phrases/stories in the same conversation
- Typical symptoms
o Reduced memory and attention
o Reduced orientation in time and place
o Reduced communication
o Difficulty finding words
o Difficulty understanding room and direction
o Apraxia
o General action failure
- Difficulty with actions requiring planning, thinking, abstraction, judgement, and execution ability, e.g.
o Paying bills
o Control own economy
o Control own medications
- Altered behavior and emotion
o Some have depressive symptoms, anxiety, and withdrawal
o Others can be suspicious, have delusions or visual hallucinations
o Restlessness, alternating irritability and apathy
o Altered sleep rhythm
- Motoric symptoms are common in late dementia
o Muscle stiffness, balance problems, incontinens

Classification

- Important to investigate all patients with dementia as many causes are treatable in practice (10-15% can
be reversed!)

- Based on cause:
o Degenerative
§ Pure dementia
• Alzheimer’s disease (60%)
• Frontotemporal/Pick’s disease (5%)
§ Dementia plus syndromes
• Dementia with Lewy bodies (10%)
• Parkinsons disease with dementia
• Corticobasal degeneration
• Progressive supranuclear palsy
• Huntington’s disease
o Cerebrovascular disease (20%)
§ Multiple infarct dementia
§ Subcortical ischemic vascular dementia
§ Chronic subdural hematomas
§ Cerebral amyloid angiopathy
§ CADASIL
o Structural disorders
§ Normal pressure hydrocephalus
o Infections
§ Prion disease (Creutzfeld-Jakob disease)
§ Syphilis
§ HIV
§ Progressive multifocal leukoencephalopathy
o Nutritional
§ Wernicke Korsakoff (thiamine deficiency)
§ B12 deficiency
 o Metabolic
§ Hepatic disease
§ Thyroid disease
o Chronic inflammatory
§ Multiple sclerosis
§ Vasculitis
o Trauma
§ Head trauma
o Neoplasia and paraneoplasia
§ Frontal tumor
§ Limbic encephalitis
o Mixed forms:
§ Alzheimer + vascular encephalopathy
- Based on site
o Useful in clinical classification, but only limited value in predicting underlying pathology

Investigation and diagnosis

- History:
o Establish:
§ Rate of intellectual decline
§ Impairment of social function
§ General health and relevant disorders (e.g. stroke, head injury)
§ Nutrition status
§ Drug history
§ Family history of dementia
- Tests to assess intellectual function
o Designed to check:
§ Memory
§ Abstract thought
§ Judgement
§ Specific focal cortical functions
- Mini mental status examination (MMSE)
- Other neurological examination of note:
o Focal signs
o Involuntary movements
o Pseudobulbar signs
o Primitive reflexes (present in dementia)
§ Pout reflex (tap lips with tendon hammer – pout response)
§ Grasp reflex
§ Gabellar reflex
§ Palmomental reflex (scratch palm – contraction mentalis muscle)
- As indicated:
o VDRL, HIV, SPECT, CT head in dementia
- Indications for CT head:
o same as for delirium, +:age < 60, rapid onset (unexplained decline in cognition or function over 1-
2 months), dementia of relatively short duration (< 2y), recent significant head trauma,
unexplained neurological symptoms (new onset of severe headache/seizures)
- Diagnosis requires presence of significant cognitive decline from previous level of performance in one or
more cognitive domains (complex attention, executive function, learning and memory, language,
perceptual-motor, or social cognition) based on:
o Concern of the individual or knowledgable informant AND
o A substantial impairment in cognitive performance either documented by standardized
neuropsychological testing, or quantified clinical assessment
DSM5 criteria major neurocognitive disorder

- A) evidence of 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, or
social cognition) based on
o 1. Concern of the individual, a knowledgeable informant, or the clinician that there has been a
significant decline in cognitive function; and
o 2. Substantial impairment in cognitive performance, preferably documented bby standardized
neuropsychological testing, or, in its absence, another quantified clinical assessment
- B) Cognitive deficits interfere with independence in everyday activities (i.e. at a minimum, requiring
assistance with complex instrumental activities of daily living such as paying bills or managing medications)
o Note: if do not interfere in B, and impairments are mild-moderate in A, considered “mild cognitive
disorder”
- C) cognitive deficits do not occur exclusively in the context of a delirium
- D) cognitive deficits are not better explained by another mental disorder (e.g. MDD, schizophrenia)

- Specify cause:

ICD-10 dementia

1. Worsening memory compared to earlier, esp related to recent past

- Exception: early stage frontotemporal dementia and other rare dementia diseases
2. At least one other cognitive function reduced compared to earlier
- E.g. orientation in time or place, communication ability, logical thinking, ability to plan and/or evaluate
3. Reduced ability to function in the daily life
- Due to reduced cognitive function, no longer able to work in normal environment and complete daily tasks
4. Altered behavior or personality
- E.g. can become passive, lack initiative, agitated or suspicious
5. Last more than 6 months
6. Normal consciousness
- Exception: severe dementia

- Grade:
o Mild: needs reminders but otherwise independent in daily living
o Moderate: needs personal assistance for some daily needs
o Severe: personal assistance for most daily needs

Management

- Treat underlying medical problems and prevent others

- Provide orientation cues for patient (e.g. clock, calendar)
- Provide education and support for patient and family (e.g. daytime programs, respite care, support groups,
home care)
- Consider long-term care plan (nursing home) and power of attorney/living will
- Infor ministry of transportation about patients inability to drive safely
- Consider pharmacological therapy
o Cholinesterase inhibitors (e.g. donepezil, rivastigmine, galantamine) for mild to moderate disease
o NMDA receptor antagonists (e.g. memantine) for moderate to severe disease
o Low-dose neuroleptics (e.g. risperidone, quetiapine), antidepressants or trazodone if behavioral
or emotional symptoms prominent – start low, go slow
o Reassess pharmacotherapy every 3 months
Alzheimer’s disease

- Most common cause of dementia

- Less than 10% are familial
- Separate early (<65y) vs late (>65y) presentation

Predisposing factors and risk factors

- Older age
- Low education level
- Genetic predisposition
o Many genes involved
o Downs syndrome is strongly associated with early debut alzheimers
- Modifiable
o Depression
o Physical inactivity
o Lack of social network
o Lifestyle with few cognitive challenges
- Factors predisposing for vascular dementia which also increase risk Alzheimer
o Most likely due to fact that subclinical Alzheimer presents clinically with cerebrovascular events
that are not enough by themselves to manifest as vascular dementia
o HTN, hypercholesterolemia and DM

Protecting factors

- Moderate alcohol intake

- Mediterranean diet and regular exercise seems like independent protective factors associated with lower
incidence of dementia
- Social and mental activity

Etiology

- Defect in amyloid precursor protein (APP)

o Defect in APP causing deposition of abnormal amyloid (beta-amyloid protein) in hippocampus
o The amyloid aggregates are also called senile plaques.
o Also seen in normal ageing but markedly increased concentration in Alzheimers disease
o The gene for APP is on chr 21, and certain mutations in this gene is assumed to be the causes of
inherited alzheimers disease
o The deposition of Abeta also seem connected to the genes presenilin 1 (PSEN1) and 2 (PSEN2),
which are on chr 14 and 1
- AD inherited Alzheimer disease
o 0,5% of cases, usually present before 65 y
o 50% have mutations in one of the three genes: PSEN1, PSEN2, and APP
§ Can be tested for
- Late debut Alzheimer’s
o 90-95% of cases
o Most likely several genes involved in the susceptibility for development of alzheimer, although in
this case genetic testing are not recommended due to damaging psychological effects and
because no treatment available
- Apolipoprotein E-polymorphism (chr 19, Apo-E-epsilon 4 allele)
o E4 allele increases risk of “sporadic alzheimer with early debut”
o Lifetime risk for Alzheimer in ApoE-c4 homozygote is >50%, heterozygote is 20-30%
o Factors shown to affect APOE-gene include herpes infection, low lipid levels, head traumas,
estrogen replacement therapy, and female gender
- Gene mutation leading to altered TREM2 function seems to increase risk of normal, late presenting
Alzheimer disease
o TREM2 have anti-inflammatory effect in the brain
- Neurofibrillary tangles
o Intranneuronal lesions of phosphorylated and aggregated tau protein
o In normal neurons tau protein functions aid in microtubule assembly and stabilization. In AD, tau
becomes hyperphosphorylated and aggregates to form paired helical filament (PHF) tau, a major
component of neurofibrillary tangles within the neuronal cytoplasm
o Aggregation of tau protein and disturbance in cytoskeleton are early changes in the pathogenesis
of Alzheimer disease and correlate well with loss of cognitive function
- Infectious?
o Reason for hypothesis is increased incidence of Alzheimer in neurosurgeons (2,5x increased risk)
and life-partners (1,6x increased risk)
o May be response to an infection
o Esp herpesvirus 6 and 7 that are implicated as potential causes

Pathology

- Lesions:
o Neuritic plaque:
§ Complex EC lesion
§ Aggregates of filaments with a central core of amyloid
§ Found in hippocampus and parietal lobes
o Neurofibrillary tangle
§ IC lesion
§ Paired helical strands of tau protein
§ Mainly affecting pyramidal cells of cortex
- Associated with neuronal loss and granulovacuolar degeneration
- The brain is small with atrophy most evident in the superior and middle temporal gyri
- Subcortical origins of cholinergic projections are also involved

Pathophysiology

- Loss of cholinergic function

o Obduction shows reduction in cholinergic markers and marked loss of neurons in locus coeruleus
- Loss of neurotransmitter function
o Loss of other neurotransmitter function, incl 5-HT and NE, also have central role in disease
development
o Glutamate system also involved
- Brain atrophy
o Esp hippocampus region and medial temporal lobe
§ Caused by reduction in nr and size of synapses + loss of neurons
o Macroscopic diffuse cerebrocortical atrophy

Clinical features

- Symptoms:
o See above
o Typically loss of memory >6m and normal consciousness, reduced orientation, logical thinking,
planning, language and communication
o General action failure, altered behavior, function loss
o Reduced consciousness is late sign

Diagnosis

- Clinical
 o Likely Alzheimer disease:
§ Fulfill dementia criteria
§ Insidious onset over months-years
§ Certain worsening of cognitive function
§ Initial symptoms and most marked symptoms are either amnestic (reduced ability to
learn and memory for new things, disorientation in time and place) or non-amnestic
(visualspatial, language, executive function)
§ Lack of:
• Cerebrovascular disease
• Typical characteristics of Lewy body dementia, frontotemporal dementia, and
progressive aphasia
• Other diseases or drugs that can affect cognition
- Information from friends/relatives are important
- Imaging and lab used to exclude reversible causes of cognitive failure
- Functional imaging and biomarkers for Alzheimer research

Management

- Organization of supportive care is most important.

- No drugs can affect the development of dementia
- Goal:
o Create best possible quality of life for patient and family
o Improve cognitive functions such as memory, orientation, attention, and concentration
o Reduce behavioral disturbances and psychological problems such as wandering, aggression,
anxiety, depression, and psyschosis
- Medications
o Indications:
§ Mild-moderate Alzheimer:
• Cholinesterase inhibitors (donepezil, rivastigmin, galantamin)
§ Severe alzheimers
• Mementin (NMDA receptor antagonist)
o Anxiolytics/hypnotics should be avoided if possible
o Psychiatric symptoms should first be treated without drugs
o Consider need for analgesics

Vascular dementia

- Dementia caused by cerebrovascular or cardiovascular disease causing brain damage of functional

disturbance
- ICD-10 definition: Demetia caused by brain infarct and due to vascular disease, incl HTN vasculopathy of
the brain. The infarcts are usually small but have cumulative effect. Usually present late in life.
- Different criterias which vary and not necessarily correlate that well (e.g. some incl hemorrhagic lesions).
Most criteria demand proof by image of cardiovascular disease and/or an anamnesis that includes factors
associated with stroka and stroke within timeframe of presentation of symptoms.
- Most common cause of dementia after alzheimers
- Usually present late in life, often together with Alzheimer

Risk factors

- Age > 60 (most important risk factor for both dementia and stroke)
- Obesity/overweight
- HTN
- Smoking
- Afib
- DM (some studies)
- Alcoholism (some studies)
- Hypercholesterolemia (risk factor stroke, not necessarily dementia)
Etiology and pathogenesis

- Classification
o Multiinfarct dementia
§ Multiple cerebral infarcts which together result in widespread brain damage
o Infarct in critical areas
§ E.g. paretal lobe, thalamus, singular gyrus
o Lacunar dementia
§ Caused by small infarcts in deep in the brain
§ Cause small cavitary lesions in brain parenchyma, esp internal capsule, deep gray nuclei
and white substance
o Chronic subcortical ischemia
§ Binswangers disease
• Subgroup subcortical vascular dementia caused by lipo- and fibrohyalinosis in
small vessels and diffuse lesions in white matter
o Amyloid angiopathy
§ Very rare variant of vascular dementia caused by amyloid angiopathy
§ Leads to amyloid deposits in vessels, which can result both in intracranial hemorrhage
and ischemic vasculoptathy
§ This is also associated with Alzheimer
- Alternaltive classification
o Cortical
o Subcortical
o Mixed

- Cerebrovascular disease can cause both focal and diffuse brain pathology
o Focal disease occur in relation to thrombotic or embolic vascular occlusions
§ Areas of the brain esp associate dwith development of dementia include white matter in
the hemispheres and the deep nuclei (esp striatum and thalamus)
o Diffuse disease is most often caused by chronic HTN
- Seems that multiple cerebrovascular lesions often occur in pt with Alzheimer dementia
o Possibly due to synergistic pathogenetic factors

Clinical features

- Two usual presentations:

o Loss of cognitive function as an immediate complication of stroke
o Loss of cognitive function without stroke, where imaging confirm vascular brain damage

- Symptoms:
o Prev stroke, problems with problem solving, apathy, disinhibition, problems with information
processing, problems with attention, memory problems, focal neurological signs, gait problems,
fluctuating symptoms, stepwise worsening (esp multi-infarct dementia), weakening
psychomotorium, loss of executive function, changes in personality, depression (up to 20%),
hallucinations (late sign)

Diagnosis

- Investigate vascular cause of dementia

- Imaging (CT, MRI)
- EKG
- Lab
o WBC, plt, ASAT, ALAT, kidney function, inflammatory markers, B12, homocysteine, folate,
electrolytes, plasma proteins, glucose, lipid profile
o Borrelia antibodies if inficated, other serological tests
- Different classification systems (ICD, DSM, AHA etc)
o Some include hemorrhagic lesions, others don’t
o Most require imaging proof of cerebrovascular disease and/or anamnestic data compatible with
stroke and temporarily association btw stroke and debut of cognitive failure
- Hachinski ischemic score
o Points:
§ Sudden presentation (2 pt.), stepwise worsening (1 pt.), fluctuating course (2 pt.),
worsening during nighth (1 pt.), relatively well maintained personality characteristics (1
pt), depression (1 pt), somatic upsets (1 pt.), emotional liability (1 pt.), prev stroke (2 pt.),
confirmed comorbid atherosclerosis ( 1 pt), focal neurological symptoms (2 pt.), focal
neurological signs (2 pt.)
o Score:
§ If 7 or more points – specificity around 90% for vascular dementia

Management

- Control and management of cardiovascular risk factors (secondary prophylaxis)

o Anti-plt / anticoagulation if indicated for other vascular diseases
- Supportive care
- If mixed alzheimer-vascular dementia – same guidelines as for Alzheimer

Frontotemporal dementia (FTD, prev “Picks disease”)

- Type of dementia caused by atrophy of frontal and/or temporal lobe

- Most common cause of dementia in pt <50y. 4th most common cause of dementia after Alzheimer,
vascular dementia, and dementia with Lewy bodies
- Most often present around 50y, can present as early as 30s and as late as 90s

Etiology and pathogenesis

- An important/relevant genetic component is found in 10-20%

o AD inheritance
o Most commonly involve gene encoding microtubule-associated tau protein on chr 17
o Another is associated with a mutation in chr 3
- In most cases there are not found any external causes of the disease
- Characteristic histopathology: loss of neruons, gliosis, swelling of neurons (Pick cells), argentophil neuronal
inclusions (Pick bodies)

Clinical features

- Symptoms
o Early symptoms dominated by altered behavior and personality, non-cirtical and indifferent
behavior, lack of insight into own disese, loss of empathy
o Memory often intact
- Signs
o Cognitive failure and altered behavior
o Cortical atrophy most marked in frontotemporal lobe is seen on imaging

Classification

- Behavioral variant FTD

o Altered emotional reaction pattern: apathy and/or disinhibition
o Lack of inhibition: social unacceptable behavior, laugh at wrong time, impulsive, non-critical
o Apathy and lack of initiation
o Reduced sympathy or empathy: reduced interest in family, friends, reduced social interests in
general
o Lack insight in own disease
 o Often maintained memory and orientation ability in early stage of disease
- Primary progressive aphasia: Further classified into 3 different classes
o Nonfluent/agrammatic
§ Reduced speech production
§ Progressive increasing problems with speech, speech becomes tense and incoherent
§ Some may have problems producing sounds, alternaltively words may be pronounced
wrong
§ Some may develop probllems with voluntary mimetic muscles, alternaltively they may
not be able to swallow on command
§ Can be associated with development of atypical parkinsonism or motor-neuron disease
o Semantic
§ Reduced memory for words, and don’t understand the meaning of common words
§ Often fluent language but difficulties with remembering names, use nonprecise words
and explanations, and show lack of understanding of the words meaning
o Logopenic
§ Struggle to find words or altered phonology

Diagnosis

- Clinic
- Imaging (MR, CT, PET, or SPECT)
- Genetic studies (inherited FTD)

Management

- Supportive therapy
- Nothing can affect development of dementia
- Medications have limited effect
o Cholinesterase inhibitors and memantin are not used (in fact they are “weakly contraindicated)
- Symptomatic treatment (limited evidence)
o SSRI may reduce change inn behavior, can also be indicated in case of depression or anxiety

Prognosis

- Early presentation is associated with worse prognosis

o 25% of younger patients with dementia need 24h care 1y after diagnosis
- Dementia in general is associated with high mortality (most related to pneumonia)
- In case of FTD the prognosis vary some with the type
o Worse prognosis if comoned with motor neuron disease (often die within 3-5y)
o Semantic type often live more than 10y

Lewy body dementia (dementia with lewy bodies, DLB)

- Chronic progressive neurodegenerative disease characterized by

o Reduced and fluctuating cognitive function
o Visual hallucinations (clear and detailed)
o Spontaneous Parkinson symptoms
o Disturbed REM sleep
o Hypersensitivity for antipsychotics
- 10-15% all cases of dementia in Norway (third most common type)
- Often comorbid alzheimers and vascular etiology

Risk factors

- Strong predisposition:
o Old age
- Weak predisposition:
 o Male gender
o Familiar DLB (AD > AR)
- Autonomic dysfunction
o Prolonged orthostatic reaction may mark faster progression of DLB

Etiology and pathogenesis

- First steps in pathogenesis is not known, may involve; toxic protein aggregation, abnormal
phosphorylation, other molecular mechanisms like formation of organic nitro-compounds, inflammation,
and oxidative stress
- Lewy bodies:
o Intraneuronal eosinophilic inclusion bodies composed of aggregated proteins (alpha-synuclein,
ubiquitin etc)
o Alpha-synuclein seem most important
§ Both parkinsons and Lewy bodies are “synucleinopathies”
§ Means they are neurodegenerative conditions with abnormal aggregations of alpha-
synuclein
§ Alpha-synuclein is neurotoxic and most likely the cause of damage. One theory states
that encapsulation is mechanism of protecting the brain from alpha-synuclein
§ Its still uncertain whether lewy-bodies have neuroprotective or neurotoxic effects
- Localization lewy bodies
o Esp substantia nigra, but also other cortical areas like locus ceruleus (NE), raphe-nuclei (5-HT),
dorsal vagus nuclei, and other parts of ANS
o In the cortex lewy bodies are found mainly in the frontal and temporal association cortex and
limbic system (presence of cortical lewy bodies correlate with development of dementia)
- Lewy bodies works as markers for neuronal loss
o Presence of lewy bodies in nigrostriatum is associated with parkinsons disease, lewy bodies in
autonomic ganglia is associated with postural hypotension, and in the limbic cortex and neocortex
lewy bodies are associated with cognitive failure and psychosis
- Reduced cholinergic neurotransmission
o Like Alzheimer, reduction in cholinergic neutrotransmission is central
o Correlate with degree cognitive failure and visual hallucination

Clinical features

- Symptoms
o Can mimic delirium with fluctuating confusion, attention deficits, psychiatric symptoms and
cognitive failure
- Signs
o Visuospatial and executive difficulties onn neuropsychologocial tests
o Usually one or more parkinsons symptoms
o Cognitive failure, but MMSE not sensitive in early phase

Diagnosis

- Criteria:
o Essential:
§ Dementia
o Core:
§ Marked fluctuation in cognitive function, attention and alertness
§ Repeated visual hallucinations which are often clear and detailed
§ REM sleep disturbances (defect in muscle relaxation – often vivid movements during
sleep, shout, gesticulate. Early sign!)
§ One or more of cardinal symptoms of parkinsonism (TRAP)
o Features supporting diagnosis
 § Hypersensitivity toward antipsychotics, postural instability, falling tendancy, syncope or
other attacks with loss of consciousness, marked ANS dysfunction (e.g. constipation,
orthostatic hypotension, urine incontinence), hypersomnia, hyposmia, non-visual
hallucinations, systematic delusions, apathy, anxiety, depression
o Indicative biomarkers
§ Reduced dopamine transporter uptake (DAT scan)
§ Abnormally low uptake of 123iodine-MIBG myocardiscintigraphy
§ Polysomnographic conformation of REM sleep without atonia
o Supportive biomarkers
§ Structures on mid temporal lobe relatively maintained (CT/MRI)
§ Generally low uptake on SPECT/PET perfusion/metabolic scan with reduced occipital
activity and cingulate high sign on FDG-PET?
§ Increase slow activity posteriorly on EEG with periodic fluctuations in pre-alpha/theta-
area
- Diagnosis DLB should be made if:
o Dementia present before or together with parkinsonism
- Probably DLB if:
o Two or more core criteria
o One core criteria + one or more indicative biomarkers
- Possible DLB if:
o Only one core criteria without indicative biomarkers
o One or more indicative markers only
- Dementia in parkinsons disease
o Dementia in a patient with diagnosed parkinsons
o 1-year rule: characteristic motor symptoms with parkisons have been present for at least 1 year
before dementia symptoms

Management

- Supportive care
- Cholinesterase inhibitors may have effect
o May improve cognitive functions and ADL-function
o May be associated with SE, e.g. some increased risk parkinsonian symptoms
- Levodopa
o May be indicated if marked parkinsonism
- Avoid antipsychotica if possible
o If pt is treated with antiparkinsonian drugs or drugs that can cause psychiatric side effects – first
consider dose reduction
o In most cases are traditional antipsychotics absolutely contraindicated in DLB due to risk of
worsening parkinsonism
o 50% have hypersensitivity for atypical antipsychotics (increased rigidty, immobilization, confusion,
sedation, fall tendency)

Creutzfeldt-Jaob disease

- Rare degenerative fatal brain disorder caused by prion proteins causing spongiform changes, astrocytosis,
and neuronal loss
o Prion proteins have a normal form and an infectious form, which result from conversion of the
protein from alpha-helix (normal) to beta-pleated sheath (abnormal); these abnormally folded
proteins aggregate leading to neuronal loss
- Most forms are sporadic (85%), hereditary (5-10%), and acquired (<1%)
- Investigations: CSF analysis, MRI brain (cortical and/or subcortical FLAIR changes), EEG (periodic
complexes)
- Definitive diagnosis: brain biopsy
- Tx: none
Differential

Aphasia

- Acquired disturbance of language characterized by errors in language production, writing, comprehension,

or reading
- Nneuroanatomy:
o Broca’s area (posterior inferior frontal lobe)
§ Involved in language production (expressive)
o Wernicke’s area (posterior superior temporal lobe)
§ Involved in comprehension of language (receptive)
o Angular gyrus
§ Responsible for relaying written visual stimuli to Wernicke’s area for reading
comprehension
o Arcuate fasciculus
§ Association bundle connecting Wernicke and Broca’s area
- Aphasia localizes the lesion to the dominant hemisphere
o >99% of right-handed people have left hemisphere language representation
o 70% of left-handed people have left hemisphere language representation, 15% have right
hemisphere representation, and 15% have bilateral representation
- Assessment of language:
o Assessment of context
§ Handedness (writing, drawing, toothbrush, scissors), education level, native language,
learning difficulties
o Assessment of aphasia
§ Spontaneous speech (fluency, paraphasias, repetition, naming, comprehension –
auditory and reading, writing, neologism)
- Classification:

Apraxia

- Inability to perform skilled voluntary motor sequences that cannot be accounted for by weakness, ataxia,
sensory loss, impaired comprehension, or inattention
- Clinicopathological correlations:
Agnosia

- Disorder in the recognition of the significance of sensory stimuli in the presence of intact sensation and
naming
- Clinicopathological correlations:

Comparison dementia, delirium, and pseudodementia of depression

27. Disorders of childhood and adolescence: diagnostic criteria of psychiaric disorders
usually first evidet in infancy, childhood, or adolescence

- Typical onset:
o Any age group:
§ Organic mental symptoms
• Treat the original somatic disease; brain tumor, epilepsy, delirium, drug effect
ect
o <3y: developmental disorders (boys > girls)
§ Intellectual dissabiltiy
§ Motor disorders
§ Communication disorders
§ ASD
§ Rarely disorders connected to emotional problems; feeding and eating disorders, sleep-
wake disorders, conditions that may be a focus of clinical attention (abuse and neglect)
o 3-8 y: still predominant developmental disorders, other:
§ Neurodevelopmental disorders:
• Specific learning disorder, ADHD, tic disorders (e.g. tourettes)
§ Disruptive
§ Impulse-contorl
§ Conduct disorders
§ Other emotional or affection related disorders:
• Elimination disorders: enuresis, encopresis
• Anxiety disorders: separation anxiety disorder, selective mutism
• Depressive disorders
• Trauma- and stressor-related disorders
• Somatic symptom and related disorders
• Dissociative disorders
• Obsessive compulsive and related disorders
• Gender dysphoria
o 8-12 years: rates still higher among boys, but approach each other
§ Developmental disorders may be recognized in this age group
§ More common: disruptive, impulse-control, and conduct disorders
• Connected to these substance-related and addictive disorders appear
§ Prevalence of emotional disorders are progressively rising
§ Bipolar with related disorders and schizophrenia spectrum and other psychotic disorders
are still rare but prevalence is rising
§ Feeding and eating disorders that earlier showed very various symptoms are getting to
be kore typical and similar to the typical anorexia nervosa
o From 13y: prevalence rates equals, then become higher in women (as in adults)
§ Developmental disorders if prev not diagnosed
• Intellectual disabilities
• ASD
• ADHD
§ Neurodevelopmental disorders that has been diagnosed earlier can lead to difficulties
§ Typical disorders in adult psychiatry become more and more common
§ When the symptoms of disruptive, impulse-control, and conduct disorders hold up, it can
lead to deviant lifestyle
• Substance-related and addictive disorders
• Antisocial personality disorder evolves
§ A diagnosis of a personality disorder cant be set up before 18y, but typical symptoms and
behaviors of PDs (e.g. borderline personality disorder) can be observed
Intellectual disability or intellectual developmental disorder

- 2% US population
- 85% have mild ID, meaning that they are just a little slower than average to learn new information or skills.
o With the right support, most will be able to live independently as adults

- Defined as significantly subnormal intellectual functioning for a childs developmental age, existing
concurrently with deficits in adaptive behaviors (self-care, home-living, communication, and social
interactions).
o i.e. someone with ID have limitations in two areas:
§ 1) intellectual functioning: low IQ (refers to a persons ability to learn, reason, make
decisions, and solve problems)
§ 2) adaptive behaviors: skills necessary for day-to-day life (communication, interact with
others, take care of oneself)
- Defined statistically as cognitive perforamance that has two SD below mean (roughly below 3rd percentile)
of the general population as measured o standardized intelligence testing.

Differential diagnoses of mental retardation

- Early alterations of embryonic development

o Sporadic events affecting embryogenesis, usually stable developmental challenge
o Chromosomal changes (e.g. Downs)
o Prenatal influences (e.g. substance abuse, teratogenic medications, intrauterine TORCH
infections)
- Unknown cause:
o No definite issue is identified, or multiple elements present, non of which is diagnostic (may be
multifactorial)
o Almost 1/3 of individuals with MR don’t have readily identifiable reasons for their disability
- Environmental and social problems
o Dynamic influences, commonly associated with other challenges
o Deprivation (neglect)
o Parental mental illness
o Environmental intoxication (e.g. significant lead intoxication)
- Pregnancy problems and perinatal morbidity
o Impingement on normal intrauterine development or delivery; neurologic abnormalities frequent,
challenges are stable or occasionally worsening
o Fetal malnutrition and placental insufficiency
o Perinatal complications (e.g. prematurity, birth asphyxia, birth trauma)
- Hereditary disorders
o Preconceptual origin, variable expression in the individual infant, multiple somatic effects,
frequently a progressive or degenerative course
o Inborn errors of metabolism (e.g. Tay-Sachs disease, Hunter disease, PKU)
o Single-gene abnormalities (e.g. neurofibromatosis or tuberous sclerosis)
o Other chromosomal aberrations (e.g. fragile X syndrome, deletion mutations such as prader willi
syndrome)
o Polygenic familial sydromes (pervasive developmental disorders)
- Acquired childhood illness
o Acute modification of developmental status, variable potential for functional recovery
o Infections (all can ultimately lead to brain damage, but most significant are encephalitis and
meningitis)
o Cranial trauma (accidental or child abuse)
o Accidents (e.g. near-drowning, electrocution)
o Environmental intoxications (prototype is lead poisoning)
DSM5

- Intellectual disability (intellectual development disorder) is a disorder with onset during the developmental
period that includes both intellectual and adaptive functioning deficits in conceptual, social, and practical
domains. The following three criteria must be met
o A) Deficits in intellectual functions, such as reasoning, problem solving, planning, abstract
thinking, judgment, academic learning, and learning from experience, confirmed by both clinical
assessment and individualized, standardized intelligence testing
o B) Deficits in adaptive functioning that result in failure to meet developmental and sociocultural
standards for personal independence and social responsibility. Without ongoing support, the
adaptive deficits limit functioning in one or more activities of daily life, such as communication,
social participation, and independent living, across multiple environments, such as home, school,
work, and community
o C) onset of intellectual and adaptive deficits during developmental period
- Specificy
o Mild
o Moderate
o Severe
o Profound
- NB:
o Diagnostic term intellectual disability is equivalent term for the ICD-11 diagnosis of intellectual
developmental disorder.

Levels of mental retardation

- WISC-IV: Weschler intelligence scale for children

- NB: caution must be exercised in interpretation because these categories don’t reflect actual fuctional level
of the tested individual

- Classification based on IQ alone has been largely replaced based on the level of support needed:
o Intermittent – desnt require constant support
o Limited – ongoing support of varying intensity
o Extensive – daily and ongoing consistent levels of support
o Pervasive – high level of support for all activities of daily living

Clinical manifestations

- Mild MR correlates with socioeconomic status , profound MR does not.

- Earlier the cognitive slowing is recognized, the more severe the deviation from normal is likely to be

- Low IQ combined with limitations in social, language, and self-help skills

- Seizures, psychiatric disorders, and behavioral disorders (e.g. explosive outburtss) may be present
- Factors that predispose to unacceptable behavior and impaired ability to communicate
- A MR adolescent may dvelop depression when socially rejected
Diagnosis

- History (perinatal, developmental, neurological, and family history) identifies infants at risk
- Isolated delays in sitting or walking (gross motor skills) and in pincer grasp or writing (fine motor skills) may
indicate a neuromuscular disorder
- Specific lab tests are performed depending on the cause

- Three factors:
o Interview with the parents
o Observation of the child
o Testing of intelligence and adaptive behaviors
- After diagnosis is made, a team will assess the childs particular strengths and weaknesses to help
determine how much nad what kind of support the child will need to succeed at home, in school and in the
community

Management

- Identify functional strengths and weaknesses for purposes of medical and habilitative therapies
- Family support, counceling. Integration into normal society as much as possible
- Developmental retardation due to a perinatal insult may be overcome in a good learning environment!

Communication disorders

Autism spectrum disorders

- ASD encompasses disorders prev known as autistic disorder (classic autism), childhood disintegrative
disorder, pervasive developmental disorder-not-otherwise specified, and aspberger disorder
- Biologically based neurodevelopmental disorder characterized by impairment in two major domains
o 1) deficits in social communication and social interaction
§ Delays and deviations in language development are one of the most common presenting
complaints of parents
§ Often lack intent to communicate
§ Features:
• Social reciprocity (interaction deficits) – may be unaware of other children, may
lack empathy, not interested in imitating others
• Joint attention – may lack spontaneous seeking to share enjoyment, interest, or
achievements with other
• Nonverbal communication – difficulty interpret behaviours such as facial
expression, gestures, and body postures.
o Parents may notice that baby resist cuddling, avoids eye contact etc.
• Social relationships – no interest in freindships
o 2) restricted repetitive patterns of behavior, interest, and activities
§ Hypo- or hypersensitivity to sensory input is also core symptom
§ Features:
• Stereotyped behavior – stereotyped and repetitive motor monnerisms or
complex whole body movements (e.g. swaying, finger flapping/twisting, rocking
etc)
• Insistence on sameness – same routine every day, e.g. need to always eat
particular foods in a specific order
• Restricted interest – preoccupation with one or more stereotyped and
restricted patterns. E.g. in older can be wheater, dates, schedules, licence
paltes, pokemon etc.
- Symptoms are most commonly recognized in 2nd year of live (may be earlier and later)
- Associated conditions:
o Intellectual impairment
o Language impairment – lack, delay
- Pathogenesis:
 o Not completely understood, general consensus is that ASD is caused by genetic factors that alter
brain developint, specifically neural connectivity.
- Dx: based on developmental history and observation
- Management:
o Goals: maximize functioning, move child towards independence, and improve QOL
o Behavioral therapy, speech and language therapy, physical and occupational therapy and drug
therapy
§ Drug may help relieve symptoms
§ Antipsychotic drugs – risperidone, aripiprazile
• May help relive ritualistic, self-injurious and aggressive behavior
§ SSRIs – ritualistic behavior,
§ Mood stabiilizers (e.g. valproate) for self-injury and outburst behavior

DSM5

- A) Persistent deficits in social communication and social interaction across multiple contexts, as
manifested by the following, currently or by history
o 1. Deficits in social-emotional reciprocity, ranging, for example, from abnormal social approach
and failure of normal back-and-forth conversation; to reduce sharing of interests, emotions, or
affect; to failure to initiate or respond to social interactions
o 2. Deficits in nonverbal communicative behaviors used for social interaction, ranging, for example,
from poorly integrated verbal and nonverbal communication; to abnormalities in eye cntact and
body language or deficits in understanding and use of gestures, to a total lack of facial expression
and nonverbal communication
o 3. Deficits in developing, maintaining, and understanding relationships, ranging, for example, from
difficulties adjusting behavior to suit various social contexts; to difficulties in sharing imaginative
play or in making friends; to absence of interest in peers.
- Specify current severity (based on social communication impairments and restricted, repetitive patterns of
behavior).
- B) restricted, repetitive patterns of behavior, interests, or activities, as manifested by at least two of the
following, currently or by history
o 1. Stereotyped or repetitive motor movements, use of objects or speech (e.g. simple motor
stereotypes, lining up toys or flipping objects, echolalia, idiosyncratic phrases)
o 2. Insistence on sameness, inflexible adherence to routines, or ritualized patterns of verbal or
nonverbal behavior (e.g. extreme distress at small changes, difficulties with transitions, rigid
thinking patterns, greeting rituals, need to take same route or eat same food every day)
o 3. Highly restricted, fixated interests that are abnormal in intensity or focus (e.g. strong
attachment to or preoccupation with unusual objects, excessively circumscribed or perseverative
interests)
o 4. Hyper- or hyporeactivity to sensory input or unusual interest in sensory aspects of the
environment (e.g. apparent indifference to pain/temperature, adverse response to specific
sounds or textures, excessive smelling or touching of objects, visual fascination with lights or
movement)
- C) symptoms must be present in the early developmental period (but may not become fully manifest until
social demands exceed limited capacities, or may be masked by learned strategies in later life)
- D) symptoms cause clinically significant impairment in social, occupational, or other important areas of
current functioning
- E) these disturbances are not better explained by intellectual disability or global developmental delay.
Intellectual disability and autism spectrum disorder frequently co-occur; to make comorbid dioagnoses of
autism spectrum disorder and intellectual disability, social communications should be below that expected
for general developmental level
- Specifiy if:
o With or without accompanying intellectual impairment
o With or without accompanying language impairment
o Associated with a known medical or genetic condition or environmental factor
o With catatonia)
ADHD

- One of the most common neuropsychiatric disorders of childhood and adolsescence, often persists into
adulthood (can also have ADHD in adulthood without having it in childhood)
- Manifest as symptoms of hyperactivity, impuslivivty, and/or inattention.
- Affect cognitive, academic, behavioral, emotional and social functioning

- Affects 9% of school aged children and 2 % of adults

- Often co-occur with other emotional, behaviorar, language and learing disorders
- Etiology:
o Final common pathway of complex brain and developmental processes
o Environmental component (maternal factors, trauma) and genetic component
o May be related to disturbance in dopamine system

- Clinical features – can be either predominantly inattentive or predominantly hyperactive/impulsivity

o Hyperactivity and impulsivity – typically observed from 4y, peak 8y (hypeactive symptoms
decline, impusivity may persist throughout life)
§ Excessive fidgetiness (e.g. tapping hands or feet)
§ Difficulty remaining seated when sitting is required (e.g. school, work)
§ Feeling of restlessness (in adolescence), or inappriopriate running around or
climbing (children)
§ Difficulty playing quietly
§ Excessive talking
§ Difficulty waiting turns
§ Blurting out answers too quickly
§ Interruption or intrusion of others
o Inattention
§ Careless mistakes
§ Difficulty maintaining attention in play, school, home activities
§ Fails to follow through (homework, chores etc)
§ Difficulty organizing tasks, activities, belongings
§ Avoids tasks that require conisistent mental effort
§ Loses objects required for tasks or activities (e.g. school books)
§ Easily distracted by irrelevant stimuli
§ Fortgetfullness in routine activities
- Impaired functioning.
o In order to meet criteria for ADHD, core symptoms must impair functioning in academic,
social or occupational activities

- Diagnosis:
o DSM-5:
§ Children <17 y require >6 symotoms of hyperactivity and impulsivity or > 6
symptoms of inattention
§ >17 y requires 5 or more
§ Symptoms must:
• Often occur
• Be present in more than one setting
• Persist for at least 6m
• Be present before age 12
• Impair function
• Be excessive for the developmental level of the child
o ADHD subtype:
§ Depending on predominant symptoms, can change over time
• Predominantly inattentive
• Predomininatly hyperactive-impulsive
• Combined 6 (or 5) or more symptoms of both!
- Management:
o Behavioral interventions
§ E.g. positive reinforcement, time-out, response-cost (e.g. no tv if kid do something),
token ecomony (combination of positive reinforcement and response cost)
§ Preferred as initial intervention for preschool children
o Pharmacotherapy
§ 1st line for school-aged children and adolsescents
§ Noradrenergic reuptake inhibitors: atomoxetine
§ Psychostimulants: methylphenidate, amphetamine
o Combinatuion therapy
§ i.e. the two above
o School-based interventions
§ May include provision of tutoring or resource room support, classroom modification,
accommodation etc.
o Social skill training
§ E.g. groups, similar interventions
o Psychotherapy interventions
§ Unlike behavioral interventions these are directed towards the child and designed to
change the childs emotional status or thought pattern
§ Generally only if coesisting conditions
Specific learning disorders
Motor disorders
28. Interviewing and assessment incl special assessment of children

- A comprehensive evaluation of a child is composed of interviews with the parents, the child, and other
family members
- Psychiatric evaluations of children are rarely initiated by the child, so clinicians must obtain information
from the family and the school to understand the reasons for the evaluation
- Assessment of a child or adolescent incudes identifying the reasons for referral; assessing the nature and
extent of the childs psychological and behavioral difficulties; and determining family, school, and
developmental factors that may be influencing the childs emotional well-being
- Steps:
o 1. Full description of current concerns and psychiatric and medical anamnnesis
§ Done with parents for school-aged children, adolescents may do it alone
o 2. Direct interview and observation of the child
o 3. Psychological testing (when indicated)

Clinical interviews
- Clinicians must be familiar with normal development to place the childs responses in proper perspective
(e.g. normal with temper tantrums when 2y, not when 17y)
- Need to develop a rapport so that the child is comfortable
- Should ask about childs of the purpose of the interwiew and should ask what the parents have told the
child. If the child appears confused about reason for the interwiew the examiner may opt to summarize
the parents cocerns in a developmentally appropriate and supportive manner
- During the interview of the child, the clinician seeks to learn about the childs relationships with family
members and peers, academic achievement and peer relationships in school, and the child’s pleasurable
activities
- Clinician must also determine whether that child is safe in his or her environment
- Towards the end, the child may be asked in an open-ended manner whether he or she would like to bring
up anything else

- Infants and young children

o Usually begin with parents present (frightening situation)
o Reasons for referral; irritability, difficulty being consoled, eating disturbances, poor weight gain,
sleep disturbances, developmental delay etc.
o Clinician assess areas of functioning including motor development, activity level, verbal
communication, ability to engage in play, problem-solving skills, adaption to daily routines,
relationships, and social responsiveness
o Observations of play reveal a childs developmental level and reflect the childs emotional state
and preoccupations
§ < 18 m – “peek-a-boo” interaction
§ 18m- 3y – observe in playroom
§ >2 y – symbolic play with toys, revealing more in this mode
§ < 6 y – puppets and dolls, can direct questions to the dolls rather than the child
- School-age children
o Some conversate with ease with adults, others are hampered by fear, anxiety, poor verbal skills,
or oppositional behavior. They can usually tolerate a 45 min session
o Part of interview can be reserved for unstructured play, and various toys can be made available to
capture the childs interest and to elicit themes and feelings.
o Initial part of interview explores the childs understading for the reason for the meeting.
§ Clinician should confirm that its not due to “bad behavior” or that the child is “in trouble”
o Techniques that can facilitate disclosure of feelings include
§ Drawing - asking the child to draw peers, family members, or anything else that comes to
mind. The child can then be questioned about the drawings.
§ Reveal three wishes
§ Describe best and worse of their lives
§ Partiall open-ended questions
 § Indirect commentary – “I once new a child who felt very sad when he moved away from
all his friends”
§ Compare moods/feelings by rating 1-10
- Adolescents
o Usually have distinct ideas about why the evaluation was intiated, ad can usually give
chronological account of recent events leading to the evaluation, although some may disagree
with the need for the evaluation
o Some adolescents approach the interview with apprehension or hostility, but open up when it
becomes evident that the clinician is neither punitive nor judgemenntal
o Every interview should include an exploration of suicidal thoughts, assaultive behavior, psychotic
symptoms, substance use, and knowledge of safe sexual practices along with a sexual history
- Family interview
o Purpose is to observe the attitudes and behavior of the parents toward the patient and the
responses of the children to their parents
o Clinicians job is to maintain a nonthreatening atmosphere in which each member of the family
can speak freely without feeling that the clinician is taking sides with any particular member
- Parents
o Necessary to get a chronological picture of the childs growth and development. A thorough
developmental history and details of any stressors or important events that have influenced the
childs development must be elicited. The parents view of the family dynamics, their marital
history, and their own emotional adjustment are also elicited

Diagnostic instruments
- Aid in collection of information in a systematic way, but cannot replace clinical interviews, because clinical
interviews are superior in the understanding of chronology of symptoms, the interplay of environmental
stressors and emotional responses, and developemental issues.

- Diagnostic interviews
o Either to child or their parents
o Typically designed to elicit sufficient information on various aspects of functioning in order to
determine whether DSM5 criteria are met
o Semistructured interviews – help clarify answers to questions about the symptoms
§ K-SADS (Kiddie schedule for affective disorders and schizophrenia)
§ child and adolescent psychiatric assessment (CAPA)
• covers disruptive behavior disorders, mood disorders, anxiety disorders, eating
disorders, sleep disorders etc.
• focuses on 3 months before interview, called the “primary period”.
o Structured interviews (“respondent-based”) – provide scripts for the interviewer without
interpreatation of the patient responses during the interview process
§ NIMH DISC-IV (national institute of mental health interview schedule for children version
IV)
§ ChIPS (childrens interview for psychiatric syndromes)
§ DICA (diagnostic interview for children and adolescents)
o Other
§ Use of picture as cues along with accompanying questions to elicit information about
symptoms
• E.g. odminic-R and the pcitoral instrument for children and adolescents (PICA-III-
R)
- Questionnaires
o Can cover broad range of symptom areas (e.g. Achenbach child behavior checklist) or they can be
focused on a particular type of symptomatology (e.g. Connors parent rating scale for ADHD)
o Achenbach child behavior checklist
§ Presents items related to mood, frustration tolerance, hyperactivity, oppositional
disorder, anxiety, and various other behaviors
§ The parent version consists of 118 items to be rated 0 (not true), 1 (sometimes true), or 2
(very true).
 § Checklist identifies specific problem areas that might otherwise be overlooked, and may
pointn out areas in which the childs behavior deviates from that of normal children of
the same age group

Components of the childs psychiatric evaluation

- Includes a description of the reason for the referral, the childs past and present functioning, and any test
results

1. Identifying data
- Identified patient and family members
- Source of referral
- Informants

2. History
- Chief complaint
- History of present illness
- Developmental history and milestones
- Psychiatric history
- Medical history, incl immunizations
- Family social history and parents marital status
- Educational histry and current school functioning
- Peer relationship history
- Current family functioning
- Family psychiatric and medical histories
- Current physical examination

3. Mental status examination

- Physical appearance
o Size, grooming, bruising, facial expression etc.
- Parent-child interaction
- Separation and reunion
- Orientation to time, place, and person
o Impairment can reflect organic damage, low intelligence, or a thought disorder
- Speech and language
- Mood
o Sad expression, lack of appropriate smiling, anxiety, euphoria
o Persistent themes in play and fantasy also reflect the childs mood
- Affect
o Should note the childs range of emotional expressivity, appropriateness of affect to thought
content, ability to move smoothly from one affect to another, and sudden labile emotional shifts
- Thought process and content
o Considers loosening of associations, excessive magical thinking, perseveration, echolalia, the
ability to distinguish fantasy from reality, sentence coherence, and the ability to reason logically.
Considers delusons, obsessions, themes, fears, wishes, preoccupations, and interests
o Suicidal ideation
o Aggressive thoughts and homicidal ideation
o Perceptual disturbances
- Social relatedness
o Appropriateness of the childs response to the interviewer, general level of social skills, eye
contact, and degree of familiarity or withdrawal in the interview process
- Motor behavior
- Cognition
o Assess a childs intellectual functioning and problem solving abilities. An approximate level of
intelligence can be estimated by the childs general information, vocabulary, and comprehension
o For a specific assessment of the childs cognitive abilities, the examiner can use a standardized test
- Memory
 o School-age children should be able to remember three objects after 5 min and to repeat five digits
forward and three digits backward
o An obvious inability to repeat digits or to add simple numbers may reflect brain damage, mental
retardation, or learning disabilities
- Judgment and insight
o The childs view of the problems, reactions to them, and suggested solutions may give the clinician
a good idea of the childs judgemennt and insight

4. Neuropsychiatric examination (when applicable)

- Indications:
o Suspected psychiatric disorder that coexist with neuropsychiatric impairment
o Psychiatric symptoms that may be caused by neuropsychiatric dysfunction
o Neurologic disorder
- Combines information from neurological, neuropsychiological testing, and mental status examinations
o Neurological testing – identify asymmetrical abnormal signs (hard signs) that may indicate lesions
in the brain
o Physical examination – presence of particular syndromes (e.g. FAS, Downs)
- …

5. Developmental, psychological, and educational testing

- Psychological testing, structured developmental assessments and achievement testing are valuable I
evaluating a childs developmental level, intellectual functioning, and academic difficulties. A measure of
adaptive functioning (incl the childs competence in communication, daily living skills, socialization, and
motor skills) is the most definitive way to determine the level of intellectual disability in a child
- Developmental tests for infants and preschoolers (down to 2m age)
o E.g. Denver developmental screening test, gesell infant scale etc.
o When used in very young infants, the tests focus on sensorimotor and social responses to a
variety of objects and interactions. When used with older infants and preschoolers, emphasis is
placed on language acquisition
o An infans score is not a reliable way to predict a childs future IQ in most cases, but can be valuble
in detecting developmental deviation and mental retardation and in raising suspicions of a
developmental disorder.
- Intelligence tests for school-age children and adolescents
o Wechsler intelligence scale for children (third edition, WISC-III-R) – most common
§ 6-17y, yields a verbal IQ, performance IQ, and a combined full-scale IQ
§ The verbal subset consist of vocabulary information, arithmetic, similarities,
comprehension, and digits span (supplemental) categories
§ The performance subtests include block design, picture completion, picture
arrangement, object assembly, coding, mazes (supplemental), and symbol search
(supplemental).
§ Each subcategpry is scored from 1-19, with 10 being the average score
§ Average full-scale IQ is 100
• Above 120 is superior or very superior range, 110-119 is high average, 90-109 is
average, 80-90 is low average range, 70-80 borderline intellectual function
§ Because a large part of intelligence testing measures abilities used in academic setting,
the breakdown of the WISC-III-R can also be helpful in pointing out skills in which a child
is weak and may benefit from remedial education.
- Personality tests
o Not much use in making diagnoses, but can be helpful in eliciting themes and fantasies.
o Rorschach test (bilaterally symmetrical ink blots) – hypothesis is that the childs interpretation of
the vague stimui reflects basic characteristics of personality.
- Educational tests
o Wide-range achievemtn test-revised
§ Test yields a score htat is compared with average expected score for the childs
chronological age and grade level
- Biophysical formulation
 o Integrate all of the information obtained into a formulation that takes into account the biological
predisposition, psychodynamic factors, environmental stressors, and life events that have led to
the childs current level of functioning.
o Psychiatric disorders and any specific physical, neuromotor, or developmental abnormalities must
be considered in the formulation of etiologic factors for current impairment. The clinicians
conclusion are an integration of clinical information along with data from standardized
psychological and developmental assessments
o The psychiatric formulation includes an assessment of family function as well as the
appropriateness of the childs educational setting
o A determination of the childs overall safety in his or her current situation is made
o Any suspected maltreatment must be reported to the local child protective service agency
o The child’s overall well-being regarding growth, development, and academic and play activities is
considered

6. Formulation and summary

7. DSM5 diagnosis
8. Recommendations and treatment plan