Psychopathology

Question 1

Erikson’s 8 stages of development

Answer 1

1: trust vs mistrust (infancy to 18 mo)
2: Autonomy vs Shame and doubt (18 mo-3)
3: Initiative vs Guilt (3-5)
4: Industry vs Inferiority (6-11)
5: Identity vs Confusion (12-18)
6: Intimacy vs Isolation (18-40)
7: Generativity vs Stagnation (40-65)
8: Integrity vs Despair (65-)

Question 2

mood disorder in DSM-5-TR

Answer 2

• Depressive disorders
• Bipolar and related disorders

Question 3

Depressive disorders

Answer 3

• Disruptive mood dysregulation disorder (in children up to 12 years old)
• Major depressive disorder
• persistent depressive disorder (parenthical alternative wording ‘dysthymia’ removed in DSM-V-TR)
• premenstrual dysphoric disorder

Question 4

Bipolar and related disorders

Answer 4

• Bipolar I disorder
• Bipolar II disorder
• Cyclothymic disorder

Question 5

Distinguishing clinical depression from sadness

Answer 5

• More pervasive and persistent; mood doesn’t pick up with activities
  usually experienced as pleasant
• Mood change may occur apparently without precipitating events or out
  of proportion to circumstances
• Ability to function is significantly impaired
• Cognitive, somatic & behavioural changes as well as change in mood
• Quality of mood change may be different from normal sadness: feeling
  ‘strange’, ‘engulfed’ or ‘empty’ or ‘emotionally dead’

Question 6

Major Depressive episode diagnostic criteria (DSM-5-TR) 1-5

Answer 6

• requires 5 or more of the following for at least two weeks at least one symptom is 1) or 2)
  1. Depressed mood most of the day, nearly every day.
• Subjective report or observation
• In children and adolescents may be irritable mood
  2. Markedly diminished interest or pleasure all or almost all activities, most of the day nearly every day.
• Subjective report or observation
  3. A significant loss or gain of weight without attempt to diet, or a persistent increase or decrease in
  appetite nearly every day (more than 5% body weight in a month).
  4. Insomnia or hypersomnia nearly every day.
  5. Psychomotor agitation or retardation nearly every day. (Excessive agitation or slowing down of
  movement response, observable by others)

Question 7

Major Depressive Episode
Diagnostic criteria (DSM-5-TR) 6-9

Answer 7

6. Fatigue or loss of energy nearly every day.
7. Feelings of worthlessness or excessive or inappropriate guilt nearly
   every day (not merely self-reproach or guilt about being sick).
8. Reduced ability to concentrate or think clearly, or make decisions,
   nearly every day.
   * Subjective report or observation.
9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal
   ideation without a specific plan, or a suicide plan or attempt.

Question 8

Major Depressive Episode
Diagnostic criteria (DSM-5-TR) B and C

Answer 8

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 physiological effects of a
substance or another medical condition.

Question 9

Major Depressive episode: Differentiate from:

Answer 9

• ordinary sadness
• grief/responses to significant loss
  ▫ Consider preoccupation with worthlessness; intensity experienced in waves;
  possibility of lighter moments; symptoms (e.g., guilt) not directly related to loss
  ▫ Clinical judgment re: major depressive episode in addition to grief response
• Dementia:
  ▫ Consider onset and pre-morbid state, temporal sequencing of depressive &
  cognitive symptoms, course of illness and treatment response
  ▫ Dementia will be discussed further later in the unit
• Prolonged grief disorder differential diagnosis added in DSM-V-TR

Question 10

Major Depressive Disorder Diagnostic Criteria (DSM-5-TR)

Answer 10

• one or more depressive episode(s) (single episode/recurrent)
• clinically significant distress or impairment
• never had a manic or hypomanic episode
• specifiers include:
  = with peripartum onset
  = with seasonal pattern
  = with psychotic features
  = with anxious distress

Question 11

Persistent Depressive Disorder
Diagnostic criteria (DSM-5-TR) A and B

Answer 11

A. Depressed mood most of the day, more days than not, for at least 2
years
▫ In children, only one year, and can be irritable mood
B. Presence, while depressed, of two or more of the following:
▫ Poor appetite or overeating
▫ Insomnia or hypersomnia
▫ Low energy or fatigue
▫ Low self-esteem
▫ Poor concentration or difficulty making decisions
▫ Feelings of hopelessness

Question 12

persistent depressive disorder diagnostic criteria (DSM-5-TR) specifiers include

Answer 12

• with anxious distress
• with melancholic features
• with persistent major depressive episode
• with intermittent major depressive episodes
• mild
• moderate
• severe

Question 13

premenstrual dysphoric disorder diagnostic criteria (DSM-5-TR)
essential features

Answer 13

• mood lability
• irritability
• dysphoria
• anxiety symptoms
• symptoms occur repeatedly during the pre-menstrual phase of the cycle
• symptoms remit around the onset of menses or shortly after
  >significant distress or interference with work, school, relationships etc.

Question 14

classifiction of bipolar disorders in DSM-5-TR Bipolar I

Answer 14

• one or more manic episodes
• depressive episodes common but not required for diagnosis

Question 15

classifiction of bipolar disorders in DSM-5-TR Bipolar II

Answer 15

• at least one hypomanic episode
  ▫ At least one major depressive episode
  ▫ No manic episodes

Question 16

classifiction of bipolar disorders in DSM-5-TR Cyclothymic disorder

Answer 16

▫ Chronic but less severe symptoms
 Persistent symptoms (at least 2 years; 1 year for children/adolescents)
 Numerous periods of hypomanic symptoms not severe enough to meet criteria for hypomanic episode
 Numerous periods of depressive symptoms not severe enough to meet criteria for major depressive
episode

Question 17

Diagnostic Criteria (DSM-5-TR) Manic episode A. B.

Answer 17

A. A distinct period of abnormally and persistently elevated, expansive, or irritable mood and
abnormally and persistently increased goal-directed activity or energy, lasting at least one week, and
present most of the day, nearly every day (or any duration if hospitalisation is necessary)
B. During the period of mood disturbance and increased energy or activity, three or more of the
following symptoms (four if mood is only irritable) are present to a significant degree and represent a
noticeable change from usual behaviour:
▫ Inflated self-esteem or grandiosity
▫ Decreased need for sleep (e.g., feels rested after 3 hours)
▫ More talkative than usual pressure to keep talking
▫ Flight of ideas or subjective experience that thoughts are racing
▫ Distractibility
▫ Increase in goal-directed activity (socially, at work or school, or sexually) or psychomotor agitation
▫ Excessive engagement in activities with high potential for painful consequences (e.g. spending sprees,
foolish business investments)

Question 18

Diagnostic Criteria (DSM-5-TR) Manic episode C. D.

Answer 18

C. The mood disturbance is sufficiently severe to cause marked
impairment in social or occupational functioning or to necessitate
hospitalisation 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 (e.g., a drug of abuse, a medication, other treatment) or to
another medical condition

Question 19

Diagnostic Criteria (DSM-5-TR) hypomanic episode A. B.

Answer 19

A. A distinct period of abnormally and persistently elevated, expansive, or irritable mood and
abnormally and persistently increased goal-directed activity or energy, lasting at least four
consecutive days, and present most of the day, nearly every day.
B. During the period of mood disturbance and increased energy or activity, three or more of the
following symptoms (four if mood is only irritable) have persisted, represent a noticeable change
from usual behaviour, and have been present to a significant degree:
▫ Inflated self-esteem or grandiosity
▫ Decreased need for sleep (e.g., feels rested after 3 hours)
▫ More talkative than usual pressure to keep talking
▫ Flight of ideas or subjective experience that thoughts are racing
▫ Distractibility
▫ Increase in goal-directed activity (socially, at work or school, or sexually) or psychomotor agitation
▫ Excessive engagement in activities with high potential for painful consequences (e.g. spending sprees,
foolish business investments)

Question 20

Diagnostic Criteria (DSM-5-TR) hypomanic episode C. D. E. F.

Answer 20

C. The episode is associated with an unequivocal change in functioning
that is uncharacteristic of the individual when not symptomatic.
D. The disturbance in mood and the change in functioning are observable
by others.
E. The episode is not severe enough to cause marked impairment in social
or occupational functioning or to necessitate hospitalisation. (If there are
psychotic features, the episode is, by definition, manic.)
F. The episode is not attributable to the physiological effects of a
substance

Question 21

Diagnostic Criteria (DSM-5-TR) Cyclothymic disorder A. B. C.

Answer 21

A. For at least two years (at least one year in children and adolescents) there have been numerous
periods with hypomanic symptoms that do not meet criteria for a hypomanic episode and
numerous periods with depressive symptoms that do not meet criteria for a depressive episode.
B. During the above two-year period (one year in children and adolescents), the hypomanic and
depressive periods have been present for at least half the time and the individual has not been
without the symptoms for more than two months at a time.
C. Criteria for a major depressive, manic, or hypomanic episode have never been met.

Question 22

Diagnostic Criteria (DSM-5-TR) Cyclothymic disorder D. E. F.

Answer 22

D. The symptoms in Criterion A are not better explained by schizoaffective disorder, schizophrenia,
schizophreniform disorder, delusional disorder, or other specified or unspecified schizophrenia
spectrum and other psychotic disorder.
E. Symptoms not attributable to physiological substance or other medical condition.
F. Symptoms cause clinically significant distress or impairment in social, occupational, or other
important areas of functioning.

Question 23

Bipolar disorder Course and outcome

Answer 23

▫ Often begins with a depressive episode
▫ Onset 15-24 years
▫ Prognosis mixed (40-50% have sustained recovery)
▫ Remission: two months with minimal or no symptoms

Question 24

Depressive disorder course and outcome

Answer 24

▫ Data based on samples in treatment
▫ Most recover from initial episode
▫ Variation in long-term course
 From rarely in remission
 To years of remission between episodes/ single episode
▫ Average episodes over lifetime: 5 or 6

Question 25

general social determinants of depressive disorder

Answer 25

• Depressive disorder rates higher for those:
  ▫ Not being married or in a defacto relationship
  ▫ With lower level of education
  ▫ Not being in the labour force
• Serious stressful life events such as loss

Question 26

mood disorder statistics

Answer 26

• About 1.5 million (7.5%) Australians aged 16-85 reported having an affective
  disorder (e.g., depressive episode) in the previous 12 months
• Bipolar Disorder around 2%
• Gender differences
  ▫ Research consistently shows higher rate of depressive episode in women, Australia
  (5.7%) than in men (4.1%)
  ▫ Minor gender differences for bipolar disorder
• Age differences in affective disorders
  ▫ 10.4% of males and 16.7% of females aged 16-24 years
  ▫ There is a trend for the prevalence of affective disorders to decrease as people age
  https://www.abs.gov.au/statistics/health/mental-health/national-study-mental-h
  ealth-and-wellbeing/latest-release

Question 27

social determinants adolescents 14-17 the mental health of children and adolescents

Answer 27

• Depressive Disorder
  ▫ Household income threshold, prevalence of major depressive disorder
  highest (3.8%) in families in the lowest household income bracket
  ▫ Higher in families with a sole parent or carer not in employment (6.9%)
  compared with families with two parents or carers both in employment
  (1.8%)
  ▫ Higher in step families (4.7%), and families with one parent or carer (5.5%)
  ▫ Poor family functioning (11.6%)
  ▫ Area of residence and parent education were not significant

Question 28

etiology: social factors and severe stress, Brown and Harris’ studies of women

Answer 28

• Depression usually triggered by highly stressful life event(s) (rated as ‘severe’
  event)
  ▫ Why did some women suffer depression after severe event and others did not?
• Some women more vulnerable to developing depression: Vulnerability factors:
  ▫ Loss of parent in childhood
  ▫ 3 or more children under 14 living at home
  ▫ Absence of intimate and supportive relationship with partner
• Some severe events more likely to trigger depression, i.e. when event involved:
  ▫ Humiliation
  ▫ Entrapment

Question 29

Theoretical Perspectives: cause of depressive disorders Behavioural

Answer 29

• Behavioural
  ▫ Lewinsohn’s theory: Loss of positive reinforcements, extinction, interpersonal
  relationships reinforcing depressed behaviour

Question 30

Theoretical Perspectives: cause of depressive disorders Cognitive

Answer 30

• Cognitive
  ▫ Beck: Depressed mood is the product of negative thinking (not vice versa):
   distortion and errors in thinking,
   selective recall of events with negative consequences,
   depressive schemas (revolving around inadequacy, failure, loss, worthlessness)
  guide the person’s perceptions and interpretations
  ▫ Seligman: Learned helplessness
• Beck’s negative cognitive triad

Question 31

Schemas

Answer 31

cognitive frame work which people perceive their life through

Question 32

Theoretical Perspectives: cause of depressive disorders Psychodynamic

Answer 32

• Psychodynamic
  ▫ Freud: Anger turned inward, triggered by loss
  ▫ Early loss experiences may sensitise person to later loss
  ▫ Harsh expectations internalised early in life leading to self-criticism and
  sense of failure
  ▫ Bibring: Put more emphasis on low self-esteem and helplessness
  ▫ Blatt: 2 forms of depression:
   One precipitated by perceived failure
   One precipitated by loss

Question 33

Theoretical Perspectives: cause of depressive disorders Biological

Answer 33

• Biological
  ▫ Genetic factors
   In major depressive disorder: influence person’s sensitivity to environmental
  stress
   Greater role in bipolar disorder
  ▫ Neurotransmitters
   Role likely to be complex and interactive
   Anti-depressant medications impact on serotonin, norepinephrine, dopamine
  ▫ Neuroendocrine system
   Hormones regulate response to stress

Question 34

Treatment: Depressive Disorder

Answer 34

• Psychotherapy
  ▫ Psychodynamic
  ▫ Cognitive-behavioural
  ▫ Interpersonal
• Medication
  ▫ SSRIs
  ▫ Tricyclics
  ▫ MAO inhibitors
• Psychotherapy and medication combined

Question 35

Treatment: Bipolar disorders

Answer 35

• Medication: Mood stabilisers
• Assistance to maintain steady biological rhythms
  ▫ Sleep-wake cycle
• Evidence based psychological therapies combined with medication
• Seasonal mood disorders: Light therapy

Question 36

The Nature of Anxiety

Answer 36

Physiological aspects
* Psychological aspects
* Often related to situations of uncertainty
* Anxiety may be adaptive and is normal; serves an alerting function;
arousal aspect can be energising
* Too much anxiety can disrupt thinking and performance

Question 37

When does anxiety become an anxiety disorder?

Answer 37

• Consider
• Severity/intensity of anxiety
• Duration of anxiety
• Pervasiveness of anxiety
• Extent to which anxiety can be managed or controlled by the person
• Extent to which anxiety is out of proportion to the situation
• Extent to which anxiety leads to a state of self-preoccupation or a
  primary focus on the anxiety itself

Question 38

List of Anxiety Disorders in DSM

Answer 38

• Separation Anxiety Disorder
• Selective Mutism
• Specific Phobia
• Social Anxiety Disorder (Parenthetical alternative name ‘Social phobia’ removed in DSM-V-
  TR)
• Panic Disorder
• Agoraphobia
• Generalised Anxiety Disorder
• Substance/Medication-induced Anxiety Disorder
• Anxiety Disorder Due to Another Medical Condition
• Other Specified Anxiety Disorder
• Unspecified Anxiety Disorder

Question 39

Changes from DSM-IV-TR to DSM-V

Answer 39

• Formerly listed under Anxiety Disorders (in DSM-IV-TR)
  ▫ Obsessive-Compulsive Disorder
  ▫ Post-traumatic Stress disorder
• These diagnoses now listed under categories of:
  ▫ Obsessive-Compulsive and Related Disorders
  ▫ Trauma- and Stressor-Related Disorders
• Linked diagnosis of ‘Panic Disorder with Agoraphobia’ now removed
• Now listed as separate disorders
  ▫ Agoraphobia
  ▫ Panic disorder

Question 40

Generalised Anxiety Disorder (GAD)

Answer 40

• Excessive anxiety and worry
  ▫ more days than not for 6 months
  ▫ about a number of events/issues (such as work or school performance)
• Difficulty controlling the worry
• Accompanied by three of:
  ▫ restlessness or feeling on the edge,
  ▫ easily tired,
  ▫ difficult to concentrate,
  ▫ irritability,
  ▫ muscle tension,
  ▫ sleep disturbance
• Clinically significant distress or impairment in occupational or social functioning

Question 41

Panic Attack
(not in itself a disorder)

Answer 41

• Abrupt surge of intense fear or discomfort reaching a peak within
  minutes with 4 or more of the list of symptoms (next slide)
• Can occur with a range of disorders

Question 42

Panic Attack - 4 or more of the following symptoms:

Answer 42

▫ Heart palpitations or accelerated heart rate
▫ Sweating
▫ Trembling or shaking
▫ Shortness of breath
▫ Feeling of choking
▫ Chest pain or discomfort
▫ Nausea or abdominal pain
▫ Feeling dizzy, lightheaded or faint
▫ Chills or heat sensations
▫ Numbness or tingling
▫ Derealisation or depersonalization
▫ Fear of losing control, going crazy
▫ Fear of dying

Question 43

Panic Disorder

Answer 43

• Recurrent unexpected panic attacks (as defined in previous slides)
• Followed by 1 month of concern about
  ▫ having more attacks
  ▫ implications of the attack
  ▫ significant change in behaviour related to the attacks
• Not attributable to physiological effects of a substance or another
  medical condition
• Not better explained by another mental disorder

Question 44

Agoraphobia

Answer 44

• Marked fear or anxiety about two of:
  ▫ Using public transport
  ▫ Being in open spaces
  ▫ Being in enclosed spaces
  ▫ Standing in line or being in a crowd
  ▫ Being outside of the home alone
• Fear or avoidance because escape is difficult or help not available if panic or other
  embarrassing symptoms
• Agoraphobic situations
  ▫ Almost always provoke fear/anxiety
  ▫ Are actively avoided or endured with great distress
• Typically lasting for 6 months or more

Question 45

Specific Phobia

Answer 45

• Intense fear or anxiety
• Cued (consistently) by specific object or situation
• Leading to an avoidance of the particular stimulus
• Fear/anxiety/avoidance out of proportion to actual danger & to
  sociocultural context
• Persistent, typically lasting 6 months
• Clinically significant distress or impairment

Question 46

Social anxiety disorder (social phobia)

Answer 46

• Marked & consistent fear or anxiety about 1 or more social situations in
  which person is exposed to possible scrutiny by others
• Fear that actions or anxiety symptoms will be negatively evaluated
  (person will feel humiliated or embarrassed)
• The social situations are avoided or endured with marked distress
• Anxiety is out of proportion to actual threat
• Persistent, typically lasting for 6 months or more

Question 47

Etiological Perspectives (Anxiety)

Answer 47

• Evolutionary perspective:
  ▫ Anxiety and fear adaptive in many situations
  ▫ Mobilise responses that help person survive danger (fight or flight)
  ▫ Are anxiety symptoms a product of dysregulation in these response
  systems?

Question 48

A core idea: anxiety related to danger situations

Answer 48

• Evolutionary perspective notes role of anxiety and fear in mobilising
  response to external danger
• Freud thought anxiety was a signal of an internal danger situation
  (signals the likelihood of psychological pain related to inner conflicts,
  impulses getting out of control or impending losses)
• Anxiety more related to danger (lack of security or lack of control) while
  depression more related to loss (lack of hope) – there is some research
  to support this

Question 49

Psychodynamic and attachment perspectives

Answer 49

• Focus on role of early childhood experience in development of
  (vulnerability to) anxiety disorders
• Psychodynamic: Anxiety precipitated by intrapsychic conflicts &
  anticipated danger that someone or something important will be lost
• Attachment: Insecure attachment patterns leave person vulnerable to
  anxiety (that attachment figure will be unavailable when needed)
• Research suggests that:
  ▫ stressful life events and
  ▫ childhood adversity
• Contribute to the development of anxiety disorders

Question 50

Behavioural perspectives

Answer 50

Symptoms based on prior learning
* Inappropriate classical conditioning or modeling/observational learning
* People with specific phobias often report learning them from
experience
* Predisposition or preparedness in humans for some fears (e.g., heights,
snakes, storms)
* Learning fear responses through imitation of others

Question 51

Cognitive perspectives

Answer 51

• Anxiety stems from maladaptive thought patterns and beliefs associated with
  ▫ vigilant attention to threatening cues and possible dangers
  ▫ misinterpretations of actions
  ▫ misinterpretation of body sensations (eg in panic disorder)
• Perception of control over events → less anxiety
  ▫ Sense of uncontrollability → more anxiety
• Cycle where fearful expectations → anxious/preoccupied self-evaluation →
  more arousal & attention to perceived threat → impaired performance &/or
  avoidance
• Attempts to suppress a thought (or associated emotion) may make the thought
  more intrusive (relevant to OCD?)

Question 52

Biological Perspectives

Answer 52

• Some evidence of genetic risk factors but not highly specific (not a
  different set of genes for each disorder) nor completely non-specific
  ▫ Heredity plays a role but comparatively modest
  ▫ GAD, panic & agoraphobia vs specific phobia?
• Investigation of neuro-anatomical pathways (especially limbic system)
  associated with emotional responses eg fear & panic
• OCD seems to involve different areas of the brain
• Neurochemistry:
  ▫ Role of neurotransmitters eg serotonin seems to dampen stress responses

Question 53

Obsessive-Compulsive and Related Disorders
DSM-5-TR

Answer 53

• Obsessive-Compulsive Disorder (was in Anxiety Disorders in DSM-IV)
• Body Dysmorphic Disorder (was in Somatoform Disorders in DSM-IV)
• Hoarding Disorder (new disorder added in DSM-V - no longer a subtype
  of OCD)
• Trichotillomania (Hair-Pulling Disorder)
  ▫ (Was in Impulse Control Disorders in DSM-IV)
• Excoriation Disorder (Skin-Picking disorder) (new in DSM-5)
• A new chapter in DSM-V
  ▫ Disorders related to OCD through obsessions or compulsions

Question 54

Obsessive-Compulsive and Related Disorders

Answer 54

• Characterised by:
  ▫ Intrusive/repetitive internal experiences (these may be thoughts, images
  or urges)
  ▫ Distress related to the intrusive experiences
  ▫ Compulsive behaviours.
• Often the belief about the meaning of the internal experience and the
  context in which it occurs are important to the person’s distress and
  compulsions.

Question 55

Obsession

Answer 55

• Recurrent and persistent ideas, thoughts, urges or images that are
  experienced as intrusive and unwanted
• Usually cause anxiety or distress
• The individual attempts to ignore or suppress the thoughts, urges or
  images, or to neutralise them with another thought or action
  (performing compulsion)

Question 56

Compulsion

Answer 56

• Repetitive behaviors or mental acts performed in response to
  obsessions or according to rules that must be applied rigidly.
• Aimed at reducing or preventing anxiety or distress, or preventing a
  dreaded event or situation. Not connected in a realistic way with what
  they are designed to neutralize or prevent, or are clearly excessive
   High anxiety ensues if prevented from completing the action

Question 57

Obsessive-Compulsive Disorder DSM-5-TR

Answer 57

• Presence of obsessions or compulsions (often both)
• Symptoms are time-consuming (e.g., more than 1 hour a day), cause marked
  distress and/or impairment in social, occupational or other important functioning
• Not due to a substance, or medical condition
• Nor better explained by another mental disorder
  ▫ Specify if
   Good or fair insight
   Poor insight
   Absent insight/delusional beliefs
  ▫ Specify if tic-related

Question 58

OCD

Answer 58

• Common types of obsessions and compulsions:
  ▫ Symmetry/exactness
  ▫ Forbidden thought aggressive/sexual/religious
  ▫ Cleaning/contamination
• Mean age of onset (US data) 19.5 years
  ▫ 25% by 14 years; onset after 35 years is unusual
• Onset is typically gradual
• Chronic without treatment
  ▫ reduces quality of life
• Common comorbidities:
  ▫ Anxiety, depressive disorder, tic disorder

Question 59

OCD Components

Answer 59

• Not-Just-Right (NJR) (Coles et al. 2003)
• The sense that an error is occurring (“it’s not juuuust right”)
• Common with order and symmetry but not restricted to this
• Difficult to describe (error-detection process may be outside awareness)
• Thought-Action Fusion (TAF) (Thompson-Hollands et al. 2014)
• Moral TAF – having the thought is morally equivalent (or almost!) to the act that the thought represents e.g. an intrusive
  thought about sex with a child is morally equivalent to having sex with a child.
• Likelihood TAF – having the thought increases the likelihood of the thought actually happening.

Question 60

Neurobiology/anatomy of OCD

Answer 60

• Early observation of obsessions/
  compulsions after encephalitis
  lethargica
  ▫ basal ganglia lesions
• Dysregulation of serotonin implicated
  in formation of obsess/comp
• Increased frontal and subcortical
  activity
  ▫ Orbitofrontal Cortex, Anterior Cingulate
  Cortex, Thalamus and Caudate
  “brain lock” Schwartz et al especially
  in right hemisphere
  “a prefrontal cortico-striato-thalamic brain
  system”

Question 61

Cognition in OCD

Answer 61

• Not-Just-Right (NJR) (Coles et al. 2003)
• The sense that an error is occurring (“it’s not juuuust right”)
• Common with order and symmetry but not restricted to this
• Difficult to describe (error-detection process may be outside awareness)
• Thought-Action Fusion (TAF) (Thompson-Hollands et al. 2014)
• Moral TAF – having the thought is morally equivalent (or almost!) to the act that the thought represents e.g. an intrusive
  thought about sex with a child is morally equivalent to having sex with a child.
• Likelihood TAF – having the thought increases the likelihood of the thought actually happening.

Question 62

Neurobiology/anatomy of OCD

Answer 62

• Early observation of obsessions/
  compulsions after encephalitis
  lethargica
  ▫ basal ganglia lesions
• Dysregulation of serotonin implicated
  in formation of obsess/comp
• Increased frontal and subcortical
  activity
  ▫ Orbitofrontal Cortex, Anterior Cingulate
  Cortex, Thalamus and Caudate
  “brain lock” Schwartz et al especially
  in right hemisphere
  “a prefrontal cortico-striato-thalamic brain
  system”

Question 63

Cognition in OCD

Answer 63

• Deficits generally related to fronto-striatal dysfunction
• Deficits seen in tasks mediated by frontal lobes  executive dysfunction
  ▫ Set shifting; idea generation; inhibition difficulties
• Little evidence of basic attentional deficits
  ▫ “Deficits” on attention tasks driven by slow speed of processing
• Visuospatial dysfunction including reduced visual-spatial memory
• Verbal working memory and declarative memory unimpaired
  ▫ Memory performance reduced on tasks requiring higher level organisation/ strategies to
  encode information
   executive aspects of memory

Question 64

OCD Components

Answer 64

• Personal Implications (Tolin et al., 2003)
• Beliefs about safety (“Things/I must be dangerous…”)
• Beliefs about morality/character (“What kind of a person….”)
• Beliefs about perfection/errors (“I must do things a certain way…”)
• External Implications (Tolin et al., 2003)
• Beliefs about the safety of others (“If I don’t act, someone will get hurt…”)
• Beliefs about responsibility (“I am responsible for others…”

Question 65

Body Dysmorphic
Disorder

Answer 65

• Preoccupation with perceived
  defects.
• Repetitive behaviours in response to
  concerns.
• Distress and impairment.

Question 66

Trichotillomania

Answer 66

• Recurrent, automatic or irresistible hair pulling.

Question 67

Excoriation Disorder

Answer 67

• Recurrent, automatic or irresistible skin-picking.

Question 68

Schizophrenia Spectrum and Other Psychotic Disorders in DSM-
5-TR

Answer 68

• Schizotypal (personality) disorder
• Delusional disorder
• Brief psychotic disorder
• Schizophreniform disorder
• Schizophrenia
• Schizoaffective disorder
• Substance/medication-induced psychotic disorder
• Psychotic disorder due to another medical condition
• Catatonic features/disorders
• Other (specified/unspecified)

Question 69

Key Features of Psychotic Disorders

Answer 69

• Positive Symptoms:
  ▫ Delusions
  ▫ Hallucinations
  ▫ Disorganised thinking
  ▫ Grossly disorganised/abnormal motor behaviour (including catatonia)
• Negative symptoms
• Note that a diagnosis of a psychotic disorder requires a pattern of
  symptoms, not just one symptom

Question 70

Concept of Positive and Negative Symptoms

Answer 70

• It is usual today to think about two sets of psychotic symptoms, positive
  and negative.
• Positive symptoms are active manifestations of abnormal experience.
  These include hallucinations, delusions and thought disorder.
• Negative symptoms, on the other hand, are deficits in normal
  behavior/experience, such as less emotional expression, less speech,
  less interest or motivation.
  ▫ Often significant in schizophrenia but less prominent in other psychotic
  disorders

Question 71

Delusions (***)

Answer 71

• False beliefs which are held in a very fixed way, not amenable to
  argument
• Typically personal - not shared by other members of the person’s family
  or cultural group; often the person is quite preoccupied with these
  beliefs
• Note that delusions involve a disorder of beliefs

Question 72

Types of Delusions

Answer 72

• Paranoid/persecutory - unrealistic belief that someone is plotting against you, trying to harm
  you; evidence for the belief is very personalised or idiosyncratic
• Grandiose - belief that one has special powers, special significance or has been given a
  special mission
• Somatic - clearly unrealistic, often bizarre belief about one’s body (not just a
  hypochondriacal concern)
• Delusions of reference – belief that events, communications etc are referring to you
• Delusions of control - belief that one is controlled by mysterious, external forces
• Thought insertion – belief that someone is putting thoughts into one’s head
• Thought withdrawal – belief that thoughts have been removed by an outside force
• Thought broadcasting – belief that others can hear one’s thoughts
• (bizarre vs non bizarre)

Question 73

Hallucinations

Answer 73

• The person sees, hears, feels, smells or tastes something which is not actually there:
  ▫ Visual
  ▫ Auditory
  ▫ Tactile
  ▫ Olfactory
  ▫ Taste
• Note that hallucinations involve a disorder of perception
• Auditory hallucinations are particularly common in psychosis, and often take the
  form of voices
• Person is generally unaware that the hallucinations are not real

Question 74

Disorganised Thinking

Answer 74

• This is generally inferred from the person’s speech
• Derailment /Idiosyncratic associations: The way one idea or thought
  follows another is unusual and idiosyncratic
• Tangential speech: Answers to questions only obliquely related to
  question
• Incoherent speech
• Must be severe enough to substantially impair effective communication
  and ability to concentrate

Question 75

Disorganised Motor Behaviour and/or Catatonia

Answer 75

• Grossly disorganised or abnormal behaviour
  ▫ Unpredictable agitation
  ▫ Childlike ‘silliness’
  ▫ Difficulties with goal-directed behaviour & ADL
• Catatonia
  ▫ Unusual immobility or rigidity, posturing
  ▫ Mutism
  ▫ Excitement/ apparently purposeless overactivity
  ▫ Stereotyped movements
  ▫ Echoing/mimicking of speech (echolalia) or movement (echopraxia)
  ▫ DSM-5 argues catatonia is under-recognised & introduces use of a catatonia specifier
  across a wider range of disorders

Question 76

Negative Symptoms

Answer 76

• Diminished emotional expression (blunted affect or affective flattening)
  – reduced expression of emotion
  ▫ Facial; tone of voice; eye contact; gesture
• Avolition - difficulty getting motivated or initiating activities
• Alogia (poverty of ideas) – diminished speech output
• Anhedonia – decreased capacity to experience pleasure
• Social withdrawal

Question 77

DSM-5-TR Diagnostic Criteria for Schizophrenia

Answer 77

A. Two or more of the following, each present for a significant portion of time during
a one-month period (or less if successfully treated). At least 1 of these must be (1),
(2) or (3):
1. Delusions
2. Hallucinations
3. Disorganised speech (e.g., frequent derailment or incoherence)
4. Grossly disorganised or catatonic behavior
5. Negative symptoms (diminished emotional expression or avolition)
B. Significant impairment in social/occupational functioning or self-care
C. Continuous signs persist for at least six months
(D & E: differentiate from other disorders and effects of a substance)

Question 78

Phases of an Episode of Schizophrenia (***)

Answer 78

1. Prodromal (onset stage, early signs, some changes in feelings, thoughts, perceptions)
   * Attenuated psychotic symptoms
   * 85% go through 1-2 year prodromal phase
2. Active or acute (clear psychotic symptoms)
3. Residual (acute symptoms have resolved but still attenuated signs of disorder or
   negative symptoms remain)
   * Depression is common in residual stage
4. Remission or recovery (50% of people will reach this stage)

Question 79

Delusional Disorder

Answer 79

• Presence of delusion(s) persisting for at least 1 month
• Never met Criterion A for schizophrenia
• Apart from impact of delusions, functioning not markedly impaired and
  not obviously bizarre or odd
• Mood episodes have been brief or absent compared with duration of
  delusions
• Not due to physiological effects of a substance (e.g., cocaine) or a
  general medical condition (e.g., Alzheimer’s disease) and not better
  explained by another mental disorder

Question 80

Delusional Disorder- Types (Specifiers)

Answer 80

• Based on central theme of delusion
  ▫ Erotomanic: That another person is in love with you
  ▫ Grandiose: Having great (but unrecognised) worth, powers, knowledge etc
  ▫ Jealous: That the person’s spouse /sexual partner is unfaithful
  ▫ Persecutory: That someone is conspiring against or being malevolent
  towards you or a loved one
  ▫ Somatic: Delusion of a physical defect or disease
  ▫ Mixed: Characterised by more than one delusion
  ▫ Unspecified
• Specify if ‘with bizarre content’

Question 81

Brief Psychotic Disorder

Answer 81

• Psychotic symptoms last for at least one day but less than one month
• Eventual return to premorbid level of functioning
• Replaced an earlier diagnostic category of Brief Reactive Psychosis
  which referred to psychotic symptoms which were a reaction to
  significant stress.
• Specify:
  ▫ With or without marked stressor(s) (brief reactive psychosis)
  ▫ Without marked stressor(s)
  ▫ With peripartum onset
  ▫ With catatonia

Question 82

Schizophreniform Disorder

Answer 82

• Symptoms as for schizophrenia but different duration
  ▫ The episode lasts at least 1 month but less than 6 months
• The term ‘first-episode psychosis’ may be used early in illness states to
  avoid ‘labelling’ young adults with schizophrenia.

Question 83

Schizoaffective Disorder

Answer 83

• Mixture of mood and psychotic symptoms
  ▫ Period during which there is a major mood episode concurrent with
  Criterion A of schizophrenia
• Psychotic symptoms do not only occur in the context of a mood episode

Question 84

Substance/Medication-Induced Psychotic Disorder

Answer 84

• Presence of (prominent) hallucinations and/or delusions
  ▫ Developed during, or soon after, substance intoxication or withdrawal
  ▫ The substance/medication is capable of producing the symptoms
• Not better explained by a psychotic disorder that is not
  substance/medication-induced
  ▫ e.g., Substance/medication-induced disorder will normally resolve within a
  month after intoxication or withdrawal
• Distinguish from:
  ▫ Substance withdrawal ‘with perceptual disturbances’

Question 85

Mood Disorders with Psychotic Features
(listed under Mood disorders in DSM-5-TR)

Answer 85

• Bipolar disorder, with psychotic features
• Major depressive disorder, with psychotic features
• Psychotic symptoms (hallucinations and/or delusions) only occur in the
  context of a mood episode
  ▫ (i.e., during manic or depressive states)

Question 86

Epidemiology
Schizophrenia and Related Psychotic Disorders

Answer 86

• Lifetime prevalence: approx 0.8 to 1%
• Onset is typically (but not only) between 15-28
• Recent evidence suggests men may be more likely than women to
  develop schizophrenia (contrary to long-held view of equal prevalence)
• Occurs in cultures/countries across the world

Question 87

Gender Differences

Answer 87

• Males more likely to have:
  ▫ Earlier onset
  ▫ Poor premorbid social functioning
  ▫ Pattern of negative symptoms
  ▫ Chronic course
  ▫ Note ‘more likely’ does not mean always

Question 88

Schizophrenia: Course and Recovery

Answer 88

• Long term follow-up studies suggest:
  ▫ Approx 50% acute onset (vs gradual onset)
  ▫ Approx 50% undulating course - exacerbations and remissions (vs stable or
  simple course)
• Long-term outcome is variable, ranging from recovered or mild
  impairment through moderate to severe impairment
• Problematic issue:
  ▫ How to measure/assess outcome
  ▫ Aspects of outcome (e.g. symptoms, social function, work) not highly
  correlated

Question 89

Course and Recovery (continued)

Answer 89

• More favourable outcome associated with:
  ▫ Acute onset
  ▫ Shorter duration of untreated psychosis
  ▫ Undulating course
  ▫ Fewer relapses
  ▫ Female gender
   For long-term outcome
   No clear difference for recovery from first episode
  ▫ In developing countries (vs developed)

Question 90

Treatment – Antipsychotic Medication

Answer 90

• 1st generation antipsychotics (e.g., Chlorpromazine/Largactil)
  ▫ In approximately 25% of sufferers, symptoms not improved
   Term ‘treatment-resistant’ refers to condition not person
  ▫ Side effects:
   Extrapyramidal symptoms (muscular rigidity, restlessness)
   Tardive dyskinesia after long-term use
• 2nd generation/Atypical antipsychotics (e.g., Clozapine)
  ▫ Symptom relief for many who found earlier antipsychotics ineffective
  ▫ Fewer motor side effects
  ▫ But other side effects (e.g., weight gain and medical risks)

Question 91

Treatment (continued) Schizo

Answer 91

• Maintenance medication reduces relapse rates
  ▫ How long to maintain for?
• Anti-psychotic medications tend to subdue positive symptoms, but have
  less impact on negative symptoms. Negative symptoms seem to
  respond better to intensive psychosocial treatment
• Hospitalisation – quite common in acute episode

Question 92

Treatment - Psychosocial interventions (Schizo)

Answer 92

• Psychoeducation
  ▫ Including medication compliance
• Psychosocial rehabilitation
  ▫ Social skills and assisted living
• Case management services
• Housing/occupational assistance
• Cognitive behavioural therapy for voices and information processing
• Supportive therapy
• Treatment of comorbid or “dual diagnosis”
• Family interventions

Question 93

Treatment - Issues (Schizo)

Answer 93

• Importance of early intervention
• Prodromal phase may be 1-2 years
• Delay between onset and treatment may be 1-2 years
• Most improve when treated
• Most ~ 75% will experience relapse and recovery
• High risk of suicide
• Non compliance with medication
• Consent to treatment
• Psychological therapy only when stable

Question 94

Schizophrenia and the brain

Answer 94

• Although results vary, most studies have found that the brains of
  people with schizophrenia weigh less than the brains of others
• Enlarged ventricles
• Lower volume of grey matter
• Reduction in the number of neurons in the PFC
• Thinner cortex in the medial temporal regions
• Abnormalities in the organization of neurons in the hippocampus

Question 95

Schizophrenia:
a neurodevelopmental disorder

Answer 95

• Subtle physical abnormalities indicative of early (foetal) developmental
  disturbance
  Schizophrenia more likely in those with adverse pre- or perinatal events
• Pregnancy complications
• Foetal growth retardation; low birth weight
• Delivery complications/interventions
• Correlation b/w Scz and serologically confirmed maternal infections like flu
• Prenatal hypoxic-ischaemic damage
• Neuronal loss in temporal lobes/hippocampus
• Synaptic pruning in adolescence may reduce connections in already affected areas
• Interaction of environmental and genetic factors

Question 96

Genetics of schizophrenia

Answer 96

• Sekar et al., (2016)
• Complement component 4 (c4) gene
• Increased c4 activity associated
  with greater pruning of
  synapses postnatally
• Mediated by an immune
  response?
• Pruning associated with grey
  matter loss during adolescence
• coinciding with onset?
• Greater grey matter loss seen
  in young people with
  schizophrenia 

Question 97

Brain morphology in schizophrenia

Answer 97

• No one “schizophrenic” lesion in the brain
• Slight decrease in overall grey matter and
  white matter volume
• Ventricular enlargement
• Reduced hippocampal volume
• Malformations of midline structures
• Cavum septum pellucidum 
• Abnormalities of cingulate gyrus
• Abnormalities evident in 1st episode
  patients
   Suggest a neurodevelopmental basis to
  illness

Question 98

Relationship between Brain
structure & symptoms in
schizophrenia

Answer 98

• Severity of auditory hallucinations
  associated with degree of grey
  matter loss in auditory cortex &
  PFC (Gaser et al., 2004).
• Functional abnormalities present
  in at risk adolescents who later
  develop Sz (Whalley et al., 2006)
• Reduced activation of frontal
  regions both at rest and during
  cognitive tasks during fMRI (Hill
  et al., 2004)
• Reduced blood flow in the
  anterior cingulate during
  attentional tasks seen on PET
  (Yucel et al., 2002)

Question 99

Cognitive effects of schizophrenia 1

Answer 99

• Present at onset of illness
• Appear unrelated to positive symptoms
• Do not appear to change substantially over
  time
• State dependent?
• Decline over time?
• Static/neurodevelopmental?
• Not just related to medication
• Atypical antipsychotics may be neuroprotective
• Attention, EF and memory dysfunction
  common
• Greatest impact on ADLs

Question 100

Cognitive effects of schizophrenia 2

Answer 100

• The prodromal period (Brewer et al., 2005)
• Ultra high risk study of 98 young people  38 later developed psychosis; cf. 34 controls
• Overall lack of impairment in UHR group  general cognitive impairment not part of
  prodrome
• BUT lower non-verbal IQ abilities and impaired verbal memory
• Frontally mediated memory processes affected before onset of psychosis
• First episode psychosis
• Associated with acute functional deterioration in cognitive functioning
• Magnitude of impairment similar to that seen in chronic illness
• Association between negative symptoms and cognitive deficits at first episode

Question 101

Cognitive effects of schizophrenia 3

Answer 101

• Chronic schizophrenia
• Generally believed that cognition does not appear to decline significantly over time
• Cognitive effects of neuroleptic/ antipsychotic drugs make such judgments difficult
• Polydrug Tx  greater cog impairment, but ?? causative
• Sponheim et al., (2010)
• 41 recent onset vs 106 chronic patients
• Most cognitive abilities comparable over time
• Some timed problem solving and fine motor tasks appear to decline
• Chan et al., (2014)
• 26 patients with chronic severe Sz vs 34 patients with behavioural variant
  frontotemporal dementia
• Performance on 6 cognitive domains compared
• > 85% overlap between groups in most cognitive domains

Question 102

What is Personality and Personality Disorder?

Answer 102

• PERSONALITY: ‘enduring patterns of thinking and behaviour that define
  the person and distinguish him or her from other people’ including
  ‘ways of expressing emotion’ and ‘patterns of thinking about ourselves
  and other people’ (Oltmanns & Emery, 2012, p.219)
• When enduring personality patterns interfere with the person’s ability
  to get on with others and to carry out social roles including work roles –
  these patterns can be viewed as a form of psychological dysfunction ie
  as a mental health problem

Question 103

General Personality Disorder defined in DSM-5-TR

Answer 103

• Enduring pattern of inner experience and behaviour that deviates markedly from
  expectations of the individual’s culture. Pattern is manifested in 2 or more of:
  ▫ Cognition (ways of perceiving or interpreting)
  ▫ Affectivity (emotional responses)
  ▫ Interpersonal functioning
  ▫ Impulse control
• Inflexible and pervasive over many situations
• Clinically significant distress or impairment in functioning
• Stable over time and of long duration, with onset in adolescence or early adulthood
• Not better accounted for by another disorder, effects of a substance or a general
  medical condition

Question 104

DSM-5-TR (Personality)

Answer 104

• The DSM has typically had a categorical approach to personality
  disorders
  ▫ What are some limitations of this?
• However, an alternative dimensional model was proposed in the DSM-5
  (in Section III), involving:
  ▫ Level of personality functioning
  ▫ Pathological personality traits
  ▫ Pervasiveness and stability
  ▫ Alternative explanations for personality pathology

Question 105

Alternative Model Listed in DSM-5-TR as ‘Emerging’

Answer 105

• Greater emphasis on personality functioning, core self and personality traits
• Rating of impairment on Self and Interpersonal Functioning (Identity, Self-direction,
  Empathy & Intimacy)
• Six personality disorder types
  ▫ Antisocial/Psychopathic
  ▫ Avoidant
  ▫ Borderline
  ▫ Obsessive-Compulsive
  ▫ Schizotypal
  ▫ Narcissistic
• But diagnosis can also be based on patterns of personality traits (e.g. Detachment;
  Antagonism; Disinhibition)

Question 106

Challenges in Diagnosis

Answer 106

• Personality disorders could be seen as involving maladaptive or extreme
  variations on the ordinary range of personality characteristics
  ▫ When does a “quirk” or variation become a personality disorder?
• Personality disorders
  ▫ Are a controversial diagnostic category
  ▫ Can be difficult to define and identify reliably
   Can have significant overlap with each other
  ▫ Can lead to significant stigma, even amongst mental health professionals

Question 107

Controversy: Gender Differences

Answer 107

• Men diagnosed with a personality disorder tend to display traits
  characterized as more aggressive, structured, self-assertive and detached
• Women tend to present with characteristics that are more submissive,
  emotional and insecure
• Criteria gender bias
  ▫ For instance, histrionic PD may be thought of as extreme “stereotypical female”,
  ▫ No “macho” disorder
  ▫ Dependent personality disorder but no independent personality disorder

Question 108

Arguments for Change in Approach to Personality Disorder
Diagnosis

Answer 108

• Excessive co-morbidity among current DSM personality disorders
• Limited validity for some existing types
• Arbitrary diagnostic thresholds in DSM (i.e., number of criteria necessary)
• Current DSM PD diagnoses not particularly stable over time (personality
  traits more stable than disorders)
• Replacement of behavioural PD criteria with traits is anticipated to result
  in greater diagnostic stability
• Use of a dimensional rating of types recognizes that personality
  psychopathology occurs on continua

Question 109

ICD-11 Classification of PDs (Bach & First, 2018)

Answer 109

• Takes an alternative approach to the categorical model of the DSM
• Focuses on the impairment of self and interpersonal personality functioning
  ▫ SELF - sense of identity, self worth, accuracy of personal evaluation, & capacity for self-direction
  ▫ INTERPERSONAL - interest in engaging in r/ships with others, ability to understand and appreciate
  others’ perspectives, develop and maintain close and mutually satisfying relationships, and manage
  conflict
• Classified according to severity
  ▫ “Personality Difficulty”, “Mild PD”, “Moderate PD”, “Severe PD”
• May also be specified with one or more prominent trait qualifiers “Negative Affectivity”,
  “Detachment”, “Dissociality”, “Disinhibition” and “Anankastia” (excessive preoccupation with
  orderliness, perfectionism and control)
• Suggested as helpful in informing clinical prognosis and intensity of treatment, and trait
  classifiers characterized as helpful in selecting focus and style of treatment.

Question 110

Other Perspective on Personality: Five Factor Model

Answer 110

• “Big Five”; one of the most researched personality models:
  ▫ Openness to experience (imaginative, curious, creative
  ▫ Conscientiousness (organised thorough, reliable)
  ▫ Extraversion (talkative, assertive, active)
  ▫ Agreeableness (kind, trusting, warm)
  ▫ Neuroticism (even-tempered)
• Cross-cultural research establishes the universal nature of the five
  dimensions

Question 111

DSM-5-TR: 10 Personality Disorders in 3 Clusters

Answer 111

• Cluster A (Odd or eccentric)
  ▫ Paranoid
  ▫ Schizoid
  ▫ Schizotypal
• Cluster B (Dramatic, emotional or erratic)
  ▫ Antisocial
  ▫ Borderline
  ▫ Histrionic
  ▫ Narcissistic
• Cluster C (Anxious or fearful)
  ▫ Avoidant
  ▫ Dependent
  ▫ Obsessive-compulsive

Question 112

Cluster A (personality)

Answer 112

• Paranoid Personality Disorder
  ▫ Pervasive distrust and suspiciousness of others such that their motives are
  interpreted as malevolent
• Schizoid Personality Disorder
  ▫ Pervasive pattern of detachment from social relationships and a restricted
  range of emotional expression
• Schizotypal Personality Disorder
  ▫ Pervasive pattern of social and interpersonal deficits marked by acute
  discomfort with reduced capacity for close relationships, as well as by
  cognitive or perceptual distortions and eccentricities of behaviour

Question 113

Cluster A: Paranoid Personality Disorder

Answer 113

• A pervasive distrust and suspiciousness of others
  ▫ The motives of others are interpreted as malevolent,
  ▫ beginning by early adulthood
  ▫ present in a variety of contexts, as indicated by four (or more) of list (next slide)
• Not occurring only during a psychotic disorder such as Schizophrenia or
  mood disorder with psychotic features
• Not due to the direct physiological effects of a general medical condition
• Criteria may be met prior to the onset of Schizophrenia, in this case -
  Paranoid Personality Disorder (Premorbid)

Question 114

Paranoid Personality Disorder (cont.) Criteria

Answer 114

• Four or more of the following:
  ▫ Suspects, without sufficient basis, that others are exploiting, harming or deceiving him or
  her
  ▫ Preoccupied with unjustified doubts about the loyalty or trustworthiness of friends or
  associates
  ▫ Reluctant to confide in others because of unwarranted fear that the information will be
  used maliciously against him or her
  ▫ Reads hidden demeaning or threatening meanings into benign remarks or events
  ▫ Persistently bears grudges, i.e., is unforgiving of insults, injuries, or slights
  ▫ Perceives attacks on his or her character or reputation that are not apparent to others
  and is quick to react angrily or to counterattack
  ▫ Recurrent suspicions, without justification, regarding fidelity of spouse or sexual partner

Question 115

Paranoid Personality Disorder: Presentation and Treatment

Answer 115

• Unlikely to come for help due to lack of trust
• Unlikely to stay in therapy due to difficulty making an alliance
• Little research available
• Presentation:
  ▫ May be argumentative, complaining or quiet
  ▫ Sensitive to criticism
  ▫ Increases any risk of suicide or violent behaviour
  ▫ Often poor quality of life

Question 116

Cluster A: Schizotypal Personality Disorder

Answer 116

• Pervasive pattern of social and interpersonal deficits marked by
  ▫ Acute discomfort with and reduced capacity for close relationships
  ▫ And cognitive or perceptual distortions and eccentricities of behaviour
• As indicated by 5 or more of:
  ▫ Ideas of reference (not delusions of reference)
  ▫ Odd beliefs or magical thinking inconsistent with cultural norms
  ▫ Unusual perceptual experiences
  ▫ Odd thinking and speech
  ▫ Suspiciousness or paranoid ideas
  ▫ Inappropriate or constricted affect
  ▫ Odd or eccentric behaviour or appearance
  ▫ Lack of close friends other than first degree relatives
  ▫ Excessive social anxiety (associated with paranoid fears rather than negative views of self)

Question 117

Schizotypal Personality Disorder (Clinical description and course)

Answer 117

• Clinical description:
  ▫ Psychotic like but not psychotic symptoms i.e: can know their ideas of
  reference are unlikely to be true
  ▫ Social deficits
  ▫ Strange ideas, little emotional expression, odd behaviours
• Course: Chronic, some people develop schizophrenia
• Not culturally or sub culturally sanctioned behaviour (such as speaking
  in tongues)

Question 118

Schizotypal Personality Disorder (cause and treatment)

Answer 118

• Cause:
  ▫ Is this a phenotype of a schizophrenia genotype?
  ▫ Symptoms have been associated with childhood maltreatment (Berenbaum et al,
  2008)
  ▫ May be mild to moderate cognitive deficits in memory and learning (Siever &
  Davis, 2004)
• Treatment
  ▫ 30-50% of treatment seekers have depression
  ▫ Research is in early stages, treatment such as antipsychotic medication,
  community support, behaviour therapy and social skills training (Nordentoft et al,
  2006; Correll et al, 2011)

Question 119

Cluster B

Answer 119

Dramatic, emotional, or erratic

• Antisocial Personality Disorder
  ▫ Disregard for and violation of the rights of others
• Borderline Personality Disorder
  ▫ Instability of interpersonal relationships, self-image, affects and control of
  impulses
• Histrionic Personality Disorder
  ▫ Pervasive pattern of excessive emotionality and attention-seeking
• Narcissistic Personality Disorder
  ▫ Pervasive pattern of grandiosity, need for admiration, and lack of empathy

Question 120

Cluster B: Narcissistic Personality Disorder

Answer 120

• Pervasive pattern of grandiosity (fantasy or behaviour), need for admiration and lack of empathy, five or
  more of:
• Grandiose sense of self-importance (exaggerates achievements and talents, expects to be recognized
  as superior without commensurate achievements)
• Preoccupied with fantasies of unlimited success, power, brilliance, beauty, or ideal love
• Believes that he or she is “special” and unique, can only be understood by, or should associate with,
  other special or high-status people ( or institutions)
• Requires excessive admiration
• Strong sense of entitlement (unreasonable expectations of especially favourable treatment or
  automatic compliance with expectations
• Exploitative of others (takes advantage of others to achieve own ends)
• Lacks empathy
• Often envious of others or believes that others are envious of him or her
• Regularly shows arrogant, haughty behaviors or attitudes

Question 121

Cluster B: Antisocial Personality Disorder

Answer 121

• Pervasive pattern of disregard for and violation of the rights of others occurring since
  age of 15, as indicated by 3 or more of:
  ▫ Failure to conform to norms re lawful behaviour as in repeatedly performing acts which
  are grounds for arrest
  ▫ Deceitfulness – repeated lying; aliases; conning others for profit or pleasure
  ▫ Impulsivity or failure to plan ahead
  ▫ Irritability or aggressiveness – repeated fights/assaults
  ▫ Reckless disregard for safety of self or others
  ▫ Consistent irresponsibility – in work or financial obligations
  ▫ Lack of remorse – indifference or rationalising re treating others badly
• Aged 18 or above
• Evidence of conduct disorder before age of 15

Question 122

Antisocial Personality Disorder: Developmental Questions

Answer 122

• There is a developmental aspect of antisocial behaviour. Many adults
  with Antisocial PD had conduct disorder as children, the combination of
  conduct disorder and ADHD may increase the risk of developing
  Antisocial personality disorder
• Conduct disorder can apply to children if present before age 10:
  childhood onset type and to adolescents if the onset is after age 10:
  adolescent onset type
• DSM 5 has a new subtype conduct disorder: “with a callous-
  unemotional presentation”

Question 123

Debates: Antisocial Personality Disorder

Answer 123

• Cleckley (1941-1982) developed the concept of the psychopathic personality
  ▫ Hare et al built on Cleckley’s descriptive work and developed an assessment
  tool including: glibness/superficial charm, grandiose sense of self worth,
  pathological lying, conning/manipulative, lack of remorse, lack of empathy
  ▫ Earlier DSM versions used observable behaviours and legal consequences,
  rather than personality traits
  ▫ DSM 5 has moved back towards Cleckley/Hare, however, the diagnosis may be
  less reliable
• Meloy – current definition of anti-social personality disorder too broad;
  need category for more extreme sadistic ‘psychopaths’

Question 124

Debates: Antisocial Personality Disorder (cont.)

Answer 124

• Do DSM-5 criteria blur the distinction between anti-social personality
  disorder and criminality?
• Not all people with Antisocial PD are aggressive
• Those who get trouble with the law may be lower in IQ
• Are there some occupations in which these characteristics are useful?
• In general those with higher scores on psychopathy commit more
  crimes, more violent crime and show more recidivism (Widiger, 2006)

Question 125

Antisocial Personality Disorder: Causes

Answer 125

• Gene-environment interaction
  ▫ Genetic predisposition
  ▫ Environmental triggers
• Neurobiology
  ▫ Arousal hypotheses
   Underarousal
   Fearlessness
• Psychosocial/developmental influences
  ▫ Parents may give in to persistent aggressive acts
  ▫ Lower parental monitoring, parental depression, less parental involvement (less
  role modelling)

Question 126

Antisocial Personality Disorder: Treatment

Answer 126

• Unlikely to seek on own
• High recidivism
• Incarceration
• Early intervention & Prevention
  ▫ Parent training
  ▫ Rewards for pro-social behaviors
  ▫ Skills training
  ▫ Improve social competence

Question 127

Cluster B: Borderline Personality Disorder

Answer 127

• Pervasive pattern of instability of interpersonal relationships, self-image, & affects, and
  marked impulsivity, indicated by 5 or more of:
  ▫ Frantic efforts to avoid real or imaged abandonment
  ▫ Unstable & intense interpersonal relationships alternating between idealisation and devaluation
  ▫ Identity disturbance: markedly & persistently unstable self-image or sense of self
  ▫ Impulsivity in 2 areas that are potentially self-damaging (eg spending, substance abuse, reckless
  driving, sexual behavior, binge eating)
  ▫ Recurrent suicidal behavior/threats or self-harming
  ▫ Affective instability – marked reactivity of mood
  ▫ Chronic feelings of emptiness
  ▫ Inappropriate, intense anger or difficulty controlling anger
  ▫ Transient, stress-related paranoid ideation or dissociative symptoms

Question 128

BPD Clinical description

Answer 128

• Commonly seen in clinical settings, stably unstable?
• Patterns of instability, emotion dysfunction
  ▫ Intense moods
  ▫ Turbulent relationships
• Impulsivity
• Poor self-image
• Self-mutilation
• Suicidal gestures

Question 129

Spectrum - Emphasis on risk from serious self-harm or suicide,
and particularly complex needs

Answer 129

• When someone deliberately hurts themselves as a way of coping, others
  find it hard to understand. Unfortunately, because so little is known or
  understood about BPD, many people will at some stage come face to
  face with the prejudice and discrimination that result from this. This can
  be extremely alienating. It is vital to remember that BPD is a genuine
  condition and that help is available.

Question 130

BPD Clinical Description

Answer 130

• Comorbidity: suicide (6%), depression (20%), bipolar (40%), substance
  abuse (67%), eating disorder –bulimia (25% of those with bulimia have
  BPD)
• Frequently present with social disorganisation; relationships, housing,
  finances, work
• Counter transference issues in treatment
• Possible discrimination from treating services
• People with BPD usually improve in 30s to 40s

Question 131

NHMRC 2012 Clinical Practice Guideline for the Management of
Borderline Personality Disorder

Answer 131

• Overall recommendations: health professionals at all levels of the healthcare
  system and within each type of service setting should:
  ▫ Acknowledge that BPD treatment is a legitimate use of healthcare services
  ▫ Be able to recognise BPD presentations
  ▫ Be aware of general principles of care for people with BPD and specific effective BPD
  treatments
  ▫ Provide appropriate care (including non-specific mental health management,
  specific treatments for BPD and treatment for co-occurring mental illness) according
  to their level of training and skill
  ▫ Refer the person to a specialised BPD service or other services as indicated
  ▫ Undertake continuing professional development to maintain and enhance their skills

Question 132

BPD (causes)

Answer 132

• Causes
  ▫ Genetic/biological components
   Serotonin
   Limbic network
  ▫ Cognitive biases
  ▫ Early childhood experience
   Neglect
   Trauma
   Abuse
• An Integrative Model

Question 133

Cluster C

Answer 133

Characterised by anxious/fearful
* Avoidant Personality Disorder
▫ Pervasive pattern of social inhibition, feelings of inadequacy and hypersensitivity
to negative evaluation
* Dependent Personality Disorder
▫ Pervasive pattern of submissive and clinging behaviour related to an excessive
need to be taken care of by others
* Obsessive-Compulsive Personality Disorder
▫ Pervasive pattern of preoccupation with orderliness, perfectionism and control (at
the expense of flexibility, openness, and efficiency)

Question 134

Obsessive-Compulsive Personality Disorder

Answer 134

• Pervasive pattern of preoccupation with orderliness, perfectionism, and mental and
  interpersonal control, at the expense of flexibility, openness, and efficiency. Four or more of
  the following:
  ▫ Preoccupied with details, rules, lists, order, organisation or schedules to the extent that the major
  point of the activity is lost
  ▫ Perfectionism interferes with task completion
  ▫ Excessively devoted to work and productivity to the exclusion of leisure and friendship (not by
  economic necessity)
  ▫ Overconscientious, scrupulous, inflexible re morality, ethics or values
  ▫ Unable to discard worn out or worthless objects even when they have no sentimental value
  ▫ Reluctant to delegate tasks unless they submit to his or her rules
  ▫ Miserly spending style towards self and others
  ▫ Rigidity and stubbornness

Question 135

Epidemiology of Personality Disorders

Answer 135

• Often not included in major epidemiological studies
• Self-report of signs and symptoms may not be reliable
• Prevalence reported in recent studies focused on PDs
  ▫ For any (at least one) PD: Approx 10% (Lenzenweger, 2007)
   But rates can vary depending on statistical procedures eg Coid (2006): 4.4%
  ▫ Relative prevalence of Clusters, A, B & C varies across studies
  ▫ Most common in community samples: Obsessive-compulsive PD (2-4% in most studies)
   But Lenzenweger found higher rates of Avoidant & Schizoid PDs
  ▫ Borderline PD is the most common in clinic samples (estimates vary from 11% to 30%) but
  approx 1.4% in community
• High co-morbidity
  ▫ Among categories of personality disorder
  ▫ Between PD and major depression, substance dependence and anxiety disorder

Question 136

Causal/Contributing Factors (personality disorders) (***)

Answer 136

• Note paucity of research re some disorders
• CLUSTER A: paranoid, schizoid, schizotypal
  ▫ Some evidence of genetic factors
  ▫ especially for Schizotypal – idea of ‘schizophrenia spectrum’
• CLUSTER B: antisocial, borderline, histrionic, narcissistic
  ▫ Role of family problems, parental loss & separation
  ▫ History of physical or sexual abuse or neglect
  ▫ For anti-social PD, combination of genetic factors and adverse environmental circumstances
• CLUSTER C: avoidant, dependent, obsessive-compulsive
  ▫ Social & psychological factors
  ▫ Early relationship history
  ▫ Avoidant – on spectrum with social phobia?

Question 137

General Personality Disorder Treatment

Answer 137

• Often insufficiently researched
• CLUSTER A: paranoid, schizoid, schizotypal
  ▫ May not present for treatment unless for co-morbid disorder
  ▫ Medication and/or supportive interventions may be helpful
• CLUSTER B: borderline, histrionic, narcissistic
  ▫ Psychotherapy may be helpful, including for Borderline:
   Dialectical Behaviour Therapy (Linehan)
   Mentalisation-Based Therapy (Bateman & Fonagy)
  ▫ Crisis management may be needed
  ▫ Medication may be indicated at times (often for co-morbid conditions)

Question 138

General Personality Disorder Treatment continued

Answer 138

• CLUSTER B: Antisocial
  ▫ Tend not to seek treatment
  ▫ unless legally mandated
  ▫ Debate about treatability (perhaps varies with severity?)
• CLUSTER C: Avoidant, dependent, obsessive-compulsive
  ▫ Psychotherapy may be helpful
• Spectrum
  ▫ http://www.spectrumbpd.com.au/

Question 139

Trauma- and Stressor-Related Disorders

Answer 139

• Reactive Attachment Disorder (children)
• Disinhibited Social Engagement Disorder (children)
• Posttraumatic Stress Disorder (PTSD)
• Acute Stress Disorder
• Adjustment Disorders
• Prolonged Grief Disorder (new diagnosis added in DSM-V-TR)
• Other specified and unspecified

Question 140

Acute Stress Disorder and PTSD in DSM-5: Key Changes from
DSM-4-TR

Answer 140

• Moved from the chapter about Anxiety Disorders
• Identifiable traumatic event or stressor induced the disorder
• PTSD:
  ▫ 4 clusters (prev. 3)
  ▫ Avoidance/numbing divided into avoidance and negative alterations in cognition
• Developmentally sensitive criteria for children aged 6 and younger
• Not necessary to have intrusion symptoms in Acute Stress Disorder
• Distinguished by duration: Acute Stress Disorder 3 days - 1 month, PTSD at least 1 month
• Trauma: Experienced, witnessed, experienced indirectly
• Does not require an assessment of the individual’s initial subjective response
• Delayed onset now called delayed expression

Question 141

Trauma Exposure and PTSD

Answer 141

• Exposure to a potentially traumatic event (PTE) is a common experience, with up
  to 75% likely to experience at least one PTE during their lifetime
• PTEs involve exposure to an event involving threat, actual or perceived, to the
  life or physical safety of the individual, their loved ones or those around them
• Can be experienced on a single occasion or repeatedly
• However, not everyone goes on to develop PTSD
• (Australian Guidelines for the Treatment of Acute Stress Disorder and
  Posttraumatic Stress Disorder, approved by NHMRC)

Question 142

PTSD Criteria DSM-5-TR

Answer 142

• Event
• Intrusion Symptoms (1+)
• Persistent avoidance (1+)
• Negative alterations in cognitions & mood (2+)
• Marked alterations in arousal & reactivity (2+)
• Duration of disturbance (B,C,D & E) is more than 1 month
• Rule out postconcussive syndrome, traumatic brain injury
• Specify
  ▫ With dissociative symptoms:
   Depersonalization (an outside observer of one’s mental processes or body) and/or
   Derealization (unreality of surroundings)
  ▫ With delayed expression
   full criteria not met until at least 6 months after the even

Question 143

PTSD Criterion A - Event For adults, adolescents, and children older than six:

Answer 143

• For adults, adolescents, and children older than six:
• A. Exposure to actual or threatened death, serious injury, or sexual violence in one (or more) of
  the following ways:
  1. Directly experiencing the event
  2. Witnessing the event as it occurred to others
  3. Learning that the event occurred to a close family member or close friend. In cases of actual or
  threatened death of a family member or friend, the event(s) must have been violent or
  accidental
  4. Experiencing repeated or extreme exposure to aversive details of the event (e.g. first
  responders collecting human remains, police officers repeatedly exposed to details of child
  abuse)
• Note: Criterion A4 does not apply to exposure through electronic media, television, movies, or
  pictures, unless this exposure is work related.

Question 144

PTSD and Children – Criterion A: Event For children aged six years and younger, trauma exposure may occur
through:

Answer 144

• A. Exposure to actual or threatened death, serious injury, or sexual
  violence in one (or more) of the following ways:
  1. Directly experiencing the event
  2. Witnessing the event as it occurred to others, especially primary
  caregivers
  3. Learning that the event occurred to a parent or caregiver

Question 145

TSD DSM-5-TR Criterion B

Answer 145

• Presence of one (or more) of the following intrusion symptoms associated with
  the traumatic event(s), beginning after the traumatic event(s) occurred:
  ▫ Recurrent, involuntary, and intrusive distressing memories of the traumatic event(s)
  ▫ Recurrent distressing dreams in which the content and/or affect of the dream are
  related to the traumatic event(s)
  ▫ Dissociative reactions (e.g. flashbacks) in which the individual feels or acts as if the
  traumatic event(s) were recurring
  ▫ Intense or prolonged psychological distress at exposure to internal or external cues
  that symbolize or resemble an aspect of the traumatic event(s)
  ▫ Marked physiological reactions to internal or external cues that symbolize or
  resemble an aspect of the traumatic event(s)

Question 146

PTSD DSM-5 Criterion C

Answer 146

• Persistent avoidance of stimuli associated with the traumatic event(s),
  beginning after the traumatic event(s) occurred, as evidenced by one or
  both:
  ▫ Avoidance of or efforts to avoid distressing memories, thoughts, or feelings
  about or closely associated with the traumatic event(s)
  ▫ 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)

Question 147

PTSD DSM-5 Criterion D

Answer 147

• 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:
  ▫ Inability to remember an important aspect of the traumatic event(s) (typically due to
  dissociative amnesia, not due to other factors such as head injury, alcohol or drugs)
  ▫ Persistent and exaggerated negative beliefs or expectations about oneself, others, or the world
  ▫ Persistent, distorted cognitions about the cause or consequences of the traumatic event(s) that
  lead to self or other blame
  ▫ Persistent negative emotional state (fear, horror, anger, guilt, shame)
  ▫ Markedly diminished interest or participation in significant activities
  ▫ Feelings of detachment or estrangement from others
  ▫ Persistent inability to experience positive emotions (happiness, satisfaction, love)

Question 148

PTSD DSM-5 Criterion E

Answer 148

• 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:
  ▫ Irritable behaviour and angry outbursts (little or no provocation) typically
  expressed as verbal or physical aggression towards people or objects
  ▫ Reckless or self-destructive behaviour
  ▫ Hypervigilance
  ▫ Exaggerated startle response
  ▫ Problems with concentration
  ▫ Sleep disturbance

Question 149

Acute Stress Disorder

Answer 149

Exposure to actual or threatened death, serious injury or sexual violence
* Nine or more symptoms in total from any of 5 categories:
▫ Intrusion symptoms
▫ Negative mood
▫ Dissociative symptoms
▫ Avoidance symptoms
▫ Arousal symptoms
* Duration of disturbance at least 3 days & up to one month after
traumatic event

Question 150

Adjustment Disorder

Answer 150

• Development of emotional or behavioural symptoms in response to an identifiable stressor(s),
  occurring within 3 months of onset of stressor
• Clinically significant: marked distress out of proportion to stressor and context, and/or
  impairment in functioning
• Not representing normal bereavement
• Once the stressor, or its consequences have terminated, symptoms do not persist for more
  than 6 months
• Specify:
  ▫ With depressed mood
  ▫ With anxiety
  ▫ With mixed anxiety and depressed mood
  ▫ With disturbance of conduct
  ▫ With mixed disturbance of emotions & conduct

Question 151

Prolonged Grief Disorder (added in DSM-V-TR) Criteria A, and B

Answer 151

• A. The death, at least 12 months ago, of a person who was close to the bereaved individual (for children and adolescents, at least 6 months ago)
• B. Since the death, the development of a persistent grief response characterized by one or both of the following
  symptoms (most days for at least one month):
  ▫ Intense yearning/longing for the deceased person
  ▫ Preoccupation with thoughts or memories of the deceased person (in children and adolescents, preoccupation may
  focus on death circumstances)

Question 152

Prolonged Grief Disorder (added in DSM-V-TR) Criteria C

Answer 152

• C. Since the death, at least 3 of the following symptoms (most days for at least one month):
  ▫ Identity disruption (e.g., feeling as though part of oneself died)
  ▫ Marked sense of disbelief about the death
  ▫ Avoidance of reminders that the person is dead (in children and adolescents, efforts to avoid reminders)
  ▫ Intense emotional pain (e.g., anger, bitterness, sorrow)
  ▫ Difficulty reintegrating into one’s relationships and activities
  ▫ Emotional numbness (absence or marked reduction of emotional experience)
  ▫ Feeling that life is meaningless
  ▫ Intense loneliness

Question 153

Prolonged Grief Disorder (added in DSM-V-TR) Criteria D, E, and F

Answer 153

• D. Clinically significant distress or impairment in areas of functioning
• E. The duration and severity of the bereavement reaction clearly exceed expected social, cultural, or religious norms
  for the individual’s culture and context
• F. Not better explained by another disorder or medical condition

Question 154

Disorders of Neglect

Answer 154

• Reactive Attachment Disorder
• Disinhibited Social Engagement Disorder

Question 155

Reactive Attachment Disorder Criteria A and B

Answer 155

A. A consistent pattern of inhibited and emotionally withdrawn behaviour towards adult caregivers, including:
▫ Rarely or minimally seeking comfort when distressed
▫ Rarely or minimally responding to comfort when distressed
B. Persistent social and emotional disturbance including two of:
▫ Minimal social and emotional responsiveness to others
▫ Limited positive affect
▫ Episodes of unexplained irritability, sadness, or fearfulness

Question 156

Reactive Attachment Disorder Criteria C, D, E, F, G

Answer 156

C. The child has experienced a pattern of extremes of insufficient care including at least one of:
▫ Social neglect or deprivation
▫ Repeated changes of primary caregivers
▫ Rearing in unusual settings that severely limit opportunities to form selective attachments
D. The care in Criterion C is presumed to be responsible for behaviour in Criterion A
E. Criteria not met for Autism Spectrum Disorder.
F. Onset before age 5.
G. Developmental age of at least 9 months.

Question 157

Disinhibited Social Engagement Disorder Criteria A and B

Answer 157

A. A pattern of behaviour in which a child actively approaches and interacts with unfamiliar adults and
exhibits at least two of:
* Reduced or absent reticence in approaching and interacting with unfamiliar adults
* Overly familiar verbal or physical behaviour
* Diminished or absent checking back with adult caregiver after venturing away
* Willingness to go off with unfamiliar adult with little or no hesitation
B. Behaviours in Criterion A are not limited to impulsivity but include socially disinhibited behaviour.

Question 158

Disinhibited Social Engagement Disorder Criteria C, D, E

Answer 158

C. . The child has experienced a pattern of extremes of insufficient care including at least one of:
▫ Social neglect or deprivation
▫ Repeated changes of primary caregivers
▫ Rearing in unusual settings that severely limit opportunities to form selective attachments
D. The care in Criterion C is presumed to be responsible for behaviour in Criterion A
E. Developmental age of at least 9 months.

Question 159

Complex Posttraumatic Stress Disorder
(not in DSM-5-TR, but in ICD-11)

Answer 159

• Judith Herman (1992) argued:
• Diagnostic criteria for PTSD derived mainly from survivors of
  circumscribed traumatic events (combat, disaster, rape)
• Prolonged, repeated trauma, involving totalitarian control, leads to
  more complex syndrome with more fundamental personality changes
• Adult survivors of prolonged childhood abuse often given other
  diagnoses instead of a trauma-related diagnosis

Question 160

Complex PTSD involves alterations in:

Answer 160

• Affect regulation e.g. dysphoria, self-injury, explosiveness
• Consciousness e.g. dissociation
• Self-perception e.g. helplessness, guilt
• Perception of perpetrator e.g. preoccupation with, idealization
• Relations with others e.g. distrust, withdrawal, failures of self-protection
• Systems of meaning e.g. despair, loss of faith

Question 161

Developmental Trauma Disorder

Answer 161

• Not in DSM – was proposed but not accepted
• Bessel van der Kolk developed this concept
• Similar to PTSD but broader definition of traumatic event, broader range
  of symptoms, and broader effects on functioning
• Could assist with treating children who have experienced multiple
  traumatic incidents, such as ongoing issues in care and attachment, but
  do not meet criteria for existing Trauma and Stressor-Related Disorders

Question 162

Adverse Childhood Experiences Questionnaire

Answer 162

• Ten questions about adverse experiences in childhood
• Research suggests that those who answer yes to four or more are at
  increased risk of a range of physical and mental health problems, not
  just PTSD
• Suggests limitations to the PTSD diagnosis in considering the impact of
  trauma on individuals
• https://acestoohigh.com/got-your-ace-score/

Question 163

Gender Differences PTSD

Answer 163

• Women are more likely than men to have PTSD, and to have it for a
  longer duration
  ▫ What are some potential reasons for this?

Question 164

Anatomy of the frontal cortex 1 Lateral view

Answer 164

Question 165

Anatomy of the frontal cortex ventral view

Answer 165

Question 166

Anatomy of the frontal cortex medial view

Answer 166

Question 167

Symptoms of frontal lobe dysfunction

Answer 167

Motor symptoms
 Primary motor area
 Impaired ability to move contralateral
part of body specific to lesion
 Premotor and Supplementary
motor areas:
 Acute-impairment of voluntary
movement
 Residual deficits in rapid planned
movements
 Frontal eye fields:
 Oculomotor deficits (eye movement)
 Broca’s area
 Broca’s aphasia
Sensory and perceptual
symptoms
 Orbitofrontal cortex: impaired
odour memory/discrimination
Behavioural symptoms of PFC
damage

Question 168

Summary of Major symptoms of frontal lobe damage

Answer 168

Question 169

What are executive functions?

Answer 169

Behavioural control
 Initiation
 Maintenance
 Attentional processes
 Cessation
Goal-directed behaviour
 Planning
 Prospective memory
Self-monitoring
Task-switching
Multi-tasking
Among many others…

Question 170

MENTAL FLEXIBILITY
AND IDEA GENERATION

Answer 170

Convergent vs.
Divergent Thinking
 Convergent thinking:
Only one answer to the
question
 Divergent thinking:
Number and variety of
responses to a single
question
 Frontal-lobe-lesion
patients are impaired on
divergent thinking
 Posterior lesions 
reliable IQ decrements
(convergent thinking)

Question 171

DORSOLATERAL
PREFRONTAL CORTEX
(DLPFC)

Answer 171

Left DLPFC associated with response selection and
specification
 Links to posterior parietal regions
 Both have connections with basal ganglia, cingulate, superior colliculus
Affects all cognitive domains

Question 172

Damage to the DLPFC:

Answer 172

 Poor judgement/ planning/ organisation
 Motor programming/ sequencing deficits
 Cognitive impersistence; reduced self-care
 Behaviour may become obsessive, ritualised
DLPFC volumes reduced in schizophrenia

Question 173

ORBITOFRONTAL
CORTEX (OFC)

Answer 173

Orbitofrontal cortex  disinhibited
behaviour (e.g. Phineas Gage)
 Regulation of social and emotional
behaviour

Question 174

Damage to OFC:

Answer 174

 Changed “personality”; lewdness;
jocularity
 Poor impulse control  Emotional lability;
irritability; distractibility
Large bilateral lesions cause
“frontal release” symptoms (re-
emergence of primitive reflexes, e.g. sucking)
Loss of ability for empathy  loss
of somatic markers (feelings in the body
associated with emotions)

Question 175

ANTERIOR CINGULATE GYRUS
(MEDIAL FRONTAL)

Answer 175

Mesial-frontal (anterior cingulate)  apathy
 ACC involved in monitoring/ coordinating the
involvement of other brain regions required for a
particular action
 Activated during intentional/volitional movement

Question 176

Damage to ACC:

Answer 176

 Poor initiation of behaviour
 Reduced speech output (mutism) and motor activity
 When both affected  akinetic mutism
 Slowed speed of processing/ bradyphrenia
 May appear depressed but emotional dysphoria/
expression lacking
 Urinary incontinence

Question 177

SELF-AWARENESS AND
THE PREFRONTAL
CORTEX

Answer 177

Autonoetic
Awareness
 Self-knowledge
 Binds together the
awareness of oneself as
continuous entity
through time
 Impairment in
autonoetic awareness 
deficit of behavioural
self-regulation
 Medial or ventral frontal
injury  loss of self-
knowledge and struggles
in daily life

Question 178

THEORY OF MIND AND THE
FRONTAL LOBES

Answer 178

ToM is the ability to infer the
intentions and mental states of
other people
 False belief task
Happe et al (1999): R FL damage
in adults results in poor ToM with
otherwise unimpaired reasoning
Stuss et al (2001): FL damage in
adults associated with reduced
ability to detect deception
Rowe et al (2001): adults with L
or R FL lesions fail the false
belief task
The Eyes Test (Baron-Cohen)

Question 179

HOW CAN WE STUDY
EMOTION?

Answer 179

“Emotions have traditionally
been regarded as extras in
psychology, not as serious
mental functions like perception,
language, thinking, learning”.
(Oatley & Jenkins, 1996)
Historically emotions have not
been seen as accessible to
objective study
Self-report is subjective by its
nature
Physiological methods tell us
only how the body reacts to an
emotional state
BUT: emotional states are brain
states

Question 180

THE EMOTIONAL BRAIN:
LIMBIC SYSTEM

Answer 180

Question 181

INTERACTION OF
COGNITION AND EMOTION

Answer 181

Emotional material more easily remembered
 Cahill & McGaugh (1995)
Two routes to emotional experience
Direct, fast, subcortical route  primary emotions
 “basic” emotional responses: instincts
Indirect, slower, cortical route  secondary
emotions
 Individualised
 Conscious, explicit

Question 182

FEAR CONDITIONING AND
THE AMYGDALA

Answer 182

Amygdala is the “sensory gateway” to the emotions
(Aggleton & Mishkin, 1986)
 Neuroanatomy of primary fear  amygdala
Classical conditioning of fear responses
 Conditioned fear responses still active even when
amygdala disconnected from cortex
 learning/maintenance of fear is subcortical
Selective lesioning of amygdala causes differential
effects on fear response
 Central nucleus ablation causes loss of autonomic fear
reaction
Sensory information via thalamus to amygdala with
no cortical evaluation: thalamo-amygdala circuit

Question 183

CORTICAL STRUCTURES
AND EMOTION

Answer 183

Posterior areas (occipital and parietal lobes)
Recognition of emotion in facial expressions
Fusiform gyrus  static aspects of faces
Superior temporal gyrus  dynamic aspects of
faces  emotional content
Frontal areas such as orbitofrontal cortex
Rolls (1999): OFC involved in making
evaluations/corrections of stimulus-response
associations
 i.e. inhibition of prepotent responses
OFC allows us to evaluate “somatic markers” of
experiences, assisting in decision-making
(Damasio, 1994)  Somatic Marker Hypothesis

Question 184

CORTICAL STRUCTURES
AND EMOTION

Answer 184

Frontal areas involved in
“higher” cortical processing
of social emotional
experience  secondary
emotions
Highly personal/
individualised
 Shame, embarrassment, anxiety
Require a personal evaluation
of situation at the cortical
level before being assigned
an emotional response
 thalamo-cortico-amygdala
circuit

Question 185

WHAT IS AMNESIA?

Answer 185

A very substantial or
complete loss of memory
function
Anterograde amnesia
 Inability to form new
memories
Retrograde amnesia
 Inability to access old
memories
Possible to have both
 Early recovery period after
TBI
 Later stages of dementia

Question 186

HENRY MOLAISON:
THE CASE OF HM

Answer 186

Intractable temporal lobe
epilepsy
Bilateral temporal lobectomy in
1953 when 27 years old
 Part of hippocampal complex
removed, and rest disconnected from
other brain regions (removal of
entorhinal cortex)
18 mo later: demonstrated
memory difficulties
 Still reported his age as 27
 Could not remember people minutes after
meeting them
 Could not form new long-term memories
Biographical knowledge up to the
time of the surgery was intact

Question 187

HM’S MEMORY DEFICITS

Answer 187

Extended Digit Span task
 Digit span + 1: STA memory task
 HM’s digit span prior to surgery was 7
(typical adult); same after surgery,
BUT…
Corsi Block tapping: a ST visual
memory task
 HM had a normal span, BUT…
Good memory for events/
information learned prior to
surgery
 HM had a dense global
anterograde amnesia (***)
 Not all memories are created
(and stored) equally

Question 188

MULTIPLE MEMORY
SYSTEMS

Answer 188

Question 189

TEMPORAL PROFILE OF
MEMORY DISORDER

Answer 189

Anterograde Amnesia
 Inability to acquire new memories
 Post-Traumatic Amnesia
 Global Anterograde Amnesia
 Impairment in the ability to form new memories across a variety
of areas
Retrograde Amnesia
 Inability to access old memories
 May be incomplete—older memories accessible
but more recent memories are not
Time-Dependent Retrograde Amnesia
 Commonly produced by traumatic brain injury
 Severity of injury determines how far back in time
the amnesia extends
 The “temporal gradient” aka Ribot’s Law
 More recent memories affected more than older memories

Question 190

LONG TERM EXPLICIT
MEMORY

Answer 190

Explicit memory
 Events, facts, and episodic
memories
 Conscious intentional remembering
 “Top-down” processing
 Episodic memory
 Autobiographic
 Person’s recall of singular personal
events
 H.M. and M.L. (see text) could not
make new episodic memories
 Semantic Memory
 All nonautobiographical knowledge
—knowledge about the world
 Intact in H.M.
 Does not depend on medial-
temporal lobe–ventral-prefrontal-
lobe memory system that subserves
episodic memory

Question 191

HM AND IMPLICIT
MEMORY

Answer 191

Some of HM’s (and other
amnesiacs’) memory
abilities were retained
 Spared skill learning 
procedural memory
 Mirror tracing task
 Mirror reading
Learning occurs in the
absence of episodic recall
Memory for skill, but not
when learning occurred

Question 192

NEURAL SUBSTRATES
OF IMPLICIT MEMORY

Answer 192

Basal ganglia
 Reduced habit learning  procedural
memory
 Huntington’s and Parkinson’s Diseases
Amygdala
 Fear conditioning
Premotor cortex (procedural)
Cerebellum (procedural)
Diencephalon
 Thalamic nuclei; Mammillary bodies
Basal forebrain  Numerous
small nuclei

Question 193

CAUSES OF AMNESIC
SYNDROMES

Answer 193

Traumatic brain injury
Neurological disorders
 Dementia
Cerebrovascular accident
(stroke)
Hypoxic events
Infections e.g. herpes
simplex encephalitis  
Neurosurgery i.e. HM
Korsakoff Syndrome

Question 194

KORSAKOFF SYNDROME:
ALCOHOL AND MEMORY

Answer 194

Due to chronic alcoholism 
vitamin B1 (thiamine) deficiency
Degeneration of diencephalic
regions
 Mammillary bodies
 Neural circuit with hippocampus
Damage is bilateral
Anterograde and retrograde
amnesia
Confabulation (attempt to fill gaps in memory by creating false memories) is a frequent
symptom
Implicit learning is often
retained
IQ largely intact, but EF and
memory impaaired

Question 195

HERPES SIMPLEX
ENCEPHALITIS

Answer 195

Herpes simplex virus infection of the brain
Untreated 70-80% mortality rate
 Treated, ~50% moderate to severe neurological deficit
Enters brain via olfactory tract or trigeminal nerve
Haemorrhagic effect on brain
 Medial temporal lobes, hippocampus, orbitofrontal cortex,
among other areas
Bilateral effects although can be assymetrical
Most common neuropsychological deficit is dense
global anterograde amnesia
 Anomic aphasia  semantic dementia-like presentation
Nomic = naming

Question 196

NORMAL AGEING AND
COGNITION

Answer 196

Patterns of ageing differ for different abilities:
 Crystallised intelligence remains more stable with
advancing years (semantic LTM)
 Fluid intelligence declines with age
 Speed of mental processing slows down
Attention deficits with more complex tasks ()
Memory
 Greater effort required to learn new skills
 STAM remains intact; WM declines
 Decline in episodic memory ()
 Normal procedural/implicit memory processes
Executive functions/mental flexibility declines (**)
 More likely to “stick with what you know”

Question 197

BRAIN CHANGES IN
NORMAL AGEING

Answer 197

Loss of grey matter with
increased age
 Not uniform across the cortex
Prefrontal cortex most affected
 Up to 5% loss per decade after 20
years ()
 Lateral PFC ~1% per year ()
More posterior regions less so
(i.e. occipital lobe relatively
unchanged)
Striatal areas (3% loss/decade)
and caudate (0.75%) affected
Methodological issue  data
from cross-sectional research

Question 198

BRAIN CHANGES IN
NORMAL AGEING

Answer 198

White matter density
reduced
 Increased incidence of
WM lesions
All areas show loss of
density
 PFC & anteriorCC more so
Frontal white matter
changes a specifically
age-related change 
not any worse in AlzD

Question 199

MILD COGNITIVE
IMPAIRMENT (MCI)
MILD NEUROCOGNITIVE
DISORDER (DSM-5-TR)

Answer 199

An intermediate stage between normal age
related cognitive change and dementia
MCI can affect any area of cognitive
functioning; most research focuses on
amnesic-MCI
 Deficits in both encoding and retrieval of new info as
with Alzheimer’s
 Only memory function affected  not dementia
People identified with MCI have greater risk
of developing dementia but not all do
 Research looking at ways to predict transition

Question 200

MAJOR NEUROCOGNITIVE
DISORDER (DSM-5-TR)

Answer 200

Called dementia in DSM-IV-TR
1. Evidence of significant cognitive
decline from a previous level of
performance in one or more
cognitive domains — such as
complex attention, executive
function, learning, memory,
language, perceptual-motor or
social cognition.
This evidence should consist of:
- Concern of the individual, a knowledgeable
informant (such as a friend or family
member), or the clinician that there’s been
a significant decline in cognitive function;
and
- A substantial impairment in cognitive
performance, preferably documented by
standardized neuropsychological testing. Or
if neuropsychological testing isn’t available,
another type of qualified assessment.
2. The cognitive deficits interfere
with independence in everyday
activities (e.g., at a minimum,
requiring assistance with
complex instrumental activities
of daily living, such as paying
bills or managing medications).
3. The cognitive deficits don’t
occur exclusively in context of a
delirium, and are not better
explained by another mental
disorder.
SPECIFY whether due to
Alzheimers, FTD, PD, HD, Lewy
Body Dementia…
MINOR neurocognitive disorder
exists when the symptoms DO NOT
significantly interfere with ADLs

Question 201

Different types of dementia

Answer 201

Question 202

ALZHEIMER’S DISEASE
(AD)

Answer 202

Most frequent dementia type (>
50%)
Age of onset usually > 65
Prevalence
 Australia 2012 (AIHW): 353, 800 people
(~10% of people > 65; ~30% of people
>85 years)
 25, 100 with younger onset dementia (<65)
Insidious onset, continuing decline
Diagnosis is one of exclusion
 Requires medical investigation for
reversible causes of cognitive impairment

Question 203

NEUROPATHOLOGY OF
AD

Answer 203

Two major neuropathogical findings
- Patient “Auguste D”, 51 years
- β-amyloid plaques found mainly in fronto-temporal cortex (***)
- Neurofibrillary tangles due to accumulation of tau protein
Primary areas affected are cortical
- Subcortical regions also affected early
- Basal forebrain cholinergic complex
Non specific pathology
- Downs Syndrome (chromosome 21 also codes for β-amyloid)
=Earlier onset of AD symptoms in DS
- Seen in older people without dementia

Question 204

CAUSES OF
ALZHEIMER’S DISEASE

Answer 204

Acetylcholine depleted in basal
forebrain cholinergic complex  loss
of nucleus basalis of Meynert
 AD patients show a greater drop in ≥ 2
neurotransmitters than controls of the
same age
Genes: causative or modulatory
 ApoE gene  Modulates risk
 Role in maintenance and repair of neurons
via distribution of CNS lipids (fats)
 Some alleles have neuropathological
effects  apoE4/4
 ApoE4 allele associated with lower
glucose metabolism; even in people
without clinical signs of Alzheimer’s
disease
 Causative (early onset < 65)
 Presenilin (< 5% all early cases)
 Amyloid precursor gene (<10%)
Down syndrome and Alzheimers

Question 205

Risk and protective factors of Alzheimer

Answer 205

Question 206

CLINICAL/
NEUROPSYCHOLOGICAL
PROFILE IN AD

Answer 206

“Triad” of symptoms (***)
 Memory impairment is primary characteristic
 Word finding deficits
 Visual-spatial deficits
Patients may first present due to psychiatric
symptoms i.e. depression or anxiety or “not coping”
 Often reactive to subtle changes in cognition
Memory deficits may present as paranoia, delusions
and suspiciousness
Exacerbation of premorbid personality
characteristics
 Difficulty making diagnosis of AD

Question 207

NEUROPSYCHOLOGICAL
DEFICITS: MEMORY

Answer 207

Poor declarative learning (them to do it themselves) often the first sign (***)
 “anterograde amnesia”
Difficulties at all levels of the memory process
 Encoding, storage and retrieval
 Extreme impairment in learning new information
 Deficits in both episodic and semantic memory
Gradual loss of “semantic associations” and
conceptual knowledge about the world
 can retrieve superordinate (dog, bird) but not subordinate
(poodle, robin)
Performance intact in implicit memory tasks,
especially skills with motor or sensory components
 Implications for “rehab” or interventions/strategies

Question 208

OTHER
NEUROPSYCHOLOGICAL
DEFICITS IN AD

Answer 208

Anomia common in early stages
 With disease progression, deficits more extreme and profound
 Later comprehension as well production deficits
Visuo-spatial deficits in early to middle stages
 losing way; poor orientation in new then old environments
Executive dysfunction subtle in early stages
 perseveration, reduced flexibility, poor shifting
 poor ability to organise, plan and problem-solve
 personality changes, poor insight and monitoring own
behaviour, poor awareness of consequences
Orientation to person, time and place declines later
Poor divided and alternating attention

Question 209

TREATMENTS FOR
ALZHEIMER’S DISEASE

Answer 209

Most treatments focus on
depleted neurotransmitters
Donepezil (Aricept)
 Inhibits (acetyl)cholinesterase,
enzyme which degrades
acetylcholine  increases
circulating acetylcholine
 Mild to moderate AlzD
Memantine (Ebixa/Memanxa)
 Works (mostly) on glutamatergic
system (NMDA receptors)
 Moderate to severe AlzD
Symptomatic treatments
Experimental treatments that
remove amyloid  successful
mouse model for this

Question 210

NEUROPLASTICITY

Answer 210

The nervous system’s potential to physically or chemically modify
itself in response to environmental change and to compensate for
age-related changes and injury
 Process underpins learning in relation to all experience
Changes occur at the level of the synapse (remember long-term
potentiation)
 Experience forges synaptic pathways
 Dendritic morphology
 Dendritic spines are extensions of the neuron membrane that allow more spaces for
synapses
 Cells with few or no dendrites have limited space for inputs
 Cells with complex dendritic protrusions may have space for tens of thousands of
inputs
Therefore more dendrites – more connections
Experience leads to the generation of new neurons, plus increased
dendritic plasticity to forge new pathways and strengthen existing
ones
 London taxi drivers have larger than normal hippocampal volumes in the posterior
region

Question 211

ENRICHED EXPERIENCE
AND PLASTICITY

Answer 211

Animal studies show that environments that provide
increased social, sensory and motor experience
increases brain weight
 Neurogenesis (new neurons)
 More synapses per neuron
 More glial cells (astrocytes)
 More blood capillaries
 Higher mitochondrial volumes
These results can be inferred for human development,
but also for rehabilitation after brain injury

Question 212

NEUROPLASTICITY &
RECOVERY OF FUNCTION

Answer 212

Neuroplasticity/brain plasticity
 The ability of the brain to change its synapses and
pathways in response to changes in environment,
behaviour, neural processes or injury
Reorganisation
 Changes in cortical maps or functional organisation of
the brain that can occur when sensory input is lost i.e.
after amputation  phantom pain
Either process can be positive or negative in
outcome
 Rehabilitation/interventions following brain insult aim to
direct these inherent processes in a positive direction

Question 213

How does the brain respond to injury?

Answer 213

Question 214

Plasticity Can Be Maladaptive

Answer 214

• Exposure to mind-altering drugs produces
  alterations in dendritic length and spine
  density
  – Addicts’ behavior results in prefrontal morphology
• Other maladaptive changes in brain maps
  – Pathological pain
  – Pathological response to sickness
  – Epilepsy
  – Dementia

Question 215

Experience-Dependent Changes Interact

Answer 215

• Environment and drug interactions
  – Stimulant drugs block the dendritic changes seen
  after exposure to a complex environment
  – Complex environments can change the response
  to drugs
  – Stress
• Associated with changes in dendrite morphology and
  neurogenesis
• Interacts with experience-dependent changes in the
  brain related to drugs, brain injury, complex housing,
  etc.

Question 216

RECOVERY OF
FUNCTION

Answer 216

Recovery influenced by a variety of factors
 Severity/number of insults
 Age, premorbid cognitive status & brain integrity
 Psychological factors
 Motivation and emotional characteristics
Rehabilitation
 Restorative  repetitive exercise; effective for motor
symptoms of stroke
 Less evidence for effectiveness in cognition/language (although see
CILT next slide)
 Compensatory  training in use of compensatory
strategies for difficulties
 i.e. memory “prostheses” such as use of notebooks, reminder
apps etc

Question 217

RECOVERY OF
FUNCTION pt2 (stroke)

Answer 217

Rehabilitation for language
impairments after stroke
(National Stroke Foundation
Guidelines 2010)
 As much as possible in first 6 months
 Piggybacking on underlying neural
changes
 Start as early as tolerated
Constraint-induced
language/aphasia therapy (CILT)
 Language analogue of CI Movement
Therapy
 Constraint achieved by requiring only
speech for communication (not drawing
or pointing) and focussing on defined
parts of speech

Question 218

MOTOR SYSTEM: NOT JUST PRIMARY
MOTOR CORTEX

Answer 218

Cortico-spinal tract
Projects from cortex to spinal
cord
 Basal Ganglia
 Cerebellum
 Brainstem
 Spinal Cord
Also called the pyramidal tract
 90-95% of fibres decussate (cross
over to the other side) at the level
of the medulla in the “pyramids”
(lateral corticospinal tract  pic)
 Other 10% cross over lower in the
spinal cord (anterior or medial
corticospinal tract)

Question 219

THE NEOCORTEX: INITIATING
MOVEMENT

Answer 219

Medial structures
- Supplementary motor area
- Cingulate cortex

Question 220

APRAXIA***

Answer 220

A “disorder of skilled
[voluntary] movement not
caused by weakness,
akinesia, deafferentiation,
abnormal tone/posture or
movement disorder”*
(Heilman, 1979)
Absence of actions, or
carrying out inappropriate
actions (often when using
objects)
 no impairment of the receptive
language or the motor
apparatus
 Example: person unable to
brush own teeth
Person not usually aware
of problem (anosognosia)*
Subtypes
 Oral (buccofacial) apraxia
 Limb apraxia (see
ideational and ideomotor)
 Constructional apraxia
 Dressing apraxia
 Callosal apraxia

Question 221

CLASSIC VIEW OF
APRAXIA SUBTYPES Ideational
(dissociation) apraxia***

Answer 221

Inability to carry out a series of
movements involving some
ideational or planning aspect
 Inappropriate use of objects i.e.
person may try to light a candle
by striking a match on it
 Problems with sequencing
complex movements
Situational component in
ideational apraxia i.e. De Renzi
et al (1968) patient can use
toothbrush appropriately at
home but not when tested for
experiment
“Conceptual” apraxia  loss of
understanding of relationship
between object and its use
 i.e. using toothbrush as a razor

Question 222

Ideomotor apraxia***

Answer 222

“Inability to mime use of an
object using simple gestures,
despite normal dexterity”
(Hecaen, 1978)
 Most commonly reported apraxia
 No ideational component
 Does not involve use of an object. If
you gave them the relevant object
they could demonstrate its use
without issue
Examples: Pt is asked to mime
using a hammer
 uses own closed fist as a hammer, or
use own finger as a toothbrush when
asked to mime the normal act of
brushing teeth (i.e. instead of
pretending to hold a toothbrush

Question 223

NEUROANATOMICAL
BASIS OF APRAXIA

Answer 223

Liepman (1900; 1907)
 L hem language centres disconnected from R hem motor areas
that control fine motor skills on the L side of the body (CC
lesion??)
 L hem contains hand movement “formulas” that are disconnected
from the R hem motor cortex
Geschwind (1965)
 Disconnection between posterior language areas and motor
association areas
Hanna-Pladdy et al (2001)
 Importance of basal ganglia
Most cases of apraxia show left hemisphere damage;
symptoms more severe with anterior damage  wide
variety of cortical and subcortical regions can cause
apraxia

Question 224

EXTRAPYRAMIDAL AND
SUBCORTICAL STRUCTURES

Answer 224

“Extrapyramidal” systems
 Additional motor systems
that do not travel through
the pyramidal structures of
the medulla
 Important for involuntary
movements
 Reflexes
 Postural control
 “Readiness” activation of
muscles
Cerebellum
Basal ganglia

Question 225

CEREBELLUM INPUTS
AND OUTPUTS

Answer 225

Question 226

THE BASAL GANGLIA

Answer 226

Question 227

DISORDERS OF THE
BASAL GANGLIA: Hypokinetic disorders***

Answer 227

Parkinson’s Disease
 Loss of dopamine cells in the
substantia nigra and their
input to the basal ganglia
 Results in muscular rigidity and
difficulty initiating and
performing movements
Difficulty making
movements = hypokinetic
symptoms

Question 228

DISORDERS OF THE
BASAL GANGLIA: Hyperkinetic disorders***

Answer 228

Huntington’s Disease
 Destroys cells in the caudate and
putamen
 Results in involuntary and
exaggerated movements –
Choreiform movements
Tourette’s Syndrome
 Related to damage to the caudate
putamen
 Results in unwanted tics and
vocalizations
Involuntary movements =
hyperkinetic symptoms

Question 229

PARKINSON’S DISEASE

Answer 229

Neurodegenerative disorder
affecting mainly motor skills
 dementia also possible
Mean age of onset ~50;
male/female 2:1
 Pringsheim et al (2014) All per 100,000
 41 in 40-49 years
 107 in 50-59 years
 173 in 55-64 years
 428 in 60-69 years
 425 in 65-74 years
 1087 in 70-79 years
 1903 in >80 years
??accelerated aging
If untreated, death occurs ~10
years after onset

Question 230

MOTOR SYMPTOMS OF
PARKINSON’S DISEASE***

Answer 230

Akinesia
 Slowed movement
(bradykinesia)
 Reduced movement
(hypokinesia)
Rigidity
 Resisting passive movement
Tremor at rest
 Stress increases tremor
 Tremor less in sleep & during
voluntary action
Postural instability
Positive vs negative Sx

Question 231

COGNITIVE SYMPTOMS
OF PARKINSON’S
DISEASE

Answer 231

Psychological Sx in PD are as variable as motor Sx
A significant proportion of patients show cognitive Sx
 Emotion
 flat or blunted affect (caution re facial Sx)
 Clinically significant depressive disturbances occur in 40–50 % of patients with PD
(Rejinders et al., 2008)
 Diagnosis of anxiety disorder is also higher than the general population in people with
PD
 Bradyphrenia
 Slowed thinking
 Dementia
 Long term studies have shown 50-80% of people with PD will develop dementia (higher
than general population at a younger age)
 Associated with Lewy bodies (abnormal microscopic deposits composed chiefly of
alpha-synuclein, a protein widely found in the brain).

Question 232

NEUROPATHOLOGY AND
TREATMENT OF PD

Answer 232

Loss of the striatal
dopamine pathway
- runs from the
midbrain (substantia
nigra), to the basal
ganglia
- L-dopa, 1950s
- Stereotaxic surgery
- Deep brain
stimulation
- Cell transplantation

Question 233

SPEECH AND
LANGUAGE DISORDERS

Answer 233

Speech/language disturbances frequent after stroke 
67% of patients have aphasia, speech dyspraxia or
dysarthria acutely
Aphasia
 refers to the collective deficit in language comprehension and
production
 ~40% of all strokes produce some aphasia, at least acutely
 Lesion in language centres
 ‘Remote’ effects (oedema)
Dysphasia
 An impairment (partial loss) of language ability (used
synonymously with aphasia)
Causes
 Dementias; strokes
 Primary vs secondary language deficits
Speech dyspraxia
- motor production of speech

Question 234

PAUL
BROCA

Answer 234

1862: demonstrated the
brain lesion of his first
patient who had suffered
from “aphémie”
 Patient: M. Leborgne (“Tan”)
 Uttered only “tan” and
occasionally curses
Concluded after autopsy of
“Tan”, that the integrity of
the “left frontal convolution”
was responsible and
necessary for articulation
David Ferrier (1843-1928)
named this region “Broca’s
convolution- the motor
speech area.”

Question 235

NONFLUENT APHASIA BROCA’S
APHASIA

Answer 235

Speech in Broca’s
aphasia is telegraphic
and effortful
 Nonfluent aphasia
Grammar comprehension
affected (see example )
Word finding difficulties
Poor pronunciation
 Dysarthria (loss of control
over speech muscles)
 Speech apraxia (loss of
ability to program
articulation)  repetition
difficulties
Comprehension
deficits apparent
when meaning
depends on precise
arrangement of
words / structure
 difficulty processing
grammatical aspects of
language: agrammatism
 ‘The boy ate the cookie’
vs ‘The boy was kicked
by the girl

Question 236

NEUROANATOMY OF
BROCA’S APHASIA

Answer 236

Frontal operculum  “motor
speech area”
 Articulation deficits
 If only damage here, most
likely to resolve
Precentral gyrus
 Underlying WM
 Subcortical structures incl. BG
and thalamus
Insula
 Dronkers et al: insula damage
required for speech apraxia
 Prosody affected
 Foreign Accent Syndrome

Question 237

KARL WERNICKE

Answer 237

1874 (aged 26): published
“Der aphasische
Symptomenkompleks”
 described sensory aphasia,
localised at the temporal
lobes, as well as alexia and
agraphia
Tried to relate the various
aphasias to impaired
“psychic” processes in
different regions of the
brain
Demonstrated dominance
of left hemisphere in
language function

Question 238

FLUENT APHASIA
WERNICKE’S APHASIA

Answer 238

Both written and spoken
comprehension affected
Fluent-sounding speech,
lack of meaning (word
salad)
 Fluent aphasia
Associated with anomia-
difficulty finding labels for
things
Neologism: new non-words
Errors in producing specific
words: paraphasias
 Semantic paraphasias
 Phonemic paraphasias

Question 239

NEUROANATOMY OF
WERNICKE’S APHASIA

Answer 239

Primary auditory cortex
 Heschl’s gyrus
Wernicke’s area
 2° auditory processing area
 Evaluates input from 1° auditory
cortex with reference to semantic
word knowledge stored in
auditory-verbal memory (L
temporal lobe)
L Wernicke’s area
 Verbal, semantic information
Homologous R hem area
 Analogical reasoning  Eureka
moments
 Subordinate, related meanings of
ambiguous words
 i.e. bank  river vs money

Question 240

OTHER APHASIA
SUBTYPES***

Answer 240

Fluent
Conduction aphasia*
 Normal speech comprehension/
production, with impaired
naming/repetition of non-words
 Lesion in arcuate fasciculus*
disconnecting Broca’s and Wernicke’s
areas
Transcortical sensory aphasia
 Disconnection of W’s area from
parietal association cortex
 Speech spontaneous and fluent
sounding
Nonfluent
Transcortical motor aphasia
 Disconnection of B’s area from SMA
 Transient mutism; prosody affected;
telegraphic speech

Question 241

NEURAL CONNECTIONS
BETWEEN LANGUAGE
ZONES

Answer 241

Lesion studies in humans
Wernicke–Geschwind Model
 Word sounds are sent to the Primary Auditory Cortex
 Word meaning is represented in Wernicke’s area
 Word meaning is sent to Broca’s area via the arcuate
fasciculus
 Broca’s area sends instructions for speech
articulation to the motor cortex
 To read, visual areas send information to the angular
gyrus and to Wernicke’s or Broca’s area

Question 242

Dual Language Pathway***

Answer 242

Dorsal language pathways (phonemes)
Ventral Language pathways (semantics)

Question 243

RECOVERY FROM
APHASIA

Answer 243

Depends upon size, location and nature of
lesion:
 Initial severity of stroke
 Progressive decline with dementia
1/3 of patients recover within 3 months
Complete recovery unlikely after 6 months
 Improvements past this time due to adaptation
Mechanisms of recovery not fully understood
 Plasticity of remaining L hem?
 R hem taking greater language role?

Question 244

THE VISUAL SYSTEM 1 –
STRUCTURES OF THE EYE

Answer 244

Question 245

THE VISUAL SYSTEM 2 –
RETINA

Answer 245

Remember: Cells
found in the retina
Rods – specialised
for:
 low light levels and
B&W tones
 Low spatial acuity
Cones –
specialised for:
 Higher light levels
and colour vision
 Responsible for
higher spatial acuity

Question 246

THE VISUAL SYSTEM 3 –
BRAIN PATHWAY

Answer 246

Geniculostriate pathway (via lateral geniculate nucleus
tectopulvinar pathway (via superior colliculus)

Question 247

THE VISUAL SYSTEM 4 –
BRAIN STRUCTURES

Answer 247

V1: striate cortex
 Retinotopic map
V2-V5: prestriate (2°
association) cortex
 Basic interpretation of visual
information
V2: light, line orientation,
features of shapes
V3: movement of objects (no
colour)
V4: colour
V5 (area MT): direction of
movement

Question 248

Scotoma

Answer 248

patchy visual field
deficit caused by cortical
damage

Question 249

CORTICAL BLINDNESS
AND BLINDSIGHT

Answer 249

Cortical blindness:
loss of vision due to
bilateral destruction of
V1(striate cortex)
 Eyes undamaged. It is
Blindsight: ability to
make simple
perceptual decisions
about visual stimuli
 no conscious awareness
of the stimuli
 damage to striate cortex
Case of DB
 (Weiskrantz, 1986)
Surgery for right
occipital arterio-venous
malformation  visual
field scotoma (lower L
quadrant)
Result:
 Unaware of stimuli in L
visual field
 Some visual judgements
well above chance:
 is stick horizontal or vertical?
 is drawing a cross or circle?

Question 250

ANTON’S BLINDSIGHT

Answer 250

Preservation of other visual abilities without
awareness
 Can localise spots or bars of light
 Movement perception
 Basic colour judgements
 Form perception: preserved reach to grasp
Why/how?
 Tectopulvinar pathway intact, while geniculostriate
pathway disrupted?  basic visual processing without
higher order processing and awareness
Problem: not all people with comparable lesions
display blindsight

Question 251

ANTON’S SYNDROME
(CORTICAL BLINDNESS WITHOUT
AWARENESS OF DEFICIT)

Answer 251

Cortical blindness without awareness
 Visual anosognosia – Anosognosia = lack of insight into
impairment
 Damage to V1 (Occipital lobe)
Sufferers will affirm, often quite adamantly and in
the face of clear evidence of their blindess, that
they are capable of seeing
 Dissmiss evidence of their condition
 Use confabulation to fill in missing sensory input
 Remember confabulation is NOT lying – rather it is UNCONSCIOUS filling of
the gaps in memory or sensory experience

Question 252

THE AGNOSIAS***

Answer 252

“A failure of recognition
that cannot be
attributed to elementary
sensory defects, mental
deterioration, attentional
disturbances, aphasic
misnaming or unfam-
iliarity with sensorially
presented stimuli”
Bauer, 1993
Not a memory disorder
Can occur in most
sensory modalities (see
Martin p 215)

Question 254

APPERCEPTIVE
VISUAL AGNOSIA***

Answer 254

Inability to recognise objects
due to deficit in forming stable
perceptual (mental)
representations of the visual
stimulus
 Most commonly as a result of
damage in the RIGHT parietal or
temporal region
Patients are unable to copy
even simple drawings or match
objects although are able to
identify individual objects or
drawings
Difficulty identifying objects
from unusual perspectives

Question 255

ASSOCIATIVE VISUAL
AGNOSIA ***

Answer 255

Inability to associate
perceptual information
with semantic info
Usually modality specific
Can copy pictures, but
cannot draw from memory
 Identification of line drawing
or picture of an object is
more difficult than
identification of actual object
Left hemisphere lesions
most frequent cause

Question 256

PROSOPAGNOSIA:
A CATEGORY-SPECIFIC
VISUAL AGNOSIA ***

Answer 256

Inability to recognise familiar
faces (even ones own face)
 Instead other cures are used to
recognize friends and family, e.g.
voice
Can typically recognise objects
Damage to Fusiform face area
(FFA)
Lesion location: mostly R
hemisphere damage
 PET in healthy adults: R parieto-
temporal cortex activation in face
perception
 Not just the FFA: importance of
amygdala in emotional response to
familiar faces

Question 257

FUSIFORM NOT JUST FOR
FACES?

Answer 257

What skills do we
need to recognise
faces?
FFA activated by
categorisation and
fine-grained
distinctions
Gauthier et al.,
(2000)
 Bird watchers, car
experts
 R FFA/Occipital Activation

Question 258

VISUAL SPATIAL NEGLECT***

Answer 258

Failure to respond, report
or attend to stimuli or
events in the hemifield
contralateral to brain injury
Damage usually temporal-
parietal***
Can occur with either L or
R hem strokes
Usually involves neglect of
personal or body space
Anosognosia (unawareness
of deficit) common in
neglect

Question 259

DSM-5-TR neurodevelopmental disorders

Answer 259

A group of conditions with onset in the developmental period
◦ Often before primary school
◦ Produces impairments in personal, social, academic or occupational functioning
◦ Frequently co-occur (e.g., Autism & Intellectual Disability)
◦ Behavioural issues or differences in achieving expected milestones
Intellectual disability and specific learning disorders (separate presentation)
Communication disorders
Autism
ADHD
Motor disorders (incl tic, disorders and developmental discoordination disorder)

Question 260

Communication Disorders

Answer 260

Language
◦ Includes the form, function, and use of a conventional system of symbols
in a rule-governed manner for communication
◦ Spoken words, sign language, written words, pictures
◦ Expressive and receptive
◦ Difficulty manifest when abilities are substantially below age expectations
and significantly interfere with effective communication across all settings
(including academic achievement)
◦ Other caused of impairment must be ruled out
◦ E.g. hearing disorder, motor disorders (dysarthria), cerebral palsy, clef palate, selective mutism
etc.

Question 261

Autism Spectrum Disorder

Answer 261

Characterised by persistent deficits DIFFERENCES in social communication and
interaction across multiple contexts
Symptoms include
◦ Differences in social reciprocity, non-verbal communicative behaviours (e.g., eye contact, body
language), developing and maintaining, and understanding social relationships
◦ Restricted repetitive patterns of behavior, interests or activities
◦ E.g. stereotyped motor movements (e.g., hand flapping), insistence on sameness, highly restricted or fixated interests,
hyper (e.g. adverse response to specific textures or sounds) or hypo (apparent indifference to pain/temperature)
sensory reactivity
◦ Severity SUPPORT NEEDS should be specified
◦ Level 1 – Requiring support
◦ Level 2 – Requiring substantial support
◦ Level 3 – Requiring very substantial support

Question 262

Autism prevalence and factors

Answer 262

Prevalence rising over the past 4 decades from 1:2000 in 1980 to 1:68
estimated in 2016 in USA
◦ Australia 1:70 in 2018
Cause of increase uncertain
◦ Changes in diagnostic tools and criteria; more accurate
◦ Increased community (and clinician) recognition and awareness
◦ Epigenetic factors? Gut health?
Four times as prevalent in boys than girls
Rates fairly consistent across different races

Question 263

Autism con.

Answer 263

Can be noticeable from birth
◦ Babies avoid physical contact by arching their backs to pull away from caregivers, or by going
limp when held
In about 1/3 of children symptoms emerge at around 3 years after previous
typical development
◦ There is no scientific evidence of a link between vaccinations and autism
◦ Gerber & Offit (2009) – 20 epidemiological studies have shown that there is no link between
the measles, mumps, rubella vaccine or the preservative thimerosal and autism
◦ Studies with high statistical power across many different countries
◦ Powered to detect even a rare association – not found

Question 264

The Autistic Brain

Answer 264

Brains of autistic children appear remarkably typical
Unusual neuronal maturation rates compared to typically developing children
◦ MRI studies have shown the autistic brain is 6-10% greater in total volume
◦ Especially clear in the amygdala – fear response association with social withdrawal?
◦ Atypical connections between neural regions suggested
◦ <100 different genetic differences, so no single “autism gene”
◦ Role of epigenetics (things that cause modification of gene expression independent of the genetic code; e.g. toxins)
Treatment SUPPORTS AND ACCOMMODATIONS
◦ No medical interventions exist
◦ Psychoeducation, speech therapy, occupational therapy
◦ Psychotherapy appropriate in some contexts
◦ Intensive behavioural therapy “empirically supported” but controversial and potentially traumatic

Question 265

Tourette’s Syndrome (Gilles de
la)

Answer 265

Tic = semivoluntary actions, “fragments” of normal voluntary actions
◦ Vocal tics – e.g. sudden cries, coprolalia (uttering vulgar words)
◦ Physical tics – e.g. hitting, lunging, or jumping
Average age onset ~7 years
◦ Dx requires presence of tic(s) for at least 12mo; Boys > girls
Initially viewed as a psychiatric disorder
◦ Tic “performed” to relieve tension
Frequent comorbidities with other “fronto-striatal” disorders
◦ Obsessive Compulsive Disorder; ADHD

Question 266

Tourette’s Syndrome

Answer 266

Appears to be familial; autosomal dominant with
incomplete penetrance (means not everyone who carries the gene
will express the disorder)
Some suggestions of environmental causes i.e.
paediatric autoimmune neuropsychiatric disorder
associated with streptococcal infections (PANDAS)
 Autoimmune reaction against
streptococcus also affects basal ganglia
Additional neuropsychological deficits seen in
control and execution of motor behaviors i.e.
response execution and inhibition of prepotent
responses
Treatment: Habit Reversal Therapy
PANDAS
* Associated with tics and can be
difficult to differentiate from
Tourette’s

Question 267

Comorbidity in Tourette’s
Syndrome ***

Answer 267

~90% of TS patients have
some form of comorbid
psychopathology
Disorders affecting frontal
lobes and connections to
subcortical areas i.e. basal
ganglia
◦  frontostriatal dysfunction
Often aggregate together***
 high comorbidity
between these disorders

Question 268

Tourette’s Syndrome Neuro con

Answer 268

Basal ganglia (BG) implicated
◦ Dorsal striatum (caudate nucleus and putamen
structures of BG)
◦ Roles include mediation of cognition involving motor function,
some EF including inhibitory control and impulsivity tics
◦ Especially right hemisphere
◦ Treated with haloperidol
◦ Blocks dopamine synapses in the BG
Urge to make involuntary movements or
vocalisations may be associated with normal
“urge-to-action” features of behavior (e.g.
contagious yawning)
◦ Tics may result from activity in the brain systems
that mediate normal learning by imitation

Question 269

Epilepsy

Answer 269

Disorder causing paroxysmal electrical
discharges in the brain
◦ We all have the capacity to have a
seizure
Australia 2005: 120, 000 – 200, 000
affected; affects all ages
Higher prevalence in childhood; “grow
out of it”
◦ Most children who have a seizure do not go
on to develop epilepsy

Question 270

Classification of epilepsy

Answer 270

Genetic
◦ Resulting directly from known genetic
defect
Structural/Metabolic
◦ Brain malformations or tumors
◦ Acquired disorders such as stroke, trauma,
or infection
Unknown
◦ Formerly “idiopathic”

Question 271

Classification of seizure types

Answer 271

Tonic - muscle rigidity
Clonic - uncontrolled jerking
Focal- focused
Generalised - unspecific

Question 272

Focal seizures with awareness
retained (formerly Simple partial seizures)

Answer 272

Question 273

Focal seizures with impaired awareness
(formerly complex partial seizures)

Answer 273

Question 274

Intellectual Disability –
DSM-5-TR

Answer 274

The following 3 criteria must be met:
A. Deficits in intellectual functions confirmed by clinical assessment and standardized
intelligence testing
◦ IQ < 70 (2 standard deviations below the mean)
B. Deficits in adaptive functioning that result in failure to meet developmental and socio-
cultural standards for personal independence and social responsibility
◦ Need for support in activities of daily life
C. Onset during the developmental period
Specifiers according to severity on the basis of adaptive functioning (not IQ) in the
domains of conceptual, social, and practical abilities.
◦ mild
◦ moderate
◦ severe
◦ profound

Question 275

Specific Learning Disorders – DSM-5-TR

Answer 275

A neurodevelopmental disorder that impedes the ability to learn or use
specific academic skills which are the foundation for other academic
learning.
◦ e.g., reading (dyslexia), writing (dyslexia, dysgraphia), or arithmetic
(dyscalculia)
The learning difficulties are ‘unexpected’ in that other aspects of
development seem to be fine.
◦ i.e. in the context of an otherwise normal IQ
Early signs of learning difficulties may appear in the preschool years (e.g.,
difficulty learning names of letters or counting objects),
◦ but they can only be diagnosed reliably after starting formal education.
Disorder has persisted for at least 6 months, despite the provision of
interventions that target those difficulties

Question 276

Epidemiology of learning
disorders

Answer 276

DSM-5 states 5-15% of school aged children for all
learning disabilities combined
◦ Dyslexia 5-17% of school age children
◦ Dyscalculia ~1% according to DSM
◦ 3-6.5% according to other prevalence studies
◦ Disorder of written expression rare ON ITS OWN; frequently
comorbid with dyslexia
Male > female for dyslexia and LDs in general; M=F
dyscalculia

Question 277

Etiology of learning
disabilities

Answer 277

Assumed to be due to underlying brain impairment
◦ Not due to poor effort, poor teaching, parenting, cultural/ethnic background
◦ HOWEVER cultural/language differences can affect diagnosis and treatment
Genetic/neurobiological basis for LDs
◦ Family history of reading and/or mathematics disorders
◦ Language centres of brain affected during gestation (~5-7th month
pregnancy); Autopsy findings looking at males with dyslexia
Recent identification of at least 6 candidate genes for
dyslexia
◦ 4 of these associated with neuronal migration in prenatal brain
(rodent models)

Question 278

Operationalising learning
disabilities

Answer 278

Diagnostic criteria: see DSM-5-TR
UNTIL DSM-5 Discrepancy between overall cognitive function
and the specific cognitive function
◦ E.g. Full Scale IQ in the average range (100) and other performances
2SD below this  Reading Ability with standard score of 70 (1SD = 15
pts)
◦ OR FSIQ 110, Reading Ability 80  PROBLEM because 80 is
considered Low Average, not impaired…
DSM-5: 2SD below POPULATION MEAN + Response to intervention
Frequently associated with demoralisation, low self-esteem, social
difficulties
◦ Mild language and motor developmental delays common

Question 279

Dyslexia
(Specific learning disorder with
impairment in reading)

Answer 279

Difficulties in reading, writing, spelling and phonological
discrimination
Biological disorder - Strong suggestion of genetic aetiology
(cause)
Traditional subtypes (according to Boder’s 1973 scheme)
◦ Dysphonetic/phonological- Little or no understanding of letter-
sound relationships (grapheme-phoneme associations)
◦ Dyseidetic/surface- Inability to read words as a whole
◦ Mixed (Dysphonetic-dyseidetic): Problems in both letter sound
relationships and reading the word as a whole.
More recently  acknowledgement of broader cognitive
difficulties

Question 280

Phonologic model of dyslexia

Answer 280

Primary deficit proposed to be deficits in phonological processing  difficulties in
associating sounds with letter strings
◦ Reading is slow and effortful
Early phonological processing deficits (poor phonological awareness) associated with
later difficulties
◦ interventions targeting phonological processing assist reading development
Persons with dyslexia show reduced activation of left posterior temporal and
temporoparietal cortices (auditory processing) during phonological processing tasks on
PET and fMRI
◦ Inconsistent neural processing of sound
Other cognitive findings in dyslexia:
◦ Slowed speed of processing
◦ Short term auditory memory deficits
Phonological deficits not a universal finding: more common in languages with many
irregularities incl. English

Question 281

Visual processing difficulties in reading
disorders?

Answer 281

Visual processing difficulties seen in some with dyslexia
◦ Not the basis for disorder  vision therapy does not improve reading
◦ See RANZCO 2016 statement about vision therapy for dyslexia
Flicker fusion slower in dyslexia  involvement of magnocellular
visual system (cf parvocellular visual system)
◦ Located in inferior part of lateral geniculate nucleus; sensitive to movement,
stimulus change and spatial location
◦ Activated during saccadic eye movement  important aspect of fluent
reading
◦ In dyslexia, hypothesised that magnocellular system fails to inhibit
parvocellular system, resulting in prolonged after image that looks like a blur
when reading
Autopsy evidence from dyslexic patients shows reduction in size of
magnocellular system neurons (Galaburda and Livingstone, 1993)

Question 282

fMRI study of dyslexia (Eden et
al., 1996)

Answer 282

Control subjects
showed robust
activity in brain
region V5/MT
when viewing a
moving dot
pattern.
Almost no activity
was present in
those areas in
people with
dyslexia.

Question 283

Treatment for dyslexia

Answer 283

Peterson and Pennington (2015):
◦ “Best interventions provide intensive, explicit instruction in phoneme
awareness, the alphabetic principle and phonics, word analysis, reading fluency,
and reading comprehension (Natl. Read. Panel 2000, Snow et al. 1998). “
◦ Reading instruction in Australia has until recently deemphasised these key skills, favouring a
“whole language” approach to learning to read
Accuracy (i.e. phonemic skills) easier to remediate than fluency
◦ Fluency dependent on reading experience, which varies by reading level
A variety of training programs have been devised to stimulate plasticity in
reading-related brain systems
◦ Focus on stimulating brain regions rather than specific reading skills
◦ E.g. musical training, auditory training, sound discrimination
◦ Evidence of effectiveness in relation to improved attention, listening and reading
skills

Question 284

Attention deficit/hyperactivity
disorder

Answer 284

Grouped in DSM-5 with the Neurodevelopmental Disorders
◦ Previously grouped together with Conduct Disorder & Oppositional Defiant
Disorder
Heterogeneity in presentation  subtypes (DSM-5-TR)
◦ Predominantly Impulsive-hyperactive presentation
◦ Predominantly Inattention presentation
◦ Combined presentation
Frequently comorbid with ODD and CD
◦ anxiety and depression; learning disabilities
Developmental course: initially noted in early childhood;
persists into adulthood where 50-65% still have core
symptoms

Question 285

Causes of ADHD

Answer 285

Ultimate cause unknown
◦ Familial for some- higher incidence of ADHD or other
externalising disorder in 1st or 2nd degree relatives  may be
genetic component
◦ Associated with some other genetic and developmental disorders
i.e. FAS
Evidence of dysfunction of parietal regions, consistent with
deficits in alerting & orienting aspects of attention
Evidence for the under functioning of dopamine and
noradrenalin/norepinephrine neurotransmitter systems

Question 286

Cognitive deficits in
ADHD

Answer 286

Historical focus was on attention
deficits especially sustained and
divided attention
◦ Focus on lack of age appropriate
sustained attention (eg Douglas,
1972)
Contemporary focus on deficits
in some aspects of executive
functions
◦ links to role of frontal/basal
ganglia dysfunction (frontostriatal
system)
◦ similarity between features of
ADHD & frontal lobe
damage/disconnection

Question 287

Neuropsychological models
of ADHD

Answer 287

Posner’s attentional model and
ADHD
◦ ADHD results from dysfunction
of the vigilance attention system
 cannot sustain attention
◦ Also anterior attentional
dysfunction  poor executive
control
Barkley’s 3-tiered model of
ADHD
◦ Difficulty inhibiting prepotent
responses underlies behavioural
and cognitive deficits of ADHD