Psychopathology Flashcards

Question

general social determinants of depressive disorder

Answer 1

* 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

Answer 2

* 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

Answer 3

* 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

Answer 4

* 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

Answer 5

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

Answer 6

* 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

Answer 7

cognitive frame work which people perceive their life through

Answer 8

* 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

Answer 9

* 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

Answer 10

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

Answer 11

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

Answer 12

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

Answer 13

* 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

Answer 14

* 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

Answer 15

* 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

Answer 16

* 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

Answer 17

* 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

Answer 18

▫ 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

Answer 19

* 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

Answer 20

* 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

Answer 21

* 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

Answer 22

* 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

Answer 23

* 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?

Answer 24

* 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

Answer 25

* 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

Answer 26

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

Answer 27

* 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?)

Answer 28

* 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

Answer 29

* 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

Answer 30

* 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.

Answer 31

* 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)

Answer 32

* 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

Answer 33

* 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

Answer 34

* 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

Answer 35

* 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.

Answer 36

* 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”

Answer 37

* 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.

Answer 38

* 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”

Answer 39

* 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

Answer 40

* 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...”

Answer 41

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

Answer 42

* Recurrent, automatic or irresistible hair pulling.

Answer 43

* Recurrent, automatic or irresistible skin-picking.

Answer 44

* 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)

Answer 45

* 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

Answer 46

* 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

Answer 47

* 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

Answer 48

* 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)

Answer 49

* 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

Answer 50

* 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

Answer 51

* 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

Answer 52

* 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

Answer 53

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)

Answer 54

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)

Answer 55

* 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

Answer 56

* 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’

Answer 57

* 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

Answer 58

* 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.

Answer 59

* 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

Answer 60

* 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’

Answer 61

* 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)

Answer 62

* 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

Answer 63

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

Answer 64

* 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

Answer 65

* 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)

Answer 66

* 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)

Answer 67

* 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

Answer 68

* 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

Answer 69

* 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

Answer 70

* 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

Answer 71

* 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

Answer 72

* 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 

Answer 73

* 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

Answer 74

* 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)

Answer 75

* 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

Answer 76

* 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

Answer 77

* 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

Answer 78

* 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

Answer 79

* 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

Answer 80

* 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

Answer 81

* 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)

Answer 82

* 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

Answer 83

* 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

Answer 84

* 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

Answer 85

* 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.

Answer 86

* “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

Answer 87

* 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

Answer 88

* 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

Answer 89

* 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)

Answer 90

* 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

Answer 91

* 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

Answer 92

* 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)

Answer 93

* 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)

Answer 94

* 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)

Answer 95

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

Answer 96

* 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

Answer 97

* 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

Answer 98

* 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”

Answer 99

* 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’

Answer 100

* 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)

Answer 101

* 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)

Answer 102

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

Answer 103

* 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

Answer 104

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

Answer 105

* 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.

Answer 106

* 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

Answer 107

* 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

Answer 108

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

Answer 109

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)

Answer 110

* 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

Answer 111

* 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

Answer 112

* 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?

Answer 113

* 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)

Answer 114

* 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/

Answer 115

* 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

Answer 116

* 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

Answer 117

* 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)

Answer 118

* 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

Answer 119

* 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.

Answer 120

* 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

Answer 121

* 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)

Answer 122

* 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)

Answer 123

* 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)

Answer 124

* 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

Answer 125

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

Answer 126

* 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

Answer 127

* 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)

Answer 128

* 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

Answer 129

* 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

Answer 130

* Reactive Attachment Disorder * Disinhibited Social Engagement Disorder

Answer 131

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

Answer 132

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.

Answer 133

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.

Answer 134

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.

Answer 135

* 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

Answer 136

* 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

Answer 137

* 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

Answer 138

* 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/

Answer 139

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

Answer 140

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

Answer 141

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

Answer 142

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)

Answer 143

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

Answer 144

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

Answer 145

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

Answer 146

 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)

Answer 147

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

Answer 148

 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

Answer 149

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

Answer 150

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)

Answer 151

“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

Answer 152

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

Answer 153

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

Answer 154

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

Answer 155

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

Answer 156

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

Answer 157

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

Answer 158

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

Answer 159

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

Answer 160

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

Answer 161

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

Answer 162

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

Answer 163

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

Answer 164

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

Answer 165

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

Answer 166

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”

Answer 167

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

Answer 168

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

Answer 169

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

Answer 170

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

Answer 171

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

Answer 172

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

Answer 173

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

Answer 174

“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

Answer 175

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

Answer 176

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

Answer 177

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

Answer 178

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

Answer 179

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

Answer 180

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

Answer 181

* 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

Answer 182

* 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.

Answer 183

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

Answer 184

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

Answer 185

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)

Answer 186

Medial structures - Supplementary motor area - Cingulate cortex

Answer 187

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

Answer 188

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

Answer 189

“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

Answer 190

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

Answer 191

“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

Answer 192

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

Answer 193

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

Answer 194

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

Answer 195

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

Answer 196

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).

Answer 197

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

Answer 198

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

Answer 199

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."

Answer 200

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

Answer 201

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

Answer 202

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

Answer 203

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

Answer 204

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

Answer 205

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

Answer 206

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

Answer 207

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

Answer 208

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?

Answer 209

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

Answer 210

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

Answer 211

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

Answer 212

patchy visual field deficit caused by cortical damage

Answer 213

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?

Answer 214

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

Answer 215

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

Answer 216

“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)

Answer 217

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

Answer 218

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

Answer 219

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

Answer 220

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

Answer 221

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

Answer 222

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)

Answer 223

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.

Answer 224

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

Answer 225

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

Answer 226

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

Answer 227

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

Answer 228

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

Answer 229

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

Answer 230

~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

Answer 231

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

Answer 232

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

Answer 233

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

Answer 234

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

Answer 235

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

Answer 236

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

Answer 237

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

Answer 238

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)

Answer 239

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

Answer 240

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

Answer 241

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

Answer 242

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)

Answer 243

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.

Answer 244

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

Answer 245

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

Answer 246

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

Answer 247

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

Answer 248

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

Psychopathology Flashcards

(288 cards)