Neuropsychiatric conditions

Question 1

What are neuropsychiatric conditions?

Answer 1

• have neurological and psychiatric features that impact on cognition and behaviour.
• lots of them: ~300 psychiatric disorders in the DSM-5

• Include
– mental illnesses (schizophrenia, mood disorders, anxiety disorders)
– brain pathologies (cerebrovascular disease)
– neurodegenerative conditions (prion disease, DLB)
– Sleep disorders

Question 2

Why are neuropsychiatric conditions important to neuropsychologists? (3)

Answer 2

• affect lots of people
• Illustrate 2 way street between brain and behaviour; depression and imaging; DLB and psychiatric features
• central to many neuropsych referrals

Question 3

What is schizophrenia? (5)

Answer 3

• a disabling, persistent brain disorder that disrupts how people think, feel, behave, and interpret reality
• Probably compromises a group of disorders with heterogeneous aetiologies, and patients varying in presentations and treatment response
• Symptoms change over time
• “Schizophrenia remains one of the most common and disabling of all psychiatric disorders”
• A clinical diagnosis, diagnosis by exclusion; coming closer, but no sign or symptom pathognomic for schizophrenia

Question 4

How did the concept of schizophrenia evolve?

Answer 4

• Emil Kraepelin 1856-1926
– 1887: manic depressive psychosis vs. dementia praecox
– Dementia praecox involved hallucinations and delusions, an early change in cognition, then long-term deteriorating course

Eugen Bleuler: 1911
– “neither a question of an essential dementia, nor a necessary precociousness. I am taking the liberty of employing the word schizophrenia (to indicate) the breaking up or splitting of psychic functioning”
– Not split personality; schisms between thought, emotion and behaviour
– Primary symptoms and secondary symptoms

Question 5

What were Ernst Kretschmer’s approaches to diagnosis schizophrenia?

Answer 5

– asthenic types (“thin, tall and weak”) prone to schizophrenia;
– pyknic types (“squat and fleshy build”) prone to bipolar disorder
– asthenic types more likely to be involved in petty theft and fraud, athletic types in violent crimes, while pyknic were involved in both

Question 6

What was Kurt Schneider’s approach to diagnosing schizophrenia?

Answer 6

1 or more 1st rank symptom

a) Audible thoughts or “thought echo”
b) Voices commenting on your actions, discussing you in the 3rd person
c) Voices conversing with each other
d) Delusionally personalised perceptions
e) Thought broadcasting
f) Somatic passivity experiences
g) Withdrawal and insertion of thoughts
h) Externally driven feelings, volition and impulses

2nd rank symptoms: sudden delusional ideas, perplexity, depressive and euphoric mood changes, emotional impoverishment

Question 7

What are DSM-5 criteria for diagnosing schizophrenia? (4)

Answer 7

Positive and negative symptoms
A. 2 or more the following symptoms (1-4 are positive)
1. Delusions
2. hallucinations
3. disorganised speech
4. grossly disorganised behaviour
5. negative symptoms, eg blunted affect, alogia or avolition. Must include 1, 2, or 3, and each is present for most of a month if untreated,
B. Reduced functioning for a significant period since onset in work, relationships, self-care or expected development
C. Continuous disturbance for 6 months+, a month (untreated) of criterion A symptoms. Can include prodromal/ attenuated periods
D-F. Not due to sz affective, MDD or bipolar disorder; or drugs or medical conditions; in case of autism/ communication disorder, prominent delusions/hallucinations for 1 month

Question 8

What are delusions (Sz)?

Answer 8

• “Fixed beliefs that are not amenable to change in light of conflicting evidence.” Must be inconsistent with their cultural and educational background
• Onset may be slow or sudden
• mostly see them as self-evident. Usually don’t press them on others
• Usually hold multiple beliefs – often inconsistent, except for theme (persecutory*, referential, somatic, religious, grandiose)

Question 9

What are hallucinations in Sz?

Answer 9

• Sensory experience without stimulation of the sensory
organs.
• Auditory hallucinations most common;
– Voices very characteristic, but also hear tapping, footsteps etc.
– Content: single words, or phrases, or commands
– Some highly suggestive of schizophrenia, e.g. repeating thoughts, commenting on what the person is doing, or arguing with each other
– patients may argue with them, or try to drown them out; may or may not be able to resist commands
• Hallucinations occur in other modalities, but need to consider other causes

Question 10

What is disorganised speech in Sz?

Answer 10

• “formal thought disorder” –illogical, incoherent self expression in speech or writing
• Examples include tangentiality, derailment, neologisms and clanging
• Lack goal-directed speech; ‘word salad”

Question 11

What is Grossly disorganised/catatonic behaviour in sz?

Answer 11

• Nb not necessarily specific for scz
• Too little (very slow, frozen posture, stupor)
• Too much (bizarre frenzied, purposeless bvr eg repetitive rhythmic gestures, walking in circles)
• Bizarre affect – incongruence between what they report
feeling and what they show
• Tendency to dress inappropriately for the weather, untidy or unkempt

Question 12

What are 5 negative symptoms of sz?

Answer 12

• Affect:
– Reduced emotion from blunting to flattening
– Wooden lifeless face, apparent loss of emotional life
– can be marked contrast between internal and external
emotion; GSR vs. expressions and self-rating
• Alogia
– Poverty of speech: the quantity said is very limited. Complain their heads are empty
– Poverty of thought: amount said is ok but excessively vague, lacks useful detail
• Avolition
– Lack impulses or inclinations; may just sit and stare doing nothing if not interrupted
• Social withdrawal
• Amotivation
• Negative symptoms predict poor outcome, and are difficult to treat clinically

Question 13

Do we still use dimensions/subtypes of Sz?

Answer 13

No
– DSM 5: discontinued
• specificity, reliability, prognostic value
the symptoms arent unique to the dimensions

Question 14

What is the typical course of Sz?

Answer 14

• 1 premorbid phase 2 prodromal period (subtle symptoms) 3 frank psychosis 4 some degree of recovery
• Prodromal period “UHR/CHR phase” →symptoms in late teens/early 20s. May follow major changes e.g. moving out, deaths etc.; 2-4 year duration common, but may be weeks, and about 20 % no prodromal period
• waxing and waning, lower baseline after each episode.
Contrasts with mood disorders
• Post-psychotic depression common
• Enduring vulnerability to stress, though patterns and durations may be unclear
• Psychotic symptoms tend to stabilise but negative symptoms tend to increase

Question 15

What are the effects of predicting the onset of Sz?

Answer 15

• Benefits: “Early detection… vital in reducing dysfunction,
morbidity, and mortality.” “Benefits of early detection and
intervention consistently reported from many different countries.”
• Longer DUP ~ poorer outcome. Problem: signs often nonspecific. ↓ Concentration, motivation, sleeping, mood
~ 50 % of teens show some compatible symptoms.
• Potential “false positive” effects
– impact on life goals; side effects of medications; stigma.
– False + rates in 51 % in some studies 60-90 % in others. False rate rising
• State of play
– 200 with Attenuated Psychosis Syndrome tracked for 2 years. 30 % converted to psychosis, 21 % developed scz.
Attenuated odd ideas and disorganised communication best predictors

Question 16

What is the prognosis of Sz?

Answer 16

• “4 quarters rule:” very poor outcome; somewhat improved but requiring a lot of ongoing support; much improved, fairly
independent; good prognosis, few episodes with minimal deficits
• More recent definitions less encouraging:
• Life skills: difficulties medications (86%), preparing food (85%), shopping (78%), handling finances (61%), doing laundry (52%)
• Work: 9-12 % support themselves through employment. Varies from country to country
• 16-23 % relapse in a year (+meds) vs. 53-72 % (-meds)
• +meds 80 % relapse in 5 years; *5 -meds
• About ½ stop taking medications within two years
• 1/3 attempt suicide; 10 – 15% complete suicide

Question 17

What are 6 risk factors for a bad prognosis of Sz?

Answer 17

Male 
Paranoid subtype
Higher intelligence and premorbid social functioning
Early/recent episode
Longer duration untreated
Substance abuse

Question 18

What is the demography of Sz?

Answer 18

• Lifetime prevalence about 1 percent
• M>F
• M younger; 50+ % M vs 33 % F have first psychiatric admission before 25
• M: peak onset 15-25, F:25-35; F have a bimodal distribution, with 2nd, smaller peak in middle age.
• onset before 10 or after 60 is rare
• M may have more negative symptoms, F typically better
premorbid social functioning and better outcomes

Question 19

What is the genetic account of Sz and its limitations?

Answer 19

• adoption studies – biological not adoptive relatives
More share genetic mat that you share with someone with schizo, the more you’re at risk of getting it
• Shared abnormalities bn PwS and relatives, eg prepulse
inhibition

• under the Nazis >75 % of Germans with schizophrenia were sterilised or murdered. German incidence rate higher than Europe and America in 1970s, and now equivalent
• Reproductive rates 50 % in schizophrenia yet prevalence
is increasing
• No “schizophrenia gene” identified; lots of genes all play a small contribution

Question 20

What is the biochemical account of Sz and its support?

Answer 20

• Dopamine hypothesis – sz caused by too much DA activity? Excess in release, receptors, or sensitivity

• Support
– Drugs increasing DA activity (cocaine) mimic symptoms of psychosis
– Drugs that disrupt DA activity reduce psychotic symptoms (antipsychotics)
• Other neurochemicals also implicated

Question 21

What are 3 structural accounts of Sz?

Answer 21

• Loss of cells: whole brain (enlarged ventricles*) and specific regions eg frontal lobes and PFC, hippocampus and limbic system, thalamus, basal ganglia and cerebellum
• Loss of connectivity: not sites, but circuits. AC-basal gangliathalamocortical tract →positive symptoms, PFC circuit →negative symptoms

• Neurodevelopmental hypothesis
– 2 hit model: maldevelopment at 2 critical time points
– Congenital anomalies in brain development, e.g. disrupted brain lateralisation, lead to premorbid symptoms and “soft signs”
– Problems in adolescence: excessive pruning of synapses, loss of plasticity to adapt to changing environment

Question 22

What are the psychosocial and psychoanalytic accounts of Sz?

Answer 22

• No strong evidence for a causative role for any specific
family pattern
• Children of sz mothers more likely to develop sz if reared in adverse circumstances than stable families
• Childhood abuse or trauma – in 20 studies, ½ those with psychotic symptoms reported childhood abuse
• Higher rates of relapse in families with high levels of negative expressed emotion

Question 23

What is the influence of experience and the environment on Sz? (10)

Answer 23

Prominent variation in risk
• ?Male sex: 3 men for every two women
• 1st-2nd generation migrant, esp. if black
• Maternal malnutrition
• Maternal viruses during gestation flu, measles, herpes simplex 2
• Pregnancy and birth complications – pre-eclampsia, asphyxia, emergency C-section
• Advanced paternal age
• Urban birth or residence 2.4* risk
• Higher risk in developed nations
• Living at higher altitude, for males - ?vitamin D/ultraviolet light
• Cannabis

Question 24

What are the cognitive findings in Sz?

Answer 24

• Cognition more predictive than imaging
• Most influential symptom re outcome and QoL

WAIS-IV
Attention, working memory, executive functioning, and speed of processing

Frequently 1.5 to 2 standard deviations below average
• Speed of information processing
• Attention
• Working memory
• Learning and memory
• Language, reasoning and problem solving
• Social cognition

Question 25

What is the course of impairment in Sz?

Answer 25

• A year behind at the start of school, with some decline/slower gains by the end
• Deterioration with first episode
• mixed findings about decline vs leveling out
– Decline varied between people, and between domains over 10 years from diagnosis.
– Verbal knowledge, memory ↓
– speed, XF, visuospatial more stable

Question 26

What are 5 main types of mood disorders?

Answer 26

• Major depression (MDD/ clinical/ unipolar depression) - a
depressed mood that lasts for at least 2 weeks.
• Bipolar disorder - (manic depression) – alternating periods of feeling low (depressed) and high (manic).
• Psychotic depression - depressed mood with psychotic symptoms, e.g. hallucinations, delusions, and paranoia
• Dysthymia - a less severe depression, lasts for years
• Mixed depression and anxiety - combined symptoms

Question 27

What is BPD?

Answer 27

A. - a distinct period of abnormally and persistently elevated, expansive, or irritable mood, lasting at least 1 week. Enough to impair social/occupational functioning, need hospital. May involve delusions (esp. grandiose, persecutory) or hallucinations (esp. auditory)
B. - during the period of mood disturbance, 3+ of the following symptoms have been persistent and significant (4 if mood is only irritable):
1) increased self-esteem or grandiosity
2) decreased need for sleep
3) more talkative than usual or pressure to keep talking
4) flight of ideas; sense of racing thoughts
5) distractibility (i.e., attention too easily drawn to unimportant or irrelevant external stimuli)
6) increase in goal-directed activity (either socially, at work or school, or sexually) or psychomotor agitation
7) excessive involvement in pleasurable activities that have a high potential for painful consequences (e.g., reckless buying sprees, sexual indiscretions, business investments)

Question 28

What is the prevalence of BPD?

Answer 28

– ~ 2 % of Australians experience BPD at some stage
– Sex ratio (F:M) 1:1 for BPD I (mania and depression), but 2:1 for BPD II (milder mania, more depression)
– onset childhood to 50 years. Mean age 21, most cases 15-24. Average period from 1st symptoms to diagnosis about 12 years
– onset after 50 may relate to medical triggers like CVD

Question 29

What are the DSM-5 criteria for diagnosing MDD?

Answer 29

A. 5+ of the following for a 2 week period; represents a change from previous functioning; must include symptom 1 or 2
1. * depressed mood nearly every day
2. * Diminished interest or pleasure in all or most activities
3. Significant unintended weight loss or gain, e.g. 5 %
4. Insomnia or sleeping too much nearly every day
5. Agitation or psychomotor retardation noticed by others
6. Fatigue or loss of energy
7. Feelings of worthlessness or excessive guilt
8. ↓ ability to think or concentrate, or indecisiveness
9. Recurrent thoughts of death
B. Symptoms cause significant distress or impairment in social, occupational, other important areas
C-E. Not attributable to substances, medical conditions, or
psychiatric conditions

Question 30

What are the ABCs of MDD?

Answer 30

• Affective component
–Feelings

• Behavioural component
–Too much or too little

• Cognitive component
–Content
–Detail, inefficiency, slowing

Question 31

How does MDD present differently with age?

Answer 31

• Prior to puberty
– Weight gain; irritability; anxiety on separation; somatic complaints

• Adolescents
– Irritability; rebelliousness; conduct problems; falls in grades; change in friends

• In the elderly
– Agitation; more likely to deny expression; hypochondriacal concerns; problems in memory and concentration

Question 32

What is the course of MDD?

Answer 32

• Short-term
– ~ 50 % have full remission in 6-12 months

• Longer term
– 90 % no longer have full form 2 years later

• A recurring problem
– ⩾40–75% lifetime recurrence Chiu, 2017
– Average interval of ~ 5 years between episodes
– Some have recurrence within a year, some stay free
– With repeated episodes, common trend to shorter remissions and longer episodes

Question 33

What are the risk factors for MDD?

Answer 33

Genetic findings
• heritability ~ 40%. Increases to ~ 70% in twins with recurrent and severe major depression
• may inherit a generic liability, not a specific form of
depression

Medical factors
• low thyroid function;
• stroke, CVD, TBI, epilepsy, PD
• blood vessel disease; diabetes and/or hypertension;
• some steroid and hormonal treatments;
• chronic pain

Question 34

What is the monoamine hypothesis for MDD, its support and limitations?

Answer 34

• “MDD caused by imbalance of one or more MAs”

Support
• People and animals given drugs that reduce MAs, like reserpine, often show depression-like behaviour
• People with MDD have low levels of MAs; drug treatments
increase levels of MAs; depression eases.
• depleting dietary building blocks (precursors) of serotonin
associated with relapse in recovered patients
• People who complete suicide have lower brain stem levels
of serotonin and/or its by-products

Limitations
• Reducing precursors doesn’t make heathy people depressed
• antidepressant drugs don’t work for many
• Reserpine only induces depression in a small minority
• drugs increase MAs very fast, but changes in mood take
several weeks
• ideal/ problem levels still unknown
• Some antidepressants don’t increase synaptic MAs; some
drugs that increase MAs don’t reduce depression

Question 35

What are the cognitive theories of MDD?

Answer 35

• “depression comes from neg distortions in perception, memory, and problem solving”
• vulnerabilities formed thru observation or traumatic events triggered later by parallel experiences
• Beck’s negative cognitive triad: dysfunctional schemas (belief systems) re the self, the world, and the future
• E.g. I’m unloveable; no one loves me; no one will ever love me
• those with dysfunctional attitudes similar to Beck’s ~ 7* more likely to develop depression, and ~2 * as likely to relapse
• Chicken vs egg: maybe depression leads to depressive
thoughts, not vice versa
• CBT remains one of the most widely used and effective
methods of treating depression

Question 36

What is the Hypothalamic-pituitary-adrenal (HPA) axis hypothesis of MDD?

Answer 36

• Under stress, the HPA axis ↑ cortisol; ↑ glucose and ↓ other production like BDNF. When the crisis is over the HPA should restore normal activity
• Chronic stress leads to atrophy of PFC, hippocampus and
amygdala, possible inhibition of neurogenesis, compromised ability to “turn down” HPA axis activity
• Effect of damage to those areas - compromised ability to
process negative emotion, display adaptive behaviour, and
lose drive to engage with the environment
• HPA hyperactivity one of the most consistent findings in
depression; it resolves with successful antidepressant
treatment
• Maybe HPA axis hyperactivity not a consequence but a risk factor for depression, caused by genetic liability and early life experience

Question 37

What is the gut-brain axis hypothesis?

Answer 37

• Micronutrients may influence brain function. Depressed and healthy controls can be distinguished by gut bacteria
• Experimentally depleting rats’ gut microbiota leads to
depression-like bvr; increasing gut microbiota reverses this
• Faecal microbiota transplantation (FMT) from an anxious mouse produces anxious behaviour, FMT from a non-anxious mouse produces non-anxious behaviour
• FMT from depressed humans into rats induced bvr features of depression
• FMT for IBS from healthy to depressed people associated
with significant gains in mood

Question 38

What are the cognitive comparisons of BPD and MDD?

Answer 38

• Both characterised by cognitive dysfunction; variable findings but deficits tend to involve sustained and divided attention, speed, executive functioning, verbal learning and memory.
• ES generally greater in BPD than MDD
• Residual impairment in attention and EF:
– Some studies find comparable severity
– Some find worse verbal memory, mental flexibility and inhibitory control in BPD
• Most suggest BPD similar to MDD but more severe; EF and memory stronger in depressed patients

Question 39

What is dementia with Lewy bodies (DLB)?

Answer 39

• DLB 2nd or 3rd most common form of dementia
• hybrid of Alzheimer’s and Parkinson’s disease
• Core features:
1. Fluctuating cognition with pronounced fluctuations in concentration and attention;
2. recurrent well-formed visual hallucinations;
3. REM sleep behavioural disorder
4. One or more spontaneous motor features of parkinsonism
• Supportive features:
– severe sensitivity to antipsychotics, falls, syncope, hallucinations in other modalities, systematised delusions, apathy, anxiety and depression

Question 40

What are the visual hallucinations (VH) in DLB?

Answer 40

• Experienced by 82 % of women, 66 % of men by 79 % of
sample
• Early incidence: 22 % have VH, 26 % have parkinsonism.
But early, recent VH far more specific for diagnosis
• Recurrent, detailed, well formed.
• Typically involve people or animals intruding into the home, but also involve perceptual distortions, e.g. misidentification syndromes, seeing faces emerging out of patterns on carpets, or backgrounds like trees
• Can be enjoyable or frightening
• VH not unique to DLB, e.g. delirium and other dementias, but distinguished by early onset, persistence, non mood-congruent nature
• Hallucinations less common in other modalities
• VH correlate with greater visuospatial problems; Capgras delusion and delusional misidentification; better response to medications

Question 41

What is the basis of VH in DLB?

Answer 41

• A) Basic problem with visuoperception? But Posterior Cortical Atrophy defined by visuospatial problems due to occipito-parietal degeneration, and VH rare
• B) DLB patients typically have hypoperfusion or hypometabolism in occipital lobes, possibly due to loss of cholinergic input. Primary visual cortex malfunctioning with abnormal sensory experiences
• C) Fluctuating cognition – intrusions of dream imagery into wakefullness
• Still contentious

Question 42

Does a psychiatric symptom mean that there is a psychiatric condition?

Answer 42

• psychiatric symptom ≠ psychiatric condition. Consider:

1. Characteristics of the experience
2. Cultural context
3. Personal context: 1/3 to ½ of bereaved spouses report some level of hallucination involving the deceased