7. Neuropsychiatric Conditions Flashcards

1
Q

What is a neuropsychiatric condition?

A

A disorder that impacts substantially on brain functioning and significantly disrupts emotions, thinking and behaviour.

There are 300 psychiatric disorders in the DSM-5

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2
Q

Why are npisc conditions important to npsy?

A

They affect lots of people: 45% of Australians aged 16-85 had a mental disorder at some point,
>20% had a mental disorder in the last 12 months (this was >40% for those aged 16-24)
3.4 M consulted a professional for their mental health.

Its a 2 way street between brain and behaviour (brain changes can result in psychiatric features, and psychopathology can result in visual changes of the brain)

Central to many neuropsychological referrals (is it brain based or psychological?)

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3
Q

What is schizophrenia/

A
  • one of the most common and disabling psychiatric disorders
  • disrupts how a person interprets reality, thinks, feels and behaves
  • is a persistent brain disorder
  • difficult to work with as it comprises a group of disorders with heterogeneous aetiologies, and patients vary in presentations
  • symptoms change over time

Clinical diagnosis is done through exclusion

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4
Q

Outline the evolution of the concept of schizophrenia: Brief!

A

Kraeplin: a genetic dementia ‘praecox’ involving hallucinations and delusions, early change in cognition and long-term deterioration.

Bleuler: dementia praecox as a group of diseases (the fundamental nature is not dementia, but a disconnect of a person’s grasp on reality) - used the word ‘schizophrenia’ to indicate a fundamental split of the psyche.
Primary symptoms = 4As
- loose Associations
- disrupted Affect (emotions incongruous to situations)
- Ambivalence (intensely negative or intensively positive relationships w ppl)
- Autism (defined here as withdrawing into own world)

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5
Q

What was Ernst Kretschmer’s approach to diagnosis

A

Constitutional diagnosis –> i.e. looking at body types
- asthenic (thin, tall, weak) prone to schizophrenia
- pyknik (squat, fleshy build) prone to bipolar

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6
Q

What was Schneider’s more sensible approach to diagnosis?

A

Looked systematically at ranked symptoms: first ranked symptoms were most helpful

1st rank:
- auditory halls: thought echo - commentary about you, voices commenting on your actions, etc
- thought insertion and withdrawal
- thought broadcasting
- passivity experiences (sensation, movements, thoughts)
- delusional personalisation of perceptions

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

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7
Q

What is the DSM-5 Criteria for Diagnosis of Schizophrenia?

A

A. 2+ of the following (need to have 1, 2 or 3):
- Positive symptoms: delusions, hallucinations, disorganised speech, grossly disorganised behaviours
- Negative symptoms (blunted affect, alogia, avolition)

B. Impacts functioning (in work, relationships, self-care, or development)

C. > 6 months, or 1 month of criterion A

D-F. Not due to schizoaffective, MDD, Bipolar disorder, drugs, medical conditions, autism, etc

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8
Q

Outline Criterion A Schizophrenia symptom: Delusions

A
  • fixed beliefs that are difficult to change (even with conflicting evidence)
  • onset may be slow / sudden
  • don’t usually press them on others
  • usually hold multiple beliefs - often inconsistent except for theme (persecutory, referential, religious)
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9
Q

Outline Criterion A symptom of schizophrenia: Hallucinations

A

Sensory experience without stimulation of the sensory organs

Auditory hallucination = most common
- voices, tapping, footsteps

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10
Q

Outline Criterion A symptom of schizophrenia: Disorganised speech

A
  • illogical, incoherent self-expression in speech or writing
  • e.g. tangent rambling, lack of connectedness of thoughts, neologisms
  • lack goal directed speech
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11
Q

Outline Criterion A symptom of schizophrenia: Grossly disorganised behaviour

A
  • disconnect in the way they feel and how they are expressing themselves
  • too little (very slow, frozen posture, stupor)
  • too much (bizarre, frenzied)
  • bizarre affect (incongruence between their feelings they report and what they show)
  • tendency to dress inappropriately for the weather / unkempt
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12
Q

Outline Criterion A symptom of schizophrenia: Negative symptoms

A

Affect:
- reduced emotion from blunting to flattening
- wooden, lifeless face, apparent loss of emotional life
- marked contrast between internal and external emotion

Alogia:
- poverty of speech: the quantity said is limited
- poverty of thought: amount said is normal but excessively vague, lacks useful detail

Avolition:
- lack impulses or inclinations, may just sit and stare doing nothing if not interrupted

Social withdrawal
Amotivation

Note: Negative symptoms harder to treat clinically and predict poorer outcome

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13
Q

What are the different dimensions / subtypes of schizophrenia?

A
  • Paranoid: delusions and hallucinations (later onset)
  • Disorganised (hebephrenic): “childish silliness”
  • Catatonic: stupor and/or excited behaviours
  • Undifferentiated: hard to distinguish
  • Residual: blunting, withdrawal, psychosis mild
  • Simple deteriorative: early onset, negative symptoms, slow course
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14
Q

What does the typical course of schizophrenia like?

A
  • Premorbid phase
  • Prodromal period (subtle symptoms, late teens/ early 20s, may follow major changes, 2-4 year period) -> 20% don’t have prodromal period
  • Frank psychosis phase: a break with reality (get all the symptoms)
  • Some degree of recovery but waxing and waning with enduring vulnerability to stress, lower baseline after each episode
  • Post psychotic depression is common
  • psychotic symptoms tend to stabilise but negative symptoms tend to increase
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15
Q

How can you predict schizophrenia onset?

A

The prodromal phase allows you to predict it earlier

Intervening earlier is really valuable!
The longer DUP - the poorer outcome (issue is that signs are often non-specific: low concentration, motivation, sleeping, mood)

Potential false positive effects: so if we try intervene early mistakenly - this has consequences of being disruptive to life goals, side effects of medications, stigma.
False positive rates can be up to 50%.

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16
Q

What is the outdated 4 quarters rule?

A

That prognosis of schizophrenia was divided equally into 4:
- very poor outcome
- somewhat improved but requiring a lot of ongoing support
- much improved, fairly independent
- good prognosis, few episodes with minimal side effects

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17
Q

What are the more recent statistics on schizophrenia prognosis?

A

Current research suggests only 9-12% of people with schizophrenia can support themselves through employment.
Difficulties with:
- medication (86%)
- preparing food (85%)
- handling finances (61%)

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18
Q

What are the relapse rates of schizophrenia?

A
  • 20% relapse in a year if they take medication, compared to 60% if they don’t take medication
  • about 50% stop taking medication within 2 years
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19
Q

Suicide rates of people with schizophrenia?

A

1/3 attempt suicide, 10% complete suicide

Risk factors: male, paranoia, higher premorbid intelligence and social functioning, early / recent episode, longer duration untreated, substance abuse

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20
Q

What are the demographics for schizophrenia?

A
  • lifetime prevalence = 1%
  • M>F
  • Men tend to get it younger (50% vs 35% of women diagnosed at 25)
  • M peak onset = 15-25, F: 25-35 with a 2nd smaller peak in middle age
  • onset before 10 or after 60 is rare
  • M have more severe negative symptoms, drug use, social problems and poorer outcomes
  • F have more depressive symptoms, social functioning
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21
Q

What’s the genetic account of people with schizophrenia?

A

Risk of developing schizophrenia was highest for individuals who were identical twins with someone with schizophrenia (48%)

22
Q

What are the limitations of the genetic explanation of schizophrenia?

A
  • Under the nazis, 75% of Germans with schizophrenia were murdered / sterilised
  • German incidence rate was higher than Europe and America following (now equivalent)
  • and people with schizophrenia tend to have half the reproductive rate of the general population
  • not schizophrenia gene, lots of genes play a small contribution
23
Q

What is the biochemical account of schizophrenia?

A

Dopamine hypothesis: caused by too much dopamine activity

Evidence:
- if you increase amount of dopamine in someone’s system, it creates psychosis symptoms
- if you give drugs that reduce the amount of dopamine, it reduces those symptoms

24
Q

What is the structural account of schizophrenia?

A
  • Loss of cells in the whole brain (enlarged ventricles) and particular regions (frontal lobe, PFC, hippocampus, limbic system, thalamus, basal ganglia, cerebellum)
  • Loss of connectivity (circuits) –> AC-basal-ganglia-thalamocortical tract (linked to positive symptoms) and PFC circuit (negative symptoms)
  • Neurodevelopmental hypothesis: maldevelopment at 2 critical time points (disrupted brain lateralization and excessive pruning of synapses resulting in loss of plasticity)
25
Q

What is the psychosocial and psychoanalytical account of schizophrenia?

A

Worst theory = result of bad parenting (no evidence)

Stressful events during childhood are linked with higher rates of schizophrenia:
- kids with schizophrenic mothers are more likely to develop schizophrenia if reared in adverse circumstances
- in 20 studies, 1/2 of those with psychotic symptoms reported child abuse
- higher rates of relapse in families with high levels of negative expressed emotion

26
Q

What are some influences of experience and environment on schizophrenia?

A
  • being male (3 men for every 2 women)
  • being a 1st or 2nd gen migrant
  • maternal malnutrition
  • maternal viruses during gestation
  • advanced paternal age
  • living in urban areas
  • industrialised west
  • cannabis
27
Q

What are the cognitive findings in schizophrenia?

A

Cognitive impairment = core feature

Cognition is more predictive than imaging, and predictive of outcome / quality of life

People with schizophrenia tend to be sitting at a Mild Cognitive Impairment range (1.5-2 SD below average)

Debate about specific vs global effects (do we see problems in higher order thinking or is it pervasive?)

Mental speed, attention, working memory, learning and memory, reasoning, problem solving, social cognition are particularly impacted

28
Q

At what school age are kids who go on to develop schizophrenia showing a lag in their schooling?

A

4 years old

29
Q

When does a big deterioration occur for schizophrenia patients?

A

Big deterioration after first psychosis episode
- mixed findings about whether impairment declines or levels out

30
Q

What are some types of mood disorders?

A
  • Major Depression: a depressed mood that lasts for 2 weeks
  • Bipolar disorder (manic depression) - alternating periods of depression and mania
  • Psychotic depression (depressed mood w psychotic symptoms)
  • Dysthymia (long depression, less severe)
  • Mixed depression and anxiety
31
Q

Outline the DSM Criteria for Bipolar disorder

A

A. abnormal / elevated irritable mood (at least 1 week) enough to impair social functioning or need hospital (may involve delusions or hallucinations)

B. during mood disturbance, 3+ of following symptoms
- increased self-esteem / grandiosity
- decreased need for sleep
- inability to stop talking
- flight of ideas
- distractibility
- increase in goal directed activity or psychomotor agitation
- excessive involvement in risky pleasurable activities

32
Q

What is the prevalence of Bipolar Disorder (BPD)

A

2% of Australians
Sex ratio is even for normal BPD, but a form of BPD with more depression and milder mania more common in women (2:1)

Onset from childhood-50 years, mean = 21. Most cases 15-24.
Onset > 50 could be from a medical trigger.

From 1st symptoms to diagnosis = 12 years

33
Q

What is the prevalence of Major Depressive Disorder

A

9% of M, 13% of F have had a depressive episode -> 4% of M and 6% of F in the last 12 months

The chance of developing a depressive episode tend to happen less as you get older (most likely to get in your 20s)

34
Q

What are the DSM criteria for Major Depressive Disorder

A

A. 5+ of following for 2 week period (including first 2), representing a change of functioning:
- * depressed mood nearly every day
- * diminished interest / pleasure in activities
- unintended weight loss/gain
- insomnia / sleeping too much
- agitation / psychomotor retardation noticed by others
- fatigue / loss of energy
- feeling worthless / excessive guilt
- indecisive and low concentration
- recurrent thoughts of death

B. Significant distress or impairment

C-E. not attributable to substance, medical condition, psychiatric condition

35
Q

What are the ABCs of depression?

A

Affective component: feelings (sad)
Behavioural component: doing too much or too little
Cognitive component: thought content changes (more likely to remember negative experiences) and efficiency changes (slower, more effortful)

36
Q

Presentation and age of MDD

A

This presentation is largely sampled by white people.

< puberty: weight gain, irritability, anxiety on separation, somatic complaints

adolescents: irritability, rebelliousness, conduct problems, falls in grades, change in friends

elderly: agitation, more likely to deny, focus instead on hypochondrial concerns, problems in memory and concentration

37
Q

What is the course of MDD

A
  • 50% have full remission in 6-12 months
  • 90% no longer have full form 2 years later

Is recurring / cyclical
- 40-75% lifetime recurrence with an average interval of 5 years between episodes
- with repeated episodes: common trend to shorter remissions and longer episodes

38
Q

What are the genetic risk factors for MDD?

A

There is a genetic loading for developing MDD
- in the general population its about 40% inherited
- even more when you look at only severe recurring depression (70%)
- may inherit a genetic liability, not a specific form of depression

39
Q

What are some medical risk factors?

A

Vascular depression -> changes in blood flow and vascular disease is causally linked to late life depression.

Thyroid dysfunction, stroke, TBI, epilepsy, PD

Some steroid and hormonal treatments

Chronic pains is a reliable predictor

40
Q

What is the monoamine hypothesis in relation to MDD?

A

Monoamine = NTs involved in fight or flight (serotonin, norepinephrine, dopamine)

Hypothesis: MDD caused by imbalance of 1+ MAs

Evidence:
- if you give a drug that induces MA, you see depression like behaviour
- people with MDD have low levels of MA (if you give them drugs that increase MA, depression eases)
- if you interfere with someone’s diet (building blocks for serotonin) you see a relapse
- brains of people who complete suicide have lower levels of serotonin

41
Q

Outline the limitations of the MA hypothesis for MDD

A
  • reducing precursors does not make healthy people depressed
  • antidepressants don’t work for many
  • reserpine only induces depression in small minority
  • drugs increase MAs very quickly, but changes in mood take several weeks
  • we still don’t know what the ideal level of MA is
  • Analogy: aspirin fixes headache, but doesn’t mean headache is caused by too little aspiring
42
Q

What are some cognitive theories of depression?

A
  • comes from (-) distortions in perception, memory and problem solving (sunglass theory)
  • vulnerabilities formed by observation or traumatic events are later triggered by parallel experiences
  • Beck’s negative cognitive triad: dysfunctional schemas about - the self, the world, the future

Evidence:
- those with dysfunctional attitudes are more likely to develop depression and relapse
- But what comes first? Depressive thoughts or depression?

43
Q

What is the HPA axis hypothesis of depression?

A

Under stress, HPA increases cortisol and glucose, and reduces other production, before restoring to normal activity.

Chronic stress leads to atrophy (PFC, hippocampus, amygdala), compromising the ability to ‘turn down’ HPA axis activity. Also compromising ability to process negative emotion, display adaptive behaviour.

HPA hyperactivity = most consistent finding in depression, and resolve with successful antidepressant treatment.

But is it a consequence or a risk factor?

44
Q

What is the gut-brain axis hypothesis of MDD?

A

Gut bacteria –> NT –> mood

  • depressed and healthy controls distinguished by gut bacteria
  • depleting rats’ gut microbiota leads to depression like symptoms, and vice versa
  • microbiota translantation from an anxious mouse (and depressed humans) produces anxious behaviour (and depressed behaviour) in mice
  • transplantation of microbiota for IBS from healthy to depressed people associated with significant gains in mood
45
Q

Depression is increasingly attributed to the mix of recent events and long term risk factors such as:

A

Recent events: life stressors and drugs and alcohol
- family conflict
- interpersonal conflict
- recent loss
- poor working conditions

Personal factors:
- past bad experiences
- personality
- high anxiety
- changes in the brain
- genetic disposition

46
Q

Outline a cognitive comparison of BPD and MDD!

A

Both: characterised by cognitive dysfunction - deficits involve sustained and divided attention, speed, exec functioning, verbal learning and memory.

Effect sizes generally greater in BPD than MDD

Residual impairment in attention and executive functioning:
- some find comparable severity
- some find worse verbal memory, mental flexibility and inhibitory control in BPD

Most suggest BPD similar to MDD but more severe; executive functioning and memory stronger in depressed patients

47
Q

Outline Neuropsychiatric symptoms in degenerative conditions: Dementia with Lewy Bodies

A
  • the 2nd or 3rd most common form of dementia
  • hybrid of Alzheimer’s and Parkinson’s

4 core features:
- Fluctuating cognition with fluctuations in concentration and attention
- recurrent well-formed visual hallucinations
- REM sleep behavioural disorder
- One + spontaneous motor features of parkinsonism

Supportive features: falls, syncope, hallucinations in other modalities, systematised delusions, apathy, anxiety, depression

48
Q

Outline visual hallucinations by people with dementia with lewy bodies

A
  • recurrent, detailed, well formed ( not flashing lights)
  • typically involve people / animals, but also perceptual distortions (seeing faces emerge out of patterns on carpets, etc)
  • more common and appear earlier in women (82% of women, 66% of men and 79% overall experience visual hallucinations)
  • not usually the earliest symptom but most specific for diagnosis
  • not distinct to DLB but distinguished by early onset, persistence and non mood-congruent nature
  • greater visuo-spatial problems and delusional misidentification (this person looks identical to my wife, but its a clone of her)
49
Q

Why are people with DLB having these problems with Visual Hallucinations?

A

A) basic problem with visuoperception? but there is another condition called posterior-cortical atrophy who have same visuospatial problems and deterioration without visual hallucinations

B) a software issue - not getting enough chemicals to the bits in their brain involved with vision: DLB patients have hypoperfusion or hypometabolism in occipital lobes. Plausible, but not perfect because this would imply continuous (constant) hallucination.

C) fluctuating cognition - intrusions of dream imagery into wakefulness

50
Q

what are some considerations relevant to the idea that mental distress does not equal mental disorder

A
  1. characteristics of the experience (how unusual is it compared to other people?)
  2. cultural context (is it culturally consistent)
  3. personal context: 1/3 to 1/2 bereaved spouses report some level of hallucination involving the deceased (i.e. could it just be recent grief?)
51
Q
A