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z. z. PSY3032 Lectures - Abnormal Psychology > Week 11 Lecture 11 - Schizophrenia (DN) > Flashcards

Week 11 Lecture 11 - Schizophrenia (DN) Flashcards

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0
Q

How did Louis……make a name for himself…..????

A

anthropomorphising cats in his paintings - represented his progression of schizophrenia

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1
Q

What did an article in 1988 Nature Journal say about Schizophrenia?

A

arguably the worst disease affecting mankind

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2
Q

How does ALex describe the experience…..

A

being bombarded by stimuli in the world around them

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3
Q

History -
Behaviours referred to as madness - generally charcterise what we refer today as schizophrenic behaviours….
how did ancients treat madness?

A

if someone displayed these symptoms - possessed by evil spirits
Trephination - drill hole in skull - let evil spirits fly out….

4:32

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4
Q

Trephination

A

hole drilled in skull

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5
Q

Who was Emil Kraepelin?

A

swiss psychiatrist
first to describe dementia praecox
tried to find patterns in how symptoms cluster together
People he saw generally has early on-set & always deteriorated

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6
Q

How did Kraeplin describe dementia praecox?

A

dementia (deterioration of mental function)
praecox (young people)
- peculiar destruction of internal connections of psychic personality
- course is regular progression
- common form is idiocy
7:00

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7
Q

What was required for a diagnosis of dementia praecox?

A

early onset
deteriorating course

7:15

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8
Q

Who was Yergan Bleuler?

A 
Coined the name Schizophrenia
Shizen - split
phren - mind
thought name dementia praecox was in appropriate
he said - not all patients have deteriorating course
not all patients same but splitting was always present
Coined four A's to define disorder
- Loosening of Associations
- Ambivalence
- Autism (subtle social difficulties)
- Affective disturbance
plus accessory symptoms
8:50
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9
Q

what may have coloured the perceptions of Kraeplin at the time?

A

many of patients they were seeing may have actually had

encephalitis lethargica

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10
Q

What was Kurt Schneider’s approach to diagnosis of Schizophrenia?

A

Atherioretic diagnosis of actual symptoms (in contrast to the emerging psychoanalytic theoretical approach of Freud, Jung etc)
First-rank symptoms
Second-rate symptoms

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11
Q

What were Schneider’s first rate symptoms?

A

The core features of Schizophrenia or psychosis

  1. Auditory hallucinations (hearing voices not really there)
  2. Passivity experiences (not in control of own bodily functions)
  3. Thought echo (if I think something others will hear it)
  4. Thought withdrawal (something is sucking thoughts out of my brain)
  5. Thought insertion (some external agent is beaming thoughts into my brain)
  6. Thought broadcasting (lots of different people can hear my thoughts)
  7. Delusional perception (believing strange things that dont have a basis in reality)

11: 40
12: 00

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12
Q

What were Schneiders ‘Second-rank symptoms’?

A
  1. Other disorders of perception
  2. Sudden delusional ideas
  3. Perplexity
  4. Depressive/euphoric mood changes
  5. Emotional impoverishment
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13
Q

Which study in the 70’s examined how diagnostic processes differed between New York & London?
What were the findings?

A

US UK Cross-National Project 1974
Diagnosed as either Schizophrenia or an Affective Disorder
Project diagnosis was similar in both cities
Clinical (Hospital diagnoses)
- Strong bias to diagnose Schizophrenia in New York
- London clinical diagnoses were similar to project
12:40

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14
Q

What did John Feighner et al., propose with regard to diagnostic criteria for Schizophrenia in 1972?

A

Core features of “definite” schizophrenia

  • Delusions, hallucinations or disorganised speach
  • Unmarried
  • Poor premorbid social/work history
  • Family history
  • Absence of drugs
  • Onset before 40yrs
  • Illness must be present for 6+ months

he also had criteria for probable schizophrenia
13:50

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15
Q

Why is Robert Spitzer significant in the diagnoses of Schizophrenia?

A

Research Diagnostic Criteria for Psychosis 1973
Looked at Reliability (inter & intra rater reliability between diagnosticians
IMPT as it became basis for DSM-3
reformed diagnosis as a checklist of symptoms
Spitzer headed task force to develop DSM-3

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16
Q

Briefly outline the key people in the development of diagnostic criteria for Schizophrenia.

A

Kraeplin - emphasised course of illness

Bleuler - started to look at certain core symptoms - 4 A’s

Schneider - focussed on symptoms in an atheoretical way (1st rank/2nd rank)

Feighner - focussed on symptoms in an atheoretical way (definite/probable)

Spitzer - RDC (Research Diagnostic Criteria for Psychosis)
& DSM-3 - a menu of symptoms for diagnosis

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17
Q

DSM

A

DSM-3
DSM-4 1994 & DSM-4-TR 2000 (dominated for past 20 years)
DSM-5 2013
16:25

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18
Q

DSM-4 Criteria

A

DSM-V
2 or more symptoms for 1mnth ( 1 must be 1, 2, or 3) i.e., (primary) 1st ranked symptoms
1. Delusions
2. Hallucinations
3. Disorganised thinking/speech (formal thought disorder)
4. Disorganised/catatonic behaviour
5. Negative Symptoms

Qualifiers
Only 1 required if delusions are BIZARRE or hallucinations give RUNNING COMMENTARY or >1 voice
Symptoms have to cause social/occupational dysfunction
Continuous disturbance >6 mnths (otherwise diagnose as schizophreniform (1mth)
Cannot be explained by drug use

17:00

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19
Q

Why is there am arbitrary 6 month time frame for symptoms in order to get a diagnosis of schizophrenia?

A

Diagnosis can be quite unstable in early stages

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20
Q

What is the main difference between DSM-4-TR & DSM-5 classifications of Schizophrenia?

A

Pretty much the same except:

DSM-4-TR included Paranoid, Catatonic, Undifferentiated and Residual sub-types - these have been removed from DSM-5

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21
Q

What is the difference between diagnoses in an individual having experienced symptoms for >1month and an individual >6months

A

> 1 month - Schizophreniform

>6 months - Schizophrenia

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22
Q

How are the symptoms of Schizophrenia split in the DSM?

Are both symptom types required for a diagnoses?

A

Positive Symptoms
Negative Symptoms

No both are not required.
Positive & Negative symptoms = Diagnosis
Positive but no negative symptoms = Diagnosis
Negative but no positive symptoms = No diagnosis

22:30

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23
Q

Positive Symptoms

A

Symptoms in excess or normal experience

  • Delusions
  • Hallucinations
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24
Delusions
Persecutory - others are trying to harm (most common) Referential - belief that external stimuli are directed to oneself Grandiose - belief in ones own exceptionality Erotomanic - false belief that another is in love with him/her Nihilistic - belief that a major catastrophy will occur Somatic - preoccupations with health/organ function Bizarre - implausible e.g., thought withdrawal. insertion & delusions of control (e.g., alien control over hand)
25
Hallucinations
Most commonly Auditory but can occur in any modality Visual, Olfactory, Auditory, Somatosensory ``` Own voice spoken by another Multiple voices arguing or keeping running commentary Command hallucinations Most often derogatory 25:32 ```
26
What type of auditory hallucinations most commonly come to clinical attention?
Derogatory
27
What is the DSM-4 & 5 criteria for | Disorganised Symptoms?
Disorganised thinking (revealed through speech content) - Derailment or loose topic switching - Tangentiality (irrelevant answers) - Incoherence Disorganised behaviour - silliness, agitation, difficulty with goal-directed behaviour Catatonia (rarer) - unresponsive Above combined are Psychosis defines Shizophrenia These may be features of other disorders It is particular combination leads to diagnosis of Schizophrenia
28
What is an important point when considering Psychosis & Schizophrenia?
If one is Psychotic they do not necessarily have Schizophrenia but If one has Schizophrenia, they have to have had a Psychotic episode 29:00
29
Negative symptoms
Deficits of normal experiences or behaviour account for the most burden family find these most troubling - WITHDRAWAL Common features - Diminished emotional expression: reduction in facial exp., eye contact, prosody, mvts - Avolition: decrease in self initiated activities - Alogia: diminished speech output - Anhedonia: decreased ability to feel pleasure from positive stimuli - Associality: lack of interest in social activities Specifiers based on Chronicity & Acuteness i.e., first episode, multiple episodes, continuous Acute, partial, partial remission, remission specify if with Catatonia Severity - 4pt scale
30
What is prodromal
just before onset of illness this is when negative symptoms tend to present 33:00
31
What is the difference between Schizophrenia & Schizo-Affective Disorder?
While Mood symptoms can be experienced in Schizophrenia; in order to have a diagnosis of Schizophrenia the Psychosis had to have begun without presence of Mood symptoms Otherwise it is Schizo-Affective Disorder. 33:40
32
What are some other considerations that are not necessarily required for a diagnosis?
No single symptom is pathognomic (exists in other conditions) Mood Symptoms Cognitive Deficits Abnormal for Culture Substance abuse/dependence & depression commonly comorbid (e.g., cannibas)
33
What are some other Psychotic disorders that need to be considered when giving a diagnosis of schizophrenia?
Schizotypal personality disorder (axis2) enduring characteristic of person Schizophreniform disorder Schizoaffective disorder - psychosis & mood symptoms Brief psychotic disorder Delusional disorder - strong delusions in isolation Substance-induced psychosis
34
What are some other disorders that have similarities but are not Schizophrenia?
Bipolar 1 disorder - psychosis can occur during periods of mania or depression Major depression with psychotic features OCD, PTSD, BDD, ASD
35
How do we know the diagnoses are valid? | Distinguishing between Validity & Utility?
DSM developed to help clinicians communicate some people argue it has constrained research Helpful to view diagnostics as heuristics designed to aid clinicians
36
What is the NIMH RDoC?
Research Domain Criteria
37
What are two predictors of poorer outcome?
poor premorbid functioning poor cognition 38:15
38
What are prevalence rates for Schizophrenia?
throughout lifetime risk of developing Schizophrenia is 0.7% peak age onset - 14-28yrs (males earlier) higher in males early on - equivalent after risk period Latitude: higher rates if further from equator (linked to VitaminD) rates are higher urban than rural areas 5-6% die by suicide - 20% attempt suicide 1/3 get better - 1/3 stay same - 1/3 get worse 50:00
39
What is the Clinician's Illusion?
earlier on researchers looked at convenient samples in hospital - general population - 3mnth illness duration - clinical population - 19mnths illness duration bias sampling Perhaps prognosis isn't as bad as it seemed
40
What has changed diagnostically since awareness of early biasing of samples?
looking at early psychosis pioneered by Pat McGorry (Melbourne Aus of the Year) Proposed - forget diagnostic categories, rather look at the stage of the illness the person is at Staging Model for Psychiatric Disorders (which cuts across boundaries) Each stage has different symptom severity & can use this framework to guide how we treat patients Stage 0 - inc risk but no symptoms Stage 1a - mild reduced symptoms Stage 1b - ultra high risk Stage 2 - meet criteria for diagnosis etc. 53:30
41
What is the advantage of the Staging Model?
Not constrained by artificial diagnostic categories | enables symptom identification for appropriate treatment
42
What was an early theory - psychoanalysis
``` Theodore Lidz Family dynamics unfortunately led to schizophrenergenic mother role of family - expressed emotion no evidence for cause but plays a role in relapse ```
43
What has been the flavour of the last 70yrs in causes for schizophrenia?
Biological models - recognised by Kraeplin (looked at brain/behaviour) - Corselis
44
Functional psychosis
no clear explanation for it 101:10
45
Why is Arvid Carlsson a significant figure?
won nobel prize 2000, for dopamine (DA) showed reserpine depleted DA & affected motor control was first to suggest antipsychotics may act by blocking DA signalling 101:35
46
What did Seeman & Lee (1975) show about dopamine & psychosis?
look at clinical doses look at rats clinical dose highly correlated with ability to block D2 receptors thus D2 receptors are the target for most antipsychotic drugs therefore psychosis must arise from overactive D2 receptors 102:15
47
Where is dopamine produced in the brain? Where does it project? What is it used for?
dopamine created by neurons deep in mid-brain (top of brain stem) within VTA & Substantia Nigra project profusely throughout the brain they have very strong projections to Striatum (input structure of basal ganglia), involved in many functions, reward, motivation, motor control, cognition....... 102:55
48
What technology is used for measuring dopamine dysregulation in psychosis?
Can use PET (Positron Emission Tomogrophy) inject with a raioactive tracer, binds to molecule of interest, track its uptake in brain, measure its abundance Using tracers for molecules relating to Dopamine synthesis & receptor binding, so can measure these levels in living patients
49
What evidence exists for dopamine dysregulation in psychosis?
Elevated markers of striatal D synthesis in both prodromal and schizophrenia compared to controls IMPT - because the prodromal (risk group) also have elevated levels it shows this is not due to medication as the prodromal (at risk) group have not yet developed symptoms or taken medication - also the higher the elevation the more severe the psychosis - also only those with high D went onto develop psychosis - effect size of just under 1 (Very large)
50
What is a recent suggestion about the relationship of dopamine dysregulation to the development of psychosis?
it has been suggested it may be other upstream causes of dopamine dysregulation but dopamine changes are the common pathway 1:05:30
51
What was seen in the cerebral activity of one of the first imaging studies (PET) of the Schizophrenia inflicted brain? Ingvar & Franzen, 1974
people with schizophrenia showed reduced blood flow to the pre-frontal cortex first evidence showing something going on in schizophrenia brain
52
What did early imaging studies reveal in the Schizophrenia inflicted brain?
Increased blood flow to Pre-frontal cortex Increased Ventricles(non-specific response to brain injury) some of the first evidence showing something was going wrong in the brain of these patients
53
What has come back into vogue with the onset of imaging technologies
Brain connectivity and Dopamine will have a role, because it will influence the way different brain areas communicate Meta-analysis - Grey matter volume reduced - widely distributed cortical, sub-cortical, frontal, temporal, posterior contradicted earlier evidence suggesting it was frontal suggests its a more complicated circuit-level disorder (of brain-connectivity) first recognised by Carl Wenicke 1848-1905 implicit in Bleuler's idea of schizen (split) 1857-1939 back into vogue
54
What tainted early (1940's) genetic research into Schizophrenia by Franz Kallman? What have genetic studies shown?
German Psychiatrist - student of Ernst Rudent Nazi Psychiatrist genetic evidence devoted to trying to eliminate/sterilise afflicted this tainted much of the evidence ``` although twin & family studies do show overwhelming evidence 1% - general population 2% - 1st cousins 9% - sibling 50% - identical twin ``` Heritability 80% of variance explained by genes
55
What are the two kinds of genetic variations found in Schizophrenia?
1. Shizophrenia assoc with 'rare' yet 'high effect' number copy alterations 2. more 'common' variations inc risk just a little bit ('low effect') hundreds & thousands of combinations may exist - which can interact with environment to develop disorder 1:14
56
What is the current conversation around the Kraeplenian Dichotomy?
at biological level - seems to be a lot of overlap | many are arguing that we do away with it
57
Neurodevelopmental Hypothesis for Schizophrenia?
1987 Early insult causes changes in brain development interacts with environment increasesrisk for onset later in life
58
Risk factor epidemiology - what are some early brain insults that render brain vulnerable to developing Schizophrenia?
``` paternal age cat in house pre-natal famine obstetric complications Winter/spring birth (2nd trimester in winter, inc chance of influenza, affects brain development) 1:18 ```
59
Risk factor epidemiology - what are some 'LATER life' brain insults that render brain vulnerable to developing Schizophrenia?
migrate to new country lifetime cannabis use urban environment taking drugs that inc dopamine levels, e.g., cocaine, amphetamine drugs that act as antagonists of NMDR receptors e.g., ketamine, PCP
60
Neurodevelopmental animal model
could be born early but disorder doesn't manifest Lesion in rats changed in PFC only in adolescence credence to idea that developmentally specific avenues at which abnormalities express themselves
61
How have late brain developmental factors have been suggested to play a role in the development of Schizophrenia?
Late brain developmental factorsmay also play an impt role peak age onset = late teens/early adulthood SYNAPTIC PRUNING - born with all neurons scan age 5 = lots of grey matter (abundance of connections) overtime = lots of blue (pruned back, use it or lose it) areas of frontal lobe are last to develop IDEA: is in S that there is an abnormality in this pruning process, i.e., there is an acceleration of this process(maybe too much pruning going on)
62
Summarise the early predisposition/later maturational processes explanation for developing Schizophrenia?
Basic Model: Early insult > predisposes > interacts with later maturational processes (pruning) > leads to onset of disorder all interacts with genes & environment Neurodevelopmental > Affective Continuum No clean-cut off between Schiz & Affective, but where you are on the continuum will determine the disorder you end up getting comb. of genetic vulnerability & environmental impact on your brain circuits 125: 00
63
Give brief timeline for development of antipsychotics
1950's - Antihistamines Paul Charpentier: developed Chlorpromazine (Thorazine) later effective in treating S by 1990 - over 40 antipsychotics introduced Late 50's, early 60's:Extra-pyramidal side effects (EPS) > Motor problems 1960's - Clozapine - few EPS side effects & helped treatment-resistant patients - although led to heart problems, agranulocytosis still used today, but heavily monitored Clozapine then led to atypical antipsychotic drugs which reduce psychotic symptoms with few EPS (but have other side effects, weight gain, high blood pressure etc)
64
what was the Catie trial?
compared the efficacy of 1st and 2nd generation drugs found 2nd gen atypical just as effective both types of drugs 70% discontinued use coz of side effects 2nd phase Clozapine more effective in more severe cases MAIN POINT: no real difference in efficacy, difference is in side effects
65
1. How do antipsychotic drugs act? 2. What kind of symptoms do they effectively treat? 3. What is the time course of treatment?
1. all anti-psychotics act by blocking D2 receptors 2. Only effective in treating positive symptoms - ineffective for negative & cognitive symptoms - ineffective in 30% patients 3. treatment is ongoing, with maintenance doses
66
What difference has been found in treatment responders compared to treatment non-responders?
Treatment responders have elevated Dopamine level in Striatum maybe there is a Dopaminergic form of Psychosis (responsive to treatment) and another form of Psychosis that is not responsive 135:30ish
67
What was found in a study that looked at rate of exposure to antipsychotics & rate of change in grey matter?
Volumetric changes across a range of brain areas were more severe in medicated group compared to non-medicated this is not causative although a recent meta-analysis showed correlation between brain volume change & antipsychotic but no correlation between brain volume change & illness duration, so it could be due to medication exposure (remains unclear) monkey studies have mimicked this 136:40
68
What are some psychosocial therapies for Schizophrenia?
CBT - focussed on reappraising &/or managing symptoms Social/skills training Occupational placement Cognitive remediation in combination with pharmacological therapy they do tend to reduce relapse rates
69
Targeted brain stimulation
``` Trans-cranial magnetic stimulation auditory hallucination (temporal - wernickes area) - stimulate this area to change its function ```
70
SUMMARY
* Schizophrenia is an evolving concept - human arbitrary construct * Current criteria may describe multiple diseases (which may benefit from different treatments) * Arises from complex interactions: multiple genetic risk factors interacting with environment to impact brain development * Dopamine dysregulation plays critical role - but upstream causes may be variable/distinct (maybe treating upstream causes could be more effective) * Current treatments: generally only treat positive symptoms (so we need treatments for negative symptoms & cognitive deficits) * Psychosocial interventions in combination with medication can help reduce relapse

z. z. PSY3032 Lectures - Abnormal Psychology (20 decks)

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