Week 11 Lecture 11 - Schizophrenia (DN) Flashcards Preview

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What is prodromal

just before onset of illness
this is when negative symptoms tend to present



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.


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)


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


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


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


What is the NIMH RDoC?

Research Domain Criteria


What are two predictors of poorer outcome?

poor premorbid functioning
poor cognition



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



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


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



What is the advantage of the Staging Model?

Not constrained by artificial diagnostic categories
enables symptom identification for appropriate treatment


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


What has been the flavour of the last 70yrs in causes for schizophrenia?

Biological models
- recognised by Kraeplin (looked at brain/behaviour)
- Corselis


Functional psychosis

no clear explanation for it



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



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



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.......



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


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)


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



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


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


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


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


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


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


Neurodevelopmental Hypothesis for Schizophrenia?

Early insult causes changes in brain development
interacts with environment
increasesrisk for onset later in life


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)


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