Week 11 Lecture 11 - Schizophrenia (DN) Flashcards Preview

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

arguably the worst disease affecting mankind


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

anthropomorphising cats in his paintings - represented his progression of schizophrenia


How does ALex describe the experience.....

being bombarded by stimuli in the world around them


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

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




hole drilled in skull


Who was Emil Kraepelin?

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


How did Kraeplin describe dementia praecox?

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


What was required for a diagnosis of dementia praecox?

early onset
deteriorating course



Who was Yergan Bleuler?

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


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

many of patients they were seeing may have actually had
encephalitis lethargica


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

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


What were Schneider's first rate symptoms?

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)




What were Schneiders 'Second-rank symptoms'?

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


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

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


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

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


Why is Robert Spitzer significant in the diagnoses of Schizophrenia?

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


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

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



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


DSM-4 Criteria

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

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



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

Diagnosis can be quite unstable in early stages


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

Pretty much the same except:
DSM-4-TR included Paranoid, Catatonic, Undifferentiated and Residual sub-types - these have been removed from DSM-5


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

>1 month - Schizophreniform
>6 months - Schizophrenia


How are the symptoms of Schizophrenia split in the DSM?
Are both symptom types required for a diagnoses?

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



Positive Symptoms

Symptoms in excess or normal experience
- Delusions
- Hallucinations



- others are trying to harm (most common)
- belief that external stimuli are directed to oneself
- belief in ones own exceptionality
- false belief that another is in love with him/her
- belief that a major catastrophy will occur
- preoccupations with health/organ function
Bizarre - implausible e.g., thought withdrawal. insertion & delusions of control (e.g., alien control over hand)



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


What type of auditory hallucinations most commonly come to clinical attention?



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


What is an important point when considering Psychosis & Schizophrenia?

If one is Psychotic they do not necessarily have Schizophrenia
If one has Schizophrenia, they have to have had a Psychotic episode



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

based on Chronicity & Acuteness
i.e., first episode, multiple episodes, continuous
Acute, partial, partial remission, remission

specify if with Catatonia

Severity - 4pt scale


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


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


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)


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


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)


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


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


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



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



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


Targeted brain stimulation

Trans-cranial magnetic stimulation
auditory hallucination (temporal - wernickes area) - stimulate this area to change its function



*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

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