Abnormal Psychology 2: Schizophrenia And Delusional Disorders

Front 1

History of schiz: Jogn Haslam, Benedict Morel, Emil Kraepelin and Eugen Bleuler

Back 1

- Haslam presented first detailed clinical description of schiz

- Morel- saw that some adolescences were 'geniuses' and then became uninterested, withdrawn, thought was brain deterioration

- Kraepelon: dementia praecox- schiz like symptoms due to mental deterioration

Bleuler- introduced term schizophrenia : schizo = to split or crack, phren=mind - thought it was lack of linkage between thoughts emotions and reactions and reality

Front 2

Stats on schiz (7)

Back 2

- little less than 1% of population affected

- occupy more hospital beds than anything else

- 60-70% do not marry

- 80% use drugs

- 6% suicide

- life expectanct is reduced by 20%, increased risk of cardiovascular problems

- 100X more money is invested in breast cancer per patient (schiz receives same $ per year as asthma)- even tho costs are 2.4 billion a year

Front 3

DSM criteria for Schizophrenia (5)

Back 3

A) two or more of the following (at least 1 must be 1-3):

- delusions

- hallucinations

- disorganized speech

- disorganized /catatonic behaviour

- negative symptoms: blunted affect, alogia, avolution

B) social or occupational dysfunction (didnt reach levels expected, or see a decrease in this area)

C) continuous signs for at least 6 months

D) mood disorders with psychosis ruled out

E) not attributable to effects of a substance

Front 4

Describe the positive symptoms of Schiz

Back 4

Positive symptoms: excess of normal function
- delusions: fixed belief that people hold despite evidence to the contrary (thought insertion, thought broadcasting, thoughts being taken out of head, delusions of reference- perron is speaking directly to me)

- must be out of the norm. not everyone with delusions have schiz but 90% of schiz patients have delusions
- Hallucinations: sensory experience in the absence of external stimulus. Most common are auditory

Front 5

Describe the 2 studies on hallucinations

Back 5

1) patients pressed a button when a hallucination started and ended, and they were in fMRI. compared this to an actual auditory sound they played to the participant. Similar areas activated! When there is actual sound, there is more activation.

2)

look at people who had auditory hallucinations (involuntary) but no schizophrenia vs people who were imagining hearing voices (voluntary). Looked at SMA STS and IFG. In the people who are hallucinating, onset of activation of these areas is at the same. In the ones who simply imagined voices, it was SMA, then time delay, then STS and IFG.
A big part of SMA is to predict the consequences of our actions. In normal people, we cant tickle ourselves because the SMA knows its coming. Patients with schiz can tickle themselves because their body is not predicting the actions.

Front 6

What are the disorganized symptoms? (2)

Back 6

- Disorganized speech: failure to make sense, use of neologisms despite language structure being normal
- Disorganized and Catatonic behaviour: disruption of the goal directed activity in almost every area- Catatonia may be almost complete absence of speech or the holding of an unusual/uncomfortable position

Front 7

What are the negative symptoms (3) describe the study on affect

Back 7

- Flat, blunted affect
- alogia- reduced speech
- avolition- inability to initiate or persist in goal behaviours
- the more negative symptoms the worse the prognosis

o Study: watch movie while happy and sad—show films of the patients to observers and had them rate the emotional expression

§ Patients show less emotion than controls do, however if you ask the patients about the emotions they say that they experience the emotions and measuring it (brain activity) shows they are

Front 8

Who is at an increased risk for schiz? When is the onset?

Back 8

- older father >45-50

- certain ethnic groups ie carribean people who immigrate to England

- men may suffer from a more severe form of the disorder... estrogen thought to be protective!

- onset is in late adolescence early adulthood- onset early in men (25 vs 29)

Front 9

Schizoaffective an schizophreiform disorder

Back 9

1) have features of both schiz and severe mood disorder

2) have same criteria as schiz but shorter duration of symptoms

- for both of these the prognosis is better than for schiz

Front 10

Schiz is a ____ disorder... (2+study)

Back 10

neurodevelopmental ;

- lesion in the brain is thought to lie dormant until normal development changes occur
- these changes expose the problems that result from this brain abnormality
- Walker et al: looked at childhood home movies of people who went on to develop school. Patients showed more motor abnormalities (primarily on left side), more negative facial emotions than controls

Front 11

Is Schiz heritable? (3)

Back 11

- interviewed the adoptive and biological familes - schiz. related diagnoses found at elevated rates in the biological but not adoptive families
- the closer your genetic proximity to the affected person, the more likely you are to develop the disorder. Grandparent = risk 5%, sibling= 10%, identical twin= 48%
- genes play a role, but not 100%

Front 12

what is wrong with searching for phenotypes and genes? what are we doing now? why?

Back 12

- the phenotype we use are the psychotic symptoms- but for ex. are delusions a common class, or are they different depending on the type of delusions?

-now we are looking for genes that underlie endophenotypes, such as reduced hippo volume, deficits in smooth pursuit eye movements, verbal memory, sensory gating, etc.

Front 13

What is an endophenotype? 5 criteria?

Back 13

= any neurobiological measure related to the underlying molecular genetics of illness.

- associated with illness: present in medicated and unmedicated patients, lifelong and newly diagnosed patients
- heritable
- state independent
- endophentype and illness co-egregate in familaies
- found in unaffected family members at higher rates than in the normal populaiton

Front 14

why is dopamine dysfunction a diathesis of interest ? (3)

Back 14

- implicated at cortical and subcortical levels
- 3 major reasons: a) all effective meds for schiz. block dopamine in the striatum b) the clinically effective dse is directly related to their affinity for the DA receptor c) dopamine agonists can cause psychosis like symptoms in healthy controls and make schiz worse

Front 15

Describe the Kegels et al and Breir et al. experiments on subcortical dopamine levels

Back 15

- uses a competitive dopamine antagonist

- looked at striatum of healthy controls and schiz patients

- after depletion of dopamine, patients had significantly increased receptors in Associated striatum (as opposed to VS or SMS) compared to controls

= increased levels of subcortical dopamine

Breir et al:

- gave patients and controls amphetamine, increases dopaine

- patients released more dopamine compared to controls

-= hyperactivity of dopamine system

Front 16

describe the study that looked at cortical dopamine in schiz

Back 16

- looked at med- free (half med-naive) patients

- found a certain ligand binding to D1 was higher in patients than controls in the dlpfc

- the higher the binding, the worse their performance was on a 3 back task (decide whether the stimuli on the screen is the same as 3 back ago)

= cortical dopamine is decreased!

Front 17

dose-related psychotic symptoms

Back 17

- Looked at suspiciousness, hallucinations, and thought content

- found that in methamphetamine users, there is a 5 fold increase in likelihood of symptoms and this increased more if they also used cannabis or alcohol.

Front 18

What are some hints that it isnt a simple matter of too much /too little DA? (3)

Back 18

- many with schiz are not helped by the use of dopamine antagonists

- the drugs like neuropleptics block the DR very quickly, but symptom reduction happens after weeks

- neuropleptics are only partially helpful for negative symptoms

Front 19

Evidence of glutamate dysregulation in Schiz.

Back 19

- antagonists of the NMDA receptor given to healthy controls can cause similar symptoms as schiz patients, including negative ones

- no studies of GLU release, since we dont have a ligand to assess it in humans

Front 20

Describe the study on the drugs and PANS

Back 20

-looked at amphetamine and ketamine and looked at their effets on the Positive and Negative Symptoms Scale (PANS).

-Had Ketamine, Ketamine placebo, Amphetamine and amphetamine placebo groups -given 2 admin per test (so ket and amph placebo for ex)

- PET

- both affected the negative and positive symptoms

- administering both together gave more increase on positive symptoms that one alone, especially hallucinations

- amphetamine improved the cognitive symptoms, ketamine produced them

- ketamine affected delusions, and amphetamine grandiosity and suspiciousness

- each drug separately had an effect on the cog symptoms but no interaction effect unlike for positive symptoms

Front 21

Why might serotonin be involved in schiz? (3)

Back 21

1) LSD causes hallucinations, and it acts on the serotonin 2A receptor

2) PET study of

anti-physotic - naive patient found they had lower serotonin binding, especially in the frontal cortex

3) also found a negative correlation between binding 2A receptor and positive symptoms, but only in male patients

Front 22

Anatomical differences in schiz (6)

Back 22

1) enlarged third + lateral ventricies *** cant distinguish btwn controls + patients so is NOT an endophenotype

2) loss of brain volume (but this isnt directly causing the larger ventricles)

3) less grey matter

4) memory problems, especially declarative, and smaller hippocampus (and general temporal areas)

5) thalamus smaller, and has dif GLU DA activity

6) hypoactive prefrontal, and underactivation in PFC cognitive tasks

Front 23

Neuro-cognitive deficits in schiz (4)

Back 23

- Attention- CPT (measure of sustained attention), STROOP

- eye-tracking- smooth pursuit problems (more saccade, linked to hypoactive PFC), anti saccade (dont follow it, they cant inhibit prepotenet response!), occulomotor delayed response task

- sensorimotor gating- P50 and prepulse inhibition - looks at filtering of sensory info

- working memory- WCST, letter-number span

Front 24

How can birth complications affect schizophrenia? (3)

Back 24

- study looked at 238 cases of schiz and found preeclampsi= 2.5 X risk, vaccuum birth extraction 1.7X, malformations 2.4

- people who were in utero during the 1944/45 Dutch Hunger Winter had a 2X increased risk

- project ice storm- looked at objective+ subjective stress, cortisol, MDI (IQ): if you were in 1st or 2nd trimester, cog affects (lower MDI scores) seen at 2 years, 5 years

Front 25

Schiz and SES....study

Back 25

- lower the SES higher prevelance of schiz

- could be sociogenic hypothesis (causation) or social drift (selection)

- study looked at occupation of father, the social class of patient either before admission to hospital, at presentation, or after

- 45% of patients never attain the social class of their father, but 13% did better

- they drifted downward after diagnosis- consistent with social drift

- seen for both schiz. and affective disorders, but they didn’t see pre-morbid dydfunction in the affective disorders, so the schiz. patients prob have a lesion that causes drift after diagnosis and dysfunction before= supports neurodevelopmental hypothesis- something happens before disorder even begins, then when it takes course it causes drift

Front 26

Cannabis and Schiz.: describe the study

Back 26

- can lead to an increase in the likelihood of developing schiz.
- looked as sweetish conscripts, had 50,000 people who used cannibis
- looked at frequency of use, personality traits, and then admissions to hospitals for phsychosis ans schiz.
- related to developing schiz. in a dose-dependent manner- the more you use pot, the more the risk
- ever used it, 2X increased risk, then goes up from there
- if you used it earlier in adolescence, greater risk

Front 27

COMT Genotype and Cannabis and Schiz.

Back 27

- has a Val allele and met allele: - met/met, val/val, met/val

- Val= high activity (low dopamine), Met= low activity (high dopamine)

- implicated in dopamine metabolism in frontal and subcortical levels
- Low dopamine in frontal = high in subcortical due to reciprocal connection

- homozygous val allele seems to bring an increased risk, and this risk seems become reality in the people who use cannabis AS AN ADOLESCENT

Front 28

levels of schiz. have remained stable across world and time.

why might the illness persist if most people dont marry or have kids?

Back 28

- evolutionary reasons!

- individuals related to someone with schiz tend to have great academic success, and also some individuals with it have very high achievements

- maybe this is because creativity and intelligence is often measured by divergent thinking

- divergent thinkers have lower dopamine in thalamus, maybe representing the inability to gate out extra stimuli, and this is like what we see in schiz.
(people who are more intelligent or creative are not more likely to suffer from schiz tho.)

Front 29

Treatment for Schiz

Back 29

1) antipsychoticswork by blocking dopamine

- conventional ones work primarily on DA, and can have parkinson-like side effects
- Novel ones block DA less but also block 5HT
- patients taking novel antipsychotics have fewer extrapyramidal (motor abnormality) side effects and tend to do better overall

2) can also use psychosocial approaches one patients are controlled on medication!
- family therapy, case management, social-skills, CBT

Front 30

Does culture mater for prognosis? Why?

Back 30

- when we look at the outcome of patients in the developing countries, they do better!
- at follow-ups, many more patients are asymptomatic and there is better remission rates there than here
- this finding has remained consistent
- maybe because: greater focus on community, increased social support, extended family characteristics, easier to “return to work,” and less stigma

Front 31

What is a conspiracy theory?

Back 31

- allegations that people or organizations are plotting together in secret to achieve sinister ends through deception of the public

- no proof, less plausable than the mainstream explanation, and this explanation is not a mistake it is sinister fraud.

- violates Occams's razor- when looking at hypotheses, the one with least assumptions should be selected

- for ex. 3-40% of Americans dont believe 911

Front 32

Studies on Princess Diana and OBL

Back 32

- asked people to rate how much they subscribed to conspiracy theories about Princess Dianas death
- people who believed in one theory believed in another, even if they were mutually exclusive.

- follow up study using OBL death
- difference between people who thought he was alive vs already dead, but if you ask them if they think generally officials were engaged in a cover up they all agree- so the details of the conspiracy aren’t so important, just that there is one

Front 33

Who are the conspiracy believers?

Back 33

- distrust in authority, lower self esteem, low levels of interpersonal trust, feelings of powerlessness

- higher among blacks than whites (bc of previous events- study where blacks with syphilis not given penicillin bc wanted to study progression of disease)

- in a study, 27% of the sample believed that HIV was created by the government to wipe out blacks (especially men!) these people also used less condoms! scary as f*ck.

Front 34

Describe the global warming study

Back 34

- looked at influence of climate change conspiracy theories on the intentions to reduce ones carbon footprint

- read conspiracies vs anti conspiracies, rated their powerlessness, and looked at intended behaviour

- in proconsipracy conditions, conspiracies were endorsed more even though the word conspiracy never mentioned

- their behaviours to reduce carbon footprint was mediated by their feelings of powerlessness

- if you got the pro consiracy you wouldnt change behaviour and if you got the anti conspiracy you would

- showed the effects of conspiracy on actual behaviours and intentions

Front 35

What is the DSM diagnosis for paranoid personality disorder

Back 35

a pervasive distrust and suspiciousness of others such that their motives are interpreted as malvolent, beginning by early adulthood and present in a variety of contexts, as indicated by 4 or more of:

- suspects ofhters are exploiting, harming, deceiving them

- pre-occupied with doubts about the loyalty or trust of others

- reluctant to confide in others for fear of malicious use of info

- reads hidden, demeaning or threatenig messages into benign remarks or events

- persistently bears grudges

- perceives attack on self that others dont

- has recurrent suspicions re fidelity of partner

Front 36

Prevalence of PPD (5)

Back 36

- 2-4%

- more common in men

- may be present form childhood (especially with poor relations, social anxiety, eccentric)

- more common in relatives of schiz. patients and in those with delusional disorder (esp persecutory)

- worse if the thoughts are intransient and inflexible

Front 37

What do we think contributes to PPD (+5teps)

Back 37

externalizing attribution bias (over attribute neg events to people around them)- attentional bias toward threat-related info

Appraisal of social situation-- dysphoric self-consciousness-- hypervigilance and rumination--activation of paranoid cognition (perceptual narrowing-- exasperation of self-consciousness

Front 38

What is the DSM criteria for delusional disorder? (5) What are the specifiers ? (7)

Back 38

- presence of one or more delusions lasing 1 month or longer

- criterion A for schiz never met

- functioning not markedly impaired and behaviour not obviously bizarre

- if any manic or depressive episodes are brief

- not the effects of medical condition of substance and not BDD or OCD

Specifiers:
- erotomanic type (higher status person in love with u)
- grandiose type (inflated power/identity)
- jealous type (unfaithful spouse)
- persecutory type
- somatic type- think have med condition, insects
- mixed type- bit of everything
- unspecified type

Front 39

what are the specifiers of duration or severity for Delusional disorder?

Back 39

after one year:

- first episode- acute (in it rn), in partial remission, full remission

- multiple episodes- acute, partial remission, full

- Continuous

- can also use a quantitative assessment of severity of delusions rating 0-4 (not necessary for diagnosis)

(fun fact in DSM4 -you only needed 1 criterion A if you were having bizarre delusions (impossible ones))

Front 40

differentiate between Delusional disorder and Schiz + PPD.

What are the characheristics of a delusion? (6)

Back 40

- PPD has more flexibility -DD are adamant that they are right

- both can recognize that others think thet are irrational but they dont buy into it themselves

- schiz presents earlier than DD. DD has better general functioning than schiz.

- schiz needs 2 symptoms form criterion A- delusions and something else

Characteristics:

- unfounded

- firmly held

- resistant to change

- distressing

- interferes with social functioning

- involves personal reference

Front 41

What is the prevalence of DD? (6)

Back 41

- 1% to 2% of inpatient admissions

- lifetime is .05-.1%

- 10% of over 85

- later onset usually 40 -55 years

- Female to male ratio: 1.6:1(but no dif found in subtypes)
- men have earlier onset and poorer functionality

Front 42

List and describe the theories of delusions

Back 42

1) Psychoanalytic theory
- delusions stem from depressed sexual tendencies
- denial of the delusions, reaction formation (do opposite of what unconscious wants) - projection put thoughts onto someone else
- delusion is a coping mechanism for thoughts we dont want

2) Theory of Mind
- subject matter of DDs may be linked to TOM, especially jealousy, persecution
- problem interpreting others thoughts

3) Cognitive Theories
- jumping to conclusions: tendency to require less info before making a decision
- Peters et al looked at patients with delusions and with schiz. on reasoning taks and found patients with delusions but not with schiz. more likely to show JTC bias
- attributional bias

Front 43

Describe the Bommer & Brume study on TOM and DD

Back 43

- 21 patients with delusions

- given tests assessing TOM (cartoon pictures), WCST, Proverbs

- sig difference in perseverative errors between DDs and controls

- DDs also performed poorly on TOM and proverbs

- when they factored out cognitive dysfunction, thought the TOM deficit went away

Front 44

How does a persecutory belief begin?

Back 44

Anomalous Arousal experiences= inner- outer confusion

The explanation you select is effected by: your feelings about mental illness, social factors- support, belief flexibility

end up with belief of persucatory delusion

Front 45

How does a persecutory belief get maintained? (3)

Back 45

reinforcement (avoid the harm one say only causes relief and renforces delusion)

obtaining confirmatory evidence (attentional biases, cog biases, on-going anomolous experiences, hostility and isolation)

Discarding Disconfirmatory evidence (things that dont support your belief are reworked to fit into the delusional system)

Front 46

Neurobiological contributions to DD (3)

Back 46

- reduced grey matter in temporal and prefrontal areas

- increased DA transmission

- left hemi overactivity

Front 47

How do you treat DD?

Back 47

- difficult to treat, individual works better than group

- dont try to tell them its not a delusion necessarily, but first work on reducing the stress it causes them

4 steps:

getting them to doubt paranoid beliefs a little

recognizing delusional thoughts

processing disconfirmatory evidence

considering alternative explanations

Front 48

What are (6) correlates of good prognosis in DD?

Back 48

- females

- onset before 30

- sudden onset and short duration

- presence of precipitating factors

- high level of functioning

- persecutory, somatic and erotic more likely to seek help than grandiose and jealous

Front 49

PPD vs normal

Back 49

· Almost everyone has had paranoid thoughts from time to time

o Can be adaptive/healthy to have some sort of paranoia

· 10-15% may experience them regularly

· What is it that distinguishes paranoid thought from paranoid personality disorder

o Transience?

§ How much they come in and go out

o Flexibility?

§ Able to state that it is all in your head /might not be the case, or do you truly believe it

- individuals especially hard to get along with and are hypervigilant+ elicit behaviour from other people that supports their beliefs

- may often be involved in legal battles