Neurobiological Theories of Psychosis

Psychosis caused by neurobiology?

TESTING FOR DEFICITS

*Studies have used various tasks to assess deficits in cognitive abilities. -WCST

-Distractibility

-continuous performance

-flexible thinking

METAANALYSES

FIORAVANTI- 1275 between 1990-2003 113 studies and found consistent evidence for impairment of 

-IQ

-MEMORY

-LANGUGE

-EXECUTIVE FUNCTION

-ATTENTION

FORBES ET AL- 187 studies on working memory in SZ, phonological,visuospatial,central executive

-signfiicant evidence of deficts in working memory in ALL

KRABBENDAM- found BPD patients show simialr range of cog deficits to SZ parts but deficits in bipolar are milder. 

LIMITATIONS?

DIVERSE EFFECT SIZES MAJOR LIMITATION

SOME EFFECTS DUE TO POOR MOTIVATION? 

longitudinally? NAKAGAMI- foudn self-report measure of intrinsic motivation predicted posiitve change on neurocognitve tests over 12 months. 

how do symtpoms link to cognitve deficits?? 

*Due to distractibility it is assumed posiitve symptoms interfere with cognitive processing

FOSTER GREEN- argues that pos symptoms are not specifcally associated with deficits. 

KEEFE- 1493 patients CATIE clinical antipsychotic trial of intervention effectiveness 

-11 neurocognitive tests were administered, outcome measures in five domains

-processing speed

-reasoning

-verbal memory

working memory

vigilance and social cognition

correlation with pos= r=.08

neg-= .0.13-0.27

many studies have shown strong correlations between performamnce on neurocognitve tests and social functioning

- adolescence and early adulthood is a maxiumum risk period for the onset of psychosis 

-peak age of onset 15-24 for MALES 25-34 FEMALES- GOLDSTEIN

modern studies have confirmed this showing that peak risk is 3-4 years later in women - hafner

Bipolar disorders show simialr age prevalence but with less evidence for later onset in women 

Hafner- estrogen might be an anti psychotic 

studies show the brain prominent, progressive changes during teenage. 

assumes that psychosis is a consequence of a disorder of the developing brain that explodes into overt symtpoms during adol

HUTTENLOCHER- first demon that changes in EEG during adol reflected late loss of synapses- neural pruning. this is though to explain the high risk of psychosis in adol. 

abnormal pruning

faikure of neurointegration due to earlier brain damage 

LIMITATION

difficulty to show non-neurotypical structure precedes the onset of psychosis - chicken or the egg type scenario. 

archieve studies are a means of bypassing this issue. 

WALKER - analysed childhood home movies of future schizoprenic patients

future SZ patients, compared to siblings showed more negative emotion (girls only) and less positive emotion. some of these differences were detectable within the first years of life- WALKER

WALKER- abnormal clumsiness observed even in infancy. 

some studies show increased risk of obsetric birth complications (OBCS) in future SZ patients 

CANNON ET AL

- complications of pregnancy

-impeded foetal growth and development

-complications of delievry

odds ratio <2 

seasonal birth effect for schiz

5-10% higher risk in late winter or spring (COTTER) 

EVIDENCE FOR SCIZOVIRUS 

transmitted through household pets? - FULLER AND YOLKEN

studies tried to find link between sz and prenatal exposure to flu virus - mixed findings. 

recebt meta anal = link between sz and childhood toxoplasmosis =2.73

SOMLI found NO association between cat ownership at 13 and 18 years and psychosis later in life. 

BP= seasonal birth effect - torrey

ASSOCIATION WITH MATERNAL STARVATION DURING PREGNANY BUT NOT SERIOUS BIRTH COMPLICATIONS. 

- EVIDENCE THAT NP ABNORMALITIES SOMETIMES CAUSE PSYCHOSIS

-EFFECTS ARE SMALL

-CANNOT EXPLAIN PEAK AGE OF RISK- 60% OF PATIENTS DO NOT BECOME ILL IN ADOL OR EARLY ADULTHOOD. 

brain disease? 

hallucinations in brain = affect brain structure 

thinning of cerebral cortex

in some SZ patients outer covering of cerebrum appears thinner in certain lobes and cells have atypical organisation 

ventricular enlargement

fluid filled areas of the brain which occur larger in sz 

studies suggest that this is due to reductions in total bran tissue (cortical atrophy) 

2% reduction compared to controls- HAIJMA

CT SCANS AND MRI STUDIES REPORTED THIS ABNORMALITY IN FIRST EPISODE PATIENTS SUGGESTING IT COMES BEFORE ILLNESS. 

MCDOANLD 243 PATIENTS AND FIRST DEGREE RELATIVES WITH SZ OR BP PATIENTS WITH SZ INCREASED VENTRICULAR VOLUME AS DID RELATIVES NO EVIDENCE FOR BP. 

Mcdonald

reported both schizophrenia and bipolar patients had low volumes of white matter but sz patients uniquely had reduced volumes of grey 

rpeorted meta anal 26 MRI studies bipolar had larger right lateral ventricular volume.