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Research indicates that a number of neuroanatomical features differ between groups of people with schizophrenia and groups of matched controls.

Adult brain structureEdit

Differences in the size and structure of certain brain areas have been found in some adults diagnosed with schizophrenia. Early findings came from the discovery of ventricular enlargement (ventricles) in people diagnosed with schizophrenia with negative symptoms most prominent.[1] However, this finding has not proved particularly reliable on the level of the individual person, with considerable variation between patients. But it has been used in case studies with twins although it is a rather small percentage about 1 in a 100 cases of twins have shown that schizophrenia is genetic but it is rare. The picture we are looking at stands around 1 in 100 within the general population this is actually quite a daunting figure if for example we were looking at 700 students 7 out of them will have the mental illness.


The role of antipsychotic medication, is to lower levels of deopomine in the brain although this may supress the affects it is not a cure. which nearly all those studied had taken, in causing such abnormalities is also unclear.[2]

More recent studies have shown a large number of differences in brain structure between people with and without diagnoses of schizophrenia.[3] However, as with earlier studies, many of these differences are only reliably detected when comparing groups of people, and are unlikely to predict any differences in brain structure of an individual person with schizophrenia.

Neuropsychology and brain functionEdit

Studies using neuropsychological tests and brain imaging technologies such as fMRI and PET to examine functional differences in brain activity have shown that differences seem to most commonly occur in the frontal lobes, hippocampus, and temporal lobes.[4] These differences are heavily linked to the neurocognitive deficits which often occur with schizophrenia, particularly in areas of memory, attention, problem solving, executive function and social cognition.

Schizophrenia and the frontal lobesEdit

Schizophrenia PET scan

Data from a PET study[5] suggests that the less the frontal lobes are activated (red) during a working memory task, the greater the increase in abnormal dopamine activity in the striatum (green), thought to be related to the neurocognitive deficits in schizophrenia.

Main article: Schizophrenia - Frontal lobes
Main article: Schizophrenia - Hippocampus
Main article: Schizophrenia - Temporal lobes

Basolateral amygdalaEdit

Abnormalities in the projections from the medial prefrontal cortex to the basolateral amygdala have been observed in those with schizophrenia[citation needed].

Schizophrenia and neural integrationEdit

Electroencephalograph (EEG) recordings of persons with schizophrenia performing perception oriented tasks showed an absence of gamma band activity in the brain, indicating weak integration of critical neural networks in the brain.[6] Those who experienced intense hallucinations, delusions and disorganized thinking showed the lowest frequency synchronization. None of the drugs taken by the persons scanned had moved neural synchrony back into the gamma frequency range. Gamma band and working memory alterations may be related to alterations in interneurons that produced the neurotransmitter GABA.

There are a number of theories about how these structural differences occur:

Genetic factors in neuroanatomical developmentEdit

Developmental aspectsEdit

Perinatal brain developmentEdit

It is thought that some of the neuroanatomical features associated schizophrenia are the result of early neurodevelopment changes, due to factors during pregnancy,etc

Main article: Schizophrenia - Developmental factors

Methods of neuroanatomical study in schizophreniaEdit

With advances in neuroimaging techniques there has been an enormous growth of activity in the area over recent years.

Main article: Schizophrenia - PET studies
Main article: Schizophrenia - EEG studies

See alsoEdit

References & BibliographyEdit

  1. Johnstone EC, Crow TJ, Frith CD, Husband J, Kreel L. (1976) Cerebral ventricular size and cognitive impairment in chronic schizophrenia. Lancet, 30;2 (7992), 924-6.
  3. Flashman LA, Green MF (2004) Review of cognition and brain structure in schizophrenia: profiles, longitudinal course, and effects of treatment. Psychiatric Clinics of North America, 27 (1), 1-18, vii.
  4. Green, M.F. (2001) Schizophrenia Revealed: From Neurons to Social Interactions. New York: W.W. Norton. ISBN 0-393-70334-7
  5. Meyer-Lindenberg A, Miletich RS, Kohn PD, Esposito G, Carson RE, Quarantelli M, Weinberger DR, Berman KF (2002) Reduced prefrontal activity predicts exaggerated striatal dopaminergic function in schizophrenia. Nature Neuroscience, 5, 267-71.
  6. Spencer KM, Nestor PG, Perlmutter R, Niznikiewicz MA, Klump MC, Frumin M, Shenton ME, McCarley (2004) Neural synchrony indexes disordered perception and cognition in schizophrenia. Proceedings of the National Academy of Sciences, 101, 17288-93. (full text)

Key textsEdit


  • Frith, C. D. (1992). The cognitive neuropsychology of schizophrenia. Hillsdale, NJ: Lawrence

Erlbaum Associates, Inc.


Additional materialEdit



External linksEdit

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