Treatment of schizophreniaCognition in schizophrenia – a systematic review
Introduction
Schizophrenia is a rare, complex biological and behavioral disorder characterized by psychosis, social withdrawal, affective flattening and cognitive deficits [1]. Lately, focus on cognitive deficits has increased because of the association between daily life functions and between general outcomes [2]. Cognitive function is relatively stable longitudinally and partly independent from positive symptoms [3].
This systematic review aims to describe the current knowledge on cognitive deficits associated with the schizophrenia disorder, for example, the measurement of cognition, the neurobiology, the effect of treatment, the course of cognitive deficits in patients with schizophrenia and the association with daily life function.
Section snippets
Methods
A literature search using PubMed was conducted and relevant articles in English, Danish, Swedish, Norwegian and German published between 1980 and end June 2011 containing the keywords schizophrenia and cognition was conducted. A total of 6211 articles were screened on titles; followed by a screening of 409 abstracts; and remaining 82 articles were reviewed and 40 included in this study.
Neurobiology and genetics
The etiology of schizophrenia is unknown, and it is still debated whether to define schizophrenia as a neurodegenerative or neurodevelopmental disorder [4]. General cerebral atrophy, lateral ventricle enlargement and lack of gliosis are some of the pathological findings in patients with schizophrenia [4]. So far, cognitive deficits have not been associated with these pathological findings.
In the search for a genetic etiology, cognitive symptoms have been examined as endophenotypes for
Conclusion
Schizophrenia is probably a neurodevelopmental disorder associated with state-like psychosis symptoms and trait-like cognitive symptoms. The cognitive symptoms appear before first ever psychosis, and are to a lesser degree also present in healthy relatives, suggesting a genetic influence. The reduction in PFC activity is consistent with impairment in the cerebral circuitry in schizophrenia leading to a disruption of normal cognitive functioning; the increases in activity seen in some PFC
Conflicts of interest
R. Nielsen has received research grants from H. Lundbeck for clinical trials and speaking fees from Bristol-Myers Squibb, Astra Zeneca, Janssen & Cilag, and Lundbeck and has acted as advisor to Astra Zeneca.
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