Chapter 5.2 – Schizophrenia

Published on Jan 1, 2016
· DOI :10.1016/B978-0-12-410513-3.00022-X
Juri D. Kropotov20
Estimated H-index: 20
(RAS: Russian Academy of Sciences)
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Abstract
In contrast to Attention Deficit Hyperactivity Disorder (ADHD), schizophrenia (SZ) is a less common psychiatric condition characterized by a diverse set of symptoms including specific distortions in sensory, motor, executive, and affective systems. SZ is a result complex inheritance in which interaction of genes with environment plays a critical role. Most of SZ patients experience a lifetime disability with 10% eventually committing suicide. Positive symptoms (delusions and hallucinations) start between ages 16 and 30, are associated with dopaminergic hyperactivity and are suppressed by antipsychotic drugs via blocking dopaminergic receptors. Negative symptoms include impairments in the affective domain such abulia, anhedonia and apathy as well as impairments in cognitive domain with no medication known to reduce them. SZ is developing during prodromal phase so that defining neuromarkers of this state is of big importance for SZ prevention. No consistent changes in QEEG have been so far reported, however ERP research shows reliable decrease of many ERP components in SZ with large effect sizes. The ERP neuromarkers reflect sensory-related deficits such as failure of normally observed P50 gating effect, decrease of auditory and visual N1 waves, decrease of MMN, novelty P3, as well as cognitive related deficits such as reduction of the target P3, N2 and P3 NOGO waves, CNV and SPN. Some of these waves predict conversion to psychosis while the others predict response to antipsychotic medication. Attempts of applying tDCS for schizophrenia are rare reporting reduction of hallucination and improvement of cognitive functions. TMS has been used more widely but still needs larger multicenter studies.
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