Resting EEG deficits in accused murderers with schizophrenia
Department of Criminal Justice, California State University, Long Beach, CA 90840, USA. Psychiatry Research
(Impact Factor: 2.47).
08/2011; 194(1):85-94. DOI: 10.1016/j.pscychresns.2010.12.017
Empirical evidence continues to suggest a biologically distinct violent subtype of schizophrenia. The present study examined whether murderers with schizophrenia would demonstrate resting EEG deficits distinguishing them from both non-violent schizophrenia patients and murderers without schizophrenia. Resting EEG data were collected from five diagnostic groups (normal controls, non-murderers with schizophrenia, murderers with schizophrenia, murderers without schizophrenia, and murderers with psychiatric conditions other than schizophrenia) at a brain hospital in Nanjing, China. Murderers with schizophrenia were characterized by increased left-hemispheric fast-wave EEG activity relative to non-violent schizophrenia patients, while non-violent schizophrenia patients instead demonstrated increased diffuse slow-wave activity compared to all other groups. Results are discussed within the framework of a proposed left-hemispheric over-processing hypothesis specific to violent individuals with schizophrenia, involving left hemispheric hyperarousal deficits, which may lead to a homicidally violent schizophrenia outcome.
Available from: Steven Silverstein
- "Electroencephalographic (EEG) findings also provide evidence of specific brain abnormalities in violent offenders with schizophrenia. In a study of resting-state EEG, Schug et al. (2011) found that murderers with schizophrenia demonstrated increased lefthemispheric fast-wave EEG activity relative to nonviolent schizophrenia patients, a finding consistent with generalized overarousal. The overall conclusion from these biological studies is that: (1) studies have consistently identified brain signatures (structural and functional) of increased risk for violence in people with schizophrenia; (2) in most cases, these are similar to what is observed among violent offenders without schizophrenia (Raine, 2013); but (3) this nonspecificity should not be interpreted as indicating lack of utility. "
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ABSTRACT: Published findings on the relationship between schizophrenia and violence have been mixed, due to differences in study design and quality. In this review, we address the issue with an emphasis on characterizing who is most likely to be violent and when. We conclude that: (1) individuals with schizophrenia are at an increased risk for violence due to specific psychotic symptoms; (2) this risk is increased by brain abnormalities, psychiatric comorbidities, and demographic factors that are not specific to schizophrenia; (3) the majority of violent offenses committed by people with schizophrenia are indistinguishable from offenses committed by others; and (4) despite our knowledge of factors related to increased violence risk and the existence of effective treatments to mitigate this risk, valid risk assessment instruments for this population are lacking, and treatment strategies are rarely employed at any level of psychiatric care. In short, while most people with schizophrenia are not violent and violence committed by people with this condition accounts for only a small percentage of overall violent crime, there is nevertheless a significantly increased risk for violence among subgroups in this population. This has implications for people living with people with schizophrenia, mental health professionals, administrators of psychiatric care facilities, law enforcement personnel, the court system, and policymakers.
Available from: Sai Tikka
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ABSTRACT: Higher frequency of minor physical anomalies (MPAs) in schizophrenia provides morphological evidence for the neurodevelopmental theory. Abnormal gamma oscillations (>30Hz) seen in schizophrenia have been hypothesized to result from developmental insults. This study investigated spontaneous gamma oscillations in schizophrenia patients having higher and lower number of MPAs. Forty drug naïve/free schizophrenia patients and 20 matched healthy controls were assessed for MPAs on the Extended Waldrop Scale (EWS). All participants underwent an awake, resting 192-channel EEG recording. Spontaneous gamma spectral power and coherence were estimated in the low- (30-50Hz) and high-gamma (51-70 and 71-100Hz) bands. Significantly higher power was observed in high-MPA than healthy control group in low-gamma band over right frontal, parietal and temporal regions. Spectral power in the high-gamma band (71-100Hz) was also significantly higher in high-MPA than healthy control group over left frontal, parietal and temporal regions. Additionally, regional intra-hemispheric and inter-hemispheric coherence in low-gamma band was significantly higher in high-MPA than healthy control group. This study is the first to provide evidence of increased spontaneous gamma power and synchrony in schizophrenia patients having higher MPAs, supporting the idea that it may represent a distinct subgroup of schizophrenia having neurodevelopmental basis.
Available from: Aleksandra Rasic-Markovic
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ABSTRACT: The aim of the study was to determine the effects of early postnatal PCP treatment on
the sensitivity of pubertal and adult rats to lindane proepileptogenic effects. Rat pups were
treated with NaCl (0.9%) or PCP (10 mg/kg) at postnatal days 2, 6, 9 and 12. One control (NaCl-
35) and one experimental (PCP-35) group have received lindane (4 mg/kg) at postnatal day
35, while others received lindane at postnatal day 65 (NaCl-65 and PCP-65). One week prior
to lindane treatment three gold-plated EEG electrodes were implanted. Pubertal rats had
significantly shorter latency time. After lindane, a prompt increase in power spectral density
seen in PCP-treated groups vs. control was evident earlier in PCP-65 rats. The theta waves
were significantly increased in PCP-35 and alpha rhythm in PCP-65 rats, when compared
with corresponding controls. Postnatal PCP treatment increases the synchronization of brain
electrical activity, thus contributing to the increased susceptibility to lindane.
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