کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5721021 | 1411340 | 2017 | 9 صفحه PDF | دانلود رایگان |
BackgroundChronic cannabis use may cause neurocognitive deficits and increase the risk of psychosis. Nevertheless, the effects of cannabis use on neurocognitive functioning in schizophrenia have remained largely unspecified.MethodsHere, we studied repetition suppression of auditory event-related responses in a paired-stimulus design in a mixed sample of schizophrenia patients (n = 34) and healthy control subjects (n = 45) with chronic heavy cannabis use and schizophrenia patients (n = 33) and healthy control subjects (n = 61) without cannabis use.ResultsRepeated measures analysis yielded an overall significant reduction of P50 amplitude between first and second stimulus (p < .02), which was not different between the groups, a reduction of N100 amplitude, which was different for schizophrenia patients compared with healthy control subjects independent of cannabis use (p < .02), and a significant interaction between diagnosis and chronic cannabis use on the reduction of the P200 amplitude (p < .001). While chronic cannabis use was related with increased P200 suppression ratios in control subjects (with chronic cannabis use: 0.55 ± 0.04; without chronic cannabis use: 0.40 ± 0.03; p < .02), the reverse effect was found in schizophrenia (with chronic cannabis use: 0.36 ± 0.05; without chronic cannabis use: 0.54 ± 0.05; p < .02). This result remained significant after inclusion of potential confounders. Total lifetime cannabis use showed a significant correlation with the P200 suppression ratio in otherwise healthy control subjects (r = .28, p < .007). By contrast, the duration of time since last cannabis use was significantly correlated with the P200 suppression ratio in schizophrenia patients (r = .42, p < .002).ConclusionsIn aggregate, these diverging effects of chronic cannabis use on P200 repetition suppression may suggest underlying alterations in the endocannabinoid system in schizophrenia.
Journal: Biological Psychiatry: Cognitive Neuroscience and Neuroimaging - Volume 2, Issue 3, April 2017, Pages 263-271