دانلود رایگان مقاله انگلیسی بازداری بازگشت (IOR) در بیماران مبتلا به اسکیزوفرنیا و استفاده از کانابیس - الزویر 2019

Abstract

Research concerning the spatial orientation in patients with schizophrenia has demonstrated a state independent deficit in inhibition of return (IOR), which has been discussed as a vulnerability marker for schizophrenia. Other recent investigations on brain structure and cognitive processing have revealed less deficits in schizophrenia patients with comorbid cannabis use (SCH+CUD) compared to abstinent schizophrenia patients (SCH). It was hypothesized that these results may reflect a premorbid lower vulnerability in at least a subgroup of comorbid patients. The aim of the present study is to extend previous work by investigating IOR functioning in patients with schizophrenia and cannabis use. This in turn should supplement the existing studies on the vulnerability of this patient group. Therefore, we compared IOR functioning in four groups: 62 patients with schizophrenia and 46 healthy controls, both with and without cannabis use. Participants underwent a covert orienting of attention task (COVAT) with peripheral cues and three stimulus onset asynchronies (SOAs: 200 ms, 400 ms and 800 ms). Both schizophrenia groups displayed delayed IOR with a more pronounced IOR effect in SCH+CUD compared to SCH. In healthy controls, IOR did not seem to be significantly affected by cannabis use. Significant IOR-differences between groups were only seen between SCH patients without cannabis use and both healthy groups at SOA 400 ms. Patterns of cannabis use as well as clinical parameters of psychoses did not affect IOR. Our results may support the hypothesis of IOR as a vulnerability marker for schizophrenia and of a lower biological vulnerability in at least a subgroup of SCH+CUD.

Conclusions

To our view, cannabis is not responsible for the higher functioning in SCH+CUD patients, but it triggers schizophrenia in high functioning individuals with low vulnerability for psychosis. Following, our study contains further reference to our initial hypotheses of an average low vulnerability in SCH+CUD patients. This in fact could have implications regarding a better course of the disease compared to abstinent patients with an average higher vulnerability, if comorbid patients succeed to reduce cannabis use. Nevertheless, some aspects remain speculative, especially regarding the role of cannabis in preattentive inhibitory mechanisms. Future studies should analyze IOR in subjects with high risk of schizophrenia, prodromal or schizotypal subjects, in order to clarify the role IOR plays as a vulnerability marker. With respect to the hypotheses of average lower vulnerability in SCH+CUD patients, future research should take an additional group of SCH+CUD patients who develop cannabis use after the onset of schizophrenia into account. According to our hypotheses, such patients with late onset of cannabis use should not demonstrate higher functioning compared to abstinent patients with schizophrenia.