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.

Introduction

Neurocognition and preattentional cognitive functioning in cannabis users and in schizophrenia Cannabis use is associated with neurocognitive impairments (e.g. memory, attention and executive functioning) in healthy users. These deficits persist over the period of acute cannabis administration and in adolescent onset users, even life-long persistence seems probable (Solovij and Michie, 2007). Interestingly, impairments in healthy cannabis users are similar to those in schizophrenia patients not using cannabis (Lorenzetti et al., 2013; Yücel et al., 2008). Deficits appear in prodromal and first-episode patients, in patients with chronic schizophrenia and have also been identified in first-degree relatives (Antonova et al., 2005). Age of onset of schizophrenia was found to be inversely proportional to deficits, but the progression of deficits is not related to the number of psychotic episodes, contradicting state-dependency of cognition (Krug and Kircher, 2017; Van Assche et al., 2017). Hence, impairments are thought to represent trait markers of schizophrenia, reflecting neurobiological vulnerability. A recent review further describes preattentive processes and cognitive inhibition as neurobiological vulnerability markers of psychoses, underlying state-independent characteristics (Krug and Kircher, 2017). And similar to above mentioned findings, schizophrenia patients and healthy cannabis users commonly display deficits at prepulse inhibition (PPI) of the startle reflex (Kedzior et al., 2016; Morales-Muñoz et al., 2015), at P50 sensory gating, a neurobiological determined inhibitory mechanism (Rentzsch et al., 2011), and at mismatch negativity (MMN) (Impey et al., 2015). Superior performance in comorbid patients with schizophrenia and cannabis use Cannabis use is highly prevalent among patients with schizophrenia and some negative effects of consumption on people with psychotic disorders are well established (Hamilton, 2017). Schizophrenia patients using cannabis (SCH+CUD) present an earlier onset of psychoses (Hermle et al., 2013) and overall poor long-term outcomes (Hamilton, 2017; Schnell, 2014). Based on these findings, we would expect additive negative effects on cognition. But surprisingly, schizophrenia patients (with onset of cannabis use prior to the first psychotic episode) demonstrate similar or even better cognitive performance compared to abstinent patients (Hanna et al., 2016; Mallet et al., 2017; Schnell et al., 2012). Consistent with these findings, SCH+CUD was associated with less severe deficits compared to abstinent patients with regard to PPI (Morales-Muñoz et al., 2015), MMN (Rentzsch et al., 2011) and P50 sensory gating (Broyd et al., 2013; Rentzsch et al., 2007).

مقدمه

مصرف ماریجوانا با اختلالات عصب شناختی ( مثل اختلال حافظه ، توجه و اختلالات عملکردی ) در مصرف کنندگان غیر بیمار همراه است.این اختلالات در طول دوره مصرف شدید ماریجوانا تداوم دارند و این تداوم حتی در مورد مصرف کنندگانی که در آغاز دوره بلوغ هستند بصورت دائمی هم محتمل است.به طرز جالبی اختلالات مصرف کنندگان غیر بیمار ماریجوانا شبیه بیماران شیزوفرنیکی است که ماریجوانا مصرف نمی کنند.اختلالات در بیماران پیش از شروع علائم اصلی بیماری و بیمارانی که در دوره اول بروز علائم بیماری هستند،در بیماران مبتلا به شیزوفرنی مزمن و بیمارانی که بین بستگان درجه یک خود سابقه بیماری دارند بروز می کند.مشخص شد سن شروع شیزوفرنی با اختلالات یاد شده همبستگی معکوس دارد.اما پیشرفت اختلالات با تعداد دوره های سایکوتیک ارتباطی ندارد که این قضیه رابطه قوای شناختی و وضعیت روانی فرد را رد می کند.به همین علت اختلالات یاد شده بعنوان نشانگرهای شیزوفرنی در نظرگرفته می شوند که که خود نشان دهنده آسیب پذیری عصبی زیستی است.