Abstract

There is a high prevalence of cannabis use reported in non-affective psychosis. Early prospective longitudinal studies conclude that cannabis use is a risk factor for psychosis, and neurochemical studies on cannabis have suggested potential mechanisms for this effect. Recent advances in the field of neuroscience and genetics may have important implications for our understanding of this relationship. Importantly, we need to better understand the vulnerability × cannabis interaction to shed light on the mediators of cannabis as a risk factor for psychosis. Thus, the present study reviews recent literature on several variables relevant for understanding the relationship between cannabis and psychosis, including age of onset, cognition, brain functioning, family history, genetics, and neurological soft signs (NSS) in non-affective psychosis. Compared with non-using non-affective psychosis, the present review shows that there seem to be fewer stable cognitive deficits in patients with cannabis use and psychosis, in addition to fewer NSS and possibly more normalized brain functioning, indicating less neurobiological vulnerability for psychosis. There are, however, some familiar and genetic vulnerabilities present in the cannabis psychosis group, which may influence the cannabis pathway to psychosis by increasing sensitivity to cannabis. Furthermore, an earlier age of onset suggests a different pathway to psychosis in the cannabis-using patients. Two alternative vulnerability models are presented to integrate these seemingly paradoxical findings

Highlights

  • Prevalence and clinical implications Use of illicit drugs is common in non-affective psychosis (ICD-10 F20–29; [1]), usually seen in about half of the patients; 40–60%, ranging from 10 to 70% [2,3,4,5,6,7,8,9]

  • The results showed that most studies had found better cognitive functioning in psychosis patients with cannabis use compared with psychosis alone [110]

  • It is suggested that the pathway to psychosis via cannabis is less influenced by neurobiological vulnerability factors

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Summary

Introduction

Prevalence and clinical implications Use of illicit drugs is common in non-affective psychosis (ICD-10 F20–29; [1]), usually seen in about half of the patients; 40–60%, ranging from 10 to 70% [2,3,4,5,6,7,8,9]. Other authors, such as Schnell et al [109], suggested similar explanations at this point in time This finding prompted a review of the existing literature on the relationship between cannabis use and cognitive functioning in non-affective psychosis, and a systematic PubMed search resulted in 23 studies [110]. Patients with dual diagnosis of cannabis abuse and schizophrenia were found to be less impaired relative to schizophrenia only compared with healthy controls in regard to emotional memory and prefrontal lobe functioning [175], and showed a more normalized brain activation pattern during mental rotation in the left superior parietal region relative to schizophrenia only compared with healthy controls [176] It must be noted, that the differences between the different groups are subtle in most studies, and even group-based differences between normal controls and patients with schizophrenia and non-affective psychosis are usually subtle and of unclear clinical relevance. It can be concluded that there are some data, scarce, suggesting minor long-term effects of cannabis on brain structure in psychosis patients, but that the majority of studies show better brain functioning in this group, suggesting less neurocognitive vulnerability

Other variables mediating neurobiological vulnerability
Discussion
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