Objective The authors examined the relationship between cannabis use and the course of illness in schizophrenia over 10 years following first psychiatric hospitalization. Method We assessed 229 patients with a schizophrenia-spectrum disorder five times: during the first admission, and 6 months, 2 years, 4 years, and 10 years later. Ratings of cannabis use and psychiatric symptoms (psychotic, negative, disorganized, and depressive) were made at each assessment. Results The lifetime rate of cannabis use was 66.2%, and survival analysis revealed that this usage was associated with an earlier onset of psychosis. The rates of current use ranged from 10% to 18% across assessments. Cannabis status was moderately stable, with concordance between waves ranging rtet = 0.48 – 0.78. Mixed-effects logistic regression revealed that changes in cannabis use were associated with changes in psychotic symptoms over time even after gender, age, socio-economic status, other drug use, antipsychotic medication use, and other symptoms were controlled. Structural equation modeling indicated that the association with psychotic symptoms was bi-directional. Conclusions Cannabis use is associated with an adverse course of psychotic symptoms in schizophrenia, and vice versa, even after taking into account other clinical, substance, and demographic variables. The specificity of this relationship suggests that clinical interventions to reduce cannabis use may be best targeted at individuals with prominent psychotic symptoms.

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Previous work in the area of gesture production, has made the assumption that machines can replicate "humanlike" gestures by connecting a bounded set of salient points in the motion trajectory. Those inflection points were hypothesized to also display cognitive saliency. The purpose of this paper is to validate that claim using electroencephalography (EEG). That is, this paper attempts to find neural signatures of gestures (also referred as placeholders) in human cognition, which facilitate the understanding, learning and repetition of gestures. Further, it is discussed whether there is a direct mapping between the placeholders and kinematic salient points in the gesture trajectories. These are expressed as relationships between inflection points in the gestures' trajectories with oscillatory mu rhythms (8-12 Hz) in the EEG. This is achieved by correlating fluctuations in mu power during gesture observation with salient motion points found for each gesture. Peaks in the EEG signal at central electrodes (motor cortex; C3/Cz/C4) and occipital electrodes (visual cortex; O3/Oz/O4) were used to isolate the salient events within each gesture. We found that a linear model predicting mu peaks from motion inflections fits the data well. Increases in EEG power were detected 380 and 500ms after inflection points at occipital and central electrodes, respectively. These results suggest that coordinated activity in visual and motor cortices is sensitive to motion trajectories during gesture observation, and it is consistent with the proposal that inflection points operate as placeholders in gesture recognition.

Background: Mismatch negativity (MMN) amplitude is reliably reduced in psychotic disorders. While several studies have examined this effect in first-degree relatives of individuals with schizophrenia, few have sought to quantify deficits in relatives of individuals with other psychotic disorders. While some studies conclude that, compared to healthy subjects, first-degree relatives of schizophrenia show reduced MMN, others contradict this finding, a discrepancy which extends to two recent meta-analyses. Furthermore, though MMN is often shown to be associated with cognitive impairments and clinical symptoms in psychotic disorders, to our knowledge no studies have sought to examine these relationships in studies of first-degree relatives. Method: The present study sought to clarify the extent of MMN amplitude reductions in a large sample of siblings of individuals with diverse psychotic disorders (n=65), compared to cases with psychosis (n=220) and never psychotic comparison subjects (n=252). We further examined associations of MMN amplitude with cognition and schizotypal symptoms across these groups. Results: We found that MMN amplitude was intact in siblings compared to cases with psychosis. MMN amplitude was associated with cognition and schizotypal symptoms dimensionally across levels of familial risk. Conclusions: The present results imply that MMN amplitude reductions emerge as a result of, or in conjunction with, clinical features associated with psychosis. Such findings carry important implications for the utility of MMN amplitude as an indicator of inherited risk, and suggest that this component may be best conceptualized as a marker for clinical symptoms and cognitive impairments, rather than risk for psychosis per se.

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