Familial liability to schizophrenia, obstetric complications, neurodevelopmental delay, deterioration in pre-morbid functioning and observable motor disorders appear to contribute independently to domains of neurological dysfunction. The findings support a neurodevelopmental model of NSS in schizophrenia.

The relationship between cannabis and cognitive performance is controversial. While both acute administration and long-term cannabis use impair cognitive performance in healthy subjects, several studies have shown improved cognitive outcomes in patients with schizophrenia spectrum disorders who use cannabis. The aim of this study was to determine the relationship between lifetime cannabis use, as assessed longitudinally over 10 years of follow-up in a sample of 42 patients and 35 of their unaffected siblings, and current cognitive performance. Forty-two healthy control subjects were assessed at follow-up with the same instruments. Stepwise linear regression revealed a negative effect of longitudinal cannabis use on performance in a social cognition task in the patient group. In the sibling group, lifetime cannabis use had a negative effect on processing speed and declarative memory performance. In the control group, cannabis use per se did not predict cognitive performance; however, when adding lifetime tobacco use to the model, we found a negative association between lifetime cannabis and tobacco use and processing speed and social cognition performance. Moreover, a lower IQ associated with current cannabis use predicted worse attentional performance in the control group. The differential pattern of associations between cannabis use and cognitive performance in patients compared with siblings and controls can be explained by the negative impact of illness on cognition.

Spontaneous Parkinsonism (SP) in schizophrenia-related disorders is poorly characterized. The objective of this study was to examine the concordance and clinical validity of alternative definitions of SP in patients with nonaffective psychotic disorders. Two-hundred drug-naive patients with nonaffective psychotic disorders were examined for core parkinsonian signs, including bradykinesia, rigidity, and tremor, and diagnosed of SP according to the Simpson-Angus Scale (SAS) cutoff criterion, the UK Parkinson's disease brain bank (UKPDBB) criteria, the National Institute of Neurological Disorders and Stroke (NINDS) criteria, and criteria requiring the presence of all three core features (full syndrome criteria). Parkinsonian signs and criteria were examined in relation to a number of relevant clinical variables. The most frequent sign was rigidity (33.5%) followed by bradykinesia (16%) and tremor (12%). The prevalence rate of SP according to the SAS cutoff criterion, the UKPDBB criteria, the NINDS criteria for possible and probable SP, and the full syndrome criteria were 20.5, 13, 25.5, 18.5, and 4%, respectively. Bradykinesia was specifically related to negative symptoms, rigidity to neurological soft signs, and tremor to dyskinetic movements. The set of criteria showing more associations with clinical variables were the NINDS criteria for probable SP. Patients fulfilling these criteria had higher ratings for poor premorbid adjustment, negative symptoms, dyskinesia, neurological soft signs, and poor global treatment response than those without that diagnosis. The NINDS criteria for probable SP, i.e., presence of any two of the three core parkinsonian signs, seem to be the most suitable for clinical and research purposes.

No abstract

The diagnosis of schizophrenia and other psychotic disorders in current psychiatric classifications identifies individuals who are severely ill but who have few clinical characteristics in common. The usual picture of psychotic patients is a mixture of mood and psychotic symptoms. Fortunately, clinicians do not base their therapeutic strategies exclusively on diagnosis, but also on symptom predominance. Thus, clinicians' treatments have been dimensional in nature for years, although, until recently, their psychiatric classifications had been mainly categorical. The main principle in psychosis classification has been the Kraepelinian dichotomy, despite its lack of enduring empirical validation. Without doubt, current psychiatric classifications have made great strides in reliability and clinical utility, although these advantages have not been enough to compensate for their shortcomings concerning validity. It has recently been suggested that the Kraepelinian dichotomy may be hindering progress in neurobiological research within psychosis. Mounting evidence is now fuelling a paradigm shift in the ongoing process of review of psychiatric classifications toward the introduction of complementary dimensional indicators of psychiatric categorical diagnoses. This new approach will allow us to understand psychosis as prototypical extremes of a severity continuum. The gradients of this continuum may begin with subtle expressions in the general population, continue with milder forms in relatives of psychotic patients and subclinical cases and finally reach the prototypical forms of psychosis at the other extreme. Future complementary dimensional indicators will require sound instruments capable of reflecting a multidimensional assessment of psychopathological symptoms, polydiagnostic interviews and the assessment of a wide range of nonsymptomatic domains. These new methods of assessment merging created by the shift toward a dimensional paradigm will be applied in the forthcoming new diagnostic criteria and may allow for a phenome-wide scanning for psychosis.