Serious viral CNS infections during childhood appear to be associated with the later development of schizophrenia and nonaffective psychoses. The association with specific viruses suggests that the risk is related to infectious agents with a propensity to invade the brain parenchyma.

No abstract

No abstract

BackgroundAlcohol has been suggested to be either protective of, or not associated with Parkinson’s disease (PD). However, experimental animal studies indicate that chronic heavy alcohol consumption may have dopamine neurotoxic effects relevant for PD. We studied the association between diagnosed alcohol use disorders and PD.MethodsAll individuals in Sweden admitted with a diagnosis of an alcohol use disorder or appendicitis (reference group) between January 1, 1972 and December 31, 2008 were identified through the Swedish National Inpatient Register, and followed for up to 37 years for a diagnosis of PD. We estimated hazard ratios (HR) with 95% confidence intervals (CI) and adjusted for age and sex.ResultsWe found 1,741 (0.3%) cases of PD in the cohort of 602,930 individuals, 1,083 (0.4%) among those admitted with an alcohol use disorder and 658 (0.2%) of the individuals admitted with appendicitis. The mean follow-up time was 13.6 and 17.1 years, respectively. The HR for PD associated with an alcohol use disorder was 1.38 (CI 1.25-1.53) adjusted for age and sex. When the risk was estimated in age groups for first hospital admission with PD the highest risk was observed in the lowest age group, ≤44, HR 2.39 (0.96-5.93), adjusted for age at exposure and sex.ConclusionsA history of an alcohol use disorder conferred an increased risk of admission with a diagnosis of Parkinson’s disease in both women and men. In particular, the risk seemed higher at lower ages of first admission with Parkinson’s disease.

No abstract

No abstract

No abstract

Introduction: While evidence strongly supports a causal effect of cannabis on psychosis, it is less clear whether the symptom pattern, clinical course, and outcomes differ in cases of schizophrenia with and without a background of cannabis use. Methods: Analysis of medical records from a longitudinal follow-up of Swedish conscripts with data on cannabis use in adolescence and subsequent incidence of schizophrenia. One hundred sixty patients with schizophrenia were assessed using the OPCRIT protocol. Cases were validated for diagnosis schizophrenia according to OPCRIT. Results: Patients with a cannabis history (n = 32), compared to those without (n = 128), had an earlier age at onset, a higher number of hospital admissions and a higher total number of hospital days. There was no significant difference in type of onset and clinical symptom profiles between the groups. Conclusion:Our findings indicate that the disease burden of schizophrenia is greater in individuals who use cannabis during adolescence. Strengthening evidence on causality and teasing out long-term effects of pre-illness cannabis use from continued post-illness has clinical implications for improving schizophrenia outcomes.