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UNLABELLED: The objective of the study was to find associations between obstetric complications (OCs) history and schizophrenia course and symptoms. We analysed the obstetric and psychiatric history of 50 DSM IV schizophrenic subjects who experienced their first schizophrenia episode in adolescence, and 30 healthy controls. Obstetrical data and Apgar scores were obtained from medical records and evaluated with the Lewis and Murray Scale. Based on patients' documentation [including longitudinal evaluation with Positive and Negative Syndrome Scale (PANSS)] the symptom profile and the course of schizophrenia were determined. RESULTS: we distinguished two major groups of patients: with prominent negative and prominent positive symptoms. Schizophrenics with prominent negative symptoms and a chronic schizophrenia course had significantly more definite OCs and lower Apgar scores than patients with prominent positive symptoms and controls. Subjects who had a positive OCs history were more than four times likely to develop schizophrenia in adolescence than those without such a history (OR=4.64; 95% CI=1.29-17.51) with the likelihood of developing schizophrenia with prominent negative symptoms especially high (OR=7.31; 95% CI=1.80-29.65). An Apgar score of between 0 and 3 after birth was associated with an increased risk for developing schizophrenia (OR=2.25; 95% CI=0.56-9.12), especially with prominent negative symptoms (OR=3.71; 95% CI=0.84-16.32). The findings support the hypothesis of a role of OCs in developing early-onset schizophrenia and suggest the associations of the OCs history with a specific symptoms profile (prominent negative symptoms) and a chronic course of schizophrenia.

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A polish translation and the description of the clinical use of the novel screening tool in Alzheimer's disease, a "7 Minute Screen", is presented.

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In the paper an evaluation of basic accuracy parameters (sensitivity and specificity) of the polish version of "7 Minute Screen" as a screening tool for Alzheimer's disease is presented as well as its comparison to Mini Mental State.

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Behavioural disturbances are common in the course of dementia in Alzheimer's disease (AD) and their treatment is usually difficult. Different pharmacological and non-pharmacological options are employed basing mainly on clinical experience, still the number of well-designed, controlled studies in the field is very small. Novel, atypical neuroleptics, including risperidone might potentially be one of these options, taking into account their good safety profile and clinical efficacy in closely related syndromes. We present the results of a retrospective analysis of 57 outpatients with behavioural symptoms complicating AD treated with risperidone, either alone or in combination with one of the acetylcholinesterase inhibitor (AchEI; donepezil or rivastigmine). Seventy five percent of patients treated responded to risperidone with the usual effective dose of 0.5-1 mg/day. The influence of risperidone treatment on behavioural symptomatology was irrespective to the use of AchEI and equally well safe in both groups. The clinical response to the treatment was seen usually within first 2-3 weeks, those who did not respond early tended not to respond later on as well. Additionally, if not responding to low doses of risperidone (0.5-1 mg/day), patients usually did not respond to higher doses or could not tolerate them, mainly due to emerging extrapyramidal symptoms (EPS). Low doses of risperidone were well tolerated, with the fraction of patients experiencing EPS not achieving 10%. EPS observed, were dose dependent and tended to appear if the dose acceleration was fast. We then recommend low doses of risperidone and its slow titration if needed.

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The costs of Alzheimer's disease treatment in the era of acetylcholinesterase inhibitors use are critically discussed.

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The aetiology of Alzheimer's disease (AD) remains, despite vast progress, not fully understood. Four genes involved in the development of the disease have been identified. Three fully penetrant ones (the amyloid beta-protein precursor on chromosome 21, presenilin 1 on chromosome 14, and presenilin 2 on chromosome 1) lead to the development of relatively rare familial form of AD. Together, they account for about half of this early-onset form of the disease. One genetic risk factor--polipoprotein E-4--is associated with late-onset Alzheimer's disease while at least two others are proposed. None of these genes can be by now adopted for use as a diagnostic or predictive test for Alzheimer's disease. Apart from the above, some environmental factors are also implicated in pathogenesis of the disease with the amyloid cascade hypothesis being the most commonly accepted as central. In the presented paper we have critically reviewed a literature on etiopatogenesis of Alzheimer's disease and discussed some practical consequences of the progress in understanding the mechanism of the disease.

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