Abstract

В статье представлена проблема резистентной шизофрении и негативной симптоматики. В теоретическом и практическом аспекте описаны попытки и возможности современной фармакотерапии преодолеть данный феномен. The article presents the problem of resistant schizophrenia and negative symptomatology. In theoretical and practical aspect the attempts and possibilities of modern pharmacotherapy to overcome this phenomenon are described. Modern research demonstrates that there are no obvious pathological changes in the brain of persons with schizophrenia. Nevertheless, there is evidence that a neurodegenerative process (significant ventricular dilation, decreased cortical thickness, decreased activity according to functional imaging techniques, and a more malignant course of the disease) may underlie the prevalence of negative symptoms in schizophrenia. Based on data from this and other studies (particularly in Alzheimer's disease), the authors concluded that cerebral as an adjunctive therapy can improve cognitive function in patients with schizophrenia and predominantly negative symptoms. However, the mechanism of this therapeutic effect remains unclear. It should be noted that olanzapine (ferzapine) monotherapy also improves cognitive function in individuals with schizophrenia [9].Safety. No serious adverse events were noted in any group during the study. The most frequent adverse events, which developed in at least 10% of patients in each group, were changes regarding weight gain. The addition of 20 mL of cerebral to olanzapine (ferzapine) at doses of 5-10 mg/day was safe and well tolerated by the subjects.This study had some limitations that should be taken into account when interpreting the results. First, only those patients who had more negative than positive symptoms were included in the follow up because they were less sensitive to antipsychotics. In addition, a study with a larger patient population and different clinical characteristics should be conducted to clarify whether cerebral therapy itself is effective in reducing the severity of schizophrenia symptoms. Second, this study was conducted over a relatively short 8-week period, which is too short to realize the full therapeutic effect of cerebral. Although additional effects of cerebral on memory and other cognitive functions were noted beginning in the 2nd week of treatment, it may take longer to detect an obvious effect on negative symptoms. Only a fixed dose of cerebral was used in all patients. Although cerebral at a dose of 20 ml/day does not increase the therapeutic effcacy of olanzapine (ferzapine) in the treatment of positive and negative symptoms in schizophrenia, the results of this study suggest that it may improve cognitive function. A similar effect has been observed in the treatment of other neurological disorders. Thus, in our opinion, there is a very interesting prospect for further randomized studies combining olanzapine (ferzapine) with nootropic drugs, in particular cerebral. Further studies with different doses of cerebral over a longer period of time are needed.

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