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Amisulpride is a potent substituted benzamide antipsychotic drug claimed to improve the negative symptoms of schizophrenia, particularly at low dosage.
Sixty long-term in-patients with schizophrenia and selected for predominant negative symptoms were randomised to receive either haloperidol or amisulpride. Over a year there was systematic dose reduction, as symptoms allowed.
There were no significant differences between the treatment groups in the proportion receiving low-dose treatment, the control of positive symptoms, or ratings of social behaviour, side-effects or tardive dyskinesia. For negative symptoms, there were consistent but non-significant trends in favour of amisulpride. The amisulpride patients required significantly less anticholinergic medication.
In chronically-hospitalised in-patients with schizophrenia characterised by persistent negative symptoms, amisulpride was a well-tolerated maintenance antipsychotic medication. The drug had only a limited effect in reducing negative symptoms, which were relatively stable, enduring phenomena in this sample, despite dosage reduction.
In a sample of 120 long-stay in-patients who fulfilled DSM–III–R criteria for schizophrenia, chronic akathisia and pseudoakathisia were relatively common, with prevalence figures of 24% and 18%, respectively. Compared with patients without evidence of chronic akathisia, those patients with the condition were significantly younger, were receiving significantly higher doses of antipsychotic medication, and were more likely to be receiving a depot antipsychotic. Patients who experienced the characteristic inner restlessness and compulsion to move of akathisia also reported marked symptoms of dysphoria, namely tension, panic, irritability and impatience. The findings support the suggestion that dysphoric mood is an important feature of akathisia. Male patients appeared to be at an increased risk of pseudoakathisia. No significant relation was found between chronic akathisia and tardive dyskinesia, although there was a trend for trunk and limb dyskinesia to be commonest in patients with chronic akathisia while orofacial dyskinesia was most frequently observed in those with pseudoakathisia. Akathisia may mask the movements of tardive dyskinesia in the lower limb. There was no evidence that akathisia was associated with positive or negative symptoms of schizophrenia nor with depression.
Investigation of the relationships between negative schizophrenic symptoms, abnormal involuntary movements and age in 179 chronic schizophrenic patients confirmed that both orofacial and trunk and limb dyskinesia are associated with negative symptoms, but only orofacial dyskinesia showed a significant increase in prevalence with increasing age. Estimation of the mean age of onset of orofacial dyskinesia from the observed variation in prevalence of orofacial dyskinesia with age indicated that patients having negative symptoms tend to develop orofacial dyskinesia at an earlier age. The estimated mean age of onset was 43.6 years in patients with substantial negative symptoms, and 54.6 years in patients without substantial negative symptoms. These findings support the proposal that the pathological process underlying negative symptoms can contribute to the occurrence of both orofacial and trunk and limb dyskinesia, but, in the case of orofacial dyskinesia, there is a synergistic interaction between the pathological process underlying negative symptoms and age-related neuronal changes.
Chronic schizophrenic patients in a long stay hospital were found to have low levels of intelligence (mean IQ of 80), which was attributed to the effects of substantial intellectual deterioration on below average pre-morbid levels of functioning. Patients with the lowest IQ scores had the least severe positive symptoms but symptomatology was not related to age or extent of intellectual decline. Speed of functioning was relatively more impaired than level of intellectual functioning, with cognitive speed being more affected than motor speed. The severity of negative but not positive symptoms was significantly related to the severity of bradyphrenia (cognitive slowing), a result which would be consistent with the notion of a subcortical pathology in patients with Type II schizophrenia.
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