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Objective: This paper reports the results of risperidone treatment in seven patients (six adults and one adolescent) diagnosed as suffering from Prader-Willi syndrome (PWS) accompanied by severe behavioural disturbances. Risperidone was chosen following the failure of these patients to respond to other acknowledged modes of treatment for the psychiatric manifestations of PWS., Method: This was a prospective open-label study. Measures of Clinical Global Impression Scale (CGIS), Retrospective Overt Aggression Scale (ROAS), Aggression Score (AS) and weight were obtained during two baseline visits and again following 37 weeks of treatment with risperidone., Results: Low dosages (1-3 mg/day; 1.6 mg/day on average) of risperidone brought about notable clinical improvement with no apparent adverse side effects. All measures evaluated--general behaviour, CGIS, OAS and weight--reacted favourably to the treatment protocol., Conclusion: The preliminary results presented here suggest that risperidone is useful in treating PWS due to its positive effect on the disruptive behavioural symptoms that accompany it.

Coadministration of olanzapine, an atypical neuroleptic, with sulpiride, a selective D2 antagonist, is suggested as an efficient strategy for treating patients with resistant unremitting schizophrenia. The psychopharmacologic rationale that may account for the enhanced clinical efficacy of combining sulpiride with olanzapine and vice versa is the difference in affinity of the two drugs to brain receptors. Olanzapine affinity is related more to serotonin 5-HT2 than to dopamine-2, whereas sulpiride is considered a selective D2 blocker. The adjunction of a selective D2 antagonist to olanzapine may act as the olanzapine's augmentor by enhancing D2 blockage. This mode of treatment was introduced to six patients with chronic schizophrenia who showed noteworthy and rapid clinical improvement, supported by a decrease in their scores on the Positive and Negative Syndrome Scale and Brief Psychiatric Rating Scale. No bothersome side effects were noticed. This clinical approach is in accordance with the findings of previous reports assessing the efficacy of the combined treatment of clozapine and sulpiride. The grounds for this treatment regimen using olanzapine rather than clozapine are discussed, calling for further studies to affirm the hypothesis and clinical results.

Objective: Clozapine and risperidone were the first two antipsychotic drugs of a new class of agents for the pharmacotherapy of schizophrenia. It has been suggested that refractory schizophrenic patients who fail to respond to neither clozapine nor risperidone may respond to a combination/augmentation strategy of both medicaments., Method: Three cases of individuals with unremittent schizophrenia treated via this combination are presented. Response was evaluated by clinical follow-up and PANSS rating scale., Results: Good clinical results with no noticeable adverse side effects, ascertained by a reduction from baseline scores of the Positive and Negative Syndrome Scale (PANSS) were obtained in all three patients., Conclusion: The findings from this pilot study suggest this combination as a possible therapeutic approach for treating resistant schizophrenic patients.

Clozapine is an "atypical" antipsychotic agent for treating previously resistant schizophrenic patients. Its main advantages over "typical" neuroleptics are low incidence of extrapyramidal side effects and its capacity to induce therapeutic response in previously treated refractory patients. However, withdrawal from clozapine has been observed to lead to "atypical" clinical characteristics or a "rebound phenomenon," manifested in two interwoven clinical forms: (1) psychotic exacerbation, and (2) cholinergic rebound. The underlying pathophysiological mechanism of this phenomenon is postulated to be a result of cholinergic supersensitivity. In this paper, the "rebound phenomenon" will be discussed and exemplified by three case histories in which abrupt cessation of clozapine led to serious deterioration and psychotic exacerbation, and one case in which gradual titration from the drug was employed in order to preempt this hazardous occurrence.

We have reported the case of a patient with neuroleptic-induced akathisia who had rapid amelioration of his symptoms after treatment with the highly lipophilic beta-blocker propranolol. His symptoms had previously failed to respond to traditional pharmacologic treatment. There is clearly a need for more double-blind studies to assess the efficacy of propranolol and other beta-blockers in the treatment of this troublesome side effect of antipsychotic medications.

A letter to the editor is presented in response to the article "Jet lag and relapse of schizoaffective psychosis despite maintenance clozapine treatment," by L. K. Oyewumi.