1,721,252 research outputs found
Extrapyramidal collateral effects induced by neuroleptic agents. II. Acute extrapyramidal effects
No full textBeside tardive dyskinesia, that was discussed in the first part of the review, published in 'Psicosi' vol. 3, 1994, also acute extrapyramidal side effects have an important role in the management of antipsychotic therapy. Acute extrapyramidal side effects incidence is quite higher than that of tardive dyskinesia, and their occurrence worsens significantly patient's quality of life and compliance. Drug-induced parkinsonism, akathisia and acute dystonias can be managed with well known strategies and their reduction is one of the main target of the development of new 'atypical' antipsychotic agents. In this review we will discuss epidemiology, including risk factors, physiopathology, clinical aspects and treatment of each acute neuroleptic-induced exrapyramidal disorder. We will report also original data about the prevalence of acute extrapyramidal disorders, presented during the meeting 'Physiopathological and clinical aspects of neuroleptic-induced extrapyramidal disorders', held in Milan on November 24, 1993 at the S. Raffaele Hospital (I.R.C.C.S.) and organized by the third Chair of Clinical Psychiatry of the university of Milan and by the I.R.G.A.S.D
ANTIPSYCHOTIC-INDUCED TARDIVE-DYSKINESIA - RECOGNITION, PREVENTION AND MANAGEMENT
No full textTardive dyskinesia is an important adverse effect of antipsychotic drug treatment. It is a complex neurological syndrome, consisting of hyperkinetic, involuntary movements, mainly choreoathetoid (but also dystonic) in nature, The movements involve several body areas, and affected patients are usually unaware of the presence of the movements. Tardive dyskinesia affects about one-fifth of patients treated with antipsychotics. Epidemiological studies show that some factors such as age, institutionalisation. a psychiatric diagnosis of mood disorders and a history of acute estrapyramidal syndromes increase the risk of developing tardive dyskinesia. Treatment variables are less clearly correlated with risk, but lower doses seem to reduce the risk and new atypical antipsychotics, in particular clozapine. seem to have a reduced risk of inducing the syndrome, As the greatest factor for risk is patient vulnerability, the best way to reduce the risk of tardive dyskinesia is to use antipsychotic drugs in a conservative manner. Recognising and treating tardive dyskinesia is of paramount importance and results in a more favourable course of the disorder. Reducing antipsychotic exposure to the minimum clinically effective dose and duration increases the possibility of improvement and remission. Active treatment is required for patients with severe tardive dyskinesia, but to date no treatment has been demonstrated to be significantly effective in the majority of patients, except for the suppressive effects of antipsychotics themselves. Benzodiazepines, in particular clonazepam, and atypical antipsychotics, especially clozapine, provide some benefits. The neuroprotective effects of tocopherol (vitamin E) seem useful in some patients. Other treatments may be limited by seven adverse effects and have little proven efficacy. Nevertheless, subgroups of patients may respond to a particular treatment, suggesting the heterogeneity of this condition
Possible linkage between primary affective disorder susceptibility locus and HLA haplotypes.
No full textThe authors analyzed the concordance of sib pairs of HLA typing in cases where both sibs had affective illness and where the sibs were discordant. They detected an excess of HLA similarities in doubly affected sibs and a lack of similarities in discordant sibs. Therefore, the authors hypothesize that HLA may be linked with a primary affective disorder susceptibility locus or it may be associated with such a locus in some other way
Further studies on the major histocompatibility complex as a genetic marker for schizophrenia.
No full textOur results seem to indicate the existence of a locus in the major histocompatibity complex (MHC) region, correlated to schizophrenic illness and strictly linked to the loci HL-A and MLR. The associations found between these last loci and the disease can probably be explained by a linkage disequilibrium or a selective pressure between the allelles of the three loci. Our results also indicate that the genetic systems investigated may be useful diagnostically as a genetic marker for schizophrenia. But the real meaning of their relationships to the illness has to be further investigated
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