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Biomedical subjects

R T Owen

Publications and source records attributed to R T Owen.

18 recordsLinked to original sources
PubMed1985

A clinical assessment of zuclopenthixol dihydrochloride (Clopixol tablets) in the treatment of psychotic illness.

An open, multi-centre study was carried out in 69 patients with an acute psychotic episode to assess the efficacy and side-effects of treatment with oral zuclopenthixol dihydrochloride. Patients were treated until the acute episode was considered terminated by the clinician and, although dosage could be adjusted to allow optimum clinical response, the majority received 25 mg zuclopenthixol dihydrochloride 3-times daily throughout the trial period. Assessments were made before and during treatment using the BPRS and CGI rating scales and a check-list of side-effects. The results showed that 55 (80%) patients had a successful response to treatment. Almost half (33) of the patients responded fully to the drug within 3 weeks and by the end of 5-weeks' treatment this had increased to over 70% (49). A further 6 patients responded after 6 to 9 weeks of treatment. The drug was generally well tolerated and the majority of patients had either no side-effects or side-effects which did not overtly affect performance.

Adolescent↗
PubMed1985

Resistance to competitive neuromuscular blocking agents in burn patients: a review.

The quantitative and qualitative aspects of the phenomenon of resistance to competitive (non-depolarizing) neuromuscular blocking agents in burn patients are described. The correlates and temporal features of this resistance are discussed, in addition to therapeutic approaches and the possible mechanisms underlying the resistance.

Age Factors↗
PubMed1983

Benzodiazepine dependence. A review of the evidence.

Classical pharmacological dependence accompanied by euphoria, clinical evidence of tolerance and escalation of dosage are very rare with the benzodiazepines. However, there is now abundant evidence that prolonged administration of doses within the therapeutic range leads to true dependence in a significant minority of patients. This dependence is characterised by withdrawal symptoms on stopping treatment; these include perceptual disturbances, epileptic seizures, weight loss, insomnia and autonomic symptoms. As some of the symptoms are qualitatively different from those of anxiety neurosis, and as the withdrawal syndrome commonly lasts between 5 and 15 days, the possibility that the symptoms represent a return of pre-existing anxiety can be discounted. The withdrawal syndrome is more likely if: (a) the benzodiazepine has been taken in regular dosage for more than 4 months; (b) higher dosages have been used; (c) the drug is stopped suddenly; and (d) a short acting benzodiazepine has been taken. The withdrawal syndrome is most likely to occur when there is a rapid fall in blood benzodiazepine concentrations; this may be associated with altered sensitivity of benzodiazepine receptors. The syndrome can best be avoided by gradual reduction of dosage. The temporary prescription of other drugs, particularly beta-adrenoceptor blocking drugs, may attenuate withdrawal symptoms, but antipsychotic drugs in low dosage are of no benefit.

Anti-Anxiety Agents↗
PubMed1980

Neuropharmacological supersensitivity-clinical and experimental correlates and methodological considerations.

The effects of chronic neuroleptic treatments on spontaneous and drug-induced locomotor activity and stereotypy is reviewed. The development of tolerance in relation to supersensitivity and its biochemical and clinical correlates are discussed, in addition to central neuropharmacological studies in this area. Proposed mechanisms of supersensitivity development are discussed and suggestions for further research made.

Animals↗
PubMed1980

Intrastriatal kainic acid- a possible model for antidyskinetic/antichoreic agents?

Bilateral intrastriatal injection of kainic acid in conscious guinea-pigs induced a spectrum of behaviours comprising: biting, seizures and hyperactivity. Preliminary findings revealed that pharmacological modification of these behaviours was possible. Metoclopramide, haloperidol, reserpine, flurazepam, quipazine, propranolol and aceperone were found to be inactive or very weakly active on the biting behaviours and seizures. Intrastriatal GABA decreased seizure activity but not the biting, whilst RS86, clonazepam, oxiperomide and tiapride decreased biting and seizures. It is suggested that intrastriatal kainate-induced behaviour may be a useful model for delineating agents with antidyskinetic or antichoreic potential. However, the spectrum of behaviour is not always consistent and the mortality rate is high over the subsequent 24 hours.

Animals↗
PubMed1978

Gabaminergic and serotonergic modulation of the antidyskinetic effects of tiapride and oxiperomide in the model using 2-(N,N-dipropyl)animo-5,6-dihydroxytetralin.

The activities of oxiperomide and tiapride were compared with those of control "neuroleptic" agents in the dyskinesia model using 2-(N,N-dipropyl)amino-5,6-dihydroxytetralin to induce peri-oral movements, in order to determine whether the differential activities (oxiperomide and tiapride being comparatively more effective as antagonists) may involve striatal gabaminergic and serotonergic mechanisms. The peri-oral movements induced by the 2-aminotetralin compound (0.05 mg/kg s.c.) were antagonised by intrastriatal GABA (2.5--10 microgram bilateral) and serotonin (25--100 microgram bilateral). Sodium valproate (i.p.) had little effect but 1.25 mg/kg s.c. quipazine abolished the peri-oral dyskinesia. Subthreshold doses (i.p.) of oxiperomide and tiapride synergised with subthreshold intrastriatal doses of both GABA and serotonin, and with s.c. quipazine, to antagonise the peri-oral movements induced by the 2-aminotetralin compound. Subthreshold doses of haloperidol, sultopride, metoclopramide and pimozide failed to consistently antagonise peri-oral movements when similarly combined with GABA, serotonin or quipazine. It is suggested that, in addition to their known action on cerebral dopamine mechanisms, oxiperomide and tiapride may modify abnormal peri-oral movements by modulation of striatal gabaminergic and serotonergic mechanisms.

2-Naphthylamine↗