Opinion statementInappropriate sexual behavior (ISB) is a relatively common and potentially disruptive form of behavior in people with dementia. It can cause considerable distress and put placements and people at risk. Yet it is poorly researched and understood. In addition to non-pharmacological approaches to management, a wide range of classes of medication has been used in ISB, and the results have been reported as single cases or short series, though none has been the subject of a randomized clinical trial, in part because of the lack of a well-defined method of observing and measuring ISB, as well as the significant ethical considerations. Pharmacological treatments for which there is low-level evidence of efficacy in the literature include antidepressants, antipsychotics, anticonvulsants, cholinesterase inhibitors, hormonal agents, and beta-blockers. None of the drugs discussed here is licensed for use in ISB, and elderly people, particularly those with dementia, are at high risk of adverse effects. Caution is advised before using medication in this group of people. It is important to consider alternative non-pharmacological treatments, as well as discussing issues of ethics and consent with those involved, before initiating treatment. It is helpful to identify and monitor target symptoms. Pharmacological treatments should be started at low dose and titrated up slowly and carefully. Nevertheless, in some situations, medication may provide a useful part of a management plan for ISB.
Sexually disinhibited behaviours are quite common (prevalence 2-17%) in people with dementia, occurring with about equal frequency in men and women. Assessment of the behaviours, the contexts in which they arise and their risks is essential. It is important to manage the environment and to educate and discuss the issues with carers and families. Behavioural measures are helpful, although no specific behavioural intervention has been shown to be effective in this area. Several classes of drug may help to control the behaviours, but all are potentially harmful and none is licensed for hypersexuality in this population.Hugh Series is a consultant in the psychiatry of old age with Oxfordshire Mental Healthcare NHS Trust, working at the Warneford Hospital (Warneford Lane, Oxford OX3 7JX, UK. ). His research interests include the neurochemistry of the serotonergic system. Pilar Dégano is a clinical pharmacist, also at the Warneford Hospital.
Previous work has suggested that repeated treatment with substituted amphetamines including PCA, MDMA and d-fenfluramine produces a persistent neurodegeneration which is relatively selective for the fine serotoninergic terminals arising from the dorsal raphe nucleus. The aim of the present study was to investigate whether the acute releasing effect of d-fenfluramine might also be sensitive to lesions produced by PCA, MDMA and d-fenfluramine itself. Basal and 5-HT release evoked by d-fenfluramine or 100 mM KCl was measured by microdialysis in frontal or parietal cortex of rats 2 weeks after they had been treated with a neurodegenerative regime of PCA, MDMA, d-fenfluramine, or vehicle. In frontal cortex of vehicle controls, d-fenfluramine (10 mg/kg IP) and KCl (100 mM via microdialysis probe) evoked an increase in 5-HT of 1740% and 779% of basal, respectively. PCA pretreatment reduced d-fenfluramine-evoked 5-HT release by 90.9% while potassium-evoked release was reduced by only 66.8%. Similar results were obtained in parietal cortex. MDMA (20 mg/kg x 8) and d-fenfluramine (1.25 mg/kg x 8) pretreatment reduced d-fenfluramine-evoked release of 5-HT in frontal cortex by 45.2% and 72.0%, respectively. Overall, the present data are consistent with the hypothesis that the acute release of 5-HT evoked by d-fenfluramine occurs via those terminals destroyed by pretreatment with PCA, MDMA and d-fenfluramine, while KCl evokes release from both PCA-sensitive and PCA-insensitive terminals. The significance of these results for the interpretation of neuroendocrine data from d-fenfluramine challenge tests is discussed.
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