If this mechanism of excitotoxicity is important in HD, then treatment aimed at interfering with the cellular receptors for glutamine may retard disease progression or prevent its development in patients identified to be at risk by genetic testing. Currently, the treatment of HD is symptomatic. The mode of action of such agents is via blockade of the doparnine receptors that promote choreiform movement. Treatment with GABA-ergic and cholinergic drugs has been disappointing so far. The cognitive impairments of the disease are not helped, and may even be worsened, by neuroleptic drugs.
Depression responds to fluoxetine, tricyclic agents, lithium, and electroconvulsive therapy.
Anxiety may be treated with benzodiazepines. A Clinical Approach. Medical and Surgical Reporter. Hayden MR, Hewitt J, Stoessl AJ, et al. The combined use of positron emission tomography and DNA polymorphisms for preclinical detection of Huntington's disease.