Fluoxetine-induced Exacerbation of Chorea in Huntington’s Disease?

Introduction

Huntington’s chorea continues to pose challenges in the management of both psychiatric and neurological symptoms. The disorder, which was first described in 1872, is widely acknowledged to be due to a gene mutation that lies in the short arm of Chromosome 4. The pathology mainly affects the basal ganglia, in particular the caudate nucleus and the putamen. Wanker [10] recently wrote about the accumulation of highly insoluble intracellular protein aggregates in neuronal inclusions as a hallmark of Huntington’s disease (HD), Parkinson’s disease (PD), and several other late-onset neurodegenerative disorders. The aggregates formed generally have a fibrillar morphology, consist of individual beta-strands, and are resistant to proteolytic degradation. Myrianthopolous estimated the prevalence to be in the range of 4 to 7 per 100,000 population in the UK [6]. The inheritance is autosomal dominant, with 50 % of the offspring being affected and virtually all manifesting the disease.

Heathfield [3] concluded that the symptoms were almost equally divided between neurological and psychiatric symptoms. The neurological symptoms of chorea - hemichorea, dysarthria, ataxia, disturbance in fine motor task completion, and a conspicuous slowness of movement - are well recognized. The psychiatric symptoms of cognitive impairment giving rise to a subcortical dementia, pervasive apathy, self-neglect, marked depression, persecutory delusions, and suicide are also well known [5].

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