Abstract

Amyotrophic lateral sclerosis (ALS) or motor neuron disease is a devastating human illness of unknown aetiology. Many different disorders have been associated with certain facets of the clinical syndrome of ALS, and thus the concept of different ALS syndromes with diverse aetiologies has been proposed (Rowland 1982). It is true that certain intoxications such as lead, viral infections such as enterovirus, endocrine dysfunction such as hyperparathyroidism, genetic disturbances such as hexosaminidase deficiency, as well as other disturbances, may simulate ALS. However, these cases together comprise only a small percentage of the total number of patients presenting with sporadic amyotrophic lateral sclerosis, and do not appear to offer insights into the aetiology of the sporadic disease. Similarly, although prior trauma has been more frequently encountered in ALS patients than in controls (Kurtzke and Beebe 1980; Gawel et al. 1983), there are no data to explain how such trauma participates in either the aetiology of the disease or the pathogenesis of motoneuron destruction.

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