Abstract
A lthough the cause of amyotrophic lateral sclerosis (ALS) remains unknown, several studies indicate that aberrant calcium metabolism may play a pathogenetic role in some patients.1-4 Theoretically, calcium could exert its deleterious effect on anterior horn cell enzymatic systems that are either deficient in quantity or abnormal in activity. Alternatively, anterior horn cell membrane structure and function may be altered, allowing increased calcium influx into neurons with subsequent cell death.Neuromuscular syndromes similar to, but not identical to, classic ALS have been described in association with hyperparathyroidism.1,2 Presumably, abnormal calcium metabolism is integrated in the pathogenesis of these neuromuscular complications. Furthermore, Mallette and co-workers3 have found abnormal calcium metabolism in ALS that was not associated with parathyroid disease. Bone disorders also have been noted in association with ALS,3-6 possibly reflecting abnormal sequestration, storage, and release of calcium, as well as other heavy metals, since the major
