Four patients are described who developed sensorimotor neuropathy whil
e being treated with simvastatin and had complete or partial resolutio
n of clinical abnormalities after withdrawal of treatment. In one case
onset was within days of commencing treatment, but in two cases sympt
oms did not develop for two years. The electrophysiological and pathol
ogical features of the neuropathy were those of axonal degeneration. C
linical evidence of proximal and distal weakness and muscle fasciculat
ions and persistent abnormalities of sensory conduction after recovery
suggest the possibility of toxic damage to anterior horn cells and do
rsal root ganglia. Thirty eight other cases with symptoms suggestive o
f peripheral neuropathy have been reported to the Australian Adverse D
rug Reactions Advisory Committee, 22 of whom recovered after cessation
of treatment; in five cases there was recurrence after re-exposure to
the drug. Simvastatin should be considered among the causes of periph
eral neuropathy, and the drug should be withdrawn if patients receivin
g it develop muscle weakness or sensory disturbances.