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Statin-induced neuropathy is increasingly described. Proposed mechanisms include an alteration in cholesterol synthesis, producing a disturbance in the cholesterol-rich neuronal membrane, or in the activity of ubiquinone (coenzyme Q10), a mitochondrial respiratory chain enzyme inhibited by statins leading to neuronal damage (1). The entire class is implicated, and both polyneuropathy and mononeuropathy have been described with improvement or even complete resolution occurring with cessation of therapy (1). In all cases, clinical improvement occurred soon after statins were discontinued, and in the absence of specific clinical, biochemical, or electrophysiological characteristics, this has become the key diagnostic feature of statin-induced neuropathy. To date, autonomic features accompanying symmetrical neuropathy have not been described.
We present an 18-year-old white female with type 1 diabetes for 5 years who, over several months, developed restless legs followed by parasthesias,...