Abstract

Is it conceivable that for 40 years we have overlooked an insidious long-term levodopa treatment adverse effect, such as neuropathy, in idiopathic Parkinson disease (IPD)? In this issue of Neurology ®, Rajabally and Martey1 take up the already controversial question, recently mooted by Toth et al.,2 of the increased prevalence of neuropathy in chronic levodopa-treated IPD and its potential but tenuous link to elevated plasma levels of homocysteine (Hcy) and methylmalonic acid (MMA) and to reduced vitamin B12 levels. Even though the role of levodopa in neuropathy is still hypothetical, the clinical relevance is evident, as sensory neuropathy may contribute to impaired balance and neuropathic pain in advanced IPD. Furthermore, vitamin B12 deficiency and increased Hcy and MMA levels can be easily determined in blood, suggesting that neuropathy as a treatment-related complication may be prevented or treated by vitamin B12 and folate supplementation. But what evidence do we have to direct our clinical care efforts? Patients with IPD, particularly those with long-term levodopa treatment, may more frequently develop a neuropathy. In the cross-sectional case-control studies of Toth et al.2 and Rajabally and Martey,1 neuropathy, mostly axonal, was found clinically …

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