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Levodopa-Associated Increase of Homocysteine Levels and Sural Axonal Neurodegeneration.
Muller, Thomas MD; Renger, Kathrin MD; Kuhn, Wilfried MD
[Article] Archives of Neurology. 61(5):657-660, May 2004.

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Background: Levodopa metabolism via catechol O-methyltransferase increases levels of the neurotoxin homocysteine, which induces an axonal-accentuated degeneration in sensory peripheral nerves in vitro.

Objectives: To demonstrate associations among daily levodopa/dopa decarboxylase inhibitor intake, total homocysteine plasma (tHcy) levels, and electrophysiologic sural nerve conduction findings.

Design: We performed bilateral assessment of sensory nerve conduction velocity and sensory nerve action potentials and determined tHcy levels.

Patients: Thirty-one levodopa-treated patients with Parkinson disease (PD) and 27 control subjects.

Results: Sensory nerve action potentials significantly (P<.001) differed between PD patients and controls. No differences between sensory nerve conduction velocities of PD patients and controls appeared. We found significant differences in sensory nerve action potentials be-tween PD patients with significantly elevated tHcy levels and controls (P<.001), PD patients with tHcy levels within the reference range and those with elevated levels (P = .001), and PD patients with tHcy levels levels within the reference range and and controls (P = .04). Our sensory nerve conduction velocity results showed no significant differences. There were significant associations between tHcy levels and sensory nerve action potentials (R = -0.52; P = .002) and and sensory nerve conduction velocity (R = -0.47; P = .008). Daily levodopa/dopa decarboxylase inhibitor intake was significantly related to tHcy levels (R = 0.43; P = .02).

Conclusions: This electrophysiological sign of peripheral neuronal dysfunction may be circumstantial evidence suggesting that, to a certain extent, sensory nerve action potentials are a surrogate marker for the levodopa metabolism-induced elevation of homocysteine levels and the aggravation of the ongoing central neurodegenerative process.