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Levodopa-associated increase of homocysteine levels and sural axonal neurodegeneration.
Arch Neurol. 2004 May; 61(5):657-60.AN

Abstract

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.

Authors+Show Affiliations

Department of Neurology, St Josef Hospital, Ruhr University Bochum, Bochum, Germany. thomas.mueller@ruhr-uni-bochum.deNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

15148140

Citation

Müller, Thomas, et al. "Levodopa-associated Increase of Homocysteine Levels and Sural Axonal Neurodegeneration." Archives of Neurology, vol. 61, no. 5, 2004, pp. 657-60.
Müller T, Renger K, Kuhn W. Levodopa-associated increase of homocysteine levels and sural axonal neurodegeneration. Arch Neurol. 2004;61(5):657-60.
Müller, T., Renger, K., & Kuhn, W. (2004). Levodopa-associated increase of homocysteine levels and sural axonal neurodegeneration. Archives of Neurology, 61(5), 657-60.
Müller T, Renger K, Kuhn W. Levodopa-associated Increase of Homocysteine Levels and Sural Axonal Neurodegeneration. Arch Neurol. 2004;61(5):657-60. PubMed PMID: 15148140.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Levodopa-associated increase of homocysteine levels and sural axonal neurodegeneration. AU - Müller,Thomas, AU - Renger,Kathrin, AU - Kuhn,Wilfried, PY - 2004/5/19/pubmed PY - 2004/6/18/medline PY - 2004/5/19/entrez SP - 657 EP - 60 JF - Archives of neurology JO - Arch Neurol VL - 61 IS - 5 N2 - 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. SN - 0003-9942 UR - https://www.unboundmedicine.com/medline/citation/15148140/Levodopa_associated_increase_of_homocysteine_levels_and_sural_axonal_neurodegeneration_ L2 - https://jamanetwork.com/journals/jamaneurology/fullarticle/10.1001/archneur.61.5.657 DB - PRIME DP - Unbound Medicine ER -