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Two cases of rapid onset Parkinson's syndrome following toxic ingestion of 
ethylene glycol and methanol.

Ethylene glycol and methanol are toxic alcohols commonly found in a variety 
of commercial products. We report two cases, one associated with ethylene 
glycol and one with methanol poisoning, which both led to acute hemorrhagic 
necrosis of the basal ganglia and resulted in acute Parkinson's syndrome. It 
is unlikely that oxalate crystal deposition is the only mechanism for such 
basal ganglia necrosis, because similar findings were seen following 
methanol intoxication. We discuss other possible mechanisms that may 
contribute towards this unusual neurotoxicity. Both of our patients survived 
their toxic ingestions, but then developed acute Parkinson's syndrome within 
10 days of the ingestion. However, the patient who ingested methanol 
developed respiratory muscle stiffness/weakness, which responded poorly to 
anti-Parkinsonian drug therapy. Treatment with carbidopa/levodopa improved 
cogwheel rigidity and bradykinesia in both patients. We conclude that acute 
Parkinsonism is one of the lesser-recognized devastating complications of 
both ethylene glycol and methanol poisoning.

Keywords: ethylene glycol, acute parkinson, methanol poisoning, basal 
ganglia, methanol, acute, glycol, ethylene

Authored by Reddy NJ, Lewis LD, Gardner TB, Osterling W, Eskey CJ, 
Nierenberg DW. Section of Clinical Pharmacology and Toxicology, Dartmouth 
Medical School, Dartmouth Hitchcock Medical Center, Lebanon, New Hampshire, 
USA.

Published in Clin Pharmacol Ther. 2007 Jan;81(1):114-21. The full report is 
available online.    A subscription to the periodical may be required.

Rayilyn Brown
Director AZNPF
Arizona Chapter National Parkinson Foundation
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