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Two Cases of Rapid Onset Parkinson's Syndrome Following Toxic Ingestion of Ethylene Glycol and Methanol
Author(s) -
Reddy NJ,
Lewis LD,
Gardner TB,
Osterling W,
Eskey CJ,
Nierenberg DW
Publication year - 2007
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1038/sj.clpt.6100013
Subject(s) - parkinsonism , ingestion , medicine , ethylene glycol , anesthesia , baclofen , levodopa , methanol , methanol poisoning , acute toxicity , toxicity , parkinson's disease , chemistry , disease , organic chemistry , receptor , agonist
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. Clinical Pharmacology & Therapeutics (2007) 81 , 114–121. doi: 10.1038/sj.clpt.6100013