Since cyanide poisoning is almost always fatal, reports of surviving patients to develop neurologic signs are rare. Systemic hypoxemia was not documented with arterial bloed gases : however, significant tissue hypoxia most likely occured from the
action
of cyanide.
A 38-year-old man ingested cyanide in a suicidal attempt. He was treated and survived the poisoning episode. But one week later, he showed classic extrapyramidal symtoms and signs, characterized by gaint disturbance, bradykinesia, increased
muscle
tone,
micrographia, tremor, apraxia of eyelid opening, palilalia. These symptoms and signs continued to progress, and response to levo-dopa and anticholinergics was poor, except apraxia of eyelid opening. About 3 months later, brain MRI showed abnormal
signals (increased signal intensity on T2WI, decreased signal intensity on T1WI) in both globus pallidus and a part of putamen, but hippocompus and substantia nigra was normal. After 16 months, follow-up brain MRI showed the same findings.
Although
brainstem auditory evoked potential (BAEP) was normal, motor eveked potential (MEP) showed prolongation of central motor conduction time (CMCT) in right upper and lower extremities, then wecould suspect subtle changes in pyramidal tract. We
report
a
patient as cyanide-induced parkinsonism by history, neuroimaginsg finding, and clinical parkinsonian symptoms and signs.
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