Since cyanide poisoning is almost always fatal, reports of surviving patients to develop neurologic signs are rare. Systemic hypoxemia was not documented with arterial blood gases : however, significant tissue hypoxia most likely occurred from the action of cyanide. A38-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 symptoms and signs, characterized by pit 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 (increas ed signal intensity on T2WI, decreased signal intensity on TIWI) 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 evoked 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, neuroimaging finding, and clinical parkinsonian symptoms and signs.
Anoxia ; Apraxias ; Brain ; Brain Stem ; Cholinergic Antagonists ; Eyelids ; Follow-Up Studies ; Gases ; Globus Pallidus ; Humans ; Hypokinesia ; Lower Extremity ; Magnetic Resonance Imaging ; Neuroimaging ; Neurologic Manifestations ; Parkinsonian Disorders* ; Poisoning ; Putamen ; Pyramidal Tracts ; Substantia Nigra ; Tremor