J Korean Neurol Assoc.  1995 Dec;13(4):1041-1046.

Cyanide-induced Parkinsonism

• Kim SR
• Kim JW
• Kim SH
• park JW
• Choi KJ
• Park KW

Abstract

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.

MeSH Terms

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
Cholinergic Antagonists
Gases