The brain lesion responsible for parkinsonism after carbon monoxide poisoning.
BACKGROUND
Parkinsonism is a common neurological sequela of carbon monoxide (CO) poisoning, but its pathophysiological mechanism has yet to be clarified.


OBJECTIVE
To describe a married couple who were both affected by CO poisoning, but only 1 of whom developed CO-induced parkinsonism, and to discuss the possible underlying pathophysiological mechanism of CO-induced parkinsonism by comparing the neuroimaging findings of these patients.


METHODS
Case report from a clinical neurology department.


METHODS
A married couple experienced CO poisoning simultaneously. One month later, only the husband gradually developed delayed sequelae, including parkinsonism and intellectual impairment. On detailed neurological examination, the husband showed mild but definite rigidity and bradykinesia, while no parkinsonian signs were observed in the wife. Neuropsychological examination revealed impaired memory and attention in both patients, but they were more severe in the husband than in the wife. Magnetic resonance imaging scans of the patients' brains disclosed diffuse high-intensity white matter signals in both patients and bilateral pallidal necrosis in the wife. Dopamine transporter imaging showed that the degree of dopamine neuronal loss was comparable between these patients. Magnetic resonance spectroscopy revealed more severe white matter damage in the husband than in the wife. Thirteen months later, neurological and neuropsychological examinations showed complete recovery from parkinsonism as well as intellectual impairment. Follow-up magnetic resonance spectroscopy also suggested remarkable improvements in white matter damage.


CONCLUSIONS
These results support the role of white matter damage in producing parkinsonism after CO poisoning and highlight the possible usefulness of magnetic resonance spectroscopy in predicting delayed sequelae in patients after CO poisoning. Arch Neurol. 2000;57:1214-1218
Department of Neurology, Yonsei University College of Medicine, CPO Box 8044, Seoul, Korea.
Y H
YH
Sohn
Y
Y
Jeong
H S
HS
Kim
J H
JH
Im
J S
JS
Kim
D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000032:analysis; D001923:Brain Chemistry; D002249:Carbon Monoxide Poisoning / Q000150:complications*; D002352:Carrier Proteins / Q000032:analysis; D002794:Choline / Q000032:analysis; D003072:Cognition Disorders / Q000000981:diagnostic imaging / Q000209:etiology; D050483:Dopamine Plasma Membrane Transport Proteins; D005260:Female; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D008562:Membrane Glycoproteins; D026901:Membrane Transport Proteins; D008875:Middle Aged; D009419:Nerve Tissue Proteins; D010300:Parkinson Disease / Q000000981:diagnostic imaging / Q000209:etiology*; D010725:Phosphocreatine / Q000032:analysis; D015899:Tomography, Emission-Computed, Single-Photon
D002352:Carrier Proteins; D050483:Dopamine Plasma Membrane Transport Proteins; D008562:Membrane Glycoproteins; D026901:Membrane Transport Proteins; D009419:Nerve Tissue Proteins; D010725:Phosphocreatine; D001224:Aspartic Acid; C000179:N-acetylaspartate; D002794:Choline