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Neurological sequelae following carbon monoxide poisoning clinical course and outcome according to the clinical types and brain computed tomography scan findings
Author(s) -
Lee M. S.,
Marsden C. D.
Publication year - 1994
Publication title -
movement disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.352
H-Index - 198
eISSN - 1531-8257
pISSN - 0885-3185
DOI - 10.1002/mds.870090508
Subject(s) - carbon monoxide poisoning , coma (optics) , akinetic mutism , medicine , surgery , globus pallidus , anesthesia , hyperintensity , pediatrics , poison control , magnetic resonance imaging , radiology , disease , basal ganglia , central nervous system , physics , environmental health , optics
The prognosis for patients who survive carbon monoxide (CO) poisoning is uncertain, particularly in those who develop persistent neurological complications after recovery from the initial coma. Thirty‐one patients with the sequelae of CO poisoning, followed for a year, are described. Eight had a progressive course, and 23 had a delayed relapse after an initial recovery period of ∼20 days (range, 1–36 days). Those with a progressive course developed a persistent akinetic‐mute state, and four of the eight died. Those with the delayed relapsing course either developed a parkinsonian state with behavioral and cognitive impairment but could walk (nine cases); or progressed further to an akinetic‐mute state, and were bed‐bound (14 cases); the deterioration to either condition occured rapidly over a few days to a week. Fourteen of the patients with the delayed relapses (61%) subsequently improved, but three (13%) died. Those with a progressive course without initial recovery were younger (mean age, 37.0 years) than those with a delayed relapsing course (55.2 years; p < 0.01). The mean duration of their initial coma (9.8 days) was longer than that in delayed relapsing cases (2.0 days; p < 0.01). The mean initial CO hemoglobin level was not different in the two groups. Brain computed tomography (CT) scans were obtained at the onset of sequelae in both groups. Ten patients had a normal CT scan, 13 had white matter low‐density lesions, and four had globus pallidus low‐density lesions. These findings did not accurately predict the outcome, although all four patients who had both globus pallidus and white matter low‐density lesions at initial CT scan had a bad prognosis. Follow‐up brain CT scans were performed in eight patients; all showed progressive changes and/or new lesions, despite which three patients improved; four of the five patients with globus pallidus and white matter lowdensity lesions at follow‐up CT scan had a bad prognosis.