Neurological sequelae following carbon monoxide poisoning clinical course and outcome according to the clinical types and brain computed tomography scan findings
Identifieur interne : 005B30 ( Main/Exploration ); précédent : 005B29; suivant : 005B31Neurological sequelae following carbon monoxide poisoning clinical course and outcome according to the clinical types and brain computed tomography scan findings
Auteurs : M. S. Lee [Corée du Sud, Royaume-Uni] ; Marsden [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 1994.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
- Adolescent, Adult, Aged, Brain (pathology), Brain (vertebrata), Brain Damage, Chronic (chemically induced), Brain Damage, Chronic (diagnosis), Brain computed tomography scan, Carbon Monoxide Poisoning (complications), Carbon monoxide, Carbon monoxide poisoning, Child, Computerized axial tomography, Encephalopathy, Female, Follow-Up Studies, Human, Humans, Male, Middle Aged, Neurologic Examination (drug effects), Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (diagnosis), Poisoning, Recurrence, Sequela, Sequelae, Tomography, X-Ray Computed.
- MESH :
- chemically induced : Brain Damage, Chronic, Parkinson Disease, Secondary.
- complications : Carbon Monoxide Poisoning.
- diagnosis : Brain Damage, Chronic, Parkinson Disease, Secondary.
- drug effects : Neurologic Examination.
- pathology : Brain.
- Adolescent, Adult, Aged, Child, Female, Follow-Up Studies, Humans, Male, Middle Aged, Recurrence, Tomography, X-Ray Computed.
Abstract
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.
Url:
DOI: 10.1002/mds.870090508
Affiliations:
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Le document en format XML
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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1994">1994</date><biblScope unit="vol">9</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="550">550</biblScope><biblScope unit="page" to="558">558</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">6719B1785BFCD0A05831CAC7A772812BC6277959</idno><idno type="DOI">10.1002/mds.870090508</idno><idno type="ArticleID">MDS870090508</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Aged</term><term>Brain (pathology)</term><term>Brain (vertebrata)</term><term>Brain Damage, Chronic (chemically induced)</term><term>Brain Damage, Chronic (diagnosis)</term><term>Brain computed tomography scan</term><term>Carbon Monoxide Poisoning (complications)</term><term>Carbon monoxide</term><term>Carbon monoxide poisoning</term><term>Child</term><term>Computerized axial tomography</term><term>Encephalopathy</term><term>Female</term><term>Follow-Up Studies</term><term>Human</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Neurologic Examination (drug effects)</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (diagnosis)</term><term>Poisoning</term><term>Recurrence</term><term>Sequela</term><term>Sequelae</term><term>Tomography, X-Ray Computed</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Brain Damage, Chronic</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Carbon Monoxide Poisoning</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Brain Damage, Chronic</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Neurologic Examination</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Aged</term><term>Child</term><term>Female</term><term>Follow-Up Studies</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Recurrence</term><term>Tomography, X-Ray Computed</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Carbone monoxyde</term><term>Encéphale</term><term>Encéphalopathie</term><term>Homme</term><term>Intoxication</term><term>Séquelle</term><term>Tomodensitométrie</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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.</div></front></TEI><affiliations><list><country><li>Corée du Sud</li><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Grand Londres</li></region><settlement><li>Londres</li><li>Séoul</li></settlement></list><tree><country name="Corée du Sud"><noRegion><name sortKey="Lee, M S" sort="Lee, M S" uniqKey="Lee M" first="M. S." last="Lee">M. S. Lee</name></noRegion></country><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Lee, M S" sort="Lee, M S" uniqKey="Lee M" first="M. S." last="Lee">M. S. Lee</name></region><name sortKey="Marsden" sort="Marsden" uniqKey="Marsden" last="Marsden">Marsden</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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