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Bilateral brachial plexus injury following acute carbon monoxide poisoning
BACKGROUND: Carbon monoxide (CO) intoxication is a leading cause of severe neuropsychological impairments. Peripheral nerve injury has rarely been reported. It consists usually in a demyelinating polyneuropathy or mononeuropathy affecting mainly the lower limbs. Isolated involvement of both upper ex...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BioMed Central
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3866568/ https://www.ncbi.nlm.nih.gov/pubmed/24314014 http://dx.doi.org/10.1186/2050-6511-14-61 |
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author | Rahmani, Mounia Belaidi, Halima Benabdeljlil, Maria Bouchhab, Wafa El Jazouli, Nadia El Brini, Asmae Aidi, Saadia Ouazzani, Reda M El Alaoui Faris, Mustapha |
author_facet | Rahmani, Mounia Belaidi, Halima Benabdeljlil, Maria Bouchhab, Wafa El Jazouli, Nadia El Brini, Asmae Aidi, Saadia Ouazzani, Reda M El Alaoui Faris, Mustapha |
author_sort | Rahmani, Mounia |
collection | PubMed |
description | BACKGROUND: Carbon monoxide (CO) intoxication is a leading cause of severe neuropsychological impairments. Peripheral nerve injury has rarely been reported. It consists usually in a demyelinating polyneuropathy or mononeuropathy affecting mainly the lower limbs. Isolated involvement of both upper extremities has been described in only 4 patients related to root damage. We report the first case of bilateral brachial plexus injury following CO poisoning and review all previous CO-induced neuropathy described in literature. CASE PRESENTATION: After being unconscious for three hours, a 42 years old man experienced bilateral brachial weakness associated with edema of the face and the upper limbs. Neurological examination showed a brachial diplegia, distal vibratory, thermic and algic hypoesthesia, deep tendon areflexia in upper limbs. There was no sensory or motor deficit in lower extremities. No cognitive disturbances were detected. Creatine kinase was elevated. Electroneuromyogram patterns were compatible with the diagnosis of bilateral C5 D1 brachial axonal plexus injury predominant on the left side. Clinical course after hyperbaric oxygen therapy was marked by a complete recovery of neurological disorders. CONCLUSION: Peripheral neuropathy is an unusual complication of CO intoxication. Bilateral brachial plexus impairment is exceptional. Various mechanisms have been implicated including nerve compression secondary to rhabdomyolysis, nerve ischemia due to hypoxia and direct nerve toxicity of carbon monoxide. Prognosis is commonly excellent without any sequelae. |
format | Online Article Text |
id | pubmed-3866568 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-38665682013-12-19 Bilateral brachial plexus injury following acute carbon monoxide poisoning Rahmani, Mounia Belaidi, Halima Benabdeljlil, Maria Bouchhab, Wafa El Jazouli, Nadia El Brini, Asmae Aidi, Saadia Ouazzani, Reda M El Alaoui Faris, Mustapha BMC Pharmacol Toxicol Case Report BACKGROUND: Carbon monoxide (CO) intoxication is a leading cause of severe neuropsychological impairments. Peripheral nerve injury has rarely been reported. It consists usually in a demyelinating polyneuropathy or mononeuropathy affecting mainly the lower limbs. Isolated involvement of both upper extremities has been described in only 4 patients related to root damage. We report the first case of bilateral brachial plexus injury following CO poisoning and review all previous CO-induced neuropathy described in literature. CASE PRESENTATION: After being unconscious for three hours, a 42 years old man experienced bilateral brachial weakness associated with edema of the face and the upper limbs. Neurological examination showed a brachial diplegia, distal vibratory, thermic and algic hypoesthesia, deep tendon areflexia in upper limbs. There was no sensory or motor deficit in lower extremities. No cognitive disturbances were detected. Creatine kinase was elevated. Electroneuromyogram patterns were compatible with the diagnosis of bilateral C5 D1 brachial axonal plexus injury predominant on the left side. Clinical course after hyperbaric oxygen therapy was marked by a complete recovery of neurological disorders. CONCLUSION: Peripheral neuropathy is an unusual complication of CO intoxication. Bilateral brachial plexus impairment is exceptional. Various mechanisms have been implicated including nerve compression secondary to rhabdomyolysis, nerve ischemia due to hypoxia and direct nerve toxicity of carbon monoxide. Prognosis is commonly excellent without any sequelae. BioMed Central 2013-12-07 /pmc/articles/PMC3866568/ /pubmed/24314014 http://dx.doi.org/10.1186/2050-6511-14-61 Text en Copyright © 2013 Rahmani et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Case Report Rahmani, Mounia Belaidi, Halima Benabdeljlil, Maria Bouchhab, Wafa El Jazouli, Nadia El Brini, Asmae Aidi, Saadia Ouazzani, Reda M El Alaoui Faris, Mustapha Bilateral brachial plexus injury following acute carbon monoxide poisoning |
title | Bilateral brachial plexus injury following acute carbon monoxide poisoning |
title_full | Bilateral brachial plexus injury following acute carbon monoxide poisoning |
title_fullStr | Bilateral brachial plexus injury following acute carbon monoxide poisoning |
title_full_unstemmed | Bilateral brachial plexus injury following acute carbon monoxide poisoning |
title_short | Bilateral brachial plexus injury following acute carbon monoxide poisoning |
title_sort | bilateral brachial plexus injury following acute carbon monoxide poisoning |
topic | Case Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3866568/ https://www.ncbi.nlm.nih.gov/pubmed/24314014 http://dx.doi.org/10.1186/2050-6511-14-61 |
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