Brachial radiculopathy with intact central nervous system imaging following carbon monoxide poisoning: A case report

TL;DR

A case report shows carbon monoxide poisoning can cause isolated brachial radiculopathy without central nervous system damage, highlighting the need for peripheral nerve assessment.

Contribution

This case expands the known spectrum of CO neurotoxicity by demonstrating isolated peripheral nerve injury without CNS involvement.

Findings

The patient developed isolated C5-C7 radiculopathy with normal brain MRI after CO poisoning.

Motor axons were more affected than sensory axons, likely due to higher metabolic demands.

Hyperbaric oxygen therapy and rehabilitation led to significant motor recovery.

Abstract

•CO poisoning caused isolated C5-C7 radiculopathy with normal brain MRI, challenging CNS-focused paradigms.•Motor axons more vulnerable than sensory due to metabolic demands; positioning during unconsciousness amplified CO toxicity.•Peripheral nerve assessment crucial in CO poisoning even with normal neuroimaging to detect nerve root injury.

CO poisoning caused isolated C5-C7 radiculopathy with normal brain MRI, challenging CNS-focused paradigms.

Motor axons more vulnerable than sensory due to metabolic demands; positioning during unconsciousness amplified CO toxicity.

Peripheral nerve assessment crucial in CO poisoning even with normal neuroimaging to detect nerve root injury.

To report and analyze a unique case of selective brachial plexopathy following carbon monoxide poisoning without central nervous system involvement.

Clinical examination, laboratory tests, neuroimaging, serial electrophysiological studies, and functional assessments were performed on a 25-year-old female presenting with severe left upper extremity weakness after CO exposure. Treatment included hyperbaric oxygen therapy, steroid therapy, and rehabilitation.

Following carbon monoxide poisoning, the patient developed complete left upper extremity paralysis with selective C5-C7 motor deficits and preserved sensory function. Brain MRI showed no abnormalities. Electrophysiological studies confirmed preganglionic radiculopathy with reduced motor nerve amplitudes and normal sensory conduction. Ultrasonography demonstrated C5-C7 nerve root swelling. Following hyperbaric oxygen therapy, corticosteroids, and rehabilitation, motor function gradually recovered with distal grip strength reaching 86% of the unaffected side at 120-day follow-up.

This case demonstrates an uncommon manifestation of carbon monoxide poisoning characterized by isolated brachial radiculopathy with preserved central nervous system function on neuroimaging. These findings expand the recognized spectrum of carbon monoxide neurotoxicity.

This case expands our understanding of CO neurotoxicity beyond the traditional basal ganglia paradigm, emphasizing the importance of peripheral nervous system assessment even when central neuroimaging is normal.

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