Disclosures: Jennifer G. Leet, MD: Nothing to disclose

Case Description: A 21-year-old male sustained a severe non-traumatic anoxic brain injury involving the bilateral globus pallidus, cerebellum and deep cortical white matter after being found in his car following a drug overdose and carbon monoxide poisoning with resultant cognitive deficits and left upper limb monoplegia. His motor weakness on exam appeared confined to the left C5/6 myotomes versus the upper trunk of the brachial plexus.

Setting: There is sparse literature identifying lesions of the brain as the etiology of electromyographic findings consistent with acute denervation.

Patient: Anoxic brain injury with upper limb monoplegia.

Assessment/Results: Electromyography performed 40 days post-injury was positive for fibrillation potentials diffusely throughout the proximal left upper limb as well as left cervical paraspinal musculature in the setting of unremarkable nerve conduction studies. This could potentially be consistent with a multilevel cervical preganglionic axonal lesion. However, magnetic resonance imaging (MRI) of the cervical spine revealed intact bilateral, symmetric, and atraumatic cervical nerve roots without spinal canal compromise, neuroforaminal stenosis or evidence of spinal cord injury. MRI of the left brachial plexus could identify no abnormal nerve pathology or compression. Furthermore, fibrillation potentials were identified in the right first dorsal interosseous muscle, without electrodiagnostic evidence of right ulnar nerve lesion.

Discussion: Many severely brain injured patients sustain trauma that causes additional peripheral nerve lesions to include mononeuropathies, plexopathies, radiculopathies and nerve root avulsions. Electrodiagnostic evidence of denervation from a brain injury could potentially confound an assessment of such lesions. In cases of a global insult, such as anoxic brain injury, electrodiagnostic evidence of axonal loss may be found diffusely.

Conclusion: The etiology of the electrodiagnostic evidence of fibrillation potentials and axonal loss in this case presented are secondary to this patient’s brain injury. As far as we can discern, this is the first description of such findings specifically in an anoxic brain injury patient.

Level of Evidence: Level V

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PM&R Meeting Abstracts - https://pmrjabstracts.org/abstract/electrodiagnostic-evidence-of-axonal-loss-in-an-upper-limb-due-to-anoxic-brain-injury/