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24th Annual Pain Medicine Meeting 2025
November 13-15, 2025| JW Marriott Austin, Austin, Texas
2198286
Atypical Delayed Brachial Plexopathy with Dysautonomia: A Case of Minor Trauma with Major Sequelae
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Medically Challenging Cases
Atypical Delayed Brachial Plexopathy with Dysautonomia: A Case of Minor Trauma with Major Sequelae
Alexander Nguyen, MD; Krishna Kudaravalli, MD; Melanie Henry, MD, MPH
INTRO
•Brachial plexopathies are commonly associated with high-impact trauma with acute neurologic deficits.
•In rare instances, minor injuries can trigger a slow, insidious cascade of neurological dysfunction.
•We present a unique case of chronic brachial plexopathy with evolving dysautonomia several years after a seemingly negligible shoulder injury.
METHODS
•Consent for the report was obtained from the patient.
CASE REPORT
•36-year-old female PMH of eosinophilic esophagitis and depression presented with chronic right shoulder and clavicular pain for 3 years after attempt to force open a shut door with her body. No fracture or dislocation were noted upon initial injury, and she had an unrevealing exam with improvements in pain over the first couple months.
•At 6-9 months, she noted shoulder drooping, fatigue, radiating numbness to the spine, hand, and fingers. Scapular winging, intermittent “shocking”, right axillary and scapular hyperhidrosis, early satiety, and diarrhea followed after 1 year. She denied allodynia, swelling, skin color or temperature changes.
•MRI showed mild disc bulges at C5-C7 without spinal stenosis or neural foraminal narrowing and mild supraspinatus tendinosis.
•EMG revealed grade 3 fibrillation potentials in the trapezius without activation, concerning for right spinal accessory mononeuropathy due to disruption in nerve continuity vs. poor activation due to pain.
•MR neurogram demonstrated right trapezius and SCM muscle atrophy but no signal abnormality along the brachial plexus or spinal accessory nerve.
•She was referred to the Peripheral Nerve Injury Clinic. A stellate ganglion block was scheduled to manage pain and autonomic symptoms.
DISCUSSION
•Deafferentation from nerve injury, as well as damage to C-fibers, can lead to dysregulation of afferent and efferent pain signals, resulting in persistent neuropathic pain.
•The gradual onset of peripheral neuropathy and long-term sequelae following axonotmesis complicated early recognition.
•The development of autonomic features including hyperhidrosis, early satiety, and diarrhea suggests a sympathetically mediated pain source.
•In rare cases, neuropathies can progress to central sensitization or complex regional pain syndrome (CRPS).
•However, the absence of allodynia, swelling, and skin changes, which are hallmarks of Budapest criteria for CRPS, reduce suspicion for extensive sympathetic injury.
•Identifying the primary pain generator is imperative for developing effective treatment strategies. Conservative treatment with physical therapy, anti-inflammatories, and nerve pain medications aims to reduce inflammation and promote healing.
•Stellate ganglion blockade can be both diagnostic and therapeutic by modulating sympathetically mediated pain and alleviate autonomic dysfunction.
•Ultimately, this case demonstrates how even minor injuries can precipitate complex pathologies requiring comprehensive, individualized management.
Figure 1 Demonstration of the patient’s physical exam findings at rest and when doing a wall push.
Figure 2 MRI C-spine at C5 and T1 which reveals both sternocleidomastoid and trapezius muscle atrophy.