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1640 - The Clinical Dilemma of Managing TBI in a Patient with Myasthenia Gravis: A Case Report

Thursday, February 27, 2025

5:00 PM - 6:30 PM MST

Presenting Author(s)

UY

Usman Yaqoob, DO

Resident Physician
Jefferson Einstein Hospital
Rockaway, New Jersey, United States
AF

Ally Ferber, MD

Resident Physician
JFK Johnson Rehabilitation Institute
Edison, New Jersey, United States

Corresponding Author(s)

BG

Brian Greenwald, MD

Physician
JFK Johnson Rehabilitation Institute
Edison, New Jersey, United States

Case Diagnosis: Traumatic brain injury (TBI) complicated by Myasthenia Gravis

Case Description: 37-year-old female with a history of Myasthenia Gravis and chronic left-sided weakness presented with TBI following a motor vehicle accident. The patient had negative trauma workup and was discharged, however 2 days later began experiencing worsening left-sided weakness and new onset slurring of speech. Diagnostic imaging was negative for acute intracranial pathology and she was discharged home again. She was evaluated by outpatient physiatry and admitted to acute inpatient rehabilitation for worsening functional deficits. Shortly after admission, she was noted to be lethargic with shortness of breath, which was evaluated by neurology and diagnosed as a myasthenic crisis. She was admitted to the intensive care unit for plasmapheresis. Her NIF and VC improved with a decrease in symptom burden. She was discharged back to inpatient rehabilitation and then home.

Discussions: Microglia and astrocytes are activated during TBI, releasing pro-inflammatory cytokines such as IL-1, TNF-α, and IL-6. This inflammatory milieu can disrupt the blood-brain barrier, cause systemic inflammation, and exacerbate autoimmune conditions like MG by promoting autoantibody production and impairing neuromuscular transmission1,2. There is a temporal relationship between TBI and the exacerbation of MG symptoms. Inflammatory responses peak within hours to days post-injury and persist for weeks, triggering autoimmune reactions in predisposed individuals3 . After TBI, Menon et al. found that MG patients are particularly vulnerable to crises. In a cohort study by Zong et al., 30% of MG patients experienced a crisis within 72 hours after a TBI4,5. Considering latent pathologies is crucial in brain injury treatment. This case demonstrates how an inflammatory immune-mediated reaction can lead to an MG crisis.

Conclusions: TBI increases susceptibility to autoimmune aberrancies, thus it is important to regularly monitor clinical presentation and consider exacerbations in the setting of neurological deterioration while in acute rehabilitation.