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Neurological Rehabilitation

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

Friday, October 24, 2025
12:00 PM - 1:30 PM MT
Location: Kiosk 7

    Primary Author(s)

  • UY

    Usman Yaqoob, DO

    Resident Physician
    NYU Langone Rusk Rehabilitation
    Rockaway, New Jersey

    • Co-Author(s)

  • AF

    Ally Ferber, MD

    Resident Physician
    JFK Johnson Rehabilitation Institute
    Edison, New Jersey

  • Brian Greenwald, MD

    Medical Director
    Rehabilitation Specialists
    Fair Lawn, New Jersey

Disclosure(s):
Brian Greenwald, MD: No financial relationships to disclose
Case Diagnosis: Traumatic brain injury complicated by Myasthenia Gravis

Case Description or Program 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.

Setting: The patient was initially admitted to JFK Johnson Rehabilitation Hospital and then transferred to the ICU at JFK University Medical Center.

Assessment/Results: The patient underwent plasma exchange therapy and received a total of 5 sessions. The patient's NIF and VC were both being monitored in order to assess response of the therapy. The patient had improvement in both NIF and VC after each session of therapy.

Discussion (relevance): 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 transmission. Inflammatory responses peak within hours to days post-injury and persist for weeks. After TBI, MG patients are particularly vulnerable to crises. Studies have shown that MG patients can experience a crisis within 72 hours after a TBI . 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.