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474 - Trauma-Related Miller Fisher Variant of Guillain-Barre Syndrome: A Case Report

Thursday, February 27, 2025

5:00 PM - 6:30 PM MST

Presenting Author(s)

BO

Bartlomiej Z. Olko, MD

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

Co-Author(s)

JY

James Yun, MD

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

Robert Lee, DO

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

Daniel McBride, MD

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

Jaclyn Joki, MD

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

Case Diagnosis: 52 year old male diagnosed with Miller Fisher Syndrome (MFS).

Case Description: Patient presented after fall found to have traumatic subdural and subarachnoid hemorrhages with multiple facial and left temporal bone fracture. Hospital course was complicated by acute right upper and lower facial weakness and fluctuating mental status. Right-sided facial palsy resolved spontaneously. Subsequently, the patient developed new-onset left facial palsy with notable ptosis, ophthalmoplegia, anisocoria reactive to light and ataxic gait. CT head and encephalogram (EEG) were unremarkable. MRI brain and CT venogram was negative for acute changes and showed improved recanalization of cerebral sinuses. Lumbar puncture revealed albuminocytologic dissociation. Given the presence of multiple cranial neuropathies, areflexia, ophthalmoplegia, ataxia, and albuminocytologic dissociation, the patient was diagnosed with MFS. Treatment with intravenous immunoglobulin (IVIG) was deferred due to prior history of dural venous sinus thrombosis. Patient underwent five sessions of plasmapheresis with improvement in diplopia and extraocular movements.

Discussions: MFS is an uncommon, clinical variant of Guillain-Barre syndrome (GBS). It is estimated to occur in approximately 5-10% of GBS. MFS is classically characterized by a constellation of ophthalmoplegia, ataxia, and areflexia. Cerebrospinal fluid analysis may demonstrate albuminocytologic dissociation. Ganglioside (Gq1b) antibodies are present in 85-90% of cases. While the exact pathophysiology of GBS is not fully understood, it is thought to be the result of an autoimmune response to a preceding infection. More recent reports have shown a unique correlation between traumatic factors and the onset of GBS. Traumatic brain injuries (TBI) trigger production of inflammatory mediators likely implicated in the pathogenesis of GBS.

Conclusions: Although GBS secondary to acute TBI is a rare phenomenon, diagnosis of MFS should be considered for patients with new or worsening symptoms of TBI. Physician recognition in these patient populations is critical to prompt and appropriate therapy.