Miller Fisher Syndrome and Neuroborreliosis: A Clinical Conundrum

Abstract

SESSION TITLE: Nervous System Disorders in the ICU 2 SESSION TYPE: Affiliate Case Report Poster PRESENTED ON: Tuesday, October 31, 2017 at 01:30 PM - 02:30 PM INTRODUCTION: Miller Fisher Syndrome (MFS) is a variant of Guillain-Barre Syndrome (GBS) accounting for 5% of GBS cases. It is characterized by ophthalmoplegia, areflexia, and ataxia. Neuroborreliosis (NB) is a common complication of Lyme disease (LD), which can mimic, or even trigger GBS. We identified a rare case of MFS in a patient with acute Lyme serologies. Given the potential similarities in clinical presentation, it can be challenging to differentiate NB from MFS. CASE PRESENTATION: A 26-year-old woman presented to the Emergency Department after awakening with ptosis, ataxia, diplopia, and dysarthria. She denied any sick contacts, travel, or tick bites. Vital signs on presentation were normal. Neurological examination was significant for bilateral ptosis and ophthalmoplegia with decreased extraocular movements in all directions, normal strength, intact sensation, decreased deep tendon reflexes in all extremities, dysmetria on bilateral finger-to-nose testing, and normal plantar reflexes. Neuroimaging, which included CT head, MRI brain, MRA head and neck, and MRV brain, were unremarkable. Laboratory studies were significant for the presence of CSF Ganglioside GQ1B Ab titers at 1:3200; CSF albuminocytologic dissociation (WBC 5u/L, protein 63mg/dL); negative CSF anti-B.burgdorferi antibodies; and positive serum anti-B.burgdorferi IgM with positive 23 and 41 kDa bands on western blot. This data suggested MFS as the diagnosis. The patient was admitted to the ICU for close respiratory monitoring with serial vital capacity (VC) and negative inspiratory force (NIF) measurements. She was concurrently treated with 5 days of IVIG and ceftriaxone. Neurological improvements were observed on day 4 of her treatment. DISCUSSION: The constellation of signs and symptoms that characterize MFS are nonspecific, and can be seen in LD manifesting with cranial neuropathies. The presence of positive Lyme serologies in the setting of the classic MFS presentation can result in a diagnostic dilemma, but MFS should be ruled out as it can progress to respiratory failure. B. burgdorferi infection is rarely associated with GBS. Its potential to be an inciting factor is based on the hypothesis that it can mount autoimmune responses. Diagnosis of MFS requires CSF analysis, and is supported by the presence of albumincytologic dissociation, and Anti-GQ1b antibodies (90% sensitivity and specificity). Treatment is based on standard therapy for GBS (plasma exchange vs. IVIG). There are no specific guidelines available catered to the MFS variant. CONCLUSIONS: Our case demonstrates that although rare, B. burgdorferi infection may be a potential inciting factor for the development of GBS and MFS. In the setting of positive Lyme serologies and cranial neuropathies that include ophthalmoplegia, both LD and GBS should also be considered in the diagnosis. Reference #1: Lo YL. Clinical and immunological spectrum of the Miller Fisher syndrome. Muscle Nerve 2007; 36:615. DISCLOSURE: The following authors have nothing to disclose: Di Pan, Sung Lee, Nader Ishak Gabra, Joseph Mathew No Product/Research Disclosure Information