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Abstract Details

More than Meets the Eye: An Unusual Case of Opsoclonus-Myoclonus Syndrome Due to West-Nile Virus Encephalitis
Infectious Disease
P10 - Poster Session 10 (11:45 AM-12:45 PM)
13-007

OMS is a rare disorder that presents with arrhythmic multidirectional conjugate eye movements, diffuse or focal myoclonus, encephalopathy, and ataxia. It is mainly associated with pediatric neoplasms and adult paraneoplastic syndromes. However, it is vital to consider para-infectious causes as well. We present a compelling case of WNV encephalitis and cerebellitis causing OMS.

Present an unusual Opsoclonus-Myoclonus Syndrome (OMS) case secondary to West Nile Virus (WNV) encephalitis.

We identified this patient during routine clinical practice.

A 65-year-old man presented to the hospital with a four-day history of confusion, anomic aphasia, ataxia, and diplopia after sustaining numerous tick bites while camping. His condition continued to worsen despite treatment, later developing opsoclonus and bilateral upper extremity myoclonus. Initial brain and spine magnetic resonance imaging (MRI) revealed no significant findings. Cerebrospinal fluid (CSF) tests were obtained and included infectious, autoimmune, paraneoplastic, and demyelinating etiologies. WNV PCR yielded negative results. However, subsequent testing for WNV antibodies, including IgM and IgG, was positive, leading to the diagnosis of WNV encephalitis. A repeat brain MRI showed patchy, T2 flair hyperintense lesions of bilateral cerebellar hemispheres, suggesting cerebellitis. Treatment with corticosteroids and intravenous immunoglobulin (IVIG) led to the resolution of both opsoclonus and myoclonus, and improved mental status and gait.

OMS is a rare constellation of symptoms with multiple etiologies, including but not limited to paraneoplastic, autoimmune, and in our case, para-infectious causes. Though the pathophysiology is debated, the most supported theory lies within immune mediated dysfunction of Purkinje cells (PCs) in the cerebellum, which is supported by improvement with immunosuppressive therapy. Due to its rarity, identification of OMS may be delayed in the clinical setting. We aim to increase awareness, enabling earlier identification of the syndrome and prompt initiation of immunosuppressive therapy to optimize patient outcomes.  

Authors/Disclosures
Gavin DeFisser
PRESENTER
Mr. DeFisser has nothing to disclose.
Francesca Pastrana, MD (Saint Louis University) Dr. Pastrana has nothing to disclose.
Hanan Qaqish, MD (St. Louis University Hospital) Dr. Qaqish has nothing to disclose.
Subin Jang No disclosure on file
Adam Awad, MD Dr. Awad has nothing to disclose.
Wilson E. Rodriguez, MD Dr. Rodriguez has nothing to disclose.
Momina Soudagar-Turkey, MD (St. Louis University School of Medicine) Dr. Soudagar-Turkey has nothing to disclose.