Abstract Number ‐ 269: Brainstem Stroke Secondary to Lyme Neuroborreliosis Vasculitis

Introduction Clinical presentations of Lyme disease are variable. A rash is often the first symptom, subsequently evolving into late complications including arthritic, cardiac, and neurological manifestations. CNS pathologies of Borrelia burgdorferi are diverse and usually include meningitis, encephalitis, strokes, intracranial hemorrhages, and central and peripheral cranial neuropathies. Stroke secondary to Lyme vasculitis is a rare entity as such there are few cases reported in the literature. The presumed mechanism of cerebral ischemia is perivascular and vascular lymphocytic infiltration causing inflammation and vasculitis, resulting in a stroke. Methods We present a case of neuroborreliosis from our stroke service in a patient who presented with sudden onset of right‐sided facial droop, dizziness, and difficulty walking. Results A 53‐year‐old male tobacco smoker (his only known risk factor for stroke) presented to the emergency department with acute onset right‐sided facial paresis, difficulty walking, double vision, and trouble managing his oropharyngeal secretions. CT Head showed no acute intracranial pathology and angiography was negative for proximal large vessel occlusion. He was eligible for and received intravenous alteplase due to concerns for acute ischemic stroke. Notably, he disclosed a history of a tick bite (roughly two and half years prior) and daily headaches (for the past 1.5 months). His exam revealed bidirectional nystagmus, negative head impulse, right LMN facial nerve palsy, left‐sided face and arm numbness, and left‐sided tongue weakness. MRI brain revealed acute infract in the right medulla, leptomeningeal and bilateral cranial (3rd, 5th, and 7th) nerves enhancement. Serum Lyme IgG and IgM antibodies were positive. Lumbar puncture revealed an elevated protein with lymphocytic predominance. CSF Lyme antibody revealed 3 bands of IgG and 1 band of IgM, consistent with Lyme meningitis. Intravenous Ceftriaxone was started and his difficulty walking and cranial neuropathies improved during the hospital course. The patient required g‐tube placement and was discharged to sub‐acute rehab. A four‐month follow MRI brain showed decreased cranial nerve enhancement without new evidence of ischemia. He eventually regained the ability to swallow, and his exam had otherwise returned to baseline. Conclusions The proposed mechanism of ischemic stroke due to Lyme Neuroborreliosis is secondary to localized inflammatory vasculitis. Lyme vasculitis can present with hemorrhagic or ischemic strokes, the latter being more common and usually affecting posterior circulation, as seen in this case. Negative CTA or transcranial Doppler studies do not exclude the diagnosis of arteriopathy as stenosis primarily involves small vessels and is usually segmental. Parenchymal brain imaging often reveals multiple territory strokes, leptomeningeal, and multiple cranial nerves enhancement in contrast studies. A thorough history of tick exposure or symptoms consistent with Erythema Migrans should be obtained in suspicious cases. Notably, patients will often complain of meningitic symptoms (including headache, neck stiffness, and malaise) usually weeks to months before any stroke‐like symptoms or deficits. Our case of Lyme Neuroborreliosis presenting as stroke illustrates the importance of considering rare etiologies in younger patients without any significant cerebrovascular risk factors, especially those residing in or traveling to endemic areas.