Objective:

To present a case of subarachnoid hemorrhage attributed to central nervous system vasculitis linked to Lyme disease.

Background:

Central nervous system (CNS) vasculitis is a rare but potentially life-threatening condition characterized by inflammation of the brain's blood vessels, leading to various neurological symptoms. Lyme disease, caused by the spirochete Borrelia burgdorferi, is known for its multisystem effects, including neurological manifestations such as meningitis, encephalitis, and, in rare cases, CNS vasculitis. This case highlights an uncommon presentation of subarachnoid hemorrhage associated with Lyme-related vasculitis.

Design/Methods:

NA

Results:

A 67-year-old man with no significant past medical history presented with a sudden onset of a severe headache, described as the worst of his life. Initial imaging revealed a diffuse subarachnoid hemorrhage with significant vasculopathy. Cerebral angiography showed dysplasia in the posterior cerebral arteries (PCAs), more pronounced on the left, without evidence of flow limitation, consistent with vasculitis.

The patient had a history of substantial outdoor activity, including chopping wood and painting barns, and a prior episode of Lyme disease treated approximately 7–8 years earlier. Cerebrospinal fluid (CSF) analysis revealed an elevated Lyme index, suggestive of CNS Lyme disease. Follow-up CT angiography of the head and neck showed moderate irregularity and a beaded appearance in the bilateral proximal-to-mid PCAs. Despite these findings, a comprehensive rheumatological workup was negative.

Given the patient's clinical history, imaging findings, and significant outdoor exposure, CNS vasculitis secondary to Lyme disease was strongly considered as the underlying cause of his subarachnoid hemorrhage.

Conclusions:

This case highlights the possibility that Lyme-associated vasculitis may increase vessel wall permeability, leading to subarachnoid hemorrhage. It remains uncertain whether this phenomenon results from the direct invasion of Borrelia burgdorferi into the vessel wall or through immune-mediated mechanisms triggering vasculitis. Further studies are warranted to elucidate these mechanisms and their role in the pathogenesis of CNS vasculitis in Lyme disease.