Atypical Lyme Neuroborreliosis Presenting With Ventriculitis and Cerebritis: A Case Report

Lyme neuroborreliosis is a neurological manifestation of infection by Borrelia burgdorferi sensu lato and most commonly presents with lymphocytic meningitis, cranial neuropathy, or painful radiculitis. Central nervous system parenchymal involvement is uncommon, and ventriculitis is rarely reported. We describe a man in his late 70s who presented with acute confusion, dysarthria, and left-sided weakness following several days of severe lower-limb pain and progressive mobility impairment. His neurological status rapidly deteriorated, with secondary seizures requiring invasive mechanical ventilation and intensive care support. Laboratory evaluation demonstrated a marked systemic inflammatory response, thrombocytopenia, acute kidney injury, and cholestatic liver dysfunction. Cerebrospinal fluid (CSF) analysis revealed pleocytosis with initial neutrophilic predominance, markedly elevated protein, and preserved glucose. Routine bacterial cultures and molecular testing for common central nervous system pathogens were negative. Anti-Borrelia IgG and IgM antibodies were detected in CSF, although a paired CSF-serum antibody index was unavailable. Brain magnetic resonance imaging demonstrated inflammatory material within the occipital horns of the lateral ventricles, bilateral leptomeningeal involvement, and focal parenchymal lesions with restricted diffusion suggestive of cerebritis. In the appropriate clinical context, these findings supported a diagnosis of probable Lyme neuroborreliosis with an unusual ventriculitis-like presentation. Despite prolonged antimicrobial therapy and partial improvement in CSF and radiological inflammatory findings, neurological recovery remained limited, and the patient subsequently died following ventilator-associated pneumonia complicated by septic shock. This case illustrates an uncommon and severe central nervous system presentation potentially associated with Lyme neuroborreliosis and highlights both the diagnostic value and limitations of CSF serology when demonstration of intrathecal antibody synthesis is unavailable.