Fatal Neuroborreliosis Case: When Lyme Disease Affects the Brain

A fatal neuroborreliosis case illustrates how Lyme disease affecting the central nervous system can become life-threatening, particularly when complicated by other serious medical conditions.

Lyme neuroborreliosis typically presents with headaches and symptoms of meningitis, encephalopathy, or stroke-like neurological findings. Diagnosis is based on clinical symptoms combined with cerebrospinal fluid analysis obtained by lumbar puncture.

Key Point: Lyme neuroborreliosis can cause severe neurological complications. Early recognition and treatment are important, particularly in patients with complex medical histories.

By Dr. Daniel Cameron

Complex Medical History

The woman described in the case report had several serious underlying health conditions. These included lupus, a left-posterior parietal ventriculoperitoneal (VP) shunt for congenital hydrocephalus, and a history of migraine headaches, explains Khan.

Diagnostic testing revealed renal failure and evidence of over-shunting on brain CT imaging.

On day two of hospitalization, she suffered cardiac arrest and required defibrillation. “Dopamine and vasopressin infusion was started for bradycardia and hypotension,” writes Khan.

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Neurologic Deterioration

Brain MRI revealed an acute ischemic insult. The patient was subsequently transferred to another hospital intubated, sedated, and requiring infusions of norepinephrine and dopamine.

Additional imaging revealed multiple abnormalities. Chest CT showed bilateral pulmonary emboli and stress-induced cardiomyopathy.

A rheumatologic workup suggested the patient had discoid lupus rather than systemic lupus.

Evidence of Lyme Neuroborreliosis

A lumbar puncture revealed significant abnormalities including a pleocytosis of 318 cells per deciliter and markedly elevated protein levels of 1,208 mg/dl.

These findings suggested central nervous system inflammation consistent with Lyme neuroborreliosis.

“Lumbar puncture results revealed elevated Borrelia burgdorferi antibodies in the cerebrospinal fluid (CSF) at 1.37 (normal <0.99),” writes Khan. Blood tests for Lyme disease, however, were negative.

This pattern—positive cerebrospinal fluid antibodies with negative blood testing—illustrates some of the diagnostic challenges clinicians face when evaluating Lyme disease testing.

Outcome of the Case

Despite treatment with intravenous ceftriaxone, the patient remained ventilator-dependent and showed minimal neurological improvement.

“A goals-of-care discussion was held, and the family decided to withdraw care after a two-week hospital stay,” writes Khan.

She died shortly after being removed from the ventilator with her family at her bedside.

Clinical Perspective

Clinical Insight: Patients with Lyme neuroborreliosis often present with neurological symptoms that can resemble stroke, meningitis, or autoimmune disease. Complex medical histories—such as lupus or other chronic illnesses—may make recognition of Lyme disease more difficult.

This case highlights how multiple medical conditions can complicate the diagnosis of Lyme neuroborreliosis. The authors emphasize that severe neurologic Lyme disease may occur alongside other medical problems that obscure the diagnosis.

Although the patient had several serious comorbid conditions—including lupus and congenital hydrocephalus requiring a VP shunt—Lyme neuroborreliosis likely contributed to her neurological decline.

Maintaining clinical suspicion for Lyme disease in patients with unexplained neurological symptoms remains essential, particularly in endemic areas.