Researchers described a case of Guillain-Barré syndrome occurring in association with Lyme disease in a 61-year-old female patient, illustrating diagnostic challenges when acute inflammatory neuropathy presents alongside tick-borne infection.
The previously healthy patient presented with two weeks of fatigue followed by acute bilateral lower limb weakness and distal paresthesia one day prior to evaluation. Neurologic examination revealed symmetrical lower limb weakness graded three out of five distally and four out of five proximally, with absent ankle and knee reflexes and reduced tone. Cranial nerve and upper limb examinations were initially normal.
Initial laboratory testing showed mild leukocytosis of 12.6 × 10⁹/L and elevated C-reactive protein of 20 mg/L. Magnetic resonance imaging of the brain showed no structural abnormalities. Cerebrospinal fluid analysis demonstrated albuminocytologic dissociation, with elevated protein of 51.6 mg/dL and a white cell count of one cell per microliter, findings consistent with Guillain-Barré syndrome (GBS).
Electrophysiological testing was consistent with acute inflammatory demyelinating polyneuropathy. Sensory nerve conduction responses were preserved, while late response testing showed absent F waves in the right tibial nerve, a finding consistent with early demyelinating neuropathy. Needle electromyography revealed no abnormal spontaneous activity but showed occasional fast-firing motor unit potentials in selected upper limb and facial muscles.
A ganglioside antibody panel demonstrated anti-ganglioside antibodies, including anti-GD2 immunoglobulin M antibodies with a titre graded as (++). This finding was interpreted in the context of the patient’s clinical and electrophysiological results as supportive of immune-mediated neuropathy.
Physicians initiated a five-day course of intravenous immunoglobulin for suspected GBS. During hospitalization, the patient developed progressive weakness involving the upper limbs and bilateral lower motor neuron facial palsy, prompting evaluation for Lyme disease.
Two-tier serologic testing returned positive results, fulfilling Centers for Disease Control and Prevention criteria and indicating exposure to Borrelia burgdorferi in the appropriate clinical context.
The patient initially received oral doxycycline but discontinued treatment because of gastrointestinal intolerance. Physicians then initiated intravenous ceftriaxone for a 30-day course.
Respiratory function was closely monitored throughout hospitalization. Peak flow improved from 320 L/min at admission to 470 L/min at discharge, and forced vital capacity improved from 2,300 mL to 3,900 mL. Negative inspiratory force improved from −42 cmH₂O to −63 cmH₂O. The patient did not require ventilatory support.
Neurological function improved during treatment. The patient regained partial ambulation with a walker prior to discharge and achieved complete neurological recovery two weeks following completion of intravenous therapy.
Lyme disease can involve the nervous system during its disseminated phase and may present with cranial neuropathies, radiculopathy, or peripheral neuropathy. Approximately 40% of patients with Lyme disease develop neurologic complications during the course of infection.
The researchers noted that the emergence of bilateral facial palsy broadened the differential diagnosis and prompted serologic testing for Lyme disease, supporting a diagnosis of GBS occurring in association with Borrelia burgdorferi infection.
“Clinicians should maintain a high index of suspicion for Lyme disease in patients presenting with atypical GBS features, particularly in endemic regions, as timely recognition and combined therapeutic strategies can significantly improve outcomes,” wrote Ahmed Elnour, MBBS, of University Hospital Kerry in Tralee, Ireland, and colleagues.
The researchers reported no financial support and no conflicts of interest.
Source: Cureus
