Abstract
Background
Facial nerve palsy is the most common cranial neuropathy of Lyme neuroborreliosis (LNB), and bilateral involvement occurs in roughly 30% of Lyme facial palsy. Erythema migrans lacking central clearing is readily mistaken for cellulitis.
Introduction
Lyme neuroborreliosis is a neurologic manifestation of Lyme disease that may present with meningitis, radiculopathy, or cranial nerve palsy. Facial nerve involvement is common, but rapidly progressive bilateral facial palsy is uncommon and may complicate diagnosis, particularly when the characteristic erythema migrans rash is absent or mistaken for cellulitis.
Case: A 22-year-old man with recent military training in North Carolina and Indiana presented with headache, neck pain, intermittent limb paresthesias, and a confluent erythematous rash of the right neck without central clearing. Three weeks earlier, the rash had been diagnosed as cellulitis on CT and treated with cephalexin, with apparent improvement that reinforced the initial diagnosis. He recalled no tick bite and was afebrile, with a white cell count of 10.2 × 10⁹/L and ESR of 17 mm/h. Left facial weakness present on admission progressed to right-sided weakness on hospital day 3 the second day of intravenous ceftriaxone. Lyme serology was positive, and CSF showed lymphocytic pleocytosis with elevated protein and normal glucose. MRI of the internal auditory canals demonstrated enhancement of cranial nerves III, V, VI, and VII, yet the deficit remained confined to the facial nerves, with no ophthalmoplegia, diplopia, or trigeminal sensory loss. Corticosteroids were withheld. He received intravenous ceftriaxone followed by oral doxycycline, with complete resolution documented 14 days after discharge.
Discussion: Three lessons. Erythema migrans without central clearing mimics cellulitis, and response to an agent inactive against Borrelia is not reassurance. Contralateral progression after appropriate therapy is expected and is not treatment failure. Radiologic involvement may substantially exceed the clinical deficit, suggesting the inflammatory process is more extensive than bedside examination reveals a dissociation not previously described in bilateral LNB facial palsy.
Conclusion
Lyme neuroborreliosis should be considered in patients presenting with aseptic meningitis and progressive facial nerve palsy, particularly when the weakness is bilateral. This case demonstrates how Lyme disease may initially resemble bacterial cellulitis and highlights the importance of recognizing evolving neurologic findings, obtaining appropriate serologic and cerebrospinal fluid testing, and initiating targeted antimicrobial therapy. It also signifies that radiologic involvement of the cranial nerves can be more extensive than the bedside examination suggests. It also reminds us that steroids offer no benefit in Lyme neuroborreliosis.