Lyme neuroborreliosis (LNB) is one of the extracutaneous manifestations of Lyme disease. BWS consists of triad of painful radiculopathy, cranial neuropathy and lymphocytic pleocytosis on Cerebrospinal fluid (CSF). Presence of Lyme antibodies in CSF confirms the diagnosis, which can be supported by neuroimaging and neurophysiological studies. Treatment includes 2-4 weeks of IV ceftriaxone or oral doxycycline. We present a case of BWS presenting with nonspecific symptoms. 

A 71-year-old male, who is a frequent hiker, with history of recent dermatomal rash (T7/T8), presented to hospital with worsening back pain radiating to lower extremities. His symptoms progressed to band-like abdominal tightness, imbalance, and weakness in extremities. Neurological exam showed 4/5 weakness in right foot dorsiflexion, hyporeflexia in arms and knees with absent ankle jerks, and decreased pinprick sensation in suspended fashion. Lyme serology was negative a week before presentation. MRI brain and spine were without evidence of nerve root enhancement. Patient was empirically started on acyclovir and IVIg for suspected zoster and GBS with minimal clinical change. Initial EMG showed normal motor responses. On day 2, patient developed blurry vision. Repeat exam showed peripheral CN VII palsy. CSF analysis showed lymphocytic pleocytosis (348), elevated protein (124), and positive Lyme DNA by PCR. Serum Lyme IgG/IgM antibodies were positive. Addition of doxycycline led to significant improvement in symptoms. Follow-up EMG was suggestive for acute on chronic axonal, motor neuropathy/polyradiculopathy affecting bilateral lower extremities.  

Although prevalent in Europe, BWS is becoming more common in United states and is often misdiagnosed due to its diverse neurological presentation. Initial EMG in this patient may have been normal due to hyperacute phase of disease progress. Not only does addition of antibiotics reverse symptoms, early identification of LNB can prevent further axonal loss.