A 65‐year‐old man presented with a 4‐week history of general malaise, headaches, low‐grade fevers, and bilateral upper‐extremity pain. He denied having episodes of chills, vomiting, or photophobia. He lives in a wooded area and has had multiple tick bites in the past. He had been on ibuprofen for more than 2 weeks before his presentation. He presented on the day of admission because of “shooting pain” in his upper extremities, worsening headaches, and pain across his lower back. He denied having stool or urine incontinence. His exam was remarkable for heart rate of 56/minute, blood pressure of 141/89 mm Hg. He was afebrile and not dyspneic. He had normal chest and cardiac examination findings. His abdomen was not tender and he had no palpable masses. Rectal tone was normal. Neck was supple, although he had tenderness on palpation of his neck muscles. His speech was normal. He had no facial droop. He had reduced power in his upper extremities: grade 4 and reduced deep tendon reflexes. Power was normal in his lower extremities, and he had normal deep tendon reflexes. No rash was noted on skin examination. Lab. data revealed normal complete blood count and electrolytes. His ESR was 40. His Head CT scan was unremarkable. He had a lumbar puncture done, which revealed he had CSF protein level of 141, glucose was 49 (normal), and 162 nucleated cells with lymphocytic predominance. CSF gram stain was negative. His serum B. burgdorferi antibody level was 6.2 (positive >1.3). He was started on IV ceftriaxone for stage 2 Lyme disease due to the CSF findings and his symptoms. He did well with the antibiotic regimen. His fevers resolved within 48 hours. He regained enough strength and function in his upper extremities for him to be discharged on a total 21‐day course of ceftriaxone.
Lyme disease is tick‐borne multisystem infectious disease that commonly affects the skin, joints, and central nervous system (CNS). The CNS is involved in 10%–15% of infected individuals. The classic triad of acute early neurologic Lyme disease consists of lymphocytic meningitis, cranial neuropathy (typically facial palsy), and radiculoneuritis. These may occur alone or in combination. Banwarth syndrome is the constellation of painful radiculoneuritis, often accompanied by meningitis. This is more common in European neuroborreliosis. Lyme radiculoneuritis is reported in about 3% of CDC‐verified cases of Lyme disease. This condition is separate from the migratory arthralgia associated with 60% of cases of Lyme disease and requires a high index of suspicion for accurate diagnosis to be made. Doxycycline instead of IV ceftriaxone is used for Banwarth syndrome and other features of stage 2 Lyme disease with great success.
Radiculoneuritis is a peripheral manifestation of Lyme disease. Hospitalists have to be aware of all the clinical conditions associated Lyme disease and need to consider this condition in patients in endemic areas presenting in spring through autumn with limb and/or truncal radicular pain..
To cite this abstract:Dapaah‐Afriyie K, Bradley J. Ban What Syndrome? — Banwarth Syndrome Due to Lyme Disease. Abstract published at Hospital Medicine 2013, May 16-19, National Harbor, Md. Abstract 348. Journal of Hospital Medicine. 2013; 8 (suppl 2). https://www.shmabstracts.com/abstract/ban-what-syndrome-banwarth-syndrome-due-to-lyme-disease/. Accessed November 19, 2019.