Case Presentation:

A 63 year-old woman presented with one-week history of severe neck pain radiating to the left arm, along with two days of weakness and numbness of both upper limbs, left greater than right. She denied any symptoms suggestive of cranial nerves, lower extremity, bladder and bowel involvement or gait disturbance. She denied any unusual exertion, trauma, viral prodrome, vaccinations or rash. She was initially started on acyclovir, which was later discontinued as the pain was thought to be musculoskeletal in origin. In the upper limbs, there was grade two out of five weakness in the proximal muscles with absent deep tendon reflexes. There were no upper motor neuron signs. The remainder of the neurological examination was normal.  MRI cervical spine was negative for spinal root or cord compression. Electromyography revealed cervical root involvement. However, Lyme serology was positive with significantly elevated antibody titers; western blot IgG (5 of 10 bands) and IgM (2 of 3 bands).  Lumbar puncture revealed an elevated protein of 285 mg/dL and a lymphocytic pleocytosis of 100 WBCs with 99% lymphocytes. On further questioning, she denied any tick bite or a bull’s eye skin lesion. She was treated with oral doxycycline. Her symptoms started improving within three weeks of initiating treatment. By three months, the deep tendon reflexes had become normal and she had regained full strength.


Neck pain, arm pain and limb weakness are commonly encountered by the hospitalists. A methodical approach to evaluate these symptoms is crucial in identifying the etiology and formulating treatment. All radiculopathies and/or myelopathies are considered compressive unless proved otherwise, as the treatment for compression is surgery. Once compression is ruled out, non-compressive etiologies should be considered. Lyme disease is a common cause of non-compressive radiculopathy, which is infrequently recognized.

Lyme meningoradiculitis (Bannwarth ‘s syndrome) occurs in acute disseminated Lyme disease. Lymphocytic meningitis often occurs in patients with Lyme radiculitis or cranial neuritis. Absence of a history of tick bite and a bull’s eye skin lesion does not rule out Lyme disease.  Radicular pain affecting multiple root distribution should raise suspicion of Lyme radiculitis, necessitating confirmation of Borrelia burgdorferi infection. Herpes zoster symptoms, however, are confined to a dermatomal pattern in an immunocompetent individual, and not in a multiple root distribution as seen in this patient.

We are once again reminded about recognizing the protean manifestations of Lyme disease, which can be effectively treated.


Lyme disease is a treatable cause of non-compressive radiculopathy and should be considered once compressive etiology has been excluded.