Electrophysiologic testing indicates that the various peripheral nerve syndromes frequently overlap. All of the preceding processes excepting the one that resembles GBS usually occur as subacute or late complications of Lyme disease, several months or, rarely, years after the initial infection (in untreated cases). These late neuropathic syndromes respond less favorably to treatment than do the acute ones, and have a less certain connection to the infection (see further on). As the disease is not fatal, there are few adequate pathologic studies of the peripheral nerves in Lyme disease. The infective agent has not been demonstrated in nerve tissue, but perivascular inflammation and vasculitic changes are found in small vessels within the nerves.
Lyme polyradiculitis and Bannwarth syndrome This is perhaps the best characterized, but not the most common, group of Lyme neuropathies. A painful lumbosacral polyradiculitis has been described in Europe by the term Bannwarth syndrome (in France as Garin-Bujadoux syndrome). The pathogen in Europe is a Borrelia spirochete slightly different from the one that causes Lyme disease in North America. In Bannwarth syndrome there is an intense inflammatory reaction in the cauda equina, giving rise to sciatic and buttock pain and bladder dysfunction. Less frequently, a cervical polyradiculopathy occurs with shoulder and arm pain that cannot be distinguished on clinical grounds from brachial neuritis. Cases of
Bannwarth syndrome from North American Lyme under our care have progressed subacutely over days or weeks and involved the L2-L3-L4 roots, first one leg, then the other, and, subsequently, the midcervical roots on one or both sides. Sparing of a proximal or distal part of a limb while the adjacent part is weakened gives rise to a striking syndrome. One or more thoracic radiculopathies may be added and cause local discomfort.
The nerve conduction tests show preservation of sensory potentials, which marks the process as radicular. Headache and a marked pleocytosis (over 100 mononuclear cells/mm3) in the spinal fluid may accompany the pain and usually precedes the radiculopathies by days. Polymerase chain reaction for the detection of the organism in the CSF gives variable results, especially after several days of neurologic illness. A value above unity of CSF to serum anti-Lyme antibodies is probably a dependable indicator of acute or subacute disease, but there have been few systematic studies of this measurement. Oligoclonal bands in the CSF are common as a reflection of these antibodies.
A similar syndrome of lumbar polyradiculitis may also be caused by the herpes and Epstein-Barr viruses or more often by an opportunistic CMV infection in a patient with AIDS.
Diagnosis This is both aided and at times confused by serologic testing (see Chap. 31). The enzyme-linked immunosorbent assay (ELISA) is not altogether satisfactory because it frequently yields false-positive and, occasionally, false-negative results. Western blot testing of CSF is more specific. Information to the effect that the patient has lived in or visited an endemic area is useful, but far more compelling is evidence of a tick bite followed by the characteristic rash, or a well-defined history of nonneurologic manifestations of Lyme disease (cardiac, arthritic). Bifacial palsy in any of these clinical contexts also favors the diagnosis of Lyme.