Page 93 - Human Lyme Neuroborreliosis

Clinical Aspects 77

both cell- and humoral-mediated immune injury as a likely consequence of B.
burgdorferi infection. A variety of candidate antigens that cross-react with
constituent peripheral nerve molecules were found in sera and peripheral nerve
of affected patients with LNB [51, 89].

Acquired autonomic neuropathy in association with LNB, in which
autonomic fibers are selectively or disproportionately affected leading to
orthostatic intolerance and other dysautonomic syndromes, are also
presumably of autoimmune cause [27, 57] as suggested by the occurrence of
autonomic neuropathy after Lymerix and Connaught vaccination [90, 91].

Conclusion

The abrupt onset of acute meningoradiculoneuritis with CSF pleocytosis
and a triad of meningitis, radiculitis, and cranial neuritis in an affected patient,
weeks to months after a spreading erythroderm, so called Garin’s triad, should
prompt a vigorous search for the causative agent of Lyme disease, B.
burgdorferi. Occasional patients present with CNS involvement including
encephalopathy long after initial treatment that may be due to mild
encephalitis. Accurate diagnosis of CNS infection requires paired serum and
CSF specimens, measurement not just of CSF anti- B. burgdorferi-specific
antibody but actual intrathecal antibody production. Non-human primate
models have contributed to our understanding of the etiopathogenesis of
nervous system injury, providing clues to the complexity of clinical
presentation in human including tandem autoimmune mechanisms of injury.
The tandem occurrence of other rare degenerative or inflammatory neurologic
disorders may require further investigation to establish causality.

References

[1] Burgdorferi, W, Barbour AG, Hayes SF, et al. Lyme disease: a tick
borne spirochetosis? Science 1982; 216:1317-1319.

[2] Afzelius A. Erythema chronicum migrans. Acta Derm Venereol 1921;
2:120-125.

[3] Garin C, Bujadoux A. Paralysie par les tiques. J Med Lyon 1922;
71:765-767.

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