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Generalised motor neuron disease as an unusual manifestation of Borrelia burgdorferi infection
  1. B HEMMER,
  2. F X GLOCKER,
  3. R KAISER,
  4. C H LÜCKING
  1. Department of Neurology and Clinical Neurophysiology, University of Freiburg , Germany
  2. Department of Neurology and Clinical Neurophysiology, University of Kiel, Germany
  1. Dr Franz X Glocker, Neurologische Universitätsklinik Breisacher Strasse 64, D-79106 Freiburg, Germany.
  1. G DEUSCHL
  1. Department of Neurology and Clinical Neurophysiology, University of Freiburg , Germany
  2. Department of Neurology and Clinical Neurophysiology, University of Kiel, Germany
  1. Dr Franz X Glocker, Neurologische Universitätsklinik Breisacher Strasse 64, D-79106 Freiburg, Germany.

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Lyme borreliosis is a well known multisystem disease caused by the spirochete Borrelia burgdorferi and can produce a wide array of neurological abnormalities in humans. The most frequent are meningitis, cranial neuritis, and painful radiculoneuritis.1 Other clinical manifestations include chronic encephalomyelitis, spastic paraplegia, and axonal polyneuropathy. Our report concerns what we think to be the first case of a patient with upper and lower motor neuron disease andBorrelia burgdorferi infection of the CNS. A causal relation is strongly supported by an evaluation of the Borrelia burgdorferi specific antibody index and the patient’s favourable response to medical treatment.

Fifteen months before admission a 33 year old patient noticed weakness in his right hand followed by weakness of the left hand and a progressive gait disturbance. Although he had no pain or sensory disturbance and no history of a tick bite, an erythema migrans, or arthralgias, his physician tested him for Borrelia burgdorferi specific antibodies in the serum because he lived in an endemic region. The test disclosed high concentrations of specific IgG antibodies (1:1200, cut off <1:200). The patient was treated with doxycyclin for two weeks. A control examination performed in a different laboratory still disclosed high concentrations of specific IgG antibodies (1:160, cut off 1:40). Treatment was started again with cefotaxim (2g intravenously for five days). Six …

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