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Neuralgic amyotrophy associated with Bartonella henselae infection
  1. Cari J Stek1,
  2. Jeroen J J van Eijk2,
  3. Bart C Jacobs4,
  4. Roelien H Enting3,
  5. Herman G Sprenger1,
  6. Nens van Alfen2,
  7. Sander van Assen1
  1. 1Department of Internal Medicine, Division of Infectious Diseases, University Medical Centre, Groningen, The Netherlands
  2. 2Department of Neurology and Clinical Neurophysiology, Donders Institute for Brain Cognition and Behaviour, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands
  3. 3Department of Neurology, University Medical Centre, Groningen, The Netherlands
  4. 4Department of Neurology and Immunology, Erasmus Medical Centre, Rotterdam, The Netherlands
  1. Correspondence to Dr J J J van Eijk, 935 Department of Neurology, Donders Institute for Brain Cognition and Behaviour, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands; j.vaneijk{at}neuro.umcn.nl

https://doi.org/10.1136/jnnp.2009.191940

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    We report three patients with a brachial plexus neuropathy diagnosed as neuralgic amyotrophy (NA) preceded by a proven Bartonella henselae infection. Neuralgic amyotrophy is a disabling disease involving the brachial plexus, with attacks of severe shoulder and arm pain followed by weakness and sensory involvement.1 Several observations support the hypothesis of an immune-mediated genesis. First, brachial plexus biopsies of NA patients in the (sub)acute stage show inflammatory changes.2 3 Second, antiganglioside antibodies are reported to be associated with NA.1 4 Third, several immune-triggering events, most frequently infections (50%), are known to precede NA.1–4 Various micro-organisms preceding NA have been reported (see table 1) but not yet B henselae.

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    Table 1

    Results of literature search for micro-organisms associated with neuralgic amyotrophy

    B henselae is a Gram-negative, intracellular bacterium causing cat-scratch disease (CSD), which usually presents with fever, malaise and regional lymphadenopathy. Occasionally, neurological complications occur, most frequently neuroretinitis and encephalopathy, but also peripheral nervous system disorders.5 These complications occur 1–3 weeks from the onset of lymphadenopathy, without any signs of direct infection of the nervous system, suggesting an immune-mediated genesis.

    Infections can induce auto-immune reactions by several mechanisms. Molecular mimicry could be the underlying pathophysiological mechanism in NA, comparable with Guillain–Barré syndrome, for example. Alternatively, NA may …

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    Footnotes

    • Competing interests None.

    • Provenance and peer review Not commissioned; externally peer reviewed.