Borrelia burgdorferi seropositive chronic encephalomyelopathy: Lymeneuroborreliosis? An autopsied report
K. Kobayashi
Bok Engelsk 1997
| Utgitt | 1997
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|---|---|
| Omfang | Side 384- 390
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| Opplysninger | A 36-year-old Japanese woman presented with progressive cerebellarsigns and mental deterioration of subacute course after her returnfrom the USA. Her serum antibody to spirochete Borrelia burgdorferiwas significantly elevated. A necropsy 4 years after her initialneurological signs revealed multifocal inflammatory change in thecerebral cortex, thalamus, superior colliculus, dentate nucleus,inferior olivary nucleus and spinal cord. The lesions showedspongiform change, neuronal cell loss, astrocytosis and proliferationof activated microglial cells. The internal capsule was partiallyvacuolated and the spinal cord, notably at the thoracic level, wasdemyelinated and cavitated in the lateral funiculus. Microglial cellsaggregated within and around the spongiform lesions and microglialnodules were present in the medulla oblongata. Use of Warthin-Starrystain demonstrated silver-impregnated organisms strongly suggestingB. Burgdorferi in the central nervous tissues. The dentate nucleusand inferior olivary nucleus showed the most advanced lesions withprofound fibrillary gliosis. Occlusive vascular change was relativelymild, and fibrous thickening of the leptomeninges with lymphocyteinfiltrates was localized in the basal midbrain. The ataxic symptomswere due to the dentate and olivary nucleus lesions and mentaldeterioration was attributable to the cortical and thalamic lesions.Spongiform change, neuronal cell loss, and microglial activation arecharacteristic pathological features in the present case. Thecerebellar ataxia and subsequent mental deterioration are unusualclinical features of Lyme neuroborreliosis. Spirochete B. Burgdorferican cause focal inflammatory parenchymal change in the centralnervous tissues and the present case may be an encephalitic form ofLyme neuroborreliosis.
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| Emner |
