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莱姆病所致急性周围性面瘫——感染部位的远端神经炎

Acute peripheral facial palsy in Lyme disease -- a distal neuritis at the infection site.

作者信息

Eiffert H, Karsten A, Schlott T, Ohlenbusch A, Laskawi R, Hoppert M, Christen H-J

机构信息

Department of Bacteriology University of Göttingen, Germany.

出版信息

Neuropediatrics. 2004 Oct;35(5):267-73. doi: 10.1055/s-2004-821174.

DOI:10.1055/s-2004-821174
PMID:15534758
Abstract

AIM

Children with acute peripheral facial palsy have often suffered tick bites and/or erythema migrans in the head/neck region on the same side. With respect to the pathogenesis of neuroborreliosis this topographical association was investigated in an animal model.

METHODS

A Borrelia garinii strain, isolated from the CSF of a child with acute facial palsy, was injected in 9 rats intracutaneously in the right subauricular region. Infected rats were examined for clinical symptoms of Lyme disease, the spread of the spirochetes was investigated by PCR of necropsies (facial nerves, trigeminus nerves, heart, brain, skin) up to 47 days after infection. The nerve tissues were investigated by histology, immunohistochemistry and electron microscopy.

RESULTS

None of the rats developed a facial palsy or other symptoms of Lyme disease. Borrelia DNA was found in the heart after 5 days and in the brain after 7 days of infection up to the end of investigation (47 days), as well as in the ipsilateral peripheral nerves after 7 to 33 days. Borrelia was detected by electron microscopy near endoneural vessels of the facial nerve. Peri-, epi-, and endoneural infiltrations of macrophages, plasma cells and B cells characterized an inflammation of the facial and trigeminus nerves ipsilateral to the infection site.

CONCLUSION

An infection with Borrelia garinii in the subauricular region induces an ipsilateral neuritis of peripheral nerves. The particular vulnerability of the human facial nerve may be a result of its long intraosseus course. Thus, an inflammatory edema may injure the nerve in the canalis facialis.

摘要

目的

急性周围性面神经麻痹患儿常于同侧头颈部遭受蜱叮咬和/或出现游走性红斑。针对神经莱姆病的发病机制,在动物模型中研究了这种部位关联。

方法

从一名急性面神经麻痹患儿的脑脊液中分离出一株加氏疏螺旋体,将其注射到9只大鼠的右耳下区域皮内。对感染大鼠进行莱姆病临床症状检查,在感染后长达47天通过尸检(面神经、三叉神经、心脏、脑、皮肤)的聚合酶链反应研究螺旋体的扩散情况。通过组织学、免疫组织化学和电子显微镜对神经组织进行研究。

结果

所有大鼠均未出现面神经麻痹或其他莱姆病症状。感染后5天在心脏中发现疏螺旋体DNA,7天后直至研究结束(47天)在脑中发现,感染后7至33天在同侧周围神经中也发现。通过电子显微镜在面神经的神经内膜血管附近检测到疏螺旋体。巨噬细胞、浆细胞和B细胞的神经周、神经外膜和神经内膜浸润是感染部位同侧面神经和三叉神经炎症的特征。

结论

耳下区域加氏疏螺旋体感染可诱发同侧周围神经神经炎。人类面神经的特殊易损性可能是由于其在骨内走行较长。因此,炎症性水肿可能会损伤面神经管内的神经。

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