KASVOHERMOHALVAUS

[Bb]

Lähettäjä: Soijuv Lähetetty: 14.2.2006 10:53

Saksalaisen tutkimuksen mukaan kasvohermohalvauksen saaneilla lapsilla esiintyy useimmiten punkinpurema ja/tai ihomuutos kaulan/pään alueella. Aiheuttajana on esim.B. garinii. Tulehduksen aiheuttama turvotus vahingoittaa hermorataa. Rottakokeissa huomattiin borreliabakteerin pesiytyneen sydämeen viidessä päivässä, aivoihin viikossa ja ääreishermostoon 7 - 33 vuorokaudessa.

Kasvohalvaus saattaa esiintyä molemmin puolin kasvoja. Puolalaisen tutkimuksen mukaan molemminpuolinen kasvohalvaus on tyypillisin neuroborrelioosin oire lapsilla. Ruotsalaisen tutkimuksen mukaan ei pidä paikkaansa, että kaikki kasvohalvauksen saaneista lapsista paranisivat 100 %:sesti. Osalle jää jonkinasteisia toimnallisia häiriöitä kasvoihin.


Neuropediatrics. 2004 Oct;35(5):267-73.
Acute peripheral facial palsy in Lyme disease -- a distal neuritis at the
infection site.

Eiffert H, Karsten A, Schlott T, Ohlenbusch A, Laskawi R, Hoppert M,
Christen HJ.

Department of Bacteriology University of Gottingen, Germany.

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.

PMID: 15534758 [PubMed - indexed for MEDLINE]
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Rocz Akad Med Bialymst. 2005;50 Suppl 1:64-9.

Bilateral facial nerve palsy in the course of neuroborreliosis in children-dynamics, laboratory tests and treatment.

Mlodzikowska-Albrecht J, Zarowski M, Steinborn B, Winczewska-Wiktor A, Gurda B, Wigowska-Sowinska J.

Chair and Department of Developmental Neurology Poznan University of Medical Sciences, Poland. albrecht@amp.edu.pl

PURPOSE: Presentation of four patients with bilateral peripheral facial nerve palsy as a clinical manifestation of neuroborreliosis in children--diagnostic, treatment and prognosis.

MATERIAL AND METHODS: In 2002-2004 in The Chair and Department of Developmental Neurology, 24 children from the Wielkopolska region were admitted with diagnosis of borreliosis. Among all the children with borreliosis, confirmed by serologic examination, 4 (16.7%) demonstrated bilateral peripheral facial palsy (PFP).

We investigated the presence of IgM class and IgG class specific antibodies in the sera and cerebrospinal fluid (CSF) of 4 patients with bilateral PFP. (Detected by immunoenzymatic methods--ELISA.)

RESULTS: Before the occurrence of PFP all the children manifested unspecified systemic symptoms such as headaches, muscle and articulation pains, weakness and in two cases a mood depression. At first all patients demonstrated elevated IgM antibodies and proper levels of IgG antibodies. Control tests administered within 2-14 months later reduction of antibodies was indicated. Two patients demonstrated significant pleocytosis in CSF test, (without the meningeal symptoms). All children were treated with physiotherapeutic procedures and were administered antibiotic intravenously.

CONCLUSIONS: PFP is one of the most frequent neurological symptoms of borreliosis in children. In case of acute PFP and especially the bilateral form of PFP, neuroborreliosis is the most probable diagnosis. All children reported PFP at one side first and after several weeks the paresis of the facial nerve on the opposite side usually appeared. The clinical state of children started to improve after the introduction of physiotherapy and this process usually lasted several months.

PMID: 16119630 [PubMed - indexed for MEDLINE]
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Otol Neurotol. 2005 Jul;26(4):790-5. Related Articles, Links

Long-term outcome of facial palsy in neuroborreliosis.

Bagger-Sjoback D, Remahl S, Ericsson M.

Departments of Otolaryngology, Karolinska University Hospital, Stockholm, Sweden. dan.bagger-sjoback@ks.se

OBJECTIVES: The objectives of this study were to examine children with previous manifest neuroborreliosis and concommitant facial palsy to see whether there were any persisting symptoms and/or signs of persistent residual facial palsy. STUDY DESIGN: Open, controlled prospective study.

SETTING: Tertiary referral center (University Hospital).

PATIENTS: The study was conducted on twenty-four patients with clinically manifest neuroborreliosis and facial palsy 3 to 5 years prior to the investigation.

MAIN OUTCOME MEASURES: Results of the clinical examination using the House-Brackmann scale were compared to results from two neuro- physiological examinations (qEMG and ENoG). RESULTS: Approximately one-half of the patients with reported subjective symptoms of residual facial palsy had signs of slight dysfunction in the clinical examination using the House-Brackmann scale. There was no correlation between the subjective feeling of facial dysfunction and presence of clinical signs. Likewise, about one-half of the subjective facial dysfunction group, as well as the control group, were found to demonstrate pathological values in their neurophysiological examinations using qEMG and ENoG.

CONCLUSIONS: This study shows that the assumption is not true that all children who had neuroborreliosis with facial palsy will heal 100%. A small proportion of the children claim that several years after the infection, they have subjective symptoms of slight facial weakness on the affected side. Our study shows that some of these children, as well as some children without subjective symptoms of facial palsy, demonstrate a slight facial weakness when examined clinically. Likewise, signs of slight-to-moderate facial motor dysfunction were revealed in about half of the children with the two neurophysiological methods utilized in this study. It is interesting to note that there was no clear correlation between the presence of subjective symptoms, objective signs, and neurophysiological results.

PMID: 16015186 [PubMed - indexed for MEDLINE]