NEUROBORRELIOOSI

[Bb]

Lähettäjä: Soijuv Lähetetty: 30.8.2005 13:02

Itävaltalaisessa tutkimuksessa kuvaillaan borreliabakteerin aiheuttama keskushermoston valkean aineen tuhoutuminen (vastaavaa tapahtuu MS-taudissa).

Amerikkalaisessa tutkimuksessa apinoilla havaittiin erilaisia borreliabakteerin aiheuttamia vaurioita keskushermostossa, myös myeliinikatoa. Tutkimuksen mukaan keskushermostovauriot johtuivat mahdollisesti immuunivälitteisestä prosessista jonka krooninen infektio oli aiheuttanut.

Viimeisessä belgialaisessa tutkimuksessa todetaan borrelioosin ja kupan samankaltaisuus. Tauti mm. etenee vuosien aikana aaltomaisesti ja se voi välittyä sikiöön istukan välityksellä.


Inflammatory demyelinating neuropathy in neuroborreliosis
[Entzundliche demyelinisierende Neuropathie bei Neuroborreliose.]
Wien Med Wochenschr 1995;145(7-8 ):188-90 (ISSN: 0043-5341)
Zifko U; Wondrusch E; Machacek E; Grisold W
Neurologischen Abteilung, Kaiser-Franz-Josef-Spitals, Wien.

A patient with acute onset of radicular pain developed an asymmetric neuropathy within a few weeks. Neurophysiology and nerve biopsy findings revealed a demyelinating neuropathy. Cerebrospinal fluid showed mild pleocytosis, increased protein levels and elevated antibody titers against Borrelia burgdorferi suggesting Lyme neuroborreliosis.

Although peripheral nervous system complications of Lyme borreliosis are common, the association with chronic demyelinating neuropathy has not been described before.

Ann Neurol 1997 Mar;41(3):375-84 (ISSN: 0364-5134)
England JD; Bohm RP; Roberts ED; Philipp MT
Department of Neurology, Louisiana State University School of Medicine, New Orleans 70112, USA.

Peripheral neuropathy is a recognized but poorly understood manifestation of Lyme disease. We performed serial electrophysiological studies on 8 rhesus monkeys chronically infected with the JD1 strain of Borrelia burgdorferi and compared the results with those of similar studies on 10 uninfected control monkeys. Four infected and 2 uninfected animals underwent sural nerve biopsy. Five of the infected and 1 of the uninfected animals also had postmortem neuropathological examinations. Altogether, 5 of the infected monkeys demonstrated primarily axonal-loss-variety multifocal neuropathies. Only one nerve lesion exhibited findings compatible with demyelination. Pathologically, peripheral nerve specimens showed multifocal axonal degeneration and regeneration and occasional perivascular inflammatory cellular infiltrates without vessel wall necrosis.

Free spirochetal structures were not seen, but several macrophages exhibited positive immunostaining with a highly specific anti-B. burgdorferi, 7.5-kd lipoprotein monoclonal antibody. In the infected animals, serial analysis of serum antibodies to B. burgdorferi showed increasing numbers of IgG specificities and new IgM specificities, suggesting persistent infection. Thus, peripheral neuropathy in the form of a mononeuropathy multiplex develops frequently in rhesus monkeys chronically infected with B. burgdorferi. The pathogenesis of these nerve lesions is not yet known, but our studies suggest an immune-mediated process perhaps driven by persistent infection with B. burgdorferi.


http://intapp.medscape.com/px/medlineap ... uropathies

Detection of Borrelia burgdorferi DNA and complement membrane attack complex deposits in the sural nerve of a patient with chronic polyneuropathy and tertiary Lyme disease.

Muscle Nerve 1997 Aug;20(8 ):969-75 (ISSN: 0148-639X)
Maimone D; Villanova M; Stanta G; Bonin S; Malandrini A; Guazzi GC; Annunziata, P
Institute of Neurological Sciences, University of Siena, Italy.

We report a patient who developed a chronic sensory-motor polyneuropathy and a progressive myelopathy 4 years after a tick bite. An increased serum antibody titer to Borrelia burgdorferi suggested a diagnosis of Lyme neuroborreliosis, although a concomitant cervical spondylosis probably contributed to spinal cord damage. Treatment with ceftriaxone resulted in a marked improvement of neuropathic symptoms, providing indirect evidence of spirochetal infection. Search for B. burgdorferi DNA by polymerase chain reaction amplification on sural nerve confirmed the diagnosis, demonstrating that the spirochete localized in the peripheral nervous system. The presence of complement membrane attack complex deposits and macrophage infiltrates around epineurial vessels and within the endoneurium suggests that the neuropathy in our patient was immune-mediated.

http://intapp.medscape.com/px/medlineap ... uropathies

Multiple neurologic manifestations of Borrelia burgdorferi infection
[Les multiples manifestations neurologiques des infections a Borrelia burgdorferi.]

Rev Neurol (Paris) 1988;144(12):765-75 (ISSN: 0035-3787)
Dupuis MJ
Clinique St-Pierre, Ottignies, Belgique.

The neurological spectrum of Borrelia burgdorferi infections is still enlarging. We review epidemiological, pathological and serological data of Lyme disease. The course of the disease is divided in three stages: stage 1 during the first month is characterised by erythema chronicum migrans and associated manifestations; stage 2 includes not only the classical European meningoradiculitis but also less specific neurological symptoms: isolated lymphocytic meningitis with an acute or even relapsing course, apparently idiopathic facial palsy, neuritis of other cranial nerves, polyneuritis cranialis, Argyll-Robertson sign, peripheral nerve involvement, acute transverse myelitis, severe encephalitis, myositis.

During stage 3, three to five months or longer after the onset of the disease, chronic arthritis, acrodermatitis chronica atrophicans and various neurological symptoms can be observed: chronic neuropathy with mainly sensory or motor signs, recurrent strokes due to cerebral angiopathy and progressive encephalomyelitis; this third stage the central nervous system involvement is characterised by slowly progressive or fluctuating course during months or years, ataxic or spastic gait disorder, bladder disturbances, cranial nerve dysfunction including optic atrophy and hypoacusia, dysarthria, focal and diffuse encephalopathy. This chronic central nervous system disease can mimic multiple sclerosis, anorexia nervosa, psychic disorders or subacute presenile dementia. It is often associated with pleiocytosis, abnormal EEG and evoked potentials, sometimes multifocal and mainly periventricular white matter lesions visualised by CT or MRI, and as a rule high antibody titers against Borrelia burgdorferi. High doses of penicillin can halt the disease, sometimes induce spectacular regression of symptoms or sometimes be inefficient; ceftriaxone could be a more powerful therapy. Similarities between syphilis and Borreliosis are multiple: both of these spirochetes contain plasmids, can be transmitted through the placenta and progress for many years through successive stages, with multiorgan symptoms, including parenchymatous and vascular lesions of the central nervous system. Borrelia burgdorferi is the new great imitator.