".....However, following treatment the most distal portion of nerves
seemed to improve first--even in nerves that were intially apparently normal---suggestive of a dying back neuropathy...."

"........we have been
unable to identify either spirochetes or evidence of active inflammation in
the nerve, nor have we been able to demonstrate antibody compliment, or immune complex deposition. However, we have been struck by the rapid clinical and neurophysiologic recovery following antibiotic treatment as well as to treatment with other agents
known to cross into the nervous system......"

"....This resolution of
symptoms has occurred before there has been any appreciable drop in antibody titer, suggesting the problem is a direct effect of infection with spirochetes and not a purely immune-mediated phenomenon..."


Lyme Disease: Cause of a treatable peripheral neuropathy
Authors: Halperin, Little, Coyle, Dattwyler
Neurology 1987;37:1700

".....Of the many patients we have seen with chronic Lyme disease (most of whom had worsened despite treatment with recommended oral antibiotics) many have noted intermittent tingling paresthesias of their extremities, yet had no demonstrable neurologic deficits. These symptoms were distinctly different from, and more commonplace than, those described in the literature, leading us to study this population in greater detail.......
Materials and methods. Subjects. Between October 1985 and March 1986, 36 patients with proven late Lyme disease were evaluated in the Lyme Disease Clinic at University Hospital, SUNY, Stony Brook. All patients had clinical histories consistent with diagnosis and had immunologic evidence of reactivity to B.
burgdorferi.......Three of the 22 patients with clinical and immunological evidence of Lyme disease but without the typical history of limb paresthesias also underwent neurophysiologic testing to determine if similar abnormalities occurred in asymptomatic patients. One of these patients, a carpenter, had a history suggestive of carpal tunnel syndrome at the time his arthritis had
been most active, but these symptoms were no longer present. Another, a mechanic, had a history of left arm tingling and back pain since a driving accident in which several cervical vertebrae had been fractured. The third
had no paresthesia of any sort..........
...............Discussion. Several distinct syndromes involving the peripheral nervous system have been described in patients with Lyme disease. Although we see large numbers of patients with Lyme disease, we have only rarely observed these syndromes . None of our patients had severe radicular pain, brachial neuritis, or obvious mononeuropathy multiplex. Only one had elecrtrophysiologic findings suggestiive of a Gullian-Barre-like syndrome. ...... the electrophysiologic testing
failed
to reveal any more subtle evidence of cranial nerve dysfunction. Yet, almost one half of the patients we have seen with late Lyme disease have had neurologic difficulties, the most common of which has been the presence of intermittent paresthesias. Therefore, we believe this syndrome to be a very common entitiy, but one quite different from those previously described. We
do not believe this high incidence to be an artifact of patient selection, since these patients were all studied before this neurologic syndrome was widely appreciated, and since all were initially referred by a
rheumatologist, not a neurologist.
The reason that this syndrome has not been previosly recognized may be that the neurologic examination is usually not strikingly abnormal in these patients. In the few previous reports of neurophysiologic testing in this disease, this was performed on patients with clinical abnormalities. Because of the consistent and persistent subjective symptoms, and in spite of the normal clinical examinations, we chose to study these patients neurophysiologicallly.
.........Our observations led us to conclude that many patients with Lyme disease have significant abnormalities of the peripheral nervous system, not attributable to other causes, and that many of these abnormalities can resolve following appropriate antibiotic treatment. This syndrome clearly may evolve despite treatment with currently recommended antibiotic regimes......However, it is striking that several patients have responded to more prolonged or
higher dose penicillin regimes, as well as to treatment with other agents
known to cross into the nervous system.......
The pathogenesis of this peripheral neuropathy remains unclear. It appears to be quite separate from the CNS manifestations of Lyme disease--its occurrence does not coincide with the acute meningoencephalitis, nor does its response to treatment necessarily parallel that of encephalopathy. The neurophysiologic abnormalities are multifocal in nature such as might be seen in mononeuritis multiplex. However, following treatment the most distal portion of nerves seemed to improve first--even in nerves that were intially apparently normal---suggestive of a dying back neuropathy.....Finally, we have been
unable to identify either spirochetes or evidence of active inflammation in
the nerve, nor have we been able to demonstrate antibody compliment, or immune complex deposition. However, we have been struck by the rapid clinical and neurophysiologic recovery following antibiotic treatment. This resolution of symptoms has occurred before there has been any appreciable drop in antibody titer, suggesting the problem is a direct effect of infection with spirochetes and not a purely immune-mediated phenomenon.
This study leads to two very different but equally important sets of conclusions. First, it serves to emphasize the sesitivity and utility of neurophysiologic testing, making posssible the demonstration significant abnormalities of peripheral nerve fuction in clinically normal patients. Furthermore , the use of sequetial studies in affected patients emphasizes the utility of using patients as their own "controls," demonstrating significant changes where values before and after were both well within the rather broadly defined "normal
range".
Second, these techniques have enabled us to
characterize a clinical syndrome quite distinct from those previously
described in Lyme disease and to demonstrate that it is one of the small
number of neuropathies that is readily reversible. Since the neurophysiologic abnormalities improve with effective treatment, they have provided a quantitative, objective assessment of the efficacy of different antibiotic regimes in this disease. Since the best antibiotic regime to treat Lyme disease remains to be determined, having such a means of objectively comparing different agents will be invaluable."
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