Peripheral neuropathy in Lyme borreliosis
Author: Kindstrand, Eva
Date: 1999-12-17
Location: Birkeaulan 2, Huddinge sjukhus
Department: Institutionen för klinisk neurovetenskap, arbetsterapi och äldrevårdsforskning (NEUROTEC) / Department of Clinical Neuroscience, Occupational Therapy and Elderly Care Research (NEUROTEC)
Abstract
Tick-transmitted Lyme borreliosis (LB) is frequently associated with
manifestations from the peripheral nervous system. One aim of the thesis
was to describe the relationship between peripheral neuropathy and LB by
prospective studies of a) LB in some defined neurological conditions with
peripheral nerve engagement and b) peripheral neuropathy in the late
dermatological LB manifestation acrodermatitis chronica atrophicans
(ACA). A second aim was to evaluate the effect of antibiotic treatment on
ACA associated neuropathy in a prospective study.
Lyme neuroborreliosis (LNB) was diagnosed in 6/37 consecutive adult
patients with isolated cranial neuropathy of primarily unknown etiology.
Four patients had unilateral facial palsy and two had unilateral abducens
palsy. All patients with LNB and cranial neuropathy had associated
symptoms and/or signs, suggesting LNB, In patients with cranial
neuropathy, a careful history to elicit other LB symptoms and tick
exposure will usually identify the patients with a probable LNB as
etiology. Routine testing for borrelia serology is not indicated in
patients with cranial neuropathy without tick exposure or other
symptoms/signs of LB.
A serological screening for LB in 94 consecutive patients with
neurophysiologically verified carpal tunnel syndrome (CTS) showed no
statistically significant difference in seroposititivity prevalence
compared to 127 age- and sexmatched control persons. None of the
seropositive CTS patients had symptoms or signs, suggesting ongoing or
past LB, The results indicate that LB is not a common cause to CTS, and
routine serological screening for LB in patients with CTS does not seem
indicated.
Symptoms and signs of peripheral neuropathy were significantly more
frequent in 63 consecutive patients with untreated ACA than in 30 age-
and sexmatched control persons. Pain and paresthesia were the most
frequent symptoms and polyneuropathy the most common finding. An
exaggerated pain reaction in extremities with ACA lesions was prominent
in many patients but was considered as nociceptive and secondary to
inflammatory skin lesions.
Polyneuropathy characteristics were described in detail in 17 patients
with ACA and polyneuropathy. The clinical and neurophysiological findings
were consistent with a large fibre sensory polyneuropathy. Sural nerve
biopsy, performed in three patients, showed a mainly axonal neuropathy.
The histopathological appearance did not suggest any particular
underlying pathogenesis.
Forty-seven patients with ACA and with abnormal clinical and/or
neurophysiological findings were followed up after antibiotic treatment
with neurological, neurophysiological, dermatological and serological
controls. The therapy effect on symptoms of irritative nerve lesions,
inflammatory skin changes and serum antibody titres to Borrelia
burgdorferi was good, while there was no improvement of neuropathy signs.
The neuropathy did not progress during the follow up time. The
interpretation of these results is that the remaining neuropathy signs
after antibiotic treatment of ACA patients with borrelia induced
neuropathy are neurological sequelae and not manifestation of ongoing
borrelia infection.
List of papers:
I. Kindstrand E (1995). "Lyme borreliosis and cranial neuropathy" J Neurol 242(10): 658-663
Pubmed
II. Kindstrand E (1992). "Antibodies to Borrelia burgdorferi in patients with carpal tunnel syndrome" Acta Neurol Scand 86(1): 73-75
Pubmed
III. Kindstrand E, Nilsson BY, Hovmark A, Pirskanen R, Åsbrink E. (1997). "Peripheral neuropathy in acrodermatitis chronica atrophicans - a late Borrelia manifestation " Acta Neurol Scand 95(6): 338-345
Pubmed
IV. Kindstrand E, Nilsson BY, Hovmark A, Nennesmo I, Pirskanen R, Solders G, Åsbrink E (2000). "Polyneuropathy in late Lyme borreliosis - a clinical, neurophysiological and morphological description" Acta Neurol Scand 101(1): 47-52
Pubmed
V. Kindstrand E, Nilsson BY, Åsbrink E (1970). "Neuropathy in acrodermatitis chronica atrophicans - effects of treatment" (Manuscript)
I. Kindstrand E (1995). "Lyme borreliosis and cranial neuropathy" J Neurol 242(10): 658-663
Pubmed
II. Kindstrand E (1992). "Antibodies to Borrelia burgdorferi in patients with carpal tunnel syndrome" Acta Neurol Scand 86(1): 73-75
Pubmed
III. Kindstrand E, Nilsson BY, Hovmark A, Pirskanen R, Åsbrink E. (1997). "Peripheral neuropathy in acrodermatitis chronica atrophicans - a late Borrelia manifestation " Acta Neurol Scand 95(6): 338-345
Pubmed
IV. Kindstrand E, Nilsson BY, Hovmark A, Nennesmo I, Pirskanen R, Solders G, Åsbrink E (2000). "Polyneuropathy in late Lyme borreliosis - a clinical, neurophysiological and morphological description" Acta Neurol Scand 101(1): 47-52
Pubmed
V. Kindstrand E, Nilsson BY, Åsbrink E (1970). "Neuropathy in acrodermatitis chronica atrophicans - effects of treatment" (Manuscript)
Issue date: 1999-11-26
Publication year: 1999
ISBN: 91-628-3940-3
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