Peripheral neuropathy in Lyme borreliosis

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.