Peripheral neuropathy in acrodermatitis chronica atrophicans - effect of treatment

Abstract

Forty-seven patients with the late borrelial manifestation acrodermatitis chronica atrophicans (ACA) and with objective neurological and/or neurophysiological findings were followed up after antibiotic treatment with dermatological, serological, neurological and neurophysiological controls. Despite a good therapeutic effect on ACA lesions, specific antibody values and symptoms of irritative nerve lesions, the objective neurological and neurophysiological findings of nerve deficit remained unchanged. There was no progress of neuropathy findings during the follow-up time. Our interpretation of the results is that the remaining neuropathy signs after treatment of ACA are neurological sequelae and not manifestations of persisting Borrelia infection.

Therapy of Lyme Disease

“…Albeit there is no high quality evidence, the outcomes of the oral and the intravenous therapeutic strategy seem to be comparable. Indeed, a Swedish study on over 40 patients suffering from acrodermatitis chronica atrophicans and late neuroborreliosis with peripheral involvement showed a similar response rate on neurological manifestations between a group (21 patients) receiving oral doxycycline for 3 weeks and a group (21 patients) receiving intravenous penicillin for 2 weeks followed by oral doxycycline for other 2 weeks [50]. Similarly, another analysis of 10 patients with late neuroborreliosis with peripheral involvement showed equal improvement after 14 days of oral doxycycline as after 14 days of intravenous ceftriaxone [31].…”

“…According to some authors, intravenous penicillin (20 million U daily for 10 days) is a possible parenteral alternative to ceftriaxone [23,27,50]. Albeit there is no high quality evidence, the outcomes of the oral and the intravenous therapeutic strategy seem to be comparable.…”

A critical appraisal of the mild axonal peripheral neuropathy of late neurologic Lyme disease

“…Other neurologic conditions have been categorized by some as late neurologic manifestations (Table 1) (Fallon et al, 2008; Halperin et al, 1987, 1990; Hopf, 1975; Kindstrand et al, 1997, 2000, 2002; Kristoferitsch et al, 1988; Logigian and Steere, 1992; Logigian et al, 1990; Mygland et al, 2006, 2010; Steere et al, 1994; Wormser et al, 2006). Although it is somewhat arbitrary as to what time frame differentiates early from late onset neurologic manifestations of Lyme disease, neurologic manifestations that arise at the same time as, or after the onset of, recognized late manifestations, such as Lyme arthritis (Logigian et al, 1990; Steere et al, 1994) or acrodermatitis chronica atrophicans (ACA) (Stanek et al, 2012), certainly would be regarded as late neurologic manifestations.…”

“…Although it is somewhat arbitrary as to what time frame differentiates early from late onset neurologic manifestations of Lyme disease, neurologic manifestations that arise at the same time as, or after the onset of, recognized late manifestations, such as Lyme arthritis (Logigian et al, 1990; Steere et al, 1994) or acrodermatitis chronica atrophicans (ACA) (Stanek et al, 2012), certainly would be regarded as late neurologic manifestations. For example, more than 40% of patients with ACA develop a sensory peripheral neuropathy (Hopf, 1975; Kindstrand et al, 1997, 2000, 2002; Kristoferitsch et al, 1988; Mygland et al, 2006). Although this neuropathy may or may not be restricted to the limb with the ACA skin lesion, when the neuropathy occurs in a location other than the ipsilateral limb, it is typically less severe, indicating that it is usually not a symmetric distal neuropathy (Hopf, 1975; Kristoferitsch et al, 1988).…”

“…Although this neuropathy may or may not be restricted to the limb with the ACA skin lesion, when the neuropathy occurs in a location other than the ipsilateral limb, it is typically less severe, indicating that it is usually not a symmetric distal neuropathy (Hopf, 1975; Kristoferitsch et al, 1988). The neuropathy that occurs in association with ACA does not respond to any form of antibiotic treatment, but (oral) antibiotic therapy will prevent further progression (Hopf, 1975; Kindstrand et al, 2002; Kristoferitsch et al, 1988). …”