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Introduction Neuropathic pain is a common and disabling late complication of leprosy. We investigated the clinical and electrophysiological characteristics of neuropathic pain in leprosy patients by evaluating nerve conduction, sympathetic skin response (SSR) and A-waves. Methods Twenty one leprosy patients with neuropathic pain validated by the Douleur Neuropathique en 4 (DN4)Questionnaire were selected for study. Pain intensity was measured by the visual analog scale. Demographic and clinical data were collected for all patients. Clinical data included appraisal of the median, ulnar, radial, tibial and common peroneal nerves, assessment of the sympathetic skin response and conventional electrophysiological recordings. Results Among all electroneuromyographic presentations, multifocal mononeuropathy was still the most prevalent. Sensory loss was observed more frequently than motor deficits. As most patients presented advanced clinical forms of leprosy and were under treatment, this high mean was found and the ulnar nerve was most frequently affected. The sympathetic skin response was absent in 16 patients. Higher DN4 Questionnaire scores were observed in women and in those receiving corticosteroid therapy. These inferences are possible to be made, but our study's limitations don't allow us to be certain about it. The statistical significance found only permits us to evidence what we related on the textual part of the study. Limitations The small number of patients studied, the lack of sophisticated diagnostic methods for leprosy, as well as the difficulties in assessing nerve conduction were the main limitations of this study. Conclusion The neurophysiological and clinical findings in leprous neuropathy were modest despite the conspicuous neuropathic pain. Although electrophysiological studies are a vital tool to verify nerve damage, variations in the clinical presentation of leprosy neuropathic pain render the diagnosis challenging. Further studies are needed to describe the neurophysiological evolution of this disease. [ABSTRACT FROM AUTHOR]

Background: Peripheral nerve disease may lead to physical disability because of decreased muscle strength and/or loss of sensitivity in the dermatomes of affected peripheral nerves. Both human immunodeficiency virus (HIV)- and leprosy-affected patients can develop neurological damage; therefore, the coinfection of these diseases presents new challenges to the health care of these patients., Aims and Objective: This study aimed to investigate the motor alterations of patients coinfected with HIV and leprosy and their relationship with clinical and anthropometric characteristics, compared with individuals with isolated diseases., Materials and Methods: In this cross-sectional study, 90 individuals were divided equally into three groups: HIV/acquired immunodeficiency syndrome (AIDS) group, leprosy group and HIV/leprosy group. All individuals underwent an evaluation of muscle strength and upper limb endurance adjusted for the Brazilian standards, a palm print pressure test using a digital dynamometer and anthropometric measurements (weight, height and skin folds)., Results: The HIV/leprosy group had the highest mean body mass index, followed by the leprosy group and the HIV/AIDS group. Skinfolds were similar between the groups. Multiple linear regression, adjusted for sex and age, revealed the coinfection of HIV and leprosy as possible contributor to a worse prognosis of muscle function, highlighting the bilateral reduction in the levels of palm print compression strengths compared with isolated diseases (HIV and leprosy). High CD4 count and shorter antiretroviral therapy duration were associated with worse indices of muscle strength, such as gripping and resistance, in coinfected patients., Conclusion: Patients coinfected with HIV and leprosy exhibited greater motor damage than those with isolated diseases. Thus, motor damage may be related to the sum of the neurological manifestations of the two morbidities., Competing Interests: There are no conflicts of interest., (Copyright: © 2023 Indian Journal of Dermatology.)

Introduction Neuropathic pain is a common and disabling late complication of leprosy. We investigated the clinical and electrophysiological characteristics of neuropathic pain in leprosy patients by evaluating nerve conduction, sympathetic skin response (SSR) and A-waves. Methods Twenty one leprosy patients with neuropathic pain validated by the Douleur Neuropathique en 4 (DN4)Questionnaire were selected for study. Pain intensity was measured by the visual analog scale. Demographic and clinical data were collected for all patients. Clinical data included appraisal of the median, ulnar, radial, tibial and common peroneal nerves, assessment of the sympathetic skin response and conventional electrophysiological recordings. Results Among all electroneuromyographic presentations, multifocal mononeuropathy was still the most prevalent. Sensory loss was observed more frequently than motor deficits. As most patients presented advanced clinical forms of leprosy and were under treatment, this high mean was found and the ulnar nerve was most frequently affected. The sympathetic skin response was absent in 16 patients. Higher DN4 Questionnaire scores were observed in women and in those receiving corticosteroid therapy. These inferences are possible to be made, but our study's limitations don't allow us to be certain about it. The statistical significance found only permits us to evidence what we related on the textual part of the study. Limitations The small number of patients studied, the lack of sophisticated diagnostic methods for leprosy, as well as the difficulties in assessing nerve conduction were the main limitations of this study. Conclusion The neurophysiological and clinical findings in leprous neuropathy were modest despite the conspicuous neuropathic pain. Although electrophysiological studies are a vital tool to verify nerve damage, variations in the clinical presentation of leprosy neuropathic pain render the diagnosis challenging. Further studies are needed to describe the neurophysiological evolution of this disease.