Motor Nerve Conduction Stuoies in Leprosy

Sohi, A. S.; Kandhari, K C; Singh, Nidhi

doi:10.1111/j.1365-4362.1971.tb03727.x

Cited by 9 publications

(5 citation statements)

References 9 publications

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“…Nerve damage in leprosy is almost exclusively studied in late disease stages; no published study describes nerve changes at the early stages of the disease. However, epidemiological surveys in endemic areas reported that nerve damage occurs even among the non-diseased leprosy contacts [ 3 ], suggesting that nerve damage might commence long before the disease manifests as skin lesions. Indeed, the natural affinity of M. leprae for nerve, particularly for Schwann cells, makes it likely that nerve damage starts at a very early stage of infection.…”

Section: Introductionmentioning

confidence: 99%

M. leprae components induce nerve damage by complement activation: identification of lipoarabinomannan as the dominant complement activator

et al. 2015

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Peripheral nerve damage is the hallmark of leprosy pathology but its etiology is unclear. We previously identified the membrane attack complex (MAC) of the complement system as a key determinant of post-traumatic nerve damage and demonstrated that its inhibition is neuroprotective. Here, we determined the contribution of the MAC to nerve damage caused by Mycobacterium leprae and its components in mouse. Furthermore, we studied the association between MAC and the key M. leprae component lipoarabinomannan (LAM) in nerve biopsies of leprosy patients. Intraneural injections of M. leprae sonicate induced MAC deposition and pathological changes in the mouse nerve, whereas MAC inhibition preserved myelin and axons. Complement activation occurred mainly via the lectin pathway and the principal activator was LAM. In leprosy nerves, the extent of LAM and MAC immunoreactivity was robust and significantly higher in multibacillary compared to paucibacillary donors (p = 0.01 and p = 0.001, respectively), with a highly significant association between LAM and MAC in the diseased samples (r = 0.9601, p = 0.0001). Further, MAC co-localized with LAM on axons, pointing to a role for this M. leprae antigen in complement activation and nerve damage in leprosy. Our findings demonstrate that MAC contributes to nerve damage in a model of M. leprae-induced nerve injury and its inhibition is neuroprotective. In addition, our data identified LAM as the key pathogen associated molecule that activates complement and causes nerve damage. Taken together our data imply an important role of complement in nerve damage in leprosy and may inform the development of novel therapeutics for patients.Electronic supplementary materialThe online version of this article (doi:10.1007/s00401-015-1404-5) contains supplementary material, which is available to authorized users.

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Section: Introductionmentioning

confidence: 99%

M. leprae components induce nerve damage by complement activation: identification of lipoarabinomannan as the dominant complement activator

et al. 2015

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“…[1] Functional derangement of nerves can be shown by nerve conduction studies before the appearance of clinical signs and symptoms of the disease. [2] Nerve damage in leprosy varies from involvement of an intradermal nerve in the cutaneous patch to a major lesion in the peripheral or the cranial nerve trunk. Neural involvement can manifest itself as enlargement of the superficial nerves such as great auricular, ulnar, median, radial cutaneous, superficial peroneal, sural, and posterior tibial which are clinically palpable against the corresponding bony prominences when thickened; associated with tenderness, in case of coexistent neuritis.…”

Section: Introductionmentioning

confidence: 99%

Nerve damage in leprosy: An electrophysiological evaluation of ulnar and median nerves in patients with clinical neural deficits: A pilot study

Kar

Krishnan

Singh

et al. 2013

Indian Dermatol Online J

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Background:Leprosy involves peripheral nerves sooner or later in the course of the disease leading to gross deformities and disabilities. Sadly, by the time it becomes clinically apparent, the nerve damage is already quite advanced. However, if the preclinical damage is detected early in the course of disease, it can be prevented to a large extent.Materials and Methods:We conducted an electrophysiological pilot study on 10 patients with clinically manifest leprosy, in the Dermatology Department of Mahatma Gandhi Institute of Medical Sciences, Sewagram. This study was done to assess the nerve conduction velocity, amplitude and latency of ulnar and median nerves.Results and Conclusion:We found reduced conduction velocities besides changes in latency and amplitude in the affected nerves. Changes in sensory nerve conduction were more pronounced. Also, sensory latencies and amplitude changes were more severe than motor latencies and amplitude in those presenting with muscle palsies. However, further studies are going on to identify parameters to detect early nerve damage in leprosy.

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“…The effect of reaction is not only limited to the affected nerves, but it also involves the clinically unaffected nerves. [ 10 11 12 13 ] The main alteration has been reported to occur in the motor nerve conduction velocities, especially in the affected nerves. [ 13 ] The reason ascribed for this decrease in motor conduction velocities has been the inflammatory edema of the granuloma producing ischemia of the nerves associated with Schwann cell dysfunction.…”

Section: Discussionmentioning

confidence: 99%

“…Since the ischemia of the nerves mainly involve the larger “a” fibers, the measurement of motor conduction velocity can be taken as an index of involvement of various nerves. [ 12 14 15 ]…”

Section: Discussionmentioning

confidence: 99%

Electrophysiological study of nerves in type-II reaction in leprosy

Singh

Gupta²,

Mukhija

et al. 2017

Indian J Dermatol

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Background:Leprosy is a chronic granulomatous infection primarily affecting the peripheral nervous system, skin and reticuloendothelial system. Cutaneous nerves are severely affected in lepra reaction and this leads to morbidity.Objective:To study electrophysiological pattern of different nerves involved in Type-II reactions in leprosy.Method:The present study was undertaken in 21 leprosy patients with Type-II reactions attending in and out-patient department of Dermatology & Venereology, B.R.D. Medical College, Gorakhpur from July 2005 to October 2006. This was a prospective case control study in which 20 healthy, age and sex matched people with no evidence of any disease (particularly nerve involvement) were included.Limitation:Lesser number of cases were studied.Result:The proximal motor conduction latency was significantly prolonged in both ulnar and common peroneal nerve and proximal motor conduction velocity was also significantly reduced. On examining the values beyond 2S.D. of the control value, distal latency was not affected and only proximal conduction was affected in ulnar nerve.Conclusion:In Type II lepra reaction the motor conduction abnormalities are not prominent. Abnormalities are relatively more marked in the proximal segment.

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Motor Nerve Conduction Stuoies in Leprosy

Cited by 9 publications

References 9 publications

M. leprae components induce nerve damage by complement activation: identification of lipoarabinomannan as the dominant complement activator

M. leprae components induce nerve damage by complement activation: identification of lipoarabinomannan as the dominant complement activator

Nerve damage in leprosy: An electrophysiological evaluation of ulnar and median nerves in patients with clinical neural deficits: A pilot study

Electrophysiological study of nerves in type-II reaction in leprosy

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