Saphenous nerve transfer: A new approach to restore sensation of the sole.

BACKGROUND: Loss of protective sensation of the sole may lead to repeated trauma, chronic nonhealing ulcers, and even amputation. Saphenous nerve (SN) to posterior tibial nerve (PTN) transfer can restore sensation of the sole. METHOD: This study was conducted in a tertiary referral center in Central India. Twenty-one patients (32 feet) diagnosed with loss of sensation of the sole were included in this study. Causes of loss of sensation were Hansen's disease (n = 18), complex sciatic nerve injury (n = 1), lumbosacral spinal tumor (n = 1), and lumbosacral meningomyelocele (n = 1). Seventeen feet (14 patients) had ulcers on the sole. Preoperative and postoperative sensory tests performed on the sole included tests for touch, pain, temperature, pressure, vibration, and two-point discrimination. Results were classified as per the British Medical Research Council (MRC) scoring system. RESULTS: Seventeen patients (26 feet) were available for follow-up at 6 months after surgery. All patients had improvement in sensory parameters. Ulcers completely healed in 13 feet and reduced in size in four feet. MRC score improved from S0 in 22 feet and S1 in 10 feet to S3 + in 20 feet, S3 in four feet, and S2 in two feet. CONCLUSIONS: Sensory neurotization with SN transfer to PTN can restore protective sensation to the sole and help in the healing of ulcers.

The pathway to foot ulceration in diabetes.

It should now be possible to achieve a reduction in the incidence of foot ulceration and amputations as knowledge about pathways that result in both these events increases. However, despite the universal use of patient education and the hope of reducing the incidence of ulcers in high-risk patients, there are no appropriately designed large, randomized controlled trials actually confirming that education works. It has been recognized for some years that education as part of a multidisciplinary approach to care of the diabetic foot can help to reduce the incidence of amputations in certain settings. Ultimately, however, a reduction in neuropathic foot problems will only be achieved if we remember that the patients with neuropathic feet have lost their prime warning signal­pain­that ordinarily brings patients to their doctor. Very little training is offered to health care professionals as to how to deal with such patients. Much can be learned about the management of such patients from the treatment of individuals with leprosy: if we are to succeed, we must realize that with loss of pain there is also diminished motivation in the healing of and prevention of injury.

Recent advances in the neurophysiology of chronic pain.

UNLABELLED: The chronic pain syndrome patient has become the 'leper' of emergency medicine. There are no emergency medicine guidelines and minimal research into managing this challenging group of patients. OBJECTIVE: To summarize the recent advances in laboratory research into the development of chronic pain that have relevance to emergency management. When the level of supporting evidence is low, it is imperative that emergency physicians understand the physiology that underpins those expert opinions upon which they base their treatment strategies. METHODS: Literature was searched via Medline, Cochrane, Cinahl, and PsycINFO from 1996 to 2004, under 'chronic pain and emergency management'. Medline from 1996 was searched for 'chronic pain and prevention', 'chronic pain and emergency' and 'chronic pain'. Bibliographies were manually searched for older keynote articles. RESULTS: Advances in understanding the biochemical changes of chronic pain are paralleled by lesser known advances in delineation of the corticol processing. CONCLUSIONS: Drug manipulation causes complex action and reaction in chronic pain. Emergency physicians must also optimize cognitive and behavioural aspects of treatment to successfully manage this systemic disease.

El pie en lepra

Con el siguiente artículo los autores pretenden describir las diferentes manifestaciones clínicas que pueden aparecer en la extremidad inferior, con especial atención al pie, en pacientes de lepra en todas sus formas clínicas, tanto activos como de alta terapéutica con secuelas secundarias a la enfermedad. Se describen las manifestaciones dermatológicas, neurológicas, las alteraciones tróficas, óseas y radiológicas presentes en pacientes controlados en el Sanatorio de Fontilles. Se expone la forma actual de trabajo en el campo, con la clasificación de los pacientes en Paucibacilares y Multibacilares, el tratamiento específico de la enfermedad y los cuidados locales a realizar (AU)

Do nerve growth factor-related mechanisms contribute to loss of cutaneous nociception in leprosy?

While sensory loss in leprosy skin is the consequence of invasion by M. leprae of Schwann cells related to unmyelinated fibres, early loss of cutaneous pain sensation, even in the presence of nerve fibres and inflammation, is a hallmark of leprosy, and requires explanation. In normal skin, nerve growth factor (NGF) is produced by basal keratinocytes, and acts via its high affinity receptor (trk A) on nociceptor nerve fibres to increase their sensitivity, particularly in inflammation. We have therefore studied NGF- and trk A-like immunoreactivity in affected skin and mirror-site clinically-unaffected skin from patients with leprosy, and compared these with non-leprosy, control skin, following quantitative sensory testing at each site. Sensory tests were within normal limits in clinically-unaffected leprosy skin, but markedly abnormal in affected skin. Sub-epidermal PGP 9.5- and trk A- positive nerve fibres were reduced only in affected leprosy skin, with fewer fibres contacting keratinocytes. However, NGF-immunoreactivity in basal keratinocytes, and intra-epidermal PGP 9.5-positive nerve fibres, were reduced in both sites compared to non-leprosy controls, as were nerve fibres positive for the sensory neurone specific sodium channel SNS/PN3, which is regulated by NGF, and may mediate inflammation-induced hypersensitivity. Keratinocyte trk A expression (which mediates an autocrine role for NGF) was increased in clinically affected and unaffected skin, suggesting a compensatory mechanism secondary to reduced NGF secretion at both sites. We conclude that decreased NGF- and SNS/PN3-immunoreactivity, and loss of intra-epidermal innervation, may be found without sensory loss on quantitative testing in clinically-unaffected skin in leprosy; this appears to be a sub-clinical change, and may explain the lack of cutaneous pain with inflammation. Sensory loss occurred with reduced sub-epidermal nerve fibres in affected skin, but these still showed trk A-staining, suggesting NGF treatment may restore pain sensation.

Histological and immunological correlates of suspected leprosy lesions.

Thirty-two subjects with suspected leprosy lesions were investigated to assess various modalities of sensibility and sweat function and these were correlated with immunological and histological parameters. It was found that pain and temperature, mediated by small unmyelinated fibres were impaired in the early lesions. Impairment of sweat function was seen only when one of the modalities of sensibility was also affected. Antibodies specific to a protein (35 kDa) antigen and phenolic glycolipid 1 of Mycobacterium leprae were positive in nine and 12 cases respectively, while 15 of the 31 biopsies revealed the presence of mycobacterial antigens in these lesions. The implications of these findings are discussed.

Sensory functions in limbs of normal persons and leprosy patients with peripheral trunk damage.

The threshold to touch was tested in hands and feet of normal persons using Semmes-Weinstein graded monofilament nylons. The minimum stimulus to which response could be elicited was nylon number 3.61 in palms and 4.31 in soles. These numbers relate to the logarithm of the force applied, 3.61 corresponding to 0.217 gm force and 4.31 to 2.35 gm force respectively. The area of pain insensitivity complained by the patient more or less corresponds to that revealed by objective testing. It was interesting to observe that loss of pain sensitivity was confined to a smaller area compared to touch and thermal insensibility in the part innervated by the same nerve trunk.