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.

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.