Neuropathies of leprosy

Abstract

Neuropathies form an integral part of the symptomatology of leprosy. Neuropathies of leprosy take various forms and shapes. At one end is the cutaneous nerve involvement adjacent to the anaesthetic skin patch and the other is of symmetrical pansensory neuropathy and the devastating sensory ataxia of leprous ganglionits. Lepra reactions add to the spectrum. Hosts immunological status largely decides the clinical manifestations seen in nerves and skin. A wide array of diagnostic techniques like ultrasonography, magnetic resonance neurography, serological markers, molecular tests, skin biopsy and in selected cases, the nerve biopsy with special stains and electron microscopy are obtainable to help the clinical diagnosis. The unsuspecting clinician, lack of community awareness and limited availability of diagnostic tests are important adverse factors in the total outcome. Multi drug therapy is efficacious and corticosteroids reduce the impact of nerve damage in leprosy. The efficacy, dose and duration of corticosteroid therapy are presently inexact and other immune suppressants like azathioprine are being evaluated. Chronic disabilities and residual deficits require attention of multiple specialties. In the coming time, focus on prevention could lead to favourable results. This review will discuss the classification systems, common and uncommon clinical features, diagnostic armamentarium and therapeutic and preventive aspects of neuropathies of leprosy.

Lesão neural hansênica: Papel da neurotrofina NGF e da citocina TNFα

“…O comprometimento dos nervos periféricos é a principal consequência da hanseníase e está presente em todas as suas formas clínicas, desde a mais inicial, como a indeterminada, até as formas polares, como tuberculoide e lepromatosa. Sua fisiopatologia é obscura, devido às limitações apresentadas pelo modelo hansênico experimental, e varia de acordo com a forma clínica que o paciente apresenta (Khadilkar et al, 2021 nervos periféricos e células de Schwann induzem uma resposta imune mediada por macrófagos e outras células que eventualmente são responsáveis pelo aparecimento de lesões imuno-mediadas. Neste contexto, citocinas como TNFα, IL-6, e IL-17, podem contribuir para evolução da lesão neural (T. L. S. Aarão, de Sousa, Botelho, Fuzii, & Quaresma, 2016).…”

“…A Reação do tipo II ocorre preferencialmente em pacientes que apresentam as formas clínicas BL e LL e desenvolvem resposta Th2 associada com presença de imunocomplexos circulantes e depositados nos tecidos. Observa-se o aparecimento de novas lesões de pele eritematosas e nódulos sensíveis na face, extremidades e tronco, além de manifestações sistêmicas como febre, artrite, linfadenopatia, orquite, iridociclite e neurite grave (Geluk, 2018;Khadilkar, Patil, & Shetty, 2021).…”

The Interplay Between Neuroinfections, the Immune System and Neurological Disorders: A Focus on Africa

“…Both the innate and adaptive immune systems are involved in nerve damage during leprosy (246). Mycobacterium leprae invades and/or activates immune cells such as macrophages and T cells as well as Schwann cells, which contribute to the nerve damage that occurs during leprosy (245)(246)(247). The bacteria also infect the nerves and cause an inflammatory process that leads to the damage and the thickening of nerves in about 40 to 75% of infected individuals, which is painful most of the time (245).…”

Peripheral nerve sonography, a novel technique for improving the diagnosis of Hansen’s neuropathy

“…Pure neuritic leprosy, silent neuropathy, leprous ganglionitis and acute neuritis during lepra reactions may also occur. 2 Traditionally, the diagnosis of leprosy relies on the presence of at least one of the three cardinal signs which are hypo-aesthetic skin lesions, thickened nerves and acid-fast bacilli in skin smears. While each of these cardinal signs individually has high sensitivity and specificity, errors arise when they are not correctly identified due to incomplete, inadequate or superficial clinical examination.…”

“…At the tuberculoid end of the spectrum, nerve enlargement occurs because of granulomatous inflammation, while at the lepromatous end, infiltration of nerve fascicles with or without caseous necrosis underlies nerve enlargement. 2…”