ABSTRACT
Small fiber neuropathy (SFN) is still unknown. Characterised by neuropathic pain, it typically begins by burning feet, but could take many other expression. SFN affects the thinly myelinated Aδ and unmyelinated C-fibers, by an inherited or acquired mechanism, which could lead to paresthesia, thermoalgic disorder or autonomic dysfunction. Recent studies suggest the preponderant role of ion channels such as Nav1.7. Furthermore, erythromelalgia or burning mouth syndrome are now recognized as real SFN. Various aetiologies of SFN are described. It could be isolated or associated with diabetes, impaired glucose metabolism, vitamin deficiency, alcohol, auto-immune disease, sarcoidosis etc. Several mutations have recently been identified, like Nav1.7 channel leading to channelopathies. Diagnostic management is based primarily on clinical examination and demonstration of small fiber dysfunction. Laser evoked potentials, Sudoscan®, cutaneous biopsy are the main test, but had a difficult access. Treatment is based on multidisciplinary management, combining symptomatic treatment, psychological management and treatment of an associated etiology.
Subject(s)
Nerve Fibers/pathology , Small Fiber Neuropathy/diagnosis , Humans , Laser-Evoked Potentials/physiology , Small Fiber Neuropathy/etiology , Small Fiber Neuropathy/therapyABSTRACT
The study of the agglutinability of Xg(a + ) cells by several examples of anti-Xga and absorption-elution tests showed that the red blood cell antigen Xga is destroyed by proteases commonly used in blood group serology but not by neuraminidase.
