• J-P Lefaucheur.
• EA 4391, excitabilité nerveuse et thérapeutique, faculté de médecine de Créteil, université Paris-Est Créteil, 8, rue du Général-Sarrail, 94000 Créteil, France; Service de physiologie-explorations fonctionnelles, hôpital Henri-Mondor, Assistance publique-Hôpitaux de Paris, 51, avenue du Maréchal-de-Lattre-de-Tassigny, 94010 Créteil cedex, France. Electronic address: jean-pascal.lefaucheur@hmn.aphp.fr.
• Rev Neurol France. 2014 Dec 1;170(12):825-36.

AbstractIt is customary to consider that a purely sensory and painful neuropathy accompanied by normal electroneuromyographic examination may be or must be a small fiber neuropathy. This leads to perform specific tests, such as measuring the intra-epidermal nerve fiber density on skin biopsy or neurophysiological tests, such as evoked potentials to noxious stimuli (laser) or quantification of thermal sensory thresholds. However, these tests are only sensitive to the loss of small fibers (A-delta and C), which does not reflect the mechanisms responsible for peripheral neuropathic pain. Selective loss of small sensory fibers inherently generates a sensory deficit that does not necessarily present a painful character. Also, assigning the cause of a painful neuropathy to a small fiber neuropathy has no pathophysiological sense, although there are indirect links between these two conditions. In fact, it is not possible to explain univocally peripheral neuropathic pain, which reflects complex and diverse mechanisms, involving different types of nerve fibers. In this context, the clinical and laboratory approach must be improved to better understand the underlying mechanisms. It is imperative to interpret the data provided by laboratory tests and to correlate these data to the clinical signs and symptoms presented by the patients. Thus, one must go beyond many a priori and misinterpretations that unfortunately exist in this area at present and are not based on any solid pathophysiological basis.Copyright © 2014 Elsevier Masson SAS. All rights reserved.

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