![]() ![]() ![]() On neurological examination, impaired small fiber sensations can be detected, including thermal or pinprick hypoesthesia or hyperalgesia, and allodynia to mechanical stimulations. However, the underlying mechanisms leading to the axonal degeneration of small-diameter sensory nerves remain unclear. Recently, gain-of-function mutations of the sodium channels have been found to enhance the excitability of dorsal root ganglion neurons, which may explain the presence of neuropathic pain symptoms in patients with SFN. The pathogenesis of the development and maintenance of SFN is not completely understood. Despite being regarded as a distinct nosologic entity, SFN is either idiopathic or associated with a heterogeneous group of diseases. The natural course of SFN is highly variable, and, in some cases, large fiber neuropathy may develop. Usually, symptoms have a length-dependent distribution, but they may also present in a non-length-dependent manner. The most common clinical feature of SFN is neuropathic pain, which is often described as burning, shooting, tingling, and even pruritic. This debilitating condition usually leads to alterations in nociceptive processing, thermal sensations, and autonomic functions. Small fiber neuropathy (SFN) results from impairment of small-diameter myelinated Aδ- and unmyelinated C-fibers. ![]()
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