Peripheral neuropathic localized pain as for instance in PDN and SFN, is characterized by hyperexcitability of nociceptors, which can be inhibited by sodium channel blockers. Such hyperexcitability is based on reduced receptor threshold of the C nociceptor, leading to spontaneous discharges and to intensified nociceptor responses in response to stimulation. These phenomena lead to the classical symptoms of mechanical and heat allodynia and spontaneous burning or stinging pain [1]. These symptoms reduce the quality of sleep and life of patients suffering from painful peripheral neuropathies. The burning sensations in general seems to suggest involvement of small fibers, even in forms of compression neuropathy [2]. SFN is increasingly recognized as one of the major pathogenetic disturbances leading to burning and stinging pain in many peripheral neuropathic syndromes. Diabetes mellitus is the main cause of SFN. Glucose intolerance and the metabolic syndrome are also associated with SFN. In CIAP, sarcoidosis, Lyme disease, HIV and amyloidosis, SFN can develop [3]. Alcohol is the main toxic agent inducing SFN. SFN is therefore a secondary complication in many internal and neurological disorders. The diagnosis CIAP is dependent on the clinical impression, a length dependent neuropathy, including disturbances of the electromyography. In many CIAP patients there are complaints of burning pain, comparable to patients suffering from SNF. This supports a possible comparable pathogenesis in both groups. The diagnosis SFN rests on the clinical impression, a normal electromyography and a reduction of the small nerve fibers, as detected via a skin biopsy [4]. In indications as PDN, CIAP and perhaps also in PHN subgroups of patients therefore might be identified as suffering from SFN.