{"title":"Diabetic neuropathies and pain","authors":"A.J.M. Boulton, J.D. Ward","doi":"10.1016/S0300-595X(86)80080-9","DOIUrl":null,"url":null,"abstract":"<div><p>Many of the diabetic neuropathic syndromes are characterized by painful symptoms with a sensation of burning and associated with troublesome hyperaesthesia. It is important to distinguish between the acute and chronic forms of peripheral sensory neuropathy; while the former carries an excellent prognosis for symptomatic improvement within one year, the latter may cause persistent symptoms for many years. In contrast to the acute form, in which symptoms are particularly severe but abnormal neurological signs are minimal, patchy stocking and glove sensory loss together with peripheral small muscle wasting are often present in chronic sensorimotor neuropathy. Peripheral polyneuropathies are more common in patients with poor metabolic control, although recent evidence implicates blood glucose flux as a possible contributory factor to neuropathic pain. It is possible that blood glucose flux or altered peripheral blood flow leads to increased spontaneous activity in nociceptive afferent fibres which are present in the axonal sprouts that characterize small fibre neuropathy. In the diagnosis of the neuropathies, exclusion of other aetiological factors is of paramount importance as there is no specific diagnostic test for diabetic nerve damage. If there is no symptomatic improvement after a period of stable and optimal metabolic control together with simple analgesics, then the tricyclic drugs should be regarded as first line therapy. The rapid effect of these drugs suggests a peripheral rather than central mode of action.</p></div>","PeriodicalId":10454,"journal":{"name":"Clinics in Endocrinology and Metabolism","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1986-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0300-595X(86)80080-9","citationCount":"78","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinics in Endocrinology and Metabolism","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0300595X86800809","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 78
Abstract
Many of the diabetic neuropathic syndromes are characterized by painful symptoms with a sensation of burning and associated with troublesome hyperaesthesia. It is important to distinguish between the acute and chronic forms of peripheral sensory neuropathy; while the former carries an excellent prognosis for symptomatic improvement within one year, the latter may cause persistent symptoms for many years. In contrast to the acute form, in which symptoms are particularly severe but abnormal neurological signs are minimal, patchy stocking and glove sensory loss together with peripheral small muscle wasting are often present in chronic sensorimotor neuropathy. Peripheral polyneuropathies are more common in patients with poor metabolic control, although recent evidence implicates blood glucose flux as a possible contributory factor to neuropathic pain. It is possible that blood glucose flux or altered peripheral blood flow leads to increased spontaneous activity in nociceptive afferent fibres which are present in the axonal sprouts that characterize small fibre neuropathy. In the diagnosis of the neuropathies, exclusion of other aetiological factors is of paramount importance as there is no specific diagnostic test for diabetic nerve damage. If there is no symptomatic improvement after a period of stable and optimal metabolic control together with simple analgesics, then the tricyclic drugs should be regarded as first line therapy. The rapid effect of these drugs suggests a peripheral rather than central mode of action.