A Prospective Study of Painful Symptoms, Small‐fibre Function and Peripheral Vascular Disease in Chronic Painful Diabetic Neuropathy

Abstract

Fifty diabetic patients with chronic painful sensorimotor neuropathy were studied prospectively to clarify the natural history of this condition and the roles of small-fibre damage and concomitant peripheral vascular disease (PVD). Initially, 30 patients had no significant PVD (ankle:brachial Doppler ratio > 1.0). Pain was assessed using a visual analogue scale (0-10 cm), and small-fibre function by thermal limen (TL), heat-pain threshold (HPT), and weighted pinprick threshold (PPT). At follow-up, on average 3.6 years later (range 3.0-4.1), 11 patients had died (6 with PVD) and contact had been lost with 6. Pain scores fell in subjects without PVD (n = 24; median (range), from 4.8 (0.5-10.0) to 2.0 (0.0-9.2) cm, p < 0.001) and also in those with PVD (n = 9; from 5.1 (2.0-8.2) to 2.1 (0.0-8.0) cm, p < 0.05). Seven patients (5 without PVD) became painfree; at presentation, these 7 patients had experienced pain for a shorter period of time. Despite this symptomatic improvement, small-fibre function generally deteriorated in both groups, with significant worsening (p < 0.05) of HPT and PPT in patients without PVD, and in HPT and TL in patients with PVD. Neuropathic pain therefore tends to improve with time and can resolve completely. By contrast, small-fibre function continues to deteriorate, indicating that these peripheral measures do not predict the evolution of painful symptoms. The presence or absence of PVD does not appear to affect the natural history of neuropathic pain or its symptomatology.

Virus-Mediated Knockdown of Nav1.3 in Dorsal Root Ganglia of STZ-Induced Diabetic Rats Alleviates Tactile Allodynia

“…However, others have shown that STZinduced diabetes in rats can lead to the development of heat hyperalgesia (32). The discrepancy between these findings might be explained by the multiple pathological mechanisms that contribute to the development of diabetic neuropathic pain (for example, peripheral nerve damage, secondary vascular disease, hypoxia), such that even small changes in the pathogenesis of diabetes could produce large variations in specific sensory modalities, such as heat detection (16,33,34). For example, in studies that report normal thermal sensitivity, small DRG neurons with thinly myelinated Aδ fibers or unmyelinated C-fiber afferents, which carry thermal nociceptive information, may have been minimally unaffected, whereas in other cases of diabetes, C fibers may have become more substantially affected (35).…”

Diabetic Somatic Neuropathies

“…In a study of 36 diabetic patients with chronic, painful symptoms who were followed for an average period of 4.7 years, there was no overall change in the severity of pain scores over time, and there were no full remissions in any of those followed (244). However, other studies have observed an appreciable occurrence of remissions (243,245).…”

Concurrent activation of the somatosensory forebrain and deactivation of periaqueductal gray associated with diabetes-induced neuropathic pain

“…A frequent complication of diabetes is unremitting pain and a reduced quality of life (Benbow, et al, 1994). Patients with DM may experience a variety of aberrant sensations including spontaneous pain and hypersensitivity to mechanical or thermal stimuli, followed by the long term paradoxical loss of stimulus-evoked sensation (Benbow, et al, 1994).…”