Hyperalgesia in spontaneous and experimental animal models of diabetic neuropathy.

Abstract

Hyperactivity of nociceptive C-fibers has been recently described in diabetic BB/Wistar rats. This study assesses the association of hyperalgesia, using an analgesy-meter, with elevated glycosylated haemoglobin levels in three animal models of diabetic and nutritional neuropathies: Psammomys obesus (sand rat), streptozotocin-treated and galactose-fed rats. Pain threshold measurements (paw pressure test) and motor nerve conduction velocities were recorded in controls (n = 75), hyperinsulinaemic (n = 16), insulin-deficient (n = 46) und galactosaemic (n = 12) animals. The reproducibility of the paw pressure test, evaluated by a correlation coefficient, was statistically significant (p less than 0.001). When compared with their controls (396 +/- 18 g), the average pain threshold in young diabetic sand rats (309 +/- 17 g) was found to be markedly reduced and to correlate inversely (p less than 0.001) with their respective HbA1c levels (mean 4.9 versus 7.4%). Acute, subacute and chronic streptozotocin-diabetic rats displayed a reduction of pain threshold (p less than 0.001) associated with slowed motor nerve conduction velocities (p less than 0.001). Similarly, galactose-feeding over 4 weeks resulted in an elevation of glycosylated haemoglobin levels with significant (p less than 0.001) reductions of pain threshold and motor nerve conduction velocity. It is concluded that hyperalgesia is a constant feature of sensory dysfunction in spontaneous and experimental models of diabetic neuropathy.