Effects of decompression on behavioral, electrophysiologic, and histomorphologic recovery in a chronic sciatic nerve compression model of streptozotocin-induced diabetic rats

Abstract

Purpose: To determine susceptibility to decompression surgery in diabetic and nondiabetic peripheral neuropathy using a chronic compression neuropathy model.

Materials and methods: Twenty-four streptozotocin-induced diabetic rats were randomly divided into three groups: group I, chronic compression of the left sciatic nerve for 4 weeks with decompression; group II, similar without decompression; and group III, sham exposing the sciatic nerve only. The other 24 nondiabetic rats were assigned to groups IV-VI, which received compression-decompression, compression, and the sham operation, respectively. Mixed-nerve-elicited somatosensory evoked potentials (M-SSEPs) and compound muscle action potentials (CMAPs) were measured to verify the compression neuropathy in the posttreatment follow-up. Behavioral observations in thermal hyperalgesia tests were quantified before electrophysiologic examinations. Treated and contralateral nerves were harvested for histomorphologic analysis.

Results: Chronic compression of sciatic nerve induced significant reduction of amplitude and increment of latency of M-SSEP and CMAP in both diabetic and nondiabetic rats. Diabetic group changes were more susceptible. Decompression surgery significantly improved both sensory and motor conduction, thermal hyperalgesia, and the mean myelin diameter of the rat sciatic nerve in both diabetic and nondiabetic groups. Near full recovery of motor and sensory function occurred in the nondiabetic rats, but not in the diabetic rats 8 weeks postdecompression.

Conclusion: Behavioral, electrophysiologic, and histomorphologic findings indicate that decompression surgery is effective in both diabetic and nondiabetic peripheral neuropathy.

Keywords: compression; decompression; diabetes; rat; sciatic nerve; streptozotocin.

Figure 1

Representative compression–decompression tracings of M-SSEP of STZ-induced diabetic rats (group I) and nondiabetic rats (group IV). Note that the amplitude improved in both groups but was more significant in group IV. Abbreviations: M, months; M-SSEP, mixed-nerve-elicited somatosensory evoked potential; Op, operation day; STZ, streptozotocin; w, weeks.

Figure 2

Representative compression–decompression CMAP tracings in the STZ-induced diabetic rats (group I) and nondiabetic rats (group IV). Note that the amplitude improved in both groups but was more significant in group IV. Abbreviations: CMAP, compound muscle action potential; M, months; Op, operation day; STZ, streptozotocin; w, weeks.

Figure 3

Micrograph images of the sciatic nerve of a nondiabetic rat (A), a diabetic rat with compression only (B), and a nondiabetic rat with compression only (C). There was evidence of demyelination found in the diabetic and nondiabetic rats in the compression-only groups. Scale bar: 20 µm.

Figure 4

Micrograph images of the sciatic nerve of a nondiabetic rat (A–C) and a diabetic rat (D–F). (A, D) Compression for 4 weeks and the release groups. (B, E) The compression-only groups. (C, F) The sham surgery groups. The nondiabetic rat experiments indicated that the 4-week nerve compression-only group revealed numerous small diameter myelin that were not present in the 4-week compression and release group. The diabetic rat experiments indicated that the 4-week compression-only group showed massive deconstruction and decreased myelin thickness compared with the sham surgery group. The small diameter myelin slightly increased in the diabetic 4-week compression and release group. Scale bar: 20 µm.

Figure 5

The ratio of different diameters of myelin counted in each experimental group. Notes: **P<0.05. Group I: diabetic compression-decompression; II: diabetic compression; III: diabetic sham; IV: nondiabetic compression-decompression; V: nondiabetic compression; VI: nondiabetic sham.