Experimental chronic entrapment of the sciatic nerve in adult hamsters: an ultrastructural and morphometric study

Abstract

Entrapment neuropathy is a group of clinical disorders involving compression of a peripheral nerve and interference with nerve function mostly through traction injury. We have investigated the chronic compression of peripheral nerves as an experimental procedure for detecting changes in ultrastructural nerve morphology. Adult hamsters (Mesocricetus auratus, N = 30) were anesthetized with a 25% pentobarbital solution and received a cuff around the right sciatic nerve. Left sciatic nerves were not operated (control group). Animals survived for varying times (up to 15 weeks), after which they were sacrificed and both sciatic nerves were immediately fixed with a paraformaldehyde solution. Experimental nerves were divided into segments based upon their distance from the site of compression (proximal, entrapment and distal). Semithin and ultrathin sections were obtained and examined by light and electron microscopy. Ultrastructural changes were qualitatively described and data from semithin sections were morphometrically analyzed both in control and in compressed nerves. We observed endoneurial edema along with both perineurial and endoneurial thickening and also the existence of whorled cell-sparse structures (Renaut bodies) in the subperineurial space of compressed sciatic nerves. Morphometric analyses of myelinated axons at the compression sites displayed a remarkable increase in the number of small axons (up to 60%) in comparison with the control axonal number. The distal segment of compressed nerves presented a distinct decrease in axon number (up to 40%) comparatively to the control group. The present experimental model of nerve entrapment in adult hamsters was shown to promote consistent histopathologic alterations analogous to those found in chronic compressive neuropathies.

Immunohistochemical characterization of Renaut bodies in superficial digital nerves: further evidence supporting their perineurial cell origin

“…More than 120 years ago, Renaut himself thought they may act as ‘supportive and protective cushions’ for the nerve ( Renaut, 1881; 1899 ) , yet their precise function remains unknown. They may represent a secondary reaction to trauma because mechanical factors have been linked with their development ( Neary et al, 1975; Ortman et al, 1983; Mackinnon et al, 1986; Prinz et al, 2003; 2005 ) .…”

Periferik Sinirde Kronik Konstrüksiyon Hasarı Tedavisi Üzerine Dekompresyonun Etkisi

“…Similar microscopic findings have been reported with CCI injury in the rat, with massive degeneration of large myelinated fibers and less severe changes in small myelinated fibers and unmyelinated fibers [24][25][26] . Later Prinz et al [10] , have reported the ultrastructural changes of peripheral nerve lesions induced by chronic compression using an experimental model by light and electron microscopy myelinated axons at the compression sites displayed a remarkable increase in the number of small axons up to 60% in comparison with the normal axons. Additionally, remarkable axonal degeneration was obswerved both in central and in marginal regions of the distal to the constriction.…”

“…The injury is characterised behaviorally as mechanical allodynia and thermal hyperalgesia after a few day of the lesion. While some neurotransmitters such Substance P,CGRP and pERK play role in development of neuropathic pain [9,15] morphological changes may occur at the injury site of sciatic nerve [10,[16][17][18] , endorgan [8] or dorsal horn [9,15] which is central terminals of for nociceptive information and DRG [11] . Neuropathic pain is treated with drugs symptomatically in clinical practice [19,20] and also various agents were tested experimentally after CCI established in animals [21,22] .…”

“…carpal tunel syndrome, spinal root compression, and trigeminal neuralgia due to vascular compression [8] . Few studies have investigated the molecular mechanisms of CCI and decompression [9] whereas some studies evaluated morphological changes [10][11][12] . However experimental evidence on neuropathic pain and CCI is still lacking.…”

Proliferative and Nonproliferative Lesions of the Rat and Mouse Central and Peripheral Nervous Systems: New and Revised INHAND Terms

“…Comment: Renaut bodies have been reported in many mammals, including such common test species as rats but especially Beagle dogs (Figure 7). In rodents, the incidence of Renaut bodies as a spontaneous change is low, but their frequency may be augmented by experimental surgery 34 or manipulating housing conditions 35 to produce chronic nerve compression. In nonrodents, Renaut bodies have been observed in 2% of human superficial peroneal nerve biopsies 36 and in 36% or more of dogs in general toxicity studies, 31 suggesting that they may be a normal feature of nerve anatomy under certain conditions.…”