Effects Of Nerve Compression Research Articles

Incidental Ultrastructural Findings in the Sural Nerve and Dorsal Root Ganglion of Aged Control Sprague Dawley Rats in a Nonclinical Carcinogenicity Study.

Xenobiotic-induced peripheral nerve damage is a growing concern. Identifying relative risks that a new drug may cause peripheral nerve injury over long periods of administration is gathering importance in the evaluation of animal models. Separating out age-related changes in peripheral nerves of rats caused by compression injury from drug-induced effects has been difficult. Biopsy of the sural nerve is utilized in humans for investigations of peripheral neuropathy, because it is largely removed from the effects of nerve compression. This study used transmission electron microscopy to identify incidental findings in the sural nerves and dorsal root ganglia of aged control rats over time. The goal was to establish a baseline understanding of the range of possible changes that could be noted in controls compared to rats treated with any new investigative drug. In this evaluation, most sural nerve fibers from aged control rats had few ultrastructural abnormalities of pathologic significance. However, glycogenosomes, polyglucosan bodies, swollen mitochondria, autolysosomes, split myelin, Schwann cell processes, and endoneural macrophages with phagocytosed debris (considered an indication of ongoing degenerative changes) were occasionally noted.

Upper Extremity Nerve Entrapments

Nontraumatic pain in the shoulder, arm, and hand (brachialgia) is a common complaint in the field of musculoskeletal disorders, where nerve entrapment constitutes a possible cause. The effect of nerve compression is dose-dependent; thus, a low-level compression will only result in decreased endoneurial circulation, neural edema, and a Seddon grade IV weakness, but will not be revealed in nerve conduction or magnetic resonance imaging studies. Because of technical limitations, several clinical options to diagnose compression neuropathies in the upper extremity have been proposed. These include blinded controlled studies on manual muscle testing to delineate the level of nerve compression, and the scratch collapse test to verify the level of compression. In this article, the authors describe the clinical examination and surgical techniques for diagnosing and treating entrapments of the axillary and radial nerves. A previously published clinical triad for diagnosis of nerve compressions has been used: (1) manual muscle testing to reveal weakness in specific muscles distal to the level of nerve compression; (2) pain on compression and/or positive Tinel sign; and (3) positive scratch collapse test at the level of nerve compression. Detailed videos illustrate the examination techniques for diagnosing axillary entrapment in the shoulder and radial nerve entrapments in the upper arm and forearm (four levels), and the surgical techniques for each nerve release. The clinical triad of muscle testing, scratch-collapse test, and pain at the level of nerve compression provides the clinician with a clinical foundation for analyzing patients with brachialgia in a structured fashion.

The effect of nerve compression and capsaicin on contact heat-evoked potentials related to Aδ- and C-fibers

Brief noxious heat stimuli activate Aδ- and C-fibers and allow contact heat-evoked potentials (CHEPs) to be recorded from the scalp. Under normal conditions, only late responses related to Aδ-fibers can be recorded. This study aimed to demonstrate C-fiber responses to contact heat stimuli. A preferential A-fiber compression blockade of the superficial radial nerve was applied in 22 healthy subjects. Quality and intensity of heat-evoked pain and CHEPs were examined at baseline, during nerve compression, and during nerve compression with simultaneous application of topical capsaicin (5%). During the A-fiber block, three subjects had CHEPs with latencies below 400ms, eight subjects within 400–800ms and six subjects (29%) later than 800ms. Pain intensity to contact heat stimuli after compression was reduced and fewer subjects reported the heat stimuli as stinging. Following nerve compression and capsaicin application, ultralate CHEPs with latencies >800ms could be recorded in 13 subjects (62%), pain intensity to the contact heat stimuli was increased and the warm/hot-burning pain quality became more intense. The main results of our study are the demonstration of ultralate C-fiber-related CHEPs following A-fiber blockade in 29% of healthy subjects increasing to 62% when the blockade was combined with capsaicin. After blockade of Aδ-fibers we recorded responses with latencies in the range between the latencies of Aδ- and C-fibers suggesting release of Aδ-fibers with slower conduction velocity than normally recorded with CHEPs.

The effect of nerve compression and capsaicin on contact heat evoked potentials (CHEPs) related to Aδ and C fibers

Abstract Background/aims Brief noxious heat stimuli activate Aδ and C fibers, and contact heat evoked potentials (CHEPs) can be recorded from the scalp. Under standard conditions, late responses related to AS fibers can be recorded. This study examines C-fiber responses to contact heat stimuli. Methods A preferential A-fiber blockade by compression to the superficial radial nerve was applied in 22 healthy subjects. Quality and intensity of heat evoked pain (NRS, 0–10), and CHEPs were examined at baseline, during nerve compression, and during further nerve compression with topical capsaicin (5%). Results During the A-fiber blockade, 3 subjects had CHEPs with latencies below 400 ms, 8 subjects within 400–800 ms and 6 subjects later than 800 ms. Pain intensity to contact heat stimuli was reduced and fewer subjects reported the heat stimuli as stinging. Following acute capsaicin application, ultralate CHEPs with latencies >800 ms could be recorded in 13 subjects, pain intensity to the contact heat stimuli was increased (p <0.01) and more subjects reported the heat stimuli as being more warm/hot-burning. Conclusion The results indicate that following a compression to the superficial radial nerve, CHEPs compatible within complete A fibers or C fibers were recorded. Following sensitization with capsaicin, C-fiber responses were recorded in 62% of subjects.

Recurrent Blistering of the Fingertips as a Sign of Carpal Tunnel Syndrome: An Effect of Nerve Compression

Recurrent Blistering of the Fingertips as a Sign of Carpal Tunnel Syndrome: An Effect of Nerve Compression

Effects of nerve compression or ischaemia on conduction properties of myelinated and non-myelinated nerve fibres. An experimental study in the rabbit common peroneal nerve.

Compound action potentials of both myelinated (A) and non-myelinated (C) fibres in the common peroneal nerve of rabbits were studied during and after acute, graded compression of the nerve at 200 or 400 mmHg applied for 2 h or during ischaemia created by nitrogen inhalation or aortic occlusion. Compression of the nerve at 200 mmHg blocked the AI component (large myelinated fibres) after about 23 min, while compression at 400 mmHg shortened this time to 11 min. The A2 component (thinner myelinated fibres) had a lower conduction velocity and a higher resistance to compression. There was just a slight decrease in conduction velocity of the non-myelinated fibres when the nerves were compressed at 200 mmHg for 2 h. However, compression at 400 mmHg for 2 h induced a marked deterioration of amplitude and conduction velocity of the C-fibres. There was an incomplete restitution of function of A- and C-fibres during 2 h of recovery. The thinner myelinated fibres were more susceptible to deprivation of oxygen than the thicker ones, while non-myelinated fibres differed in response according to method of ischaemia induction. It is concluded that non-myelinated fibres are very resistant to compression and a very high pressure (greater than 400 mmHg) is needed to affect these fibres.

Effects of nerve compression on fast axonal transport in streptozotocin-induced diabetes mellitus

The hypothesis that nerves in diabetes mellitus exhibit an increased susceptibility to compression was experimentally tested. Inhibition of fast axonal transport was induced by local compression in sciatic nerves of rats with streptozotocin-induced diabetes mellitus. Fast anterograde axonal transport was measured after application of 3H-leucine to the motor neurone cell bodies in the spinal cord. The sciatic nerve was subjected to local, graded compression in vivo by a small compression chamber. The amount of accumulation of proteins was quantified by calculation of a transport block ratio. Compression at 30 mm Hg for 3 h induced a significantly greater (p less than 0.05) accumulation of axonally transported proteins at the site of compression in nerves of diabetic animals (transport block ratio: 1.01 +/- 0.35; n = 7) than in nerves of controls (0.67 +/- 0.16; n = 7). Accumulation was significantly higher in ligature experiments of both control (1.34 +/- 0.44; n = 8; p less than 0.01) and diabetic animals (1.45 +/- 0.30; n = 8; p less than 0.05), indicating that the block of transport in compressed nerves was incomplete. Neither sham compressed diabetic (0.50 +/- 0.09; n = 6) nor control (0.49 +/- 0.11; n = 6) nerves showed any block of axonal transport. The possible causes of the increased inhibition of fast axonal transport in diabetic rats are discussed. The results indicate that diabetes may lead to an increased susceptibility of peripheral nerves to compression.

Effect of nerve compression on the morphogenesis of the cholinesterase containing structures of the rat myoneural junction.

The sciatic nerve of the newborn rat was unilaterally compressed to cause temporary denervation and subsequent re-innervation of immature myoneural junctions prior to the development of postsynaptic infoldings in the rat tibialis anterior muscle. Subsequent changes in the postsynaptic structure were followed by histochemical demonstration of acetylcholinesterase activity.

Effect of Nerve Compression on Wallerian Degeneration in Vitro.

Effect of Nerve Compression on Wallerian Degeneration in Vitro.