The contribution of ischaemia and deformation to the conduction block generated by compression of the cat sciatic nerve

Abstract

SUMMARYThe pattern of conduction block induced in cat peripheral nerve by compression has been investigated electrophysiologically by recording unitary action potentials. A degree of compression, associated with chronic compression disorders in man, was applied to the cat sciatic nerve and resulted in a conduction block typified by early failure of the slow conducting myelinated axons. By contrast, a greater degree of compression, a degree more likely to result in acute compression lesions, produced a different pattern of effect, inducing early conduction failure in the fast conducting myelinated axons. These results are related to earlier studies which have shown that nerve deformation during compression has a differential action upon fast myelinated axons, while nerve ischaemia has a differential action upon slow myelinated axons.

Dehydroepiandrosterone as an enhancer of functional recovery following crush injury to rat sciatic nerve

“…14 It is known that following crush injury, compressive forces around the nerve may invaginate the myelin sheaths at the nodes of Ranvier. 20 The functional and morphological deterioration become worse due to crushrelated ischemia. With long-standing pressure, oxygen depletion may increase the permeability of the endothelium of the endoneural capillaries, leading to increased edema and the creation of endoneural compartment syndrome.…”

Pathophysiology of Peripheral Nerve Injury During Regional Anesthesia

“…The initial effect of direct compression of the nerve by the tourniquet is failure of transmission by fast conducting myelinated fibers. 52 Prolonged nerve dysfunction results from damage to the portion of the nerve under the edge of the pneumatic cuff, where the mechanical distortion of the nerve is maximal. Irreversible damage, including substantial distortion of myelin lamellae and axonal shrinkage, may ensue as early as 2 to 4 hours after tourniquet inflation,53 and predominantly affects large diameter neurons.54 Thus, the main findings of tourniquet-induced neuropathy are motor loss and diminished touch, vibration, and position sense, with preserved senses of heat, cold, and pain and the absence of spontaneous paresthesias.55 One may minimize nerve damage by using wide cuffs and inflation pressures just adequate for arterial occlusion, 56 but periodic deflation of the cuff (even as much as 10 minutes down every hour) has no beneficial effects on the compression trauma.…”

Work-Related Musculoskeletal Disorders of the Hand and Wrist: Epidemiology, Pathophysiology, and Sensorimotor Changes

“…In acute studies of anoxia, axonal conduction began to fail after approximately 11 minutes. 39,48 Pressures as low as 20 to 30 mm Hg reduce nerve blood flow, 94 so it is likely that the pressures observed in the carpal tunnel of patients with CTS (mean, 32 mm Hg) 55 may limit nerve perfusion. Motor conduction latency decreased immediately upon surgical release in patients with CTS, suggesting that pressure in the tunnel had restricted nerve perfusion prior to surgical release.…”