Structural alterations of nerve during cuff compression.

Abstract

Whether compression nerve injury is due to ischemia, direct mechanical injury, or both remains unsettled. To assess structural changes of nerve during compression, peroneal nerves of rats were compressed at various pressures for different times, and the structural alterations were stopped by simultaneous in situ and perfusion fixation. The structural changes observed during a few minutes of compression cannot be explained by ischemic injury because the pathologic alterations characteristic of ischemia take many hours to develop and in any case are different from the ones found here. The pressure-and time-related structural changes observed in the present study under the cuffwere (i) decrease in fascicular area and increase in fiber density due to expression of endoneurial fluid; (i) compression and expression of axoplasm, sometimes to the point of fiber transection; (iii) lengthening of internodes; and (iv) obscuration of nodes of Ranvier due to cleavage and displacement of myelin and overlapping of nodes by displaced loops of myelin. At the edges of the cuff the changes were (i) increase of fascicular area probably from expressed endoneurial fluid; (ii) widening of nodal gaps, perhaps mainly from translocated axonal fluid; and (iii) disordered structure of axoplasm. We suggest that the process of paranodal demyelination and axonal transection are linked, occur during the act of compression, and are due to shear forces. The initial event is expression of endoneurial fluid, followed by compression and expression of axoplasm and cleavage and displacement oflayers of myelin. Conceivably, with prolonged cuff compression ischemic injury might be found to be superimposed on mechanical injury.In humans, nerve compression injury may follow use of a tourniquet at too high a pressure, for too long a time, or from improper application; lying in one position without moving for a long time (as may occur during anesthesia, inebriation, or coma) with a limb nerve compressed against bone by a protruding ridge or hard surface; or prolonged sitting with the legs crossed or prolonged leaning on the elbows (1, 2). Excellent recovery is expected after compression injury, whereas it is usually delayed and faulty after nerve transection. This difference in outcome is usually explained by conduction block and demyelination in the former and complete fiber degeneration and faulty regeneration in the latter (3-5).The mechanisms underlying nerve compression injury have usually been attributed to ischemia (6-8), to mechanical forces (9), or to both.In the present study the structural alterations of nerve during compression were stopped by simultaneous in situ and perfusion fixation, usually during short periods of compression. We found nodal lengthening and other acute structural changes after only a few minutes of compression, which appear to explain the paranodal demyelination and axonal degeneration that are characteristic of nerve compression injury. The structural alterations that develop during acute compression are different...

Acute demyelination disrupts the molecular organization of peripheral nervous system nodes

“…It remains to be determined whether paranodal demyelination contributes to the conduction block caused by lysolecithin injections (Smith and Hall, 1980). Paranodal demyelination is also caused by wide variety of immune (Ballin and Thomas, 1969a,b;Allt, 1975;Bonnaud-Toulze and Raine, 1980), toxic (Allt, 1969;Jones and Cavanagh, 1983;Griffin et al, 1987), and mechanical (Lubinska, 1958;Ochoa, 1972;Foster et al, 1980;Dyck et al, 1990;Abe et al, 2002) agents. In spite of its potential importance, its only molecular attribute is that paranodal demyelination splits nodes into two heminodes of Na V channels (Dugandzija-Novakovic et al, 1995;Novakovic et al, 1996).…”

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

“…Dyck et al 45 found that endoneurial fluid, axoplasm, and myelin were displaced away from regions of rat peroneal nerve that were acutely pressurized. At the site of compression, there was an increase in the distance between nodes of Ranvier and distortion of myelin lamellae.…”

Regional modulation of neurofilament organization by myelination in normal axons

“…Axonal caliber is considered to be largely determined developmentally. A special role of neurofilaments in influencing caliber has been deduced from the observation that neurofilament density is relatively constant among axons of different calibers (Friede and Somarajski, 1970;Hoffman et al, 1984), although regional differences (Nixon and Logvinenko, 1986;Lasek, 1988;Price et al, 1990;Reles and Friede, I99 l), changes in axonal diseases (Parhad et al, 1987;Dyck et al, 1990) and alterations due to interrupted axon-target interactions (Hoffman et al, 1984) all indicate that neither neurofilament number nor density is fixed or immutable.…”