eMedicine Specialties > Neurology > Neuromuscular Diseases
Traumatic Peripheral Nerve Lesions
Updated: Oct 11, 2006
Introduction
Background
Evaluation and management of peripheral nerve injuries requires a thorough knowledge of neuroanatomy, neurophysiology, and electrodiagnostic medicine. The purpose of this article is not to describe the clinical features of every conceivable nerve injury. This type of information is well presented in other publications (eg, Stewart, 1993). Instead, this article emphasizes the use of various electrodiagnostic techniques in the evaluation and management of nerve injuries in general.
Pathophysiology
See History.
Clinical
History
Nerve injuries can be classified on the basis of completeness and predominant pathophysiology.- Nerve injuries first should be classified as complete or incomplete.
- Complete injuries disrupt all the neurons traversing the injured segment, causing total loss of distal motor or sensory function.
- Incomplete lesions disrupt some neurons but leave others unaffected, with some sparing of distal motor or sensory function. An incomplete nerve injury implies that at least part of the nerve remains in continuity; this has important therapeutic implications.
- Although peripheral nerves may be injured in various ways, pathophysiologic responses to trauma at the neuronal level comprise only 2—demyelination and axonal loss.
- Segmental demyelination (ie, neurapraxia): A mild stretch or compression injury may disrupt or distort the myelin sheath at the injury site, resulting in focal demyelination and leaving the axons intact. This causes a transient state of disrupted conduction along the injured segment—conduction slowing or block. Because the axons remain intact, function can be restored by focal remyelination, usually within a matter of days to weeks. This type of nerve injury is known as neurapraxia and is best considered the peripheral nervous system equivalent of "concussion."
- Axonal injury and wallerian degeneration: Injured axons undergo a highly stereotyped process known as wallerian degeneration. Axonal function is disrupted immediately after the injury, although the disconnected distal segment initially survives and conducts externally applied stimuli; over the course of the next 5-7 days, however, the distal axonal segment slowly degenerates in a centrifugal fashion and eventually becomes inexcitable. The neuron may recover subsequently by axonal regeneration from the intact cell body, which is a slow process occurring at a rate of about 1 mm/day.
- Axonal injuries that spare the supporting perineural connective tissue sheath are known as axonotmetic. The intact perineural connective tissue sheaths provide a conduit for axonal regeneration from the cell body to the target muscle, facilitating recovery. Injuries that disrupt the whole nerve, affecting both the axon and supporting connective tissue, are known as neurotmetic. These injuries are less likely to recover by axonal regeneration; they more often require surgical repair.
- Mixed injuries: Individual axons can exhibit only one of these types of pathophysiologic change; however, one injured nerve is composed of thousands of axons, and a mixed pattern of segmental demyelination and axonal loss is manifested frequently. Moreover, some axons may be affected by different pathophysiologic processes at various points along their courses. This can make assessing the type of injury very difficult, even with electrodiagnostic methods, thus confounding management (see Case study 1 in Medical/Legal Pitfalls). Recovery from mixed lesions is usually biphasic. The neurapraxic component of the injury recovers quickly by remyelination and the axonal component of the injury recovers slowly by axonal regeneration.
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| References |
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References
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Kline DG, Hudson AR. Nerve Injuries: Operative Results for Major Nerve Injuries. Philadelphia, Pa: WB;1995.
Kliot M, Slimp J. Techniques for assessment of peripheral nerve function at surgery. In: Loftus CM, Traynelis VC, eds. Intraoperative Monitoring Techniques in Neurosurgery. New York: McGraw-Hill Inc;. 1994:275-85.
Landi A, Copeland SA, Parry CB, Jones SJ. The role of somatosensory evoked potentials and nerve conduction studies in the surgical management of brachial plexus injuries. J Bone Joint Surg [Br]. Nov 1980;62-B(4):492-6. [Medline].
Stewart JD. Focal Peripheral Neuropathies. New York: Raven Press;1993.
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Wilbourn AJ. Assessment of the brachial plexus and the phrenic nerve. In: Johnson EW, Pease WS, eds. Practical Electromyography. Baltimore: Williams & Wilkins;1997:273-310.
Further Reading
Keywords
peripheral nerve injuries, complete nerve injury, incomplete nerve injury, segmental demyelination, neurapraxia, axonal injury, wallerian degeneration, axonal regeneration, focal remyelination, myelin sheath, evaluation of peripheral nerve injury, management of peripheral nerve injury, treatment of peripheral nerve injury
