History
Nerve injuries can be classified on the basis of completeness and predominant pathophysiology.
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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.
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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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Large-amplitude compound muscle action potential (CMAP) response was recorded from the right biceps muscle after intraoperative direct bipolar stimulation of the proximal right musculocutaneous nerve at low stimulus intensities (3.9 mA). The time base shown is 10 milliseconds/div and the gain is 50 mcV/div.
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Electrodiagnostic testing 1 day after the injury revealed the following: (Left) Right ulnar motor conduction study showed a normal distal amplitude with conduction block across the elbow segment (gain = 2 mV/div, time base = 2 milliseconds [ms]/div). (Second from left) Right ulnar sensory response was normal (gain = 20 mcV/div, time base = 2 ms/div). (Third from left) Right ulnar F-wave responses were absent. (Right) Needle electromyographic (EMG) examination of right abductor digiti minimi was quiet at rest but showed a single fast firing unit on attempted contraction (gain = 200 mcV/div, time base = 10 ms/div).
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Electrodiagnostic testing 3 days after the injury revealed the following: (Left) Right distal ulnar motor response is of lower amplitude than on day 1, approximately 50% of baseline (gain = 2 mV/div, time base = 5 milliseconds [ms]/div) with persistent conduction block across the elbow. (Right) Right ulnar sensory response is still normal (gain = 20 mcV/div, time base =2 ms/div).
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Electrodiagnostic testing 6 days after the injury revealed the following: (Left) Right distal ulnar motor response is less than 10% of baseline (gain = 2 mV/div, time base = 5 milliseconds [ms]/div) with persistent conduction block across the elbow. (Right) Right ulnar sensory response amplitude still is relatively preserved at 50% of baseline (gain = 20 mcV/div, time base = 1 ms/div).
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Electrodiagnostic testing 10 days after the injury revealed the following: Right ulnar motor (middle) and sensory (right) responses are absent. Needle electromyography (EMG) of first dorsal interosseus shows sparse denervation potentials with 1 fast firing unit on attempted volitional activity.
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Intraoperative nerve action potentials recorded from the lateral cord (point R) with successive stimulation (at points 1, 2, 3, 4, and 5) along the course of the musculocutaneous nerve (gain = 100 mcV/div, time base = 0.5 milliseconds [ms]/div). Normal responses are recorded from stimulation at points 1 and 2. A slight increase in latency and drop in amplitude are noted on stimulation at point 3 close to the nerve injury. Stimulation at points 4 and 5 (distal to the injury) fail to evoke a recordable response.
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A 25-year-old man had a "flail" right arm after injury in a motorcycle accident (Case study 4). Left panel: Somatosensory evoked potentials (SEPs) recorded at the scalp from stimulation of the (healthy) middle trunk (gain = 0.2 mcV/div, time base = 10 milliseconds [ms]/div). Middle panel: SEPs recorded at the scalp from stimulation of the lower trunk—no reproducible responses present (gain = 0.2 mcV/div, time base = 10 ms/div). Right panel: "Super normal" nerve action potentials recorded at the lower trunk from stimulation of the medial cord (time base = 1.5 ms/div, gain = 20 mcV/div).
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MRN of the brachial plexus. a: Abnormal signal in the brachial plexus elements on the affected (right) side. Compare to b: normal plexus on the unaffected (left) side.
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MRN image through the cervical spine showing pseudomengocele (arrows) at the site of a cervical root avulsion in a patient with traumatic brachial plexopathy.
