MECHANISMS AND CLASSIFICATION OF NERVE INJURY
The lesions of the peripheral nerves may be provoked by different agents and in different mechanisms (Tab. 19-1). The lesion can affect some or all structures of the nerve in different proportions and in different extents. For example, a cutting injury affects a small segment of the nerve trunk, whereas traction injuries provoke lesions of large extent and without clear limits. A sharp agent can cause damage of an circumscribed form whereas a gunshot injury may damage the peripheral nerves along the entire track of the projectile and areas in its surroundings. Damage of the peripheral nerves can also be chronic, provoked by long compression as in carpal tunnel syndrome, thoracic outlet syndrome, compression of the ulnar nerve in the elbow after fracture in this area and so on.
Table 19 - 1
MECHANISM OF INJURY
Laceration and contusion
Traction
Compression
Chemical lesion - injection
Thermal lesion
Electrical lesion
The peripheral nerve fibres that are composed of thousands of axons with varied dimensions, each of which reacts in a different way to the forces that may cause an injury. J. Seddon has introduced three degrees of axon injury. The temporary physiological blocking of the axon without interruption is neuropraxia. Histological changes if present, will be those of segmental demyelination without axonal injury. The motor and sensory functions rapidly return usually within minutes to hours. However, a patient with more severe neuropraxic injury may require as long as 6 weeks to recover. A common example of neuropraxic injury is partial peroneal palsy, which can result from a prolonged cross-leg position, or "Saturday night palsy" involving the posterior cord of the brachial plexus, or the radial nerve. Axonotmesis represents an interruption of the axons without the connective tissue of the nerve being touched.
Distal Wallerian degeneration follows. Complete loss of motor, sensory, and autonomic function usually occurs distal to the lesion.
However, because the nerve is still in continuity, distal growth of axonal sprouts from the point of injury is facilitated, and reinnervation is possible. This type of injury can be encountered following traction, compression, contusion and laceration wounds. Neurotmesis shows anatomic interruption of the connective tissue, as well as that of the axons with their sheaths. The clinical manifestations are similar to that of axonotmesis: complete loss of motor, sensory, and autonomic function distal to the lesion. A neurotmetic lesion requires either direct repair or grafting if nerve function is to be restored. In an injury of the nerves over a large segment, the fibres suffer to a varied extent from all three stages of injury.
According to the classification of Sunder-land, there are five grades of peripheral nerve injuries. Sunderland's grade I injury corresponds to neuropraxia. Grade Il injuries involve loss of axon continuity but preservation of the endoneurium and corresponds to the axonotmesis of Seddon's classification. The more severe nerve injuries (neurotmesis according to Seddon) are subdivided. Sunderland IIIrd degree represents loss of axonal continuity as well as of continuity of endoneural tubes. Grade IV injury comprises of the loss of axons, endoneurium, and the fascicular structure, but continuity is maintained by the epineurium. A grade V injury is a transected nerve.