Nerve Injuries: Anatomy, Pathophysiology, and Classification

Fig. 3.1 (a) Schematic drawing of the basic structure of normal peripheral nerves. (b) The essential elements of the three layers of peripheral nerves.

Nerves are subjected to trauma by many different mechanisms, traction and laceration injury being the most common traumatic mechanisms. Different, less common, and rare forms of injury can also lead to significant nerve dysfunction, pain, and disability ( ▶ Table 3.1).

**Table 3.1** Mechanisms of nerve injuries
Traction (stretch, rupture, and avulsion)
Laceration (sharp and blunt)
Entrapment
Pressure
Ischemic/compartment
Injection injury
Radiation injury
Electrical
Thermal

To be able to offer the best management in a timely fashion, it is essential to understand the different pathophysiological processes related to each mechanism of injury.

3.2 Traction Injury

Traction injury is a common mechanism of injury affecting peripheral nerves; traumatic and birth-induced plexus injuries represent classical examples of traction injury. According to the severity of injury in form of traction, pathological changes take place within the nerve. The grading of nerve injury is classically accredited to Seddon and Sunderland. Seddon ² first described three well-defined types of nerve injury: neuropraxia (conduction block), axonotmesis (neuroma-in-continuity), and neurotmesis (nerve division). Sunderland ³ followed Seddon by a five-point grading system in ascending order of severity with both anatomical and functional correlations ( ▶ Table 3.2).

**Table 3.2** Grading of peripheral nerve injuries
Sunderland grade	Seddon grade	Pathological features	Clinical outcome
I	Neuropraxia	Conduction block, myelin loss	Excellent
II	Axonotmesis	Axon loss	Very good
III		Grade II and endoneurium loss	Variable
IV		Grade III and perineurium loss	Poor/no recovery
V	Neurotmesis	Nerve trunk disruption	No recovery

These injuries may not be of uniform severity. Different grades can be present in the same segment of the nerve and different grades can be present along the course of the nerve. This classification is based on the effect of the injury on the nerve and not necessary the mechanism of injury, as this pattern can be caused by stretch, thermal, or ischemic mechanisms.

Sunderland grade I (neuropraxia) is characterized by conduction block, with usually an excellent recovery. Early in the process, the involved muscles are weak/paralyzed, and sensory loss is evident, particularly for touch and proprioception; pain is usually more resistant. Autonomic function is usually not affected. Wasting of muscles is not common and is a useful clinical clue. The exact duration of neuropraxia is debatable; however, it may range from 1 to 4 months, with an average of 2 months in most cases.

Sunderland grade II nerve injury is characterized by loss of axons with preservation of the endoneurial tube. Clinically, this is manifested by complete loss of motor, sensory, and autonomic functions. Because of the intact endoneurium, the regenerating axons find its old path and reach their targets. The time to recovery depends on the level of injury—the more proximal the lesion, the longer the time for recovery. Regenerating axons travel in a speed of 1 to 3 mm/day. Tourniquet injury is believed to be a combination of grade I and II. ⁴^, ⁵

Sunderland grade III nerve injury combines grade II and endoneurial tube disruption. The perineurium is intact or minimally involved. This pattern means that the fascicles are preserved as tubes but their inside is “messed up.” Trauma inside the fascicles may cause hemorrhage, edema, ischemia, and eventually fibrosis. Fibrosis constitutes the main barrier for the regenerating axons. The scar created also can cause rerouting of the regenerating axons, not reaching their original targets; this is more evident in mixed fascicles with motor and sensory axons compared to pure motor fascicles. This nature of mixed nerve can explain why grade III injury of the median nerve (mixed nerve) at the arm level is different from grade III injury of the radial nerve (mostly motor) at the same level. In proximal lesions, retrograde neuronal degeneration is more pronounced compared to grade II, making recovery of grade III injuries significantly worse. Also, the chance for axonal misdirection is higher, affecting the extent and quality of recovery.

Sunderland grade IV nerve injury (fascicular disruption) occurs in nerves subjected to higher forces, with complete and more severe disorganization of the fascicles ( ▶ Fig. 3.2), with no or very little recovery that is usually nonfunctional.

Fig. 3.2 Intraoperative photograph depicting the cut section in the middle of nonconducting neuroma of the sciatic nerve showing complete loss of internal architecture with the formation of dense fibrous scar.

Sunderland grade V nerve injury (neurotmesis) represents a severed, discontinuous nerve. This mode of injury is not commonly seen in traction injuries at the level of the nerve trunk and is usually caused by lacerations.

Grades I and II are not surgical lesions and usually recover spontaneously. They can be found in association with more severe lesions of grades III and IV (neuroma-in-continuity) involving other nerves. They usually show positive nerve action potential (NAP) following external neurolysis. In cases of neuroma-in-continuity (grade III and IV), the affected nerve segment is isolated; if no NAP or nerve stimulation is present, the neuroma is resected and either primarily repaired or grafted ( ▶ Fig. 3.3).

Fig. 3.3 Intraoperative photograph demonstrating the technique of slicing the nonconducting neuroma starting from the center and going proximally and distally until reaching the normal fascicular pattern for repair.

3.3 Laceration Injury

It has been estimated that laceration injury to the limbs, caused by knifes or sharp objects, causes transection of the underlying nerves in 30% of the cases. ⁶^, ⁷ This percentage depends on the injury location. Volar wrist laceration injury will cause median or ulnar nerve injury in the majority of cases. Sharp injuries to different areas of the body may not necessary transect the underlying nerve, yet can cause a temporary loss of function depending on the degree of injury. In clean sharp lacerations, there is a minimal contusive injury, bruises, or hemorrhage in the proximal and distal stumps. Both stumps form neuromas and retract and adhere to the underlying tissues. Both ends may remain attached by thin, fibrous tissue or normal part of the partially preserved fascicles ( ▶ Fig. 3.4). Retraction can progress with time because of limb movement, and usually stopped by the next distal branch. Significant retraction is usual in median and ulnar nerve injuries at the arm level because of lack of branches of both nerves at this level. Both stumps usually remain in the same plane but may change location according to the adherence to nearby tissues ( ▶ Fig. 3.5). In blunt lacerations caused by blunt objects (motor blades, machinery, chainsaw), irregular, ragged tears of the nerve trunk occur; this causes bruises and hemorrhages along both ends for some distance, making identification of healthy end difficult ( ▶ Fig. 3.6). It is a good practice to explore sharp injuries causing complete loss of function of the underlying nerves, as this gives the best chance for good recovery. In cases of blunt lacerations or contaminated wounds or large wounds with soft-tissue loss, delayed repair (4–6 weeks) is advised allowing the edematous, bruised ends of the nerve to heal and therefore delineating the zone between the normal and the abnormal parts of the nerve, allowing better reconstruction with either end-to-end or, more commonly, graft repair.

Fig. 3.4 Intraoperative photograph of sharp, near-completely lacerated common peroneal nerve 1 month following injury, showing minimal distal and proximal stump changes.

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