Anatomy and Physiology

A few basic principles underlie the anatomy of the peripheral nervous system. Each peripheral nerve is composed of fibers from more than one spinal nerve root; correspondingly, each spinal nerve contributes fibers to more than one peripheral nerve. Consequently, whereas spinal nerve lesions manifest in the clinical picture of radiculopathies with dermatomal sensory disturbances and mild to moderate weakness of muscles supplied by the spinal nerve, peripheral nerve lesions manifest in more precise borders of sensory disturbances acutely and more severe atrophy and paresis of muscles supplied solely by the peripheral nerve as time elapses.

The microscopic anatomy of the peripheral nerve comprises nerve fibers, fascicles, connective tissue (epi-, peri-, and endoneurium), blood vessels, lymphatics, and nervi nervorum (Fig. 32.1). Although the fascicular pattern may change as the nerve courses more distally, the general structure of the nerve remains constant. After a peripheral nerve is injured, a coordinated sequence of events occurs to remove the damaged tissue and ultimately initiates the regenerative process. When the nerve is disrupted, the severed ends retract owing to the elasticity of the endoneurium. Trauma to the vasa nervorum leads to robust inflammation triggering fibroblasts to proliferate to form the basis for a dense scar at the injury site: in the most severe cases, the nerve ends become markedly disorganized, with fibroblasts, macrophages, capillaries, Schwann cells, and collagen fibers within which the regenerating axons form disorganized masses known as neuromas. The degree of damage sustained by the proximal segment and neuronal cell body depends on the distance of the zone of injury from the cell body. The nucleus migrates to the periphery of the cell and select cytoplasmic elements (e.g., Nissl granules, endoplasmic reticulum) undergo chromatolysis. Cell survival relies upon the Schwann cells and trophic molecules present in the immediate environment.

FIGURE 32.1 Microscopic anatomy of the peripheral nerve.

Conversely, the distal portion of the axon undergoes Wallerian degeneration within hours after injury; this granular disintegration of the cytoskeleton and axoplasm occurs over several days to weeks, yielding empty endoneurial tubes. Early after injury, until the distal axons are totally degenerated, motor conductivity and sensory nerve potentials still can be observed in the distal segment; therefore, electrodiagnostic studies, used to predict severity of the lesion and to guide treatment recommendations, should not be performed within the first several weeks after injury.

When a peripheral nerve is injured, the accompanying muscle is denervated. Denervation leads to a series of structural changes and atrophy of the muscle if neural regeneration does not occur. Atrophy is seen as a mean 70% reduction in the cross-sectional area after 2 months.³ Sodium channels regress toward embryonic forms with altered biochemical properties, and acetylcholine receptors redistribute to cover the entire muscle surface. This supersensitivity to acetylcholine manifests clinically as spontaneous uncoordinated muscle activity, otherwise known as fibrillation. Death of muscle fibers generally does not occur, but when it does, dropout occurs between 6 and 12 months after denervation.

Pertinent History of Injury

Pertinent history regarding the timing and location of the motor and sensory disturbances is critical for an accurate assessment of the acute nerve injury. For instance, an immediate neurological deficit coincident with the injury implies direct involvement of the peripheral nerve at the site of injury. In contrast, a delayed neurological deficit implies consequent involvement of the peripheral nerve, as with reduction of fractures, injections, or tourniquet application. If the motor and sensory disturbance progressively worsens, an enlarging adjacent lesion compromising the nerve (such as a hematoma, pseudoaneurysm, or pressure from a cast or splint) must be considered and urgently addressed. Additionally, with time, a bony callus can form causing a progressive neurological deficit such as in tardy ulnar palsy.

The description of the mechanism of injury can also yield information about the severity of injury to the nerve and guide treatment. For instance, if the injury involved low/no impact such as a fall from a standing position, neurapraxia will be the likely result. In contrast, if there is high impact as in extreme sports or high-speed motor vehicle accidents, then the likely injury is axonotmesis or neuronotmesis. This classification of nerve injury described by Seddon and associates in 1943⁴ and expanded by Sunderland and colleagues in 1951⁵ (Fig. 32.2) remains useful today, although most injuries occur along the continuum of pure grades.

FIGURE 32.2 Seddon and Sunderland classifications of nerve injuries.

Nerve injuries can also be classified as preganglionic or postganglionic, with profound surgical implications (Fig. 32.3