Peripheral Nerve Injury - Clinical Tree

Introduction

Little was known about peripheral nerve repair until the American Civil War. That conflict inflicted wounds on thousands of soldiers who received care at institutions throughout the states. Many with severe trauma were admitted to Turner Lane’s Hospital in Philadelphia. Dr. Silas Weir Mitchell, a neurologist interested in the peripheral nervous system, oversaw the neurologic wards at the center. Throughout his tenure, Mitchell systematically documented multiple series of nerve injuries. His work ultimately enabled other physicians—such as Herbert Seddon and Sydney Sunderland—to expand the field into the civilian arena. Their efforts have become increasingly relevant as the annual incidence of peripheral nerve injuries has grown. Approximately 300,000 people each year experience some form of peripheral nerve trauma, and a disproportionate number of those affected are young working adults. ^, These patients’ outcomes depend largely on proper clinical assessment, operative management, and postoperative care.

Nerve Anatomy

Peripheral nerves consist of multiple connective tissue layers ( Fig. 182.1 ). The outermost layer is the epineurium, which is composed of dense, irregular tissue. The epineurium surrounds multiple fascicles—bundles of axons—as well as the blood vessels supplying the nerves. Each fascicle resides within its respective perineurium, a layer of lamellar tissue. Individual axons are bounded by a thinner, more delicate layer known as the endoneurium. Schwann cells, which myelinate the nerve fibers, exist in this space. They produce the myelin sheath; this lipid-rich membrane provides proper insulation for axons, the projections of individual neurons. Axons are the innermost units within peripheral nerves.

Classification Systems of Peripheral Nerve Injury

The neuroanatomic structure of peripheral nerves allowed physicians to devise two injury classification schemes. Seddon developed the first in 1943, describing three types of injury: neurapraxia, axonotmesis, and neurotmesis. Sunderland elaborated on Seddon’s work in 1951, extending the previous system across five grades.

Seddon

Neurapraxia

Neurapraxia involves selective segmental demyelination with a focal nerve conduction block across the lesion. The etiology is least understood but has mostly been attributed to direct mechanical compression or transient ischemia. ^, Although there may be motor or sensory loss, the axon and surrounding connective tissue remain intact, so Wallerian degeneration does not occur. This often allows for spontaneous recovery within weeks to months and typically foregoes the need for surgical intervention. Function, however, may be recovered unevenly, as axons are remyelinated at different rates and to different degrees.

Axonotmesis

Axonotmesis involves disruption of axons and demyelination while sparing the supportive connective tissue. It can be caused by direct blunt injury, fractures, dislocations, contusions, and stretch or crush injuries; it can result in motor, sensory, or autonomic paralysis. Wallerian degeneration begins within hours and continues for approximately 6 to 8 weeks. The degree of proximal axonal degeneration depends on the severity, ranging from only the first internode in mild injuries to more proximal in severe injuries. Over time, reactive Schwann cells line the remaining endoneurial tubes and provide scaffolding for axonal regeneration, which occurs at a rate of 1 mm/day. Complete regeneration is possible as long as regenerating fibers grow into their original endoneurial tubes, ensuring the original fiber pattern.

Neurotmesis

Neurotmesis involves disruption of axons, myelin sheaths, and surrounding connective tissue structures. It can be caused by severe contusions, stretch, or lacerations. These injuries involve complete severance of the nerve trunk and clinically manifest as complete loss of motor, sensory, and autonomic function in the autonomous distribution of the affected nerve. Wallerian degeneration occurs, and spontaneous regeneration is unlikely. Moreover, proximal sprouting axons that fail to reach their target tissue can form neuromas. These lesions require surgical removal of scar tissue and, if large gaps remain, repair using nerve grafts.

Sunderland

Grade I

This grade mirrors Seddon’s neurapraxia. A reversible local conduction block exists at the lesion site. The myelin sheath incurs damage, but axon continuity between nerve and end organ remains preserved. Symptoms range from mild to severe, with paresis/paralysis and minor/complete sensory loss. Proprioceptive losses usually occur first, followed by touch, temperature, and pain; cutaneous sensory changes are often transient. Complete spontaneous recovery transpires between weeks to 4 months.

Grade II

These injuries disrupt axons and myelin sheaths while sparing the endoneurium, perineurium, and epineurium. Loss of sensory, motor, and sympathetic function develops distal to the lesion in the autonomous distribution of the nerve. Wallerian degeneration ensues; in certain cases, proximal retrograde degeneration also occurs. The timing and degree of recovery depend on the extent of retrograde axonal loss and the distance from injury to target tissue. Peripheral nerves with simple branching patterns as well as pure sensory or pure motor nerves have a higher chance of successful reinnervation than mixed nerves. During regeneration, the intact proximal portion of the axon grows distally at approximately 1 mm/day within undisturbed tubules. The nerve fiber pattern remains unaltered, which ensures complete restoration of function.

Grade III

These injuries involve loss of endoneurial tube continuity without significant harm to the perineurium and epineurium. If all fascicles are damaged, the patient will experience complete loss of motor, sensory, and sympathetic function in the autonomous distribution of the nerve. If only certain fascicles are damaged, their fiber composition will determine the type and degree of impairment. Spontaneous regeneration is often limited by intrafascicular fibrosis secondary to hemorrhage, edema, vascular stasis, and ischemia. The minimal recovery that does occur can be complicated by cross-shunting, where regenerating axons enter functionally unrelated tubes and result in a new pattern of innervation in the distal end organ. Cross-shunting, in conjunction with retrograde axonal loss, can lead to chronic muscle denervation and a poorer quality of recovery. Altogether, these injuries often require surgical intervention, and even then there is rarely more than 60% to 80% of normal functional recovery.

Grade IV

These injuries involve loss of the endoneurium and perineurium while sparing the epineurium. If all funiculi are damaged, patients will experience complete loss of motor, sensory, and sympathetic function in the autonomous distribution of the nerve. Wallerian degeneration ensues in the distal stump; the incidence of retrograde degeneration and axonal loss is elevated. Severe fibrosis limits axonal regeneration, and neuromas often form. The axons that do regenerate enter the interfunicular space and either terminate blindly, reach the correct target tissue (resulting in spontaneous recovery), or infiltrate functionally unrelated tubes (leading to cross-shunting). Surgical repair is required for any possible functional recovery.

Grade V

This grade mirrors Seddon’s neurotmesis and is seen in the setting of complete nerve transection, usually from laceration or severe stretch injuries. There is complete loss of motor, sensory, and sympathetic function in the autonomous distribution of the severed nerve. Wallerian degeneration ensues in the distal stump; retrograde degeneration and axonal loss are higher than in grade IV injuries. Severe fibrosis limits regeneration, and sprouting axons may become entangled and form neuromas. The axons that do regenerate either rarely reach their target (triggering spontaneous recovery), escape into intervening tissue (causing wasteful regeneration), or infiltrate functionally unrelated tubes (leading to cross-shunting). The distal stump shrinks over time owing to denervation, and any chance of functional recovery depends on surgical repair. Complete restoration is not possible.

Clinical Assessment

History and Physical

A detailed history and physical examination remain the most important components in the evaluation of patients with suspected peripheral nerve injury. When this step is conducted thoroughly, the physician should be able to localize the lesion and characterize its severity. Pertinent details of the history include the mechanism of injury, concomitant vascular and soft tissue injuries, and the presence of risk factors for delayed regeneration, such as preexisting diabetic neuropathy. With appropriate prompting or questioning as needed, the patient should be allowed to describe his or her pain, sensory loss, and motor deficits. Particular attention should be paid to the temporal progression of the patient’s symptoms as well as any alleviating or aggravating factors.

The physical examination should include close inspection, palpation, muscle-strength grading, and sensory assessment. The examination should start with visual inspection of the affected limb. The contralateral unaffected limb should be fully exposed and used as a reference during the examination. Careful note is made of previous scars, muscle atrophy, contractures, swellings, perspiration patterns, and hair loss. If appropriate, baseline photographs may be taken for comparison on follow-up visits.

Muscle strength is assessed and described using the British Medical Research Council scale. This scale ranges from 0 to 5, with a motor score of 0 referring to the absence of visible muscle contraction, whereas a score of 5 is used to describe normal muscle function. The physician can also use this time to assess the range of motion of each muscle group as well as its bulk. Although examination of obviously paretic regions is important, a comprehensive evaluation of all regional muscles will allow for definitive localization of the nerve injury. This is especially the case for lesions lying in the brachial or lumbosacral plexus and can produce complex clinical pictures.

Sensation is graded on a six-point scale, with a score of 0 representing no sensation in the affected distribution; 5 represents normal sensation. A complete sensory examination should include an assessment of light touch, pinprick, two-point discrimination, temperature, vibration, and proprioception. A careful effort should be made to examine the autonomous region of the nerve, with minimal overlap from adjacent nerves, in order to identify the causative lesion. The contralateral limb or an unaffected region of the same limb should be used for comparison.

The physical examination can also be used to assess for nerve regeneration in patients who are being managed conservatively. Provocative testing, used to elicit transient symptoms from the injured nerve, can provide some information about the degree of recovery. The Hoffman-Tinel test is an example of this and involves invoking paresthesias along the distribution of the nerve via percussion of the injured segment. This sign is indicative of an incomplete injury, and its advancement along the distribution of the nerve may signal nerve regeneration. Similarly, the return of perspiration within the affected region is evidence of sympathetic nerve fiber regeneration.

Clinical Neurophysiologic Studies

Although the history and physical examination form the cornerstone of the assessment for patients with peripheral nerve injury, neurophysiologic studies can be used to corroborate diagnostic hypotheses and monitor recovery. A complete neurophysiologic examination must include both needle electromyography (EMG) and nerve conduction studies (NCSs). Ideally these studies are performed at least 2 to 3 weeks after the initial injury to allow sufficient time for denervational changes in the muscles to occur. Some physicians repeat the studies at the 3-month postinjury time point to assess for electrophysiologic signs of improvement. Some elect to follow the patient clinically for meaningful signs of improvement.

Electromyography

EMG assesses the pattern of electrical activity in muscles at rest and during voluntary muscle activity using needle electrodes inserted into the region of interest. It is usually normal in neuropraxic injury and abnormal in the setting of axonotmesis and neurotmesis. ^, Abnormalities in the signal manifest as changes in spontaneous electrical activity and the motor unit recruitment pattern. Relaxed muscle is usually electrically silent; however, denervated muscles may produce fibrillation potentials and positive sharp waves at rest, which reflect underlying fiber irritability. Similarly, the insertional activity generated when the needle is passed through the muscle is usually increased as a result of fiber irritability.

Voluntary muscle contraction leads to the activation of motor units. Following nerve injury, the duration, amplitude, and configuration of these motor units may change. In neuropathic disorders, the number of motor units available is decreased and the remaining units typically fire at a faster rate prior to further recruitment. As muscle reinnervation from healthy nearby axons occurs, the resultant motor units are usually polyphasic and have an increased amplitude and duration.

Nerve Conduction Studies

NCSs assess both peripheral motor and sensory nerve function by evaluation of electrical potential following nerve stimulation. Motor NCSs are performed by recording the compound muscle action potential (CMAP) produced by stimulating a motor nerve at two points along its course. In comparison, during sensory NCS, the nerve of interest is stimulated at one point and sensory nerve action potentials (SNAPs) are recorded at a different location on the nerve. These techniques allow the conduction velocity, amplitude of the propagated action potential, and the distal motor latency of the nerve to be recorded. The amplitude of the response corresponds to the quantity of depolarized fibers, and the conduction velocity reflects the speed of propagation in the largest-caliber fibers of the nerve. In the setting of neuropraxia, motor and sensory NCSs usually display evidence of conduction block due to demyelination. In comparison, axonotmetic and neurotmetic injuries are characterized by absent or reduced CMAP and SNAP amplitudes. In this case, the ratio of CMAP/SNAP amplitudes on the injured side to that on the normal side can be used to estimate axonal loss.

Standard NCSs are unable to text the proximal portion of the nerve of interest. F waves and H reflexes are additional studies that can be used to evaluate this region of the nerve. Stimulation of a motor nerve produces an orthodromic response toward the nerve terminals at the neuromuscular junction and an antidromic response toward the spinal cord. The antidromic response may induce the anterior horn cells to discharge and produce a small motor response that occurs after the initial orthodromic wave. This motor response is known as the F wave and may be abnormal in the setting of nerve injury at the root level. Stimulation of the sensory nerves can also produce waves that travel toward the spinal cord, where they synapse on anterior horn cells and trigger a motor response. This electrophysiologic correlate of the tendon stretch reflex is known as the H reflex. It is most commonly used to assess for the presence of an S1 radiculopathy.

Radiology

Imaging studies should not replace careful physical examination, but they can be used to provide greater definition to the established clinical picture.

Magnetic Resonance Imaging

Conventional MRI provides poor visualization of peripheral nerves because of their small size and the surrounding muscle and fatty tissue. Despite this, it is still possible to infer pathology from associated findings such as muscle atrophy, fatty degeneration, and increased signal on short tau inversion recovery (STIR) sequences. ^, Magnetic resonance neurography (MRN) provides excellent spatial resolution, visualizes the normal fascicular structure and pattern of the nerve, and provides information about the integrity of the nerve in patients or locations that are not amenable to NCSs. Standard MRN protocols include nonenhanced T1-weighted images (T1WI), fat-suppressed T2-weighted images (T2WI), and contrast-enhanced T1WI. Ideally these sequences are obtained on a 3T machine. The nonenhanced T1WI delineates the anatomy of the peripheral nerve and its relationship to the surrounding tissue. The latter two sequences provide more information regarding the possible pathology present. Additional sequences such diffusion tensor imaging may also be included. This uses the anisotropic diffusion properties of nerve fibers in order to track their course; its metrics have been shown to differ in healthy, damaged, and regenerating nerves. ^,

The parameters of interest from MRN examination include the size, signal intensity, fascicular pattern, and course of the nerve. Findings suggestive of injury using this modality include nerve enlargement, nerve discontinuity, loss of fascicular definition, contrast enhancement, and hyperintensity on T2WI. ^, In combination, these findings may be used to distinguish neuropraxia, axonotmesis, and neurotmesis. Neuropraxic lesions usually have no abnormalities on imaging studies. Axonotmetic and neurotmetic lesions display increased signal intensity suggestive of Wallerian degeneration; however, only the latter will have complete loss of nerve continuity. Additionally, MRN can also be used to evaluate for signs of recovery following peripheral nerve injury. This is usually reflected by normalization of signals and usually correlates with functional recovery.

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