Peripheral Nerve Trauma or Injury

Peripheral Nerve Trauma

The peripheral nervous system extends throughout the body and is subject to injury from a wide variety of traumas. Peripheral nerves transmit motor and sensory information between the CNS and the body. An individual nerve may have pure motor. pure sensory. or mixed motor and sensory functions. The key information-carrying structure of the nerve is the axon. The axon transmits informa­tion from the neuronal cell body and may measure from less than1 mm to greater than I m in length. Axons that travel a signifi­cant distance are often covered with myelin. which is a lipid-rich. electrically-insulating sheath formed by Schwann cells. Myelinated axons transmit signal much more rapidly than unmyelinated axons, because the voltage shifts and currents that define action potentials effectively jump from gap to gap over the insulated lengths of the axon.

Axons, whether myelinated or unmyelinated, travel through a collagenous connective tissue known as endoneurium. Groups of ax­ons and their endoneurium form bundles known as fascicles. Fasci­cles run through a tubular collagenous tissue known as perineurium. Groups of fascicles are suspended in mesoneurium. Fascicles and their mesoneurium run through another tubular collagenous tissue known as epineurium. The epineurium and its contents form the nerve.

There are four major mechanisms of injury to peripheral nerves. Nerves may be lacerated, stretched, compressed, or contused. Knives, passing bullets, or jagged bone fractures may lacerate nerves. Adjacent expanding hematomas or dislocated fractures may stretch nerves. Expanding hematomas, external orthoses such as casts or braces, or blunt trauma over a superficial nerve may com­press or crush nerves. Shock waves from high-velocity bullets may contuse nerves. These mechanisms of injury cause damage to the various anatomic components of the nerve. The patterns of damage are categorized below.

Certain nerve segments are particularly vulnerable to injury. The following four characteristics make a nerve segment more vulnera­ble: proximity to a joint, superficial course, passage through a con­fined space, and being fixed in position.

Types of Injury

The traditional classification system for peripheral nerve injury is the Seddon classification. Seddon described three injury patterns: neurapraxia, axonotmesis, and neurotmesis, as defined below. 'The Seddon classification provides a simple, anatomically-based ap­proach to peripheral nerve injury.

Neurapraxia. Neurapraxia is defined as the temporary failure of nerve function without physical axonal disruption. Axon degeneration does not occur. Return of normal axonal function occurs over hours to months, often in the 2- to 4-week range.

Axonotmesis. Axonotmesis is the disruption of axons and myelin. The surrounding connective tissues, including en­ doneurium, are intact. The axons degenerate proximally and distally from the area of injury. Distal degeneration is known as wallerian degeneration. Axon regeneration within the connective tissue path­ways can occur, leading to restoration of function. Axons regenerate at a rate of I mm per day. Significant functional recovery may occur

for up to 18 months. Scarring at the site of injury from connective tissue reaction can form a neuroma and interfere with regeneration.

Neurotmesis. Neurotmesis is the disruption of axons and en­ doneurial tubes. Peripheral collagenous components, such as the epineurium, may or may not be intact. Proximal and distal axonal degeneration occurs. The likelihood of effective axonal regeneration across the site of injury depends on the extent of neuroma formation and on the degree of persisting anatomic alignment of the connec­tive tissue structures. For instance, an injury may damage axons, myelin, and endoneurium, but leave perineurium intact. In this case the fascicle sheath is intact, and appropriate axonal regeneration is more likely to occur than if the sheath is interrupted.

Management of Peripheral Nerve Injury

The sensory and motor deficits should be accurately documented, Deficits are usually immediate. progressive deficit suggests a pro­cess such as an expanding hematoma, and may need early surgical exploration. Clean, sharp injuries may also benefit from early ex­ploration and reanastomosis. Most other peripheral nerve injuries should be observed. Electromyography and nerve conduction stud­ies (EMG|NCS) should be done 3 to 4 weeks post injury if deficits persist. Axon segments distal to the site of injury conduct action po­tentials normally until wallerian degeneration occurs, so EMG|NCS before 3 weeks is not informative. Continue observation if function improves. Explore the nerve surgically if no functional improvement occurs over 3 months. If intraoperative electrical testing reveals con­duction across the injury, continue observation. In the absence of conduction, the segment should be resected and end-to-end primary anastomosis attempted. Anastomoses under tension will not heal, so a nerve graft may be needed to bridge the gap between the proximal and distal nerve ends. The sural nerve is often harvested, as it car­ries only sensory fibers and leaves a minor deficit when harvested. The connective tissue structures of the nerve graft may provide a pathway for effective axonal regrowth across the injury.

Patterns of Injury

Brachial Plexus. The brachial plexus may be injured in a variety of ways. Parturition or a motorcycle accident can lead to plexus injury due to dislocation of the glenohumeral joint Attempting to arrest a fall with one's hands can lead to a stretch injury of the plexus due to abrupt movement of the shoulder girdle. A lung apex tumor, known as a Pancoast tumor, can cause compression injury to the plexus. There are many patterns of neurologic deficits pos­sible with injury to the various components of the brachial plexus, and understanding them all would require extensive neuroanatomic discussion. Two well-known eponymous syndromes are Erb's palsy and Klumpke's palsy. Injury high in the plexus to the C5 and C6 roots resulting from glenohumeral dislocation causes Erb's palsy with the characteristic( bellhop's tip) position. The arm hangs at the side, internally rotated Hand movements are not affected. in­ jury low in the plexus, to the C8 and Tl roots, resulting from stretch or compression injury, causes Klumpke's palsy with the character­istic "claw hand" deformity. There is weakness of the intrinsic hand muscles, similar to that seen with ulnar nerve injury.

Radial Nerve. The radial nerve courses through the axilla, and then laterally and posteriorly in the spiral groove of the humerus. Improper crutch use can cause damage to the axillary portion. The section of the nerve traversing the spiral groove can be damaged by humerus fractures or pressure from improper positioning during sleep. This classically occurs when the patient is intoxicated and is called Saturday night palsy .The key finding is wrist drop (i.e., weakness of hand and finger extensors. Axillary (proximal) injury causes tricep weakness in addition to wrist drop

Common Peroneal Neuropathy. 'The common peroneal nerve forms the lateral half of the sciatic nerve (the medial half be­ing the tibial nerve). It receives contributions from L4, L5, S I, and S2. It emerges as a separate nerve in the popliteal fossa and wraps laterally around the fibular neck, after which it splits to form the deep peroneal nerve and the superficial peroneal nerve. The superfi­cial, fixed location at the fibular neck makes the nerve susceptible to compression. The classic cause of traumatic peroneal neuropathy is crush injury from a car bumper striking the lateral aspect of the leg al the level of the knee. Symptoms of common peroneal neuropathy include foot drop (weakness of the tibialis anterior) and numbness over the anterolateral surface of the lower leg and dorsum of the foot. Surgical exploration of this lesion is typically unsatisfying. Rare cases may be due to compressive fibers or adhesions that may 
be lysed, with the possibility of retun of function

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