A peripheral nerve lesion is one complication of a traumatic extremity injury, since recovery of muscle and tendon activity and restoration of sensibility are essential for a functional extremity. Principles for the initial management of the traumatized extremity have been well established. A clean wound, structural alignment, and prevention of deformity are important goals. however, the more extensive and severe the injury to the involved extremity, the longer the time required for the attainment of homeostasis in the tissues. Vascular insufficiency, chronic osteomyelitis, and articular incongruity all contribute to fibrotic infiltration and decreased activity. Clinical studies of traumatic peripheral nerve injuries in humans show considerable variation because return of useful function depends as much on the total response of the extremity to the injury as on the regeneration of the injured nerve. Furthermore, peripheral nerves are only as functional as the pertinent sensory receptors and motor end plates. An overview of the traumatically injured nerve is thus presented within the context of neurologic evaluation, outcome, and global extremity injury.
The initial clinical examination is a broad assessment of functional loss designed to determine the level of peripheral nerve injury. In the conscious patient, this may be done with voluntary muscle testing and the testing of the threshold for sensibility. The voluntary muscle test, with manual grading as introduced by Robert W. Lovett's text on infantile paralysis, published in 1917, will determine the level of the nerve lesion on the basis of active and inactive muscles, as reported by Omer. Common gestures are easier to elicit in a distracted patient than sequential muscle contractions; for example, "cross your fingers" is an adequate test for intact motor function of the ulnar nerve. Passive muscle stretching will alert the examiner to a potential compartment syndrome with associated loss of peripheral nerve function. Sensibility threshold also is related to the responsiveness of the conscious patient. A tuning fork can be used to determine threshold recognition of sensibility, which then can be quantitated with either static or moving two point discrimination distance. In the unconscious patient with fractures or dislocations, the examiner should maintain a high index of suspicion for a compartment syndrome and consider electrodiagnostic studies to establish the integrity of any potentially involved peripheral nerves. The severity of the overall injury alone may dictate exploration of the extremity. This decision is usually based on the involvement of other anatomic structures in addition to the peripheral nerves, such as an abnormal angiogram or an open fracture. Magnetic resonance imaging is useful when there is a two-level extremity injury and the extent of peripheral nerve involvement is unknown. This point will be addressed later in this chapter. If an emergency operation is indicated, the nonfunctional peripheral nerve should be assessed by direct observation. A disrupted nerve should be repaired as soon as clinically practical. If debridement exposes the nerve and judgment indicates delayed repair, the nerve stumps can be tagged with fine monofilament wire sutures to prevent retraction and enhance roentgenographic identification.
Nerve Injury Classification Scheme
Seddon introduced a simple classification of traumatic nerve injuries with specific terminology: neurapraxia, axonotmesis, and neurotmesis. Sunderland identified five degrees of injury, of increasing severity, that produce loss of function. It seems logical to use three degrees of injury, however, in the clinical situation. These are: (1) a peripheral nerve so severely ,disorganized that spontaneous regeneration cannot occur. This could result from nerve division, traction, impalement, or injection with subsequent scarring. The involved segment requires excision as part of the surgical repair. This condition is termed neurotmesis by Seddon and fourth- or fifth-degree injury by Sunderland; (2) a peripheral nerve with interruption of axons and their myelin sheaths, but connective tissue planes, such as the perineurium, are maintained. There is a reduction in the number of axons available for regeneration and there may be intrafascicular bundle fibrosis. This commonly results from penetrating missiles or impalement, traction, or compression with related ischemia. This condition is termed axonotmesis by Seddon and second- or third-degree injury by Sunderland; and (3) a peripheral nerve with a segmental interruption of the myelin sheaths, but intact axons and connective tissue planes. No Wallerian degeneration occurs, and the disturbance that is responsible for blocking conduction is fully reversible. This commonly results from contusion, such as a fracture, or compression, such as "Saturday night palsy." Functional recovery occurs in weeks to months. This condition is termed neurapraxia by Seddon or a first-degree injury by Sunderland
Factors Affecting the Decision-Making Process
Age is the most significant single factor in recovery following nerve injury and suture. Almost all patients up to the age of puberty have good clinical results following nerve suture. The young patient has a greater intrinsic capacity for sensibility re-education and motor adaptability than does the older patient.
Distance from End Organ
The proximal (high) nerve injury presents a difficult dilemma with regard to both prognosis for recovery and indications for surgery. There may be considerable distance from the site of injury to the first motor point to be reinnervated. From the moment of injury, there is progressive distortion and degeneration of the distal motor and sensory end organs. Over time, distortion of the nerve distal to the site of injury occurs, with associated slowing of the regenerative process for axon regrowth. The more proximal the injury, the longer the denervation of the distal tissues and the slower the recovery of function. One should expect axon regeneration to be vigorous for the first year after injury in an adult, but if the interval between injury and end organ reinnervation is longer than 4-5 years, functional recovery will be quite limited. A proximal injury of the ulnar or sciatic nerves may be more than 20-30 cm from the most proximal end organ.
The more extensive the injury to the involved extremity, the longer the time required for the establishment of tissue homeostasis. Peripheral nerves are only as functional as their sensory receptors and muscle-tendon motor plates. A nerve gap often reflects the severity of the traumatic insult. Multiple nerve involvement is a more serious problem for functional recovery of the entire extremity than is an isolated nerve injury. Severe vascular deficiency or chronic osteomyelitis involving the soft tissue around the nerve both contribute to fibrotic infiltration and delayed healing. The incidence of nerve injuries associated with fractures is unknown. A fracture of the humerus is the fracture most likely to be associated with a nerve injury. Most injuries associated with diaphyseal (shaft) fractures leave the peripheral nerve in continuity. The radial nerve is involved in 60%, the ulnar nerve in 18%, the common peroneal nerve in 15%, and the median nerve in 6% of all neuropathies resulting from fractures. Epiphyseal-level fractures or dislocations can result in vascular disruption and nerve injury. Tight fascial constraints about joints enhance the potential for ischemic damage and traction. Nerve dysfunction occurs in 18% of knee dislocations. These are usually traction injuries that vary from neurapraxia to neurotmesis. The sciatic nerve is injured in approximately 13 % of posterior dislocations of the hip or posterior acetabular fractures. Shoulder dislocations are associated with axillary nerve stretch injuries in 5 % of cases. Infraclavicular brachial plexus injuries often accompany shoulder subluxation, whereas supraclavicular injuries are often signaled by fractures of the first rib, transverse process of the cervical spine, or the clavicle. The prognosis for spontaneous recovery is poorer for dislocations or epiphyseal-level fractures than for diaphyseal-level fractures. The prognosis is different for closed and open fracture injuries and is related to the severity of damage to the extremity. Seddon reported an 83.5% spontaneous recovery rate in 109 cases of closed fractures of the upper extremity with associated nerve injury, but only 65 % in 37 cases of open fractures with neuropathy. Omer found 83% spontaneous recovery for all neuropathies associated with fractures.
Mechanism of Injury
Nerve injury associated with traction or stretch has a poorer prognosis than does neuropathy related to fracture. Traction usually involves a long segment of the nerve trunk. Only 58% of patients with traction injuries at the knee in the presence of continuity of the peroneal nerve had functional motor recovery. Furthermore, the prognosis of traction injuries was unaffected by surgical exploration. Gunshot wounds are a fact of life in our society. Their incidence is increasing worldwide. Surgeons will therefore be dealing with these injuries more and more often. These injuries include those caused by sophisticated weapons that deliver substantial kinetic injury to tissue. High-velocity gunshot wounds can result in internal explosions and may be associated with fractured bones remote from the missile tract; however, the pressure-related disturbances related to increased missile velocity are pertinent only with deep tissue penetration by the missile. With gunshot wounds there is often a loss of function without disruption of the nerve. Sunderland studied a small series of military patients during World War II and documented spontaneous recovery in 68 % of the cases. In a prospective study of 595 gunshot wounds during the Vietnam War, Omer determined that spontaneous recovery occurred in 227 of 331 (69%) low-velocity gunshot wounds and 183 of 264 (69%) high-velocity gunshot wounds. Neurapraxia and axonotmesis injuries are approximately equal in gunshot wounds, with the clinical time scale for spontaneous recovery being 1-4 months for neurapraxia and 4-9 months for axonotmesis. Rakolta and Omer noted that spontaneous regeneration may be delayed up to 11 months without excluding the possibility of complete recovery in femoral nerve combat injuries. Low-velocity gunshot wounds result in a higher percentage of peripheral nerve axon loss (neurotmesis) than do high-velocity missile wounds. Low-velocity wounds with a smaller shock wave tend to directly involve structures such as peripheral nerves, blood vessels, and bone. Shotgun wounds have a higher percentage of associated peripheral nerve injuries than low-velocity handgun wounds. In addition, shotgun wounds require thorough debridement with early exploration of neurovascular structures and, usually, a delayed primary closure. Spontaneous recovery of peripheral nerve injuries resulting from shotgun wounds has been reported as only 45%. Lacerations, injections, and penetrating impalement are low-velocity injuries that often do not demonstrate significant spontaneous recovery from the initial injury. Lacerations with associated loss of peripheral nerve function, therefore, should be diagnosed clinically as severed nerve lesions (neurotmesis) until proven otherwise through intraoperative examination.
A disrupted peripheral nerve (neurotmesis) should be repaired as soon as clinically practical. Anastomosis should be done with adequate magnification and appropriate instruments and suture. There should be minimal circumferential and longitudinal tension at the suture line in order to avoid internal disorganization of the fascicular bundles. Epineurial suture technique may be used in all peripheral nerve injuries with single (monofascicular) or less than four (oligofascicular) bundle patterns. Fascicular bundle suture techniques may be preferred in peripheral nerves with many (polyfascicular) bundles in segment avulsion, or in chronic lesions with either a nerve gap or a neuroma-in-continuity. Current reports indicate the superiority of primary repair over delayed repair of peripheral nerves. Kline and Nulsen recorded a 72 % good or better motor recovery after primary repair of the median nerve at the wrist. Moneim and Omerls reported an 83% good or better motor recovery of the ulnar nerve after primary group fascicular repair at wrist level, whereas Birch and Raw obtained an 81 % good or better motor recovery of the median and ulnar nerves after primary repair at wrist level.
A variety of trophic factors that influence nerve regeneration have been identified. These include nerve growth factor and axon outgrowth factor. Brushart has found random evidence that reinnervation of the distal nerve stump usually occurs, with subsequent survival of correct projections and loss of mal-aligned neurons. Badalamente and Hurstl have attempted to inhibit calcium-activated neutral protease through intramuscular injections of tripeptide leupeptin. Inhibition of the calcium activated neural protease facilitates morphologic recovery in peripheral nerve injuries.
Time Frame for Recovery
The time frame for recovery following neurapraxia is 1-4 months, and following axonotmesis is 4-9 months. Proximal extremity injuries take longer to demonstrate clinical function than distal injuries, and extensive extremity injuries producing multiple nerve lesions require a longer period for return of clinical function than do injuries resulting in isolated nerve dysfunction.
Assessment of Recovery Potential
Assessing the specific etiology of the nerve injury, the level of functional loss, and the overall severity of extremity involvement will provide a clinical classification of the nerve injury and indicate the potential for spontaneous recovery. Lacerations require exploration and suture of disrupted nerves at the time of injury. A disrupted nerve should be repaired as soon as clinically practical. It is appropriate at 4 months to electively explore the clinically complete nerve lesion in high-velocity, low-velocity, and shotgun wounds above the elbow or knee, severely comminuted fractures, and fractures adjacent to joints. At this point, 100% of neurapraxia injuries and 50% of axonotmesis lesions should have recovered. However, approximately 60% of these nerves will have a neuroma-in-continuity, and a decision must be made concerning resection of the neuroma. Because the degree of functional loss is very influential in brachial plexus injuries, these should be explored somewhat earlier (perhaps at 3 months) if there has been no recovery from a clinically complete nerve lesion. The progress of regeneration cannot be assessed without evaluating functional loss and recovery. Assessment of the established peripheral neuropathy requires a series of quantitative tests that are repeated at regular intervals of approximately 12 weeks. The sensibility level related to the individual peripheral nerve and the motor strength of individual reinnervated muscles are the most important studies in the series of quantitative tests. Sensibility testing evaluates the patient's capacity for precise interpretation of sensation. All current tests that assess sensibility are related to cutaneous touch pressure; for example, the Weber two-point discrimination test is a judgment more than the recognition of sensation. The Weber-Moberg static two-point discrimination test determines if the patient can discriminate between being touched with one or two points and the minimal distance at which two points are recognized. The testing instrument can be an ordinary paper clip, a blunted eye caliper, or a Boley gauge. The normal threshold for the volar surface of the hand varies from 2-5 mm at the fingertip to 7-10 mm at the base of the palm.14,23.24 The Dellon moving two-point discrimination test is normal between 2-3 mm at the volar fingertip. Other sensibility techniques in current use include Von Frey monofilaments and the ridge sensitometer test. Functional results should be measured against the contralateral extremity. Functional sensation may be tested with the stem of a tuning fork (30 cycles per second) over the anatomical trunk of the involved peripheral nerve (Tinel's sign). This percussion stimulation begins at the distal portion of the extremity to delay the patient's potential discomfort until the positive point of the test. The voluntary muscle test used to determine muscle strength is based on the use of gravity and resistance, first devised by Lovett in 1912 as reported by Omer. The examiner grades muscle strength by palpation of the involved muscle-tendon unit and by resistance to movement of a bone-joint lever arm motored by the involved muscle. The active range of motion can be quantitated with a goniometer across an appropriate joint. Trick movements must be detected. Strength can be quantitated with the aid of resistance instruments, such as grip and pinch meters. The contralateral (if normal) extremity should be used for comparison.
Electrodiagnostic studies are more objective than clinical tests. Determination of the conduction velocity of sensory nerves is the only objective study to measure sensation. Electromyography cannot be used to predict the quantity or quality of reinnervation. These studies may become redundant if early research in nuclear magnetic resonance (NMR) spectroscopy is fruitful. Despite the most refined histochemical techniques, the nature of the critical early stages of nerve degeneration remains unclear; however, using high-field NMR, reproducible patterns of biophysical changes occurring during wallerian degeneration and nerve regeneration have been recorded. Although the NMR data may demonstrate that metabolic perturbations occur within hours after nerve injury, the corresponding histologic findings show virtually no edema and no remarkable changes in nerve morphology. The loss of spin-spin correlations in NMR studies is dramatic after 5 hours. As the nerves undergo repair and regeneration, the spin-spin correlations return, indicating that an ongoing evaluation of nerve degeneration and regeneration is feasible.
From the time of injury, the extremity is kept in a functional position and in a dynamic state. Fibrotic tissue is stretched and mobilized. The principle of active motion cannot be neglected and daily activities should be emphasized. An important aspect of treatment is the use of dynamic splints, which should be fabricated for each patient and changed whenever indicated. In the upper extremity, function will improve with a motor and sensibility re-education program. Motor re-education will prevent abnormal motor habits such as the extended and "divorced" insensible index finger following median nerve loss. Sensibility re-education should allow recovery of the full potential of the regenerating nerve.
Motor re-education consists of two phases: (1) visual monitoring of activity patterns and (2) early tendon transfers (which function as internal splints). The principles for early tendon transfers are: (1) use only one tendon and (2) use a transfer that will not result in deformity should spontaneous nerve recovery occur. For example, transfer of the pronator teres tendon to the tendon of the extensor carpi radialis brevis muscle will result in active extension of the wrist and passive mobilization of the collateral ligaments of the metacarpophalangeal joints in a patient with radial palsy. Recovery of the radial nerve will not result in a deformity.
Sensibility re-education consists of conscious handling of objects with the eyes open and then closed. The purpose is to use items in the patient's occupation, such as nails for a carpenter. Sensibility re-education is not effective if the patient cannot recognize vibratory sensation (250 cycles per second tuning fork) over the autonomous zone of the involved nerve. A timed picking-up test will quantitate improvement in a patient with median or ulnar palsy. Excellent re-education requires a team approach, including an occupational therapist, physical therapist, and brace maker (orthotist), as well as a cooperative patient and an interested surgeon.
Evaluation can be done at several levels: individual nerve recovery, extremity coordination, medical impairment and disability. This is accessed through the motor strength of individual reinnervated muscles, and the sensibility level of the individual's nerve recovery. Voluntary muscle testing is based on the use of gravity and resistance. The examiner grades muscle strength by palpation of the involved muscle-tendon unit and by resisting movement of a bone-joint lever arm motored by the involved muscle: zero (no contractibility), trace (contractility), poor (complete range of motion with gravity eliminated), fair (motion against gravity), good (motion against gravity and some resistance), and normal (complete function). The range of motion can be quantitated with a goniometer across an appropriate joint.
Sensibility is the capacity for precise interpretation of sensation. All current tests to assess sensibility are related to cutaneous touch/pressure. The static two-point discrimination test has the greater application. Normal levels are between 3-5 mm at the fingertips, and 7-10 mm at the base of the palm. Moving two-point discrimination is normal between 2-3 mm at the fingertips. Other techniques in current use include monofilaments and the ridge sensitometer. Functional levels should be measured against the contralateral (if normal) extremity.
The British scales (Tables 1, 2, and 3) are the most frequently used today. Motor recovery is based on combined motor activity. This is most useful in proximal (high) lesions (Table 2). Extremity coordination is the end product of motor and sensibility function. Grasp and pinch can be measured with dynamometers, which should be adjusted to fit the finger span of the patient. Tactile gnosis can be tested by writing numbers on a digit, identifying a coin, or palpating type or arrows. In all tests the patient's eyes are closed. The best comparison is the contralateral (if normal) extremity. The degree of medical impairment is affected by pain. A simple grading scheme has been presented: 100% = P4 (prevents all activity); 75%= P3 (prevents some activity); 50% = P2 (interferes with activity); 25% = P1 (annoying); and 0% = P0 (normal).
The best current reference for the evaluation of permanent impairment is the American Medical Association's Guides to the Evaluation of Permanent Impairment (3rd ed. [revised], 1990). This is a comprehensive publication, One must remember, however, that disability determination is an administrative and non-medical decision that defines the patient's ability to engage in personal, social, and occupational activities related to earning capacity in a given social and economic situation.
|M4||All synergic and independent movements are possible|
|M3||All important muscles act against resistance|
|M2||Return of perceptible contraction in both proximal and distal muscles|
|M1||Return of perceptible contraction in proximal muscles|
|Proximal and Distal Muscles Innervated by Peripheral Nerves|
|Proximal Muscle||Distal Muscle|
|Brachioradialis||Abductor pollicus longus|
|Extensor carpi radialis longus||Extensor pollicis longus|
|Extensor digitorum communis||Extensor indicis|
|Extensor carpi ulnaris|
|Pronator teres||Abductor pollicis brevis|
|Flexor carpi radialis|
|Flexor digitorum superficialis|
|Flexor pollicis longus|
|Flexor carpi ulnaris||Abductor digiti quinti|
|Flexor digitorum profundus (ring and little)||Interossei|
|Common Peroneal Nerve|
|Tibialis anterior||Extensor digitorum brevis|
|Extensor digitorum longus|
|Extensor hallucis longus|
|Gastrocnemius and soleus||Abductor hallucis|
|Tibialis posterior||Intrinsic muscles of sole of foot|
|Flexor digitorum longus|
|Flexor hallucis longus|
|British and Moberg Sensibility Scale|
|Two-point discrimination distance of 12 mm or less-tactile gnosis|
|Two-point discrimination distance of 12-15 mm||Fair|
|S3+||Some recovery of two-point discrimination within the autonomous area of the nerve||Poor|
|S3||Return of superficial cutaneous pain and tactile sensibility throughout the autonomous area with disappearance of any previous over-reaction||Bad|
|S2||Return of some degree of superficial cutaneous pain and tactile sensibility within the autonomous area of the nerve|
|S1||Recovery of deep cutaneous pain sensibility within the autonomous area of the nerve|
|SO||Absence of sensibility in the autonomous area of the nerve|