Nerve Architecture

Most peripheral nerves are mixed and contain motor, sensory, nociceptive, and autonomic fibers.¹ The autonomic fibers are responsible for sudomotor control, vasoreactivity, and piloerection. The main constituent of a peripheral nerve is connective tissue, which can vary from 85% in the sciatic nerve at hip level to about 25% for the peroneal nerve at fibular level.² The external sheath, the epineurium, is constituted from connective tissue with an amount of collagen and elastic fiber; it contains abundant blood vessels and protects the nerve against compression. The endoneurium provides connective tissue support for the nerve fibers. A certain degree of fiber undulation enables a physiologic amount of nerve stretch.^3,4 Nerve elongation below 12% of its resting length can be compensated for without functional damage, but venous flow is already blocked when a nerve is stretched by 8%, and a stretch of 16% produces ischemia.⁵ Attached to the epineurium is another capillarized outer gliding layer, by some referred to as the mesoneurium or paraneurium, that is traversed by vascular channels supplying the nerve. This mesoneurium also allows the nerve to glide between tissue planes during physiologic movement.^6–8 It is important to restore and retain gliding of injured nerve in order to prevent its tethering and entrapment.^4,9 The epineurium includes the internal epineurium or interfascicular epineurium, which ensheathes the fascicles. This is less compact than the external epineurium. Directly around each fascicle is the perineurium, which is constituted by perineurial cells in between circular, oblique, and longitudinal strands of collagen fibers. The perineurium is responsible for maintaining the physiologic milieu of the conducting elements, and it acts as a diffusion or blood-nerve barrier. Breaching the perineurium interferes with conduction and provokes demyelination of the contained nerve fibers.¹⁰ The role of perineurial fibroblasts in trauma appears to be underestimated because they initiate and maintain the connective tissue reaction and as such contribute to neuroma development.^11–13 Neuroma formation should be regarded as nondirected and a futile attempt at regeneration, where axons do not manage to reach the appropriate distal basal lamina and cannot reconnect to their natural target organ.

A further connective tissue layer is the endoneurium, which surrounds each myelinated fiber and groups of unmyelinated fibers. The endoneurial layer’s role in injury and repair is less well understood.

The vascular supply of peripheral nerves is abundant. At regular intervals, collateral vessels enter through the mesoneurium to connect to the nerve’s central artery.¹⁴ If a nerve is circumferentially mobilized, several of these “segmental” arteries are disconnected, and the central vessel maintains the blood supply.¹⁰ It is therefore possible to circumferentially mobilize a nerve over a relatively long stretch without putting the nerve at ischemic risk.¹⁰ Some of these extrinsic pedicles sustain vascularized nerve grafts, as in the case of the ulnar nerve.^15,16 Nerves, however, differ extensively in their vascular supply; the tibial, for example, is more richly supplied than the common peroneal nerve at knee level.¹⁷

Timing of Operative Therapy

The Schwann cells, the skin, and other target organs are rich sources of neurotrophins that are essential for the development, maturation, and maintenance of the cell bodies. Transection of a peripheral nerve leads to central cell death by deprivation of neurotrophins (i.e., nerve growth factor). Progressive neuronal death, ischemia, and fibrous proliferation are important limiting factors for useful recovery.³⁵ There is extensive evidence for progressive neuronal death to occur after a critical time window has passed. Sensory and motor neurons appear to differ in the onset of such cell loss. There is also evidence that early nerve repairs can stop this process of neuron loss.³⁶ Early repair improves the reconstructed nerve’s regenerative capacity. The efficacy of axonal regeneration is significantly affected by the amount of cell loss already present at the time of repair.^37–40 Central changes after peripheral nerve injury are more extreme in more proximal, more extensive, and more violent injuries and thus are an important factor in prognosis after repair.^22,41

When a nerve lesion is deep enough to interrupt the axons and to separate them from the cell nucleus, wallerian degeneration¹⁹ (anterograde degeneration) is the consequence. This is not a consequence exclusively of complete transection but also of profound crush or severe traction, as happens in violent blunt injuries. When there is no regeneration of axons into the distal stump, changes will occur in the target organ that over time become irreversible:^42,43 Motor end plates disappear, and the denervated muscle becomes fibrosed. Studies of central and peripheral conduction are of inestimable value in the analysis of injuries to the brachial plexus when these can be operated within 60 hours of the injury. This implies that injured nerves should be explored and repaired as soon as possible, unless there are realistic chances that the lesion bears enough potential for spontaneous regeneration to a functional level. In those cases, observation is justified. However, a favorable lesion might also progress to a less favorable one if the original cause is not addressed. Recovery is likely for the nerve accidently encircled by a suture or crushed under a plate if the cause is urgently removed. If that cause remains for days or weeks, a much more unfavorable lesion develops. One also cannot overemphasize the significance of the worsening pain and the deepening of nerve lesion caused by expanding hematoma or ischemia. The vulnerability of the lumbosacral plexus to expanding hematoma was discussed by Donaghy.⁴⁴ Nerves crushed in a swollen ischemic limb or in a tense compartment progress from conduction block to much deeper and much less favorable degenerative lesions.

Some crucial clinical insights regarding timing have been known for a long time. In 1908, Sherren examined 50 cases of acute suture performed at the London Hospital.^44a Pain sensibility recovered before touch sensibility; tactile localization continued to improve for more than 2 years. Recovery of power was rather slower. There was no recovery in only one patient, whose wound had become infected. Sherren recommended primary suture “because the prognosis after secondary suture is more unfavourable.”^44b In 1924, Platt and Bristow reviewed the late results of nerve injuries treated in the First World War and noted the “extreme perfection attained after so-called primary suture,” acknowledging that the more severe gun shot wounds of nerves were treated by secondary suture.^44c In 1937, Platt and Bristow Platt wrote, “in primary sutures performed under ideal conditions, complete recovery of motor power and recovery of protopathic sensibility at least, is to be expected … however, in more extensive wounds with widespread bruising and multiple tendon injuries, and in wounds in which infection had already secured a hold, partial or complete failure after primary suture is almost inevitable.”^44d Nine years later, Zachary and Holmes compared 55 cases of primary sutures of nerves referred to the Peripheral Nerve Injury Centre at the Wingfield-Morris Hospital, Oxford, England, during the years 1940 to 1944, with 36 “early” secondary sutures. The results of secondary suture were distinctly better. The primary repair was resected and the nerve resutured in 16 patients. Histologic examination of the resected material revealed a number of causes for the failure of the first operation: poor matching of the proximal and distal stumps; coarse suture material lodged between the stumps; separation of the stumps; and dense scar between the stumps or within the distal stump. Zachary and Holmes concluded, “Formal nerve suture should be undertaken at the earliest moment when it is possible to recognise the extent of damage to the nerve, excise the injured segment, and bring together the mobilised nerve ends without the prospect of undue post operative tension.” These early contributions came at a time when antibiotics were unavailable and when grafting of nerves was rarely performed in Great Britain.

Glasby used the freeze-thawed muscle graft (FTMG) in a series of experiments that provided evidence about the factors governing the quality of regeneration after nerve repair.⁴⁵ The findings were decisive. Regeneration was worsened by delay and also by association with arterial injury, fractures, or cavitation and hematoma.^46,47

Improved results after urgent repair have been reported for the median and ulnar nerves,^48–51 the radial nerve,⁵² the musculocutaneous nerve,⁵³ the sciatic nerve,⁵⁴ the common peroneal nerve,^55,56 and the closed traction lesion of the brachial plexus.^51,57 Kato and coworkers⁵¹ showed that recovery of function and relief of pain were decisively better in urgent repairs of the closed traction lesion of the brachial plexus. The spinal accessory nerve appears to be the one exception to the rule because it exhibits good recovery of function even after substantially delayed repairs. Uncomplicated open wounds and nerves can be left for 24 hours until an experienced surgeon can address them. When, however, a nerve injury is associated with damage to a major blood vessel, with an impending threat of peripheral ischemia, or with increasing pressure within a fascial compartment, delay is not permissible. The case is an emergency, as it is with cases of open fracture or fracture-dislocation.

Thus, the clinician must always bear in mind that the sooner the distal segment is connected to the cell body and proximal segment the better the result will be.

The primary limitation of very early repair is that there is a significant risk that even a very experienced surgeon will be unable to determine how much of the proximal and distal stump must be resected. Leaving in place any length of nerve that is irretrievably damaged is often the cause of failed repairs—such as those observed by Zachary and Holmes that had dense scar between the stumps. Because of this, when there is any component of blunt injury involved, a delay of a few weeks may be necessary.¹⁰ On the other hand, urgent operation enables detection of rupture of the perineurium, and studies of proximal and distal conduction ease the difficulties relating to the appropriate level of section.

The World War II experience with the urgent suture of nerves was dismal.^58,59 The results of delayed repair, in special units, were surprisingly good, and they fell a little short of modern series.^59A Urgent repair of nerves injured in current conflicts show promise.^66A

Classifications and Grading

Seddon distinguished among three types of nerve injury in his 1943 classification²⁰:

The implications of this classification with regard to chances for spontaneous recovery are seemingly straightforward, and the classification is easy to apply and remember. That is why it still is the most popular classification system used. In neurapraxia and axonotmesis, the prognosis for recovery is favorable, given that the cause is removed. With neurotmesis, however, there is no recovery without nerve repair. An important factor that frequently is forgotten by clinicians, who have discovered electrophysiologic signs of regeneration in an injured nerve, is that unless the cause of the lesion is removed, an initially favorable prognosis can change to a less favorable one (e.g., if an injured nerve is still compressed). And for this and various other reasons, “electrophysiologic signs of life” should never preclude surgical exploration, when it is necessary.

Sunderland’s classification system, which was introduced in 1951, is more elaborate and recognizes five degrees of severity.⁶⁰ A neurapraxic lesion is the equivalent to a Sunderland type I lesion. In principle, lesions with axonolysis (as equivalent to Seddon’s axonotmesis) are further differentiated between those that have an intact endoneurium (Sunderland type II) and those that have not (Sunderland type III). A type IV lesion denotes complete disruption of the contents of the epineurium, both connective tissue elements and axons, but with the nerve still in continuity, and a type V lesion is a severed or pulled-apart nerve that is not in continuity.

The question remains of what way classifications can actually really depict the clinical picture and as such have relevance for clinical decision making. In theory, falling in the continuum between need to graft a lesion and leaving the lesion alone after decompression and external neurolysis is a Sunderland type III lesion, in which there is considerable internal fibrosis that effectively precludes that enough sprouting axons overcome this soft tissue barrier to sprout distally in an orderly fashion. Some patients with Sunderland type III lesions recover, and some do not. This is why nerve action potential (NAP) recording is valuable for type II, III, and IV lesions. In this Sunderland classification threshold situation, there is axonolysis, the endoneurium is destroyed and fibrotic,⁶¹ and the perineurium theoretically could still be intact—and yet such a lesion has a poor chance for recovery without grafts.

In actuality, the different sectors of a lesion of the whole nerve can depict an array of injury grades, unless the lesion is neurapraxic or neurotmetic. Part of the lesion might show a gap (Sunderland type V) abutted by former nerve tissue that transformed into fibrous tissue (Sunderland type IV), and the rest of the nerve’s cross section might have axonolysed fascicles with fibrotic endoneurium (Sunderland type III). A tiny portion of the cross section, however, might conduct a compound nerve action potential because the axonal integrity of a minor portion of the fascicles is still intact. Thus the assignment of the whole nerve grades does not really reflect what should be done surgically in such a case (which would be a split repair after careful internal neurolysis in the case presented).

It helps clinical decision making with regard to surgery to simplify and distinguish a nondegenerative (focal conduction block) from a degenerative nerve^62,63 lesion with axonal division and ongoing wallerian degeneration (axonal discontinuity in all its forms: axonotmesis and neurotmesis, or the Sunderland equivalent spectrum from types II to V).⁶⁴

In the case of a complete nerve palsy in conjunction with vasomotor and sudomotor paralysis (dry, red, and warm skin) and a Tinel sign at the level of the lesion, a mere conduction block (neurapraxia, nondegenerative lesion) is highly unlikely. Neuropathic pain indicates partial destruction of a nerve’s integrity. A very vivid and strong Tinel sign at the level of the lesion points toward axon rupture.

Closed Traction Injury

A combination of the blunt mechanisms of stretch/traction and contusion/compression is a frequent cause of acute nerve injury. Traction can lead to rupture of nerve and artery. Most frequently affected by traction are the following:

If complicated by an arterial lesion, this group of injuries has an unfavorable prognosis.

The most common type of civilian nerve trauma most likely is a stretch-related injury in context with a motor vehicle crash.^66,74,75 Three percent (2.8%) of a Canadian trauma population of 5777 patients treated between 1986 and 1996 sustained associated peripheral nerve injuries (162 of 5777 patients).⁷⁴ Motor vehicle crashes were the predominant cause (46%). Eighty-three percent of the patients were male, and the mean age was 34.6 years. Seventy-five percent affected the upper extremities (121 of 162 injuries). The radial nerve was the most frequently injured nerve, with 36% (58 of 162 injuries), and the peroneal nerve was the most frequently injured lower limb nerve with 24% (39 of 162 injuries). Surgery was required in 54%. Brachial plexus injuries were identified in 1.2% of multitrauma patients presenting to the same major regional trauma facility (54 of 4538 patients seen at Sunnybrook Hospital, Toronto, Canada).⁷⁵

Open Injury with Transection

With open, complete lesions (Sunderland type V, neurotmetic), a primary reconstruction with an epineurial end-to-end suture is the objective, provided the injury is sharp. Most open lesions are caused by a knife, glass, or a surgeon’s scalpel wound.

In contrast, blunt injuries (Web Fig. 240-1), commonly caused by open fractures or penetrating missile injuries, are better approached with a delayed end-to-end suture. There is extensive tissue damage with a high risk for sepsis. Retraction of stumps is usually performed. If possible, it is helpful to gently approximate nerve stumps to each other or to adjacent structures at the first operation. The nerve stumps are readapted after resection of the stump neuromas within a 2- to 3-week interval. This form of intentionally delayed repair due to unfavorable soft tissue condition at the time of injury is termed delayed end-to-end suture.

WEB FIGURE 240-E1 Example of delayed secondary repair of blunt open sciatic nerve injury with soft tissue loss, infection, and compound femur fracture (“untidy wound”) after motorcycle accident. A, The primary wound before débridement and fracture nailing. B, Delayed secondary nerve reconstruction at middle third of the femur. Exposure of bluntly ruptured and retracted nerve, with nerve stumps on yellow rubber dam background material. C, Interpositional graft reconstruction. D, Wound closure with tissue substitute.

(A, Courtesy of the Trauma Unit “Weiden-Germany.”)

Unfortunately, the bulk of lacerating injuries (Web Fig. 240-2) are blunt and also have ragged, contused, and compressed margins, necessitating more nerve resection and graft interposition.

WEB FIGURE 240-E2 Primary repair. A, An 80% section of the femoral nerve after iatrogenic injury. The lesion was repaired 48 hours after the iatrogenic injury. B, A “tidy” laceration at the wrist that was repaired primarily.

(Copyright Rolfe Birch.)

Sharp transections can often be sutured end to end, and their prognosis is excellent.

Penetrating Missile Wounds

Penetrating missile wounds are blunt injuries and mainly result in contusion and stretch. Most are caused indirectly because the projectile trajectories do not strike the nerve in 85% of cases. However, many of the recited data in the literature have been carried over from older reports⁷⁶ and thus describe injuries caused by older and completely different firearms.^10,77–79 More current reports are related to the Serbo-Croatian wars and Middle Eastern combat activity.^66,66a,80 For example, brachial plexus lesions associated with complete loss of function have been demonstrated to benefit from surgery, particularly in those associated with injuries to C5, C6, C7, and lateral and posterior cord.^80,81 High-velocity missiles can have a direct impact but also can cause impact by the produced shock wave and by cavitation. A “near miss” creates a shock wave with instant high-pressure damage (explosion) on the way to the nerve, followed by low-pressure damage (implosion) on the way out.^10,81–84 A serious problem is the open wound. The damage with a near or close miss can range from mere neurapraxia to a complete degenerative lesion. Lesions that show no spontaneous recovery are thus usually explored with delay and then often need graft repair. Of course, pain syndromes and associated other injuries are a frequent concern. The Red Cross wound classification system is helpful for describing this type of injury.^66a,85

Iatrogenic Injury

A whole chapter of this edition is devoted to iatrogenic injury lesion complex (see Chapter 246), and there is a reason: in some centers, these lesions make up 20% to 25% of operated nerve injuries.^{67–70,86,87} Because of its importance for a nerve surgeon’s practice, some facts about this entity deserve reiteration. Despite the fact that cases of inadvertently injured nerves are not declining, and all mechanisms have been described, the appropriate treatment usually still is delayed. Treatment regimens should follow exactly those for traumatic nerve injuries of other origin. One element of delay certainly is that clinicians frequently embark on false hopes whenever a nerve injury has been induced through the hands of a physician. Whenever there is a wound over a nerve that is nonfunctional, chances come close to certainty that this nerve would benefit from exploration because it is probably cut.

History, Symptoms, and Signs

When and how an injury occurs are important aspects that guide our decision making. High-velocity injury; compound fracture and wounding; and accidental, criminal, or surgical history are likely to mean that there has been a serious lesion. The use of a knife, often enough in the hand of a surgeon, is an indication that a nerve is likely to have been partly or completely severed. The subclavian artery is ruptured in 10% of complete lesions of the brachial plexus and in as many as 30% of cases of violent traction injury of the infraclavicular brachial plexus. The incidence of arterial lesion is high after fracture-dislocations of the elbow and higher still after fracture-dislocations of the knee. Knowledge about the mechanism of an injury, the initial degree of dysfunction, and the course or lack of functional regeneration are most important aspects, which in conjunction with a detailed and systematic examination help us to localize and assign level and depth to an injury, when we cannot assess the patient initially. It is of utmost importance to judge the extent of injury, distinguishing between degenerative and nondegenerative injury, and to determine the length of the nerve and severity of the injury. The diagnosis of the extent of injury depends on history and signs on electrical examination and may involve the use of magnetic resonance imaging (MRI).

The inexperienced surgeon usually is enlightened by the opportunity to observe what a thorough and nevertheless quick systematic examination by an expert can yield with regard to exact branch localization, level and extent of injury, and potential for recovery. To detect the level, thorough knowledge of branching pattern and supplied muscles and sensory area is crucial. A helpful guide is a systematic table and scheme that is routinely used to document the findings. It is valuable to develop an individual systematic sequence of muscles to examine for each nerve, which usually follows the innervated areas and thus branches from proximal to distal. The actual steps in testing the individual muscles is something that is best learned from an expert. By far, the best guide to examination is still O’Brian’s Aids to the Examination of the Peripheral Nervous System.⁹¹ There are some “trick movements” that can compensate for loss of nerve and muscle function by activating other muscle groups supplied by different and more functional nerves.¹⁰ Thus, sometimes a complete lesion is deemed partial and followed instead of being repaired. Examples of trick movements include the following:

Muscle power is graded by most examiners according to the British Medical Research Council (BMRC) system, which has 5 grades of strength (0—complete loss of function, to 5—normal muscle power). This is documented individually for each muscle. Evaluation schemes that account for more functional aspects are useful, but they are also more complex. Such schemes need to be applied uniformly if crude interobserver differences are to be avoided. This usually requires documentation forms, which also list descriptions of the different functional grades.

The BMRC was developed by Highet for war wounds in 1943¹⁰⁰ and was later used in poliomyelitis. Thus, in the BMRC system, grade 3 is only contraction against gravity, 4 mild or moderate pressure, and 5 normal. In contrast, the Louisiana State University Hospital (LSUH) system¹⁰ grades are as follows: 1—observable contraction but not enough to overcome gravity, 2—against gravity only, 3—against gravity and mild pressure, 4—against gravity and moderate pressure, and 5—close to normal.

In the acute setting, the radial, median, and ulnar nerves are tested by asking the patient to form an O between the thumb and little finger, to give the thumbs-up sign, and to open and close the fingers like a fan.

Sensory loss is determined by response to light touch and pinprick and by the ability to localize stimuli.

Sensitivity and sympathetic function give precious clues to the completeness or extent of functional loss. Apart from weakness or paralysis of muscles, the early signs of nerve injury are alteration or loss of sensibility, vasomotor and sudomotor paralysis in the distribution of the affected nerve, and an abnormal sensitivity over the nerve at the point of injury. After severe injury of a nerve with a cutaneous sensory component, the skin in the distribution of the affected nerve is warm and dry starting within 48 hours of trauma. If possible, sensation to light touch and pinprick, vibration sense, position sense, and ability to localize stimuli should be tested and the affected area of skin recorded. Anhidrosis can easily be checked with loupes or an ophthalmoscope set on ±20 if in doubt. Warming of the skin, color change, and capillary pulsation in the fingertips indicate vasomotor paralysis. Ischemia affects the large fibers first, and thus discriminative sensibility and vibration sense are lost early.⁹² The palmar and plantar skin is scrutinized for changes in color and in sweating.

The Hoffmann-Tinel sign, as simple as it might be, is an effective means to detect the point of lesion and to monitor, or more likely rule out, any progress of recovery (see earlier).

A painful nerve is injured or compressed, or both. The occurrence of pain after injury often means that the noxious process is continuing (Web Fig. 240-3). Acute neuropathic pain is characterized by loss of sensation; by painful, spontaneous sensory symptoms throughout the nerve’s territory (dysesthesia); and by lancinating or shooting pain irradiating into the distribution of a main nerve. A constant crushing, bursting, or burning pain in the otherwise undamaged hand or foot indicates serious and continuing injury to major trunk nerves. Progression of sensory loss with a deep bursting or crushing pain within the muscles of the limb, often accompanied by allodynia, can indicate impending critical ischemia. A regular feature of injury caused by critical ischemia is neurostenalgia, which indicates continuation of the noxious process and sometimes also deepening of the lesion. Partial nerve injuries are at times excruciatingly painful. Causalgia is uncommon, and it responds well to the correct operation. Deafferentation pain is related to the death of neurons on the dorsal root ganglion (herpes zoster) or to lesions of the dorsal root of the spinal nerve.^90a

WEB FIGURE 240-E3 Bone fragment (small square and circles) that has been dissected out from brachial plexus at the retroclavicular and infraclavicular level months after the accident. The fragment maintained a “neurostenalgic picture.” The patient was complaining of ongoing severe neuropathic pain since the accident with an electrifying element, without typical features of deafferentation and without radiologic suggestion of root avulsion. Despite the clinical picture of a severe extended upper brachial plexus lesion (C5, C6, and C7), the patient was referred with considerable delay.

Joint function is extremely important to assess. The passive range of motion must be assessed and recorded.

Any soft tissue or bony injury, tendon avulsion, muscle tear, or associated vascular injury needs to be assessed and documented or ruled out.

Electrophysiology

The study of nerve conduction advises the clinician about the health of axons, about their myelination, and, when applied to the proximal stump of a nerve, about whether there is continuity between the exposed nerve and the spinal cord. Conduction across a nerve lesion indicates that at least some of the axons are intact.

After transection of a nerve, axons become inexcitable, and neuromuscular transmission fails. Direct stimulation of the nerve distal to the level of lesion elicits no response chronically. However, some conduction is maintained for some days after nerve transection. Fibrillation potentials appear as muscles are denervated, but their onset depends on the distance between the site of nerve lesion and the muscle, so there may be an interval of 2 to 3 weeks before fibrillations are seen. The reappearance of voluntary motor unit potential activity indicates that reinnervation is taking place, and the electromyographic evidence of this usually precedes clinical evidence of recovery. However, it is important to understand that “some recovery” is often not good enough to restore function. The finding of a few motor units showing reinnervation even at an early stage after injury does not imply that full recovery of a nerve will take place. In analysis of incomplete lesions of large nerve trunks, the clinician may be lulled into a sense of false security by electrodiagnostic evidence of an incomplete lesion. Such evidence should not be taken to imply that full recovery could be anticipated. Unless a nerve has been completely transected, it is likely that there will be mixed elements of neurotmesis, axonotmesis, and prolonged conduction block.

After nerve exposure, electrodiagnostic work is of inestimable value to assess whether a lesion in continuity has a chance for spontaneous recovery or will fare better with graft repair.^10,93,94 Somatosensory evoked potentials (SSEPs) can help to check for root avulsion.^95–97 NAPs for significant conduction require about 3000 to 4000 fibers of at least moderate size and some myelination across a lesion in continuity.^10,73

Imaging

The role of imaging in nerve trauma is to rule out root avulsion,^95,98,99 musculotendinous injury or tear (MRI, ultrasound), or bony injury (computed tomography [CT]), or to assess implanted metal (radiograph) in secondary nerve reconstructions. Ultrasound will gain increasing importance as an excellent means to assess whether a nerve has been torn apart or a neuroma-in-continuity has formed. Modern high-frequency ultrasound devices allow one to recognize fascicles within the nerve and, even more so, the lack of fascicles in case of internal scar (neuroma). However, fascicular continuity does not ensure, although it does favor, axonotmesis and future recovery of function.