The structure of a peripheral is shown in Fig. 94.1. The basic structure of a nerve comprises a series of axons which are grouped together to form fascicles. Groups of fascicles together form a complete nerve. The axons are covered by a loose gelatinous collagen matrix called endoneurium. This has minimal tensile strength. Schwann cells surround individual myelinated axons in many peripheral nerves and help insulate the nerve and increase conduction speed. Groups of axons arranged into fascicles are collectively surrounded by perineurium. This is a connective tissue layer with selective permeability that is thin but dense with high tensile strength. The bundles of fascicles are covered by epineurium, which represents the outer layer of the nerve. This contains collagen and elastin fibers and is surrounded by a thin loose areolar tissue called mesoneurium, which is critical for normal nerve excursion during movement. Nerve repair is most commonly performed by suturing the epineurium to reconstitute complete external nerve continuity (an epineurial repair). In some cases, grouped fascicular repair is performed instead. In this case, sutures are placed in the perineurium. When nerve injury occurs, a predictable set of processes are initiated. These are described in Fig. 94.2.1–3 Fig. 94.1 Nerve anatomy. Nerves are formed from multiple axons running in parallel. Axons are grouped together in bundles to form fascicles. Multiple fascicles collectively form the nerve. Mesoneurium Epineurium Perineurium Endoneurium Nerve fiber Microvessels Axon Fascicles Vaso nervosus Axon Basement membrane Node of Ranvier Myelin sheath Nuclei of Schwann cells
2. Jabaley ME. Current concepts of nerve repair. Clin Plast Surg 1981;8(1):33–44
3. Maggi SP, Lowe JB III, Mackinnon SE. Pathophysiology of nerve injury. Clin Plast Surg 2003;30(2):109–126 ABERRANT NERVE ANATOMY 2. Which one of the following anatomic abnormalities could account for the ability to abduct some of the fingers, despite complete median and ulnar nerve transection at the wrist? The Froment-Rauber anastomosis is a rare condition in which there is a connection between the posterior interosseous nerve (superficial radial nerve) and the ulnar nerve motor branches innervating the dorsal interossei (typically first, second, or third). This could explain why a patient could still have residual finger abduction following median and ulnar nerve division. According to Guo et al,1 Froment2 first described the distal continuation of the posterior interosseous nerve (PIN), and Rauber3 later reported a similar finding. Spinner4 subsequently referred to this anomalous connection as the Froment-Rauber nerve. The Martin-Gruber and Riche-Cannieu anastomoses involve motor connections between the ulnar and median nerves proximally and distally and lead to diagnostic confusion by masking injury when one but not both nerves is affected. The Berrettini connection is a sensory connection between the ulnar and median nerves, so it would not affect ulnar motor nerve function. Double-crush phenomenon5 refers to the scenario where nerve entrapment at one location can predispose an individual to symptoms of clinical nerve compression at another site along that same nerve despite only minimal compression at that second site. Focal compression can affect axoplasmic flow and increase the susceptibility to further minor insults elsewhere along the nerve length. An example is thoracic outlet syndrome (TOS) affecting C8/T1/medial cord, which may lower the threshold for symptoms of ulnar nerve compression at the elbow (or vice versa), producing significant symptoms despite relatively minimal compression at the either site on electrophysiological testing. In such cases, patients often benefit from decompression of the simplest site to treat in the first instance, followed by review of symptoms. Therefore, in the example above, treating the cubital tunnel despite minimal electrophysiological changes at this site may resolve both the cubital tunnel and TOS symptoms and signs without having to treat the TOS. Treatment may no longer be required at the other sites of compression, as overall nerve function is often improved, and the other site becomes asymptomatic.
4. Spinner M. Injuries to the Major Branches of Peripheral Nerves of the Forearm. 2nd ed. Philadelphia: WB Saunders; 1978
5. Upton AR, McComas AJ. The double crush in nerve entrapment syndromes. Lancet 1973;2(7825):359–362 3. After a peripheral nerve has been divided, which one of the following processes is responsible for guiding the regenerating axon to the correct distal nerve stump? Neurotropism is a process where a chemotactic gradient attracts a regenerating axon toward the correct end target at the distal nerve stump. Initially around half of axonal sprouts will make an incorrect connection and this is subsequently modified such that correct realignment is achieved. Groups of damaged axonal endings form a growth cone and these ends grow toward the distal nerve ends guided by the neurotropic factors. Neurotrophism is also important in nerve regrowth but more precisely refers to the nutritional support provided to axons connecting with the correct nerve stump. Factors include nerve growth factor, insulin-like Fig. 94.2 Nerve regeneration. A, When a myelinated axon is injured, degeneration occurs distally and for a variable distance proximally. B, Multiple regenerating fibers sprout from the proximal axon, forming a regenerating unit. A growth cone at the tip of each regenerating fiber samples the environment and advances the growth process distally. C, Schwann cells eventually myelinate the regenerating fibers. D, Because it is from a single nerve fiber, a regenerating unit that contains several fibers is formed, and each fiber is capable of functional connections. Endoneurium Basement membrane Axon Endoneurium A C B D Fibroblasts Individually myelinated sprouts Schwann cell Fibroblast Nerve fiber regeneration sprout Growth cone with filopodia Wallerian degeneration in distal nerve fiber Basement membrane Myelin sheath Axon growth factor, and epidermal growth factor. When a nerve is divided, the distal stump undergoes Wallerian degeneration. The damaged Schwann cells and macrophages form a neural tube and organize into bands called bands of Bunger. This process forms a scaffold or conduit for nerve regeneration. Proximal to the injury a process called chromatolysis occurs with axon degeneration. The main objective of nerve repair is to return continuity to the framework of damaged nerve such that organized axonal regeneration can proceed along the correct path. When incorrect alignment and excess scarring occur, a neuroma will form with disorganized nerve ends, resulting in pain and dysfunction.1
Two-point discrimination is a test of nerve density most applicable to nerve injuries and less reliable in compression neuropathies. A normal static two-point value is up to 6 mm for the volar fingertip. A moving two- point discrimination is 2 to 3 mm when testing perpendicular to the digit, moving longitudinally from proximal to distal. Specialized calipers are used to test this and the patient is asked to confirm whether they feel one or two pressure points with the caliper tips set apart at differing distances. It is important to stay on the ulna or radial aspect of the digit without crossing over, otherwise a false result will occur with sensation being due to different digital nerves. Semmes-Weinstein monofilaments are not used for two-point discrimination. They are used to measure pressure thresholds and are most applicable to compression neuropathies. They are often used in diabetic patients to assess for protective sensation in the feet. Other tests include vibration thresholds and Tinel’s sign, where tapping over a site of nerve degeneration/regeneration produces paresthesia and/or an electrical sensation.1–3
Although the nerve ends are less amenable to mobilization in the digits than more proximally, it is unlikely that there will be sufficient retraction or fibrosis to prohibit primary repair during the first week. There is no established advantage of one repair over another when comparing epineurial and grouped fascicular repairs; however, there is a balance to be struck between potentially more accurate alignment with a grouped fascicular repair and increased scarring from the foreign body reaction to suture material. In the small digital sensory nerves, it is an accepted practice to use epineurial sutures, as there are few fascicles and good alignment is readily achieved with an epineurial repair. Regardless of the technique used, bulging fascicles should be trimmed to avoid buckling of the repair and subsequent misdirection of the regenerating axons. If there is a nerve gap, it is preferable to insert a good quality graft (if >5 mm) or use a conduit to bridge a short gap (<5 mm) than to perform a tight primary repair ameliorated by flexing the digit. The digit will need to be mobilized within a few weeks, at which point there will be tension across the nerve repair site again before regeneration has occurred. Excessive tension is recognized to have a detrimental effect upon nerve regeneration; however, some tension is considered acceptable.1,2 Use of a postoperative extension blocking splint is common in the first 2 to 3 weeks following digital nerve repair; however, this should not be used as a substitute for a nerve graft or conduit where indicated.
A single sural nerve may provide 30 to 40 cm of suitable nerve graft material. Three to five individual nerve grafts, depending on the cross-sectional size of the graft, might be used in parallel for an ulnar nerve defect (often termed “cable grafting”). Anterior transposition of the ulnar nerve at the elbow can gain a small amount of additional nerve length and may well be indicated, even when nerve grafts are planned as reducing the length of the grafts would be beneficial. While the nerve may have suffered an additional zone of injury to the 4-cm defect, anterior transposition may still be appropriate to both reduce the defect length and to move the nerve repair outside the zone of injury if applicable. Vascularized nerve grafts are not common and are generally reserved for extensively scarred tissues, such as tissues that have undergone radiotherapy, or in longer defects. Nerve conduits generally perform better in smaller nerves over shorter defects, such as a 3-mm digital nerve gap.1,2
When performing direct nerve repair, there is no proven advantage in using an epineurial versus grouped fascicular technique, and a perineural technique would be technically difficult to achieve and involve an excess of foreign material. When repairing nerves that have obvious motor and sensory components with consistent topology, such as the ulnar or median nerves in the distal forearm, repairing groups of fascicles may be helpful to more accurately align motor and sensory components. In this scenario, there is likely to be clean cut with no tissue loss, so neither nerve grafting, a bridging conduit, nor significant mobilization would usually be required.1–3
For small nerve gaps in the upper limb, selection of a local nerve graft donor site is preferable; so for radial nerve repair, the lateral antebrachial cutaneous nerve is a good choice and provides 5 to 8 cm total graft length. However, the nerve is variable in cross-sectional size, and in the scenario described the defect is already 6 cm and likely requires further sharp debridement before graft inset, leaving an even longer defect. The multiple lengths of nerve graft required will therefore necessitate sural nerve harvest, which can provide 30 to 40 cm of graft. The PIN is a good option for cases where there is segmental loss of a digital nerve, as the donor site is easily accessed on the same limb, it leaves minimal morbidity, and is a good size match for digital nerves. Mobilization of a transected nerve can avoid nerve grafting, but the length of nerve gap described in this scenario cannot be closed directly unless there is significant shortening of other tissues, i.e., bone, muscle, and tendon as it may sometimes be necessary following major limb trauma. In general, up to 5 cm of humeral shortening can be tolerated in adults without significant problems with musculotendinous unit length.1 When mobilizing a nerve, it is considered acceptable to do so up to 25% of its length. Beyond this, the vascularity and function could be impaired. Other options to avoid grafting in some settings include transposition of the nerve to shorten this distance required (e.g., ulnar nerve at the elbow) or direct neurotization of the proximal nerve into a target muscle. Nerve conduits are not favored in long defects or in major nerves and are most commonly reserved for short gaps (<5 mm) in small nerves, such as in the finger.2
function? The British Medical Research Council (MRC) grading system is a useful and globally accepted approach to classify nerve function. Highet and Dellon have modified this to relate more specifically to nerve recovery following injury (Box 94.1). Motor recovery has six grades ranging from M0 (no muscle contraction) to M5 (complete recovery). Sensory recovery also has six grades, but these range from S0 (no sensory recovery) to S4 (complete recovery with two-point discrimination 2–6 mm), with S3 being split into two different grades designated S3 and S3+. This terminology allows comparison of results and accurate communication between clinicians regarding outcome following injury.1 BOX 94.1 HIGHET’S METHOD OF END-RESULT EVALUATION AS MODIFIED BY DELLON ET AL Motor recovery M0 No contraction M1 Return of perceptible contraction on both proximal muscles M2 Return of perceptible contraction in both proximal and distal muscles M3 Return of function in both proximal and distal muscles to degree that all important muscles are sufficiently powerful to act against gravity M4 Return of function as with stage M3; in addition, all synergistic and independent movements possible M5 Complete recovery Sensory recovery S0 Absence of sensory recovery S1 Recovery of deep cutaneous pain sensibility within autonomous area of nerve S2 Return of some degree of superficial cutaneous pain and tactile sensibility with autonomous area of nerve S3 Return of superficial cutaneous pain and tactile sensibility throughout autonomous area, with disappearance of any previous overresponse S3+ Return of sensibility as with stage S3; in addition, discrimination within autonomous area (7–15 mm) S4 Complete recovery (two-point discrimination, 2–6 mm) Note: In the hand, proximal muscles are defined as extrinsic and distal muscles are defined as intrinsic.