Peripheral nervedisorders

NERVE STRUCTURE AND FUNCTIONPeripheral nerves are bundles of axons conductingefferent (motor) impulses from cells in the anteriorhorn of the spinal cord to the muscles, and afferent(sensory) impulses from peripheral receptors via cellsin the posterior root ganglia to the cord. They alsoconvey sudomotor and vasomotor fibres from ganglioncells in the sympathetic chain. Some nerves arepredominantly motor, some predominantly sensory;the larger trunks are mixed, with motor and sensoryaxons running in separate bundles.Each axon is, in reality, an extension or elongatedprocess of a nerve cell, or neuron (see Chapter 10).The cell bodies of the motor neurons supplying theperipheral muscles are clustered in the anterior hornof the spinal cord; a single motor neuron with its axonmay, therefore, be more than a metre long. The cellbodies of the sensory neurons serving the trunk an

PATHOLOGY

Nerves can be injured by ischaemia, compression,traction, laceration or burning. Damage varies inseverity from transient and quickly recoverable loss offunction to complete interruption and degeneration.There may be a mixture of types of damage in the variousfascicles of a single nerve trunk.Transient ischaemiaAcute nerve compression causes numbness and tingling within 15 minutes, loss of pain sensibility after30 minutes and muscle weakness after 45 minutes.Relief of compression is followed by intense paraesthesiaelasting up to 5 minutes (the familiar ‘pins andneedles’ after a limb ‘goes to sleep’); feeling isrestored within 30 seconds and full muscle powerafter about 10 minutes. These changes are due totransient endoneurial anoxia and they leave no traceof nerve damage.NeurapraxiaSeddon (1942) coined the term ‘neurapraxia’ todescribe a reversible physiological nerve conductionblock in which there is loss of some types of sensationand muscle power followed by spontaneous recoveryafter a few days or weeks. It is due to mechanical pressurecausing segmental demyelination and is seen typicallyin ‘crutch palsy’, pressure paralysis in states ofdrunkenness (‘Saturday night palsy’) and the mildertypes of tourniquet palsy.AxonotmesisThis is a more severe form of nerve injury, seen typicallyafter closed fractures and dislocations. The term means,literally, axonal interruption. There is loss of conductionbut the nerve is in continuity and the neural tubesare intact. Distal to the lesion, and for a few millimetresretrograde, axons disintegrate and are resorbed by

phagocytes. This wallerian degeneration (named afterthe physiologist, Augustus Waller, who described theprocess in 1851) takes only a few days and is accompaniedby marked proliferation of Schwann cells andfibroblasts lining the endoneurial tubes. The denervatedtarget organs (motor end-plates and sensoryreceptors) gradually atrophy, and if they are not reinnervatedwithin 2 years they will never recover.Axonal regeneration starts within hours of nervedamage, probably encouraged by neurotropic factorsproduced by Schwann cells distal to the injury. Fromthe proximal stumps grow numerous fine unmyelinatedtendrils, many of which find their way into thecell-clogged endoneurial tubes. These axonalprocesses grow at a speed of 1–2 mm per day, thelarger fibres slowly acquiring a new myelin coat. Eventuallythey join to end-organs, which enlarge and startfunctioning

NeurotmesisIn Seddon’s original classification, neurotmesis meantdivision of the nerve trunk, such as may occur in anopen wound. It is now recognized that severe degreesof damage may be inflicted without actually dividingthe nerve. If the injury is more severe, whether thenerve is in continuity or not, recovery will not occur.As in axonotmesis, there is rapid wallerian degeneration,but here the endoneurial tubes are destroyedover a variable segment and scarring thwarts any hopeof regenerating axons entering the distal segment andregaining their target organs. Instead, regenerating

fibres mingle with proliferating Schwann cells andfibroblasts in a jumbled knot, or ‘neuroma’, at the siteof injury. Even after surgical repair, many new axonsfail to reach the distal segment, and those that do maynot find suitable Schwann tubes, or may not reach thecorrect end-organs in time, or may remain incompletelymyelinated. Function may be adequate but isnever normal.The ‘double crush’ phenomenonThere is convincing evidence that proximal compressionof a peripheral nerve renders it more susceptibleto the effects of a second, more peripheral injury. Thismay explain why peripheral entrapment syndromesare often associated with cervical or lumbar spondylosis.A similar type of ‘sensitization’ is seen in patientswith peripheral neuropathy due to diabetes or alcoholism

CLINICAL FEATURESAcute nerve injuries are easily missed, especially ifassociated with fractures or dislocations, the symptomsof which may overshadow those of the nervelesion. Always test for nerve injuries following any significanttrauma. If a nerve injury is present, it is crucialalso to look for an accompanying vascular injury.Ask the patient if there is numbness, paraesthesia ormuscle weakness in the related area. Then examinethe injured limb systematically for signs of abnormalposture (e.g. a wrist drop in radial nerve palsy), weaknessin specific muscle groups and changes in sensibility.Areas of altered sensation should be accuratelymapped. Each spinal nerve root serves a specific dermatome(see Fig. 11.3) and peripheral nerves havemore or less discrete sensory territories which areillustrated in the relevant sections of this chapter.Despite the fact that there is considerable overlap insensory boundaries, the area of altered sensibility isusually sufficiently characteristic to provide ananatomical diagnosis. Sudomotor changes may befound in the same topographic areas; the skin feels drydue to lack of sweating. If this is not obvious, the‘plastic pen test’ may help. The smooth barrel of thepen is brushed across the palmar skin: normally thereis a sense of slight stickiness, due to the thin layer ofsurface sweat, but in denervated skin the pen slipsalong smoothly with no sense of stickiness in theaffected area.The neurological examination must be repeated atintervals so as not to miss signs which appear hoursafter the original injury, or following manipulation or

operation.In chronic nerve injuries there are other characteristicsigns. The anaesthetic skin may be smooth andshiny, with evidence of diminished sensibility such ascigarette burns of the thumb in median nerve palsy orfoot ulcers with sciatic nerve palsy. Muscle groups willbe wasted and postural deformities may become fixed.Beware of trick movements which give the appearanceof motor activity where none exists.Assessment of nerve recoveryThe presence or absence of distal nerve function can berevealed by simple clinical tests of muscle power andsensitivity to light touch and pin-prick. Remember thatafter nerve injury motor recovery is slower than sensoryrecovery. More specific assessment is required to answertwo questions: How severe was the lesion? How well isthe nerve functioning now?THE DEGREE OF INJURYThe history is most helpful. A low energy injury islikely to have caused a neurapraxia; the patient shouldbe observed and recovery anticipated. A high energyinjury is more likely to have caused axonal andendoneurial disruption (Sunderland third and fourthdegree) and so recovery is less predictable. An openinjury, or a very high energy closed injury, will probablyhave divided the nerve and early exploration iscalled for.Tinel’s sign – peripheral tingling or dysaesthesiaprovoked by percussing the nerve – is important. In aneurapraxia, Tinel’s sign is negative. In axonotmesis,it is positive at the site of injury because of sensitivityof the regenerating axon sprouts. After a delay of afew days or weeks, the Tinel sign will then advance at

a rate of about 1 mm each day as the regeneratingaxons progress along the Schwann-cell tube. Motoractivity also should progress down the limb. Failure ofTinel’s sign to advance suggests a fourth or fifthdegree injury and the need for early exploration. If theTinel sign proceeds very slowly, or if muscle groupsdo not sequentially recover as expected, then a goodrecovery is unlikely and here again exploration mustbe considered.Electromyography (EMG) studies can be helpful. If amuscle loses its nerve supply, the EMG will showdenervation potentials by the third weekexcludes neurapraxia but of course it does not distinguishbetween axonotmesis and neurotmesis; thisremains a clinical distinction, but if one waits too longto decide then the target muscle may have failedirrecoverably and the answer hardly mattersASSESSMENT OF NERVE FUNCTIONTwo-point discrimination is a measure of innervationdensity. After nerve regeneration or repair, a proportionof proximal sensory axons will fail to reach theirappropriate sensory end-organ; they will either haveregenerated down the wrong Schwann-cell tube orwill be entangled in a neuroma at the site of injury.Therefore, two-point discrimination (measuredwith a bent paper clip and compared with the oppositenormal side) gives an indication of how completelythe nerve has recovered. Static two-pointdiscrimination measures slowly adapting sensors(Merkel cells) and moving two-point discriminationmeasures rapidly adapting sensors (Meissner corpusclesand pacinian corpuscles). Moving two-point discriminationis more sensitive and returns earlier.

Normal static two-point discrimination is about 6mm and moving is about 3 mm.

Threshold tests measure the threshold at which a sensoryreceptor is activated. They are more useful innerve-compression syndromes, where individual receptorsfail to send impulses centrally; two-point discriminationis preserved because the innervation density isnot affected. Fine nylon monofilaments of varyingwidths are placed perpendicularly on the skin and thesize of the lightest perceptible filament is recorded.Locognosia is the ability to localize touch and can betested with a standardized hand map.The Moberg pick-up test measures tactile gnosis. Thepatient is blindfolded and instructed to pick up andidentify nine objects as rapidly as possible.Motor power is graded on the Medical ResearchCouncil scale as:0 No contraction.1 A flicker of activity.2 Muscle contraction but unable to overcome gravity.3 Contraction able to overcome gravity.4 Contraction against resistance.5 Normal power.

PRINCIPLES OF TREATMENTNerve explorationClosed low energy injuries usually recover spontaneouslyand it is worth waiting until the most proximallysupplied muscle should have regained function.Exploration is indicated: (1) if the nerve was seen tobe divided and needs to be repaired; (2) if the type ofinjury (e.g. a knife wound or a high energy injury)suggests that the nerve has been divided or severelydamaged; (3) if recovery is inappropriately delayedand the diagnosis is in doubt.Vascular injuries, unstable fractures, contaminatedsoft tissues and tendon divisions should be dealt withbefore the nerve lesion. The incision will be long, asthe nerve must be widely exposed above and belowthe lesion before the lesion itself is repaired. Thenerve must be handled gently with suitable instruments.Bipolar diathermy and magnification are essential.An operating microscope is ideal but magnifyingloupes are better than nothing. A nerve stimulator isessential if scarring makes recognition uncertain. Ifmicrosurgical equipment and expertise are not available,then the nerve lesion should be identified andthe wound closed pending transferral to an appropriateafacility.Primary repairA divided nerve is best repaired as soon as this can bedone safely. Primary suture at the time of woundtoilet has considerable advantages: the nerve endshave not retracted much; their relative rotation is usuallyundisturbed; and there is no fibrosis.

A clean cut nerve is sutured without further preparation;a ragged cut may need paring of the stumpswith a sharp blade, but this must be kept to a minimum.The stumps are anatomically orientated andfine (10/0) sutures are inserted in the epineurium.There should be no tension on the suture line. Opinionsare divided on the value of fascicular repair withperineurial sutures.Sufficient relaxation of the tissues to permit tension-free repair can usually be obtained by positioningthe nearby joints or by mobilizing and re-routing thenerve. If this does not solve the problem then a primarynerve graft must be considered. A traction lesion– especially of the brachial plexus – may leave a gaptoo wide to close. These injuries are best dealt with inspecialized centres, where primary grafting or nervetransfer can be carried out.If a tourniquet is used it should be a pneumaticone; it must be released and bleeding stopped beforethe wound is closed.The limb is splinted in a position to ensure minimaltension on the nerve; if flexion needs to be excessive,a graft is required. The splint is retained for 3 weeksand thereafter physiotherapy is encouraged.Delayed repairLate repair, i.e. weeks or months after the injury, maybe indicated because: (1) a closed injury was left alonebut shows no sign of recovery at the expected time;(2) the diagnosis was missed and the patient presentslate; or (3) primary repair has failed. The options mustbe carefully weighed: if the patient has adapted to thefunctional loss, if it is a high lesion and re-innervation

is unlikely within the critical 2-year period, or if thereis a pure motor loss which can be treated by tendontransfers, it may be best to leave well alone. Excessivescarring and intractable joint stiffness may, likewise,make nerve repair questionable; yet in the hand it isstill worthwhile simply to regain protective sensation.The lesion is exposed, working from normal tissueabove and below towards the scarred area. When thenerve is in continuity it is difficult to know whetherresection is necessary or not. If the nerve is onlyslightly thickened and feels soft, or if there is conductionacross the lesion, resection is not advised; if the‘neuroma’ is hard and there is no conduction onnerve stimulation, it should be resected, paring backthe stumps until healthy fascicles are exposed.How to deal with the gap? The nerve must besutured without tension. The stumps may be broughttogether by gently mobilizing the proximal and distalsegments, by flexing nearby joints to relax the soft tissues,or (in the case of the ulnar nerve) by transposingthe nerve trunk to the flexor aspect of the elbow. In thisway, gaps of 2 cm in the median nerve, 4–5 cm in theulnar nerve and 6–8 cm in the sciatic nerve can usuallybe closed, the limb being splinted in the ‘relaxing’ positionfor 4–6 weeks after the operation. Elsewhere, gapsof more than 1–2 cm usually require grafting.Nerve guidesIt is now apparent that nerve gaps can regeneratethrough a tube which excludes the surrounding tissuefrom each end. The tubes can be autogenous vein,freeze-dried muscle, silicone or metal; soluble guides(flexible at body temperature) which dissolve overweeks or months are also used. This technology offers

a simple way of avoiding a nerve graft yet achievingresults which are at least as good in both digital nervesand probably in main trunks.Nerve graftingFree autogenous nerve grafts can be used to bridgegaps too large for direct suture. The sural nerve ismost commonly used; up to 40 cm can be obtainedfrom each leg. Because the nerve diameter is small,several strips may be used (cable graft). The graftshould be long enough to lie without any tension, andit should be routed through a well-vascularized bed.The graft is attached at each end either by fine suturesor with fibrin glue.It is crucial that the motor and sensory fascicles areappropriately connected by the graft. There are varioustechniques which can help. Careful inspection of thefascicular alignment, structure and vascular markings isoften helpful. Enzyme-staining techniques can be used.Vascularized grafts are used in special situations. Ifthe ulnar and median nerves are both damaged (e.g.in Volkmann’s ischaemia) a pedicle graft from theulnar nerve may be used to bridge the gap in themedian. It is also possible to use free vascularizedgrafts for certain brachial plexus lesions.Nerve transferIn root avulsions of the upper brachial plexus, tooproximal for direct repair, nerve transfer can be used.The spinal accessory nerve can be transferred to thesuprascapular nerve, and intercostal nerves can betransferred to the musculocutaneous nerve. If bicepshas failed because too much time has passed since theinjury, an entire muscle (gracilis or latissimus dorsi)can be transferred as a free flap, attached between

elbow and shoulder and then innervated by joining

PRINCIPLES OF TENDON TRANSFER ANSFER INCIPLES OF TENDON TRANSFERAssess the problemWhich muscles are missing?Which muscles are available?The donor muscle should be:expendablepowerful enoughan agonist or synergistThe recipient site should:be stablehave mobile joints and supple tissuesThe transferred tendon should be:routed subcutaneouslyplaced in a straight line of pullcapable of firm fixationThe patient should be:motivatedable to comprehend and attend hand therapyintercostal nerves or the spinal accessory nerve to thestump of the original nerve supplying that muscle.Care of paralysed partsWhile recovery is awaited the skin must be protectedfrom friction damage and burns. The joints should bemoved through their full range twice daily to preventstiffness and minimize the work required of muscleswhen they recover. ‘Dynamic’ splints may be helpful.Tendon transfersMotor recovery may not occur if the axons, regeneratingat about 1 mm per day, do not reach the musclewithin 18–24 months of injury. This is most likely

when there is a proximal injury in a nerve supplyingdistal muscles. In such circumstances, tendon transfersshould be considered. The principles can be summarizedin the Box on the previous page.Recommended transfers are discussed under theindividual nerve lesions.PROGNOSISType of lesion Neurapraxia always recovers fully;axonotmesis may or may not; neurotmesis will notunless the nerve is repaired.Level of lesion The higher the lesion, the worse theprognosis.Type of nerve Purely motor or purely sensory nervesrecover better than mixed nerves, because there is lesslikelihood of axonal confusion.Size of gap Above the critical resection length, sutureis not successful.Age Children do better than adults. Old people dopoorly.Delay in suture This is a most important adverse factor.The best results are obtained with early nerverepair. After a few months, recovery following suturebecomes progressively less likely.Associated lesions Damage to vessels, tendons andother structures makes it more difficult to obtain recoveryof a useful limb even if the nerve itself recovers.Surgical techniques Skill, experience and suitable facilitiesare needed to treat nerve injuries. If these arelacking, it is wiser to perform the essential wound toiletand then transfer the patient to a specialized centre.REGIONAL SURVEY OF NERVE