DIAGNOSIS OF THE

COMMON FORMS OF NERVE INJURY

OF THE EXTREMITIESBy

COLIN EDWARDS, M.B., B.S., M.R.C.P., D.P.M.

History-taking is the first step in diagnosis andit is useful to know how varied the causes of peri-pheral nerve injuries can be. Otherwise the truenature of a traumatic lesion sometimes may notbe suspected.The commoner ones are the result of:-

(I) Cutting and laceration.(2) Stretching, which may be sudden (e.g.

stretching of the sciatic by jumping upon theextended foot) causing fibre rupture andhaemorrhage, or prolonged (e.g. lying with thearm extended for hours above the head) causingischaemia.

(3) Contusion.(4) Concussion (including that produced by a

"near miss" when a missile passes throughneighbouring tissues without touching the nerve).

(5) Pressure (e.g. crutch and "Saturday-night"palsies).

(6) Puncture (e.g. by an injection needle).(7) Local poisoning by injected substances;

and(8) Freezing.

Loss or impairment of movement is usually thepresenting symptom of a peripheral nerve injury.But such loss may be caused by fractures, jointlesions (dislocation, inflammation, adhesions,ankylosis), muscle or tendon injuries, local in-flammatory or other swellings, and spasm, fibrosisor contracture of muscles. It may also be due tomore remote causes such as Central NervousSystem diseases, non-traumatic peripheral nervouslesions or hysteria. Care may sometimes beneeded to exclude some of these conditions, butusually the obvious paralysis of muscles followingupon trauma, with loss of sensation in the skin areasupplied by the corresponding nerve points directlyto peripheral nerve injury. Adequate diagnosis,however, involves first localising the lesion (ana-tomical diagnosis) and then an estimate of its kindand degree (pathological diagnosis). Localisingthe lesion is the simpler of the two tasks, althoughit requires a knowledge of a fairly large number ofwell-recognised facts. Many of the criteria ofpathological diagnosis are also well established,but some are still being evolved.The clearest guides to localisation are muscular

weakness or paralysis, and wasting, with accom-

panying diminution or loss of reflexes. In theabsence of an external wound or contusion near thenerve concerned these muscle changes may be theonly guide.Look first at the most peripheral muscles and

particularly those which move the hands and feet.If these are normal (indicating an intact nervesupply) it is uncommon, although not impossible,for muscles to be involved whose supply leavesthose same nerves at a more proximal level. Andproximal involvement with normal peripheralmuscles only occurs close to the actual spot wherethe nerve is injured. The state of innervation ofthe muscles moving the hands and feet gives noguide, however, to that of the limb girdle muscles,as they are supplied by comparatively short nervesarising directly from the two great plexuses.Weakness or paralysis of a muscle having been

found, one then follows the nerve proximallymuscle by muscle in the order in which their nervesof supply leave the parent trunk. The mostproximally innervated of the muscles found affectedis a useful pointer to the level of the lesion. Musclesshould be tested by seeing and palpating the actualmuscular contraction or the tensing of its tendon.Movement of a segment of a limb is not a safe test.Very similar movements can sometimes be producedby more than one muscle and they may not besupplied by the same nerve. There are also othervarieties of "false movement." Furthermore, lossof the fixating action of certain paralysed musclesmay give a false impression that other healthymuscles are weakened (e.g. the apparent weaknessof the finger flexors when there is wrist drop.)*

Impaired sensation can be useful in confirmingthe fact of involvement of a particular nerve,particularly if motor signs are slight. It is oflittle use, however, in locating the level at whichthe nerve is injured, particularly if the lesion is acomplete one, for then overlapping adjacent nervesfunction to supply skin sensation in much of thearea also supplied by the injured nerve. If thelesion is old enough even the residual anaestheticarea unaffected by the phenomenon of "overlap"

* A very useful pamphlet containing numerous illustra-tions of good methods of testing various muscles is MedicalResearch Council War Memorandum No. 7 entitled Aidsto the Investigation of Peripheral Nerve Injuries, publishedby His Majesty's Stationery Office in I942.

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POST-GRADUATE MEDICAL JOURNALmay show returning sensation due to the ingrowthof fibres from adjacent uninjured nerves.So much for general principles in localisation.Individual nerves can now be considered.Isolated lesions of the Ulnar Nerve are common,

due to its fairly superficial course, particularly "iearthe elbow. PLATE I shows a hand where thereis a severe ulnar lesion. Atrophy of the first dorsalinterosseous muscle and of the adductor pollicis isobvious from the hollowing of the first interspaceand there is some indication of clawing of the handwith hyperextension at the metacarpo-phalangealjoints and flexion at the interphalangeal joints.Such a finding would lead one to test in order theremaining interossei and the medial two lumbricals,the opponens and the abductor digiti minimi, theslips of the flexor digitorum profundus to the ringand little fingers and finally the flexor carpi ulnaris.This search would give one the most peripheralpossible site of the injury.*

Confirmatory sensory loss should be sought overthe ulnar edge of the hand and the little finger. Asin all nerve injuries, sensation of light touch will befound lost over a wider area than is pin-prick.

Isolated injury of the Median Nerve is not seenexcept as a result of penetrating wounds. Itsposition makes it less prone to injuries in generalthan either ulnar or radial. Trophic and vasomotordisturbances and causalgia are commoner inmedian nerve lesions than in any other. PLATE 2shows a right hand where there is a severe lesionof the median nerve and the normal left hand ofthe same subject. Note the atrophy of the thenarmuscles and of the pulp of the first finger. Notealso the thumb lying back in the plane of the palm.It is this falling backwards of the t.humb with hyper-extended index and middle fingers which give rise tothe term "ape-hand" in median nerve palsy. Themiddle finger in this case happens to be flexed dueto the development of a contracture. Before thisoccurred there was the usual great difficulty inflexing its two distal phalanges. Characteristicand easily elicited signs in median paralysis areinability to oppose the tips of the thumb and littlefinger so as to make a circle (opponens, and shortand long flexors pollicis), to abduct the thumb atright angles to the plane of the palm (abductorpollicis brevis) or to flex the two terminal phalangesof the index finger whilst the proximal one is heldextended (flexor digitorum profundus-lateral slip)and (flexor digitorum sublimis).

Obvious median involvement having been diag-.* It is not possible in a short article like this, to go into

detail which can be found readily in any text-book ofneuro-anatomy, but it can be taken as a rule that branchesof supply to muscles usually leave the parent nerve as itlies abreast of the muscle belly. There may be severalsuch branches to an individual muscle, e.g. the flexorcarpi ulnaris may receive as many as four.

nosed, the muscles it supplies should be tested inthe following order-distalo-proximally:--the twolateral lumbricals, the opponens and short flexorof the thumb, the short abductor of the thumb, thelateral two heads of the flexor digitorum pro-fundus, the long flexor of the thumb, the flexordigitorum sublimis, the flexor carpi radialis andthe pronator teres.

Sensory loss is to be sought over the two terminalphalanges of the index and middle fingers. If thelesion is at all severe loss of tactile sensibility ismore extensive than this and can be found overthe radial half of the palm as well.No picture of the appearance of the hand in

lesions of the Radial Nerve has been included.This nerve, of course, supplies no muscles in thehand itself, and the reader can produce the charac-teristic wrist-drop simply by relaxing the extensorsof the hand. With this as a usual initial sign, onecan confirm the fact of a radial lesion by notingthat the thumb cannot be extended in the plane ofthe palm (e.g. with the palm held flat on a table),nor can the proximal phalanges of the fingers beextended. Ascending the arm one then tests thesupinator, extensor carpi radialis longus, brachio-radialis and triceps, Sensory changes in radiallesions are limited to a small area on the back ofthe hand overlying the first and second metacarpalsand perhaps the base of the thumb.The radial nerve is apt to show extensive paraly-

sis of good prognosis after relatively trivial injuriesand. it is from the radial that one gets the moststriking examples of neurapraxia following pressureand stretching.

Musculo-Cutaneous palsy is very obvious withbiceps paralysed and brachialis largely inactive andsensory impairment over the proximal part of theradial border of the forearm. (It should be re-membered that the brachialis is also supplied by theradial). Damage to the musculo-cutaneous nerveusually occurs as part of a brachial plexus injury.

Deltoid paralysis is the outstanding sign ofAxillary Nerve lesions. PLATE 3 shows the flatten-ing of the outline of the shoulder produced whenwasting of the deltoid supervenes. Palpation ofthe muscle is particularly important when testingthe deltoid because compensatory action by thesupraspinatfis can abduct the arm and elevate itlaterally to some extent, giving a false impressionthat the deltoid is recovering. The only othermuscle the axillary nerve supplies is the teres minor.It is small and not readily tested as its functionsare not easily distinguished from those of theinfraspinatus which is supplied by the supra-scapular nerve. Axillary nerve lesions produce acharacteristic longitudinally oval area of sensoryloss about the size of a hen's egg with its lower endover the deltoid insertion.

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NERVE INJURY OF THE EXTREMITIES COLIN EDWARDS, M.B., B.S., M.R.C.P., D.P.M

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PLATE I.--Effects of an ulnar nerve lesion.(Reproduced by kind permission of Dr. C. C. Worster-Drought.)

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PLATE 2.-Effects of median nerve lesion (right) compared with normal left hand.(Reproduced by kind permission of Dr. C. C. Worster-Drought.)

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NERVE INJURY OF THE EXTREMITIES COLIN EDWARDS, M.B., B.S., M.R.C.P., D.P.M.

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PLATE 3.-Effects of axillary circumflex nerve lesion (right) comparedwith normal left shoulder.

(Reproduced by kind permission of Dr. C. C. Worster-Drought.)

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PLATE 4.-Effects of a complete sciatic nerve lesion(right) compared with a normal left leg.

(Reproduced by kind permission of Dr. C. C. Worster-Drought.)

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NERVE INJURY OF THE EXTREMITIESFrom the Brachial Plexus itself the more

important of the short branches which may beinjured and whose muscles can be tested easily,are:-

(x) from the cords of the plexus(a) the thoraco-dorsal nerve supplying the

latissimus dorsi,(b) the lateral and medial anterior thoracic

nerves supplying the pectorals.(2) from the trunks

the suprascapular nerve supplying the supraand infra spinatus muscles.

(3) from the rami or roots of the plexus(a) the long thoracic nerve supplying the

serratus anterior(b) the dorsal scapular nerve supplying the

rhomboids.

If these muscles are tested in the above order,they can give useful information about the level ofa plexus lesion. If the injury involves the lowestcervical or first dorsal roots very near their originthere may be a cervical sympathetic paralysis withproduction of Homer's syndrome (miosis, enoph-thamlos, narrowing of the palpebral fissure and,much more rarely, vasodilatation and diminutionof sweating over the face on the affected side).The three classic varieties of brachial plexus

lesion are mentioned here for completeness.(i) Lower plexus type (Klumpke's paralysis)

due to injury to the eighth cervical and first thoracicroots, caused usually by upward traction on theextended arm. This produces paralysis of all theintrinsic hand muscles and wrist and finger flexorswith sensory impairment along the ulnar borderof the hand and forearm. Occasionally there is acervical sympathetic paralysis also.

(2) Upper plexus type (Erb's paralysis) due toinjury to the fifth and sixth cervical roots, mostcommonly caused by strong downward traction onthe arm or shoulder, particularly when combinedwith forcible flexion of the neck to the oppositeside. In proximo-distal order the muscles foundaffected in this type are the spinati, the pectoralismajor (partial), latissimus dorsi, teres major,deltoid, all three anterior upper arm muscles, andthe brachio-radialis. The hand and forearmmuscles escape. Sensory impairment may befound over the outer aspect of the whole of theupper limb.

(3) Middle plexus type. This involves theposterior cord and the picture is one of combinedradial and axillary nerve paralysis with involve-ment of the nerve to the latissimus dorsi also. Itis only caused by penetrating wounds and is un-common.

Injuries of the nerves of the lower limb are muchless common than those of the upper.The Sciatic is the one most frequently involved

and PLATE 4 shows the leg and.foot in a right-sidedsciatic lesion. Note the greatly wasted calf andthe foot-drop. In complete lesions such as this,there is total paralysis below the knee and, if thelesion is sufficiently high in the buttock, a loss offlexion at the knee due to hamstring paralysis.The ankle jerk is lost but the knee jerk remains.Sensory impairment is to be sought over the wholeof the foot except the medial malleolus and thearea of the instep just in front of it, and over thelower two-thirds of the postero-lateral aspect ofthe calf.The sciatic usually divides into tibial and com-

mon peroneal branches at the upper end of thepopliteal fossa. It may do so, however, as high asthe buttock, or the two parts occasionally maynot be united into one trunk at any level. Thisis why a deep wound of the thigh may sometimesproduce a lesion of one division of the sciatic only.Common Peroneal injury shows itself by loss of

eversion of the foot (peroneus longus and brevis,supplied by its musculo-cutaneous (or superficialperoneal) branch) and also by loss of extension ofthe proximal phalanges of the toes (extensorsdigitorum brevis and longus and extensor hallucislongus) and of dorsiflexion at the ankle (tibialisanticus and long extensors of the toes), this secondgroup of muscles being supplied by its anteriortibial (deep peroneal) branch. If the lesion is highin the-thigh the supply from the common peronealnerve to the short head of the biceps may be inter-rupted. Knee and ankle jerks are unaffected.The two branches of the common peroneal may beaffected separately by penetrating wounds in theleg but this is not common. The area of sensoryloss in common peroneal lesions extends in a bandfrom the bases of the medial two toes up the middleof the top of the foot and immediately lateral tothe ridge of the tibia up to a point two or threeinches below the knee.

Lesions of the Tibial (medial popliteal) branchof the sciatic cause paralysis of all the intrinsicfoot muscles (except the short extensor of the toes)of the long flexors of the toes and great toe and ofthe other three great calf muscles. If high in thethigh its supply to the semitendinosus and bicepsmay be involved. Sensory impairment is foundon the sole and the outer border of the foot. Theankle jerk and the plantar reflex are lost.The Superior Gluteal nerve supplying the tensor

fasciae latae, the gluteus medius and the gluteusminimus, and the Inferior Gluteal nerve supplyingthe gluteus maximus are very occasionally injuredby penetrating wounds.The Obturator Nerve supplying the adductors of

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POST-GRADUATE MEDICAL JOURNALthe thigh, the obturator exterus and the graciliswhich bring about adduction and internal rotationat the hip, is rarely injured alone.

Femoral Nerve involvement produces quadricepsparalysis with loss of the knee jerk, paralysis of thesartorius, and if the lesion be high enough, paralysisof the iliacus. Its sensory area is the anterior andmedial aspect of the lower two-thirds of fhe thigh,the anterior and medial aspect of the knee and themedial aspect of the leg, the medial malleolus andthe medial part of the foot and the instep just infront of this malleolus.

Injury of the Lateral Cutaneous Nerve of theThigh may cause meralgia paraesthetica, althoughthe condition is more often of unknown origin.Its symptoms are spontaneous tingling, numbness,burning or neuralgic pain in the area supplied bythe nerve. They are made worse by activity. Onexamination there may be tenderness of the nervetrunk near the point where it enters the thigh andimpairment or distortion of sensation on testingthe skin it supplies.When diagnosing the Nature of the Lesion one

must have in mind the possible varieties. Thesefall into three groups. First is complete severingof the nerve trunk which Henry Cohen has namedNeurotmesis. It abolishes every function of thenerve.The second is the "lesion in continuity" now

named Axonotmesis, where there has been sufficientdamage to the actual nerve fibres to cause themto degenerate peripherally to the lesion but thecontinuity of the nerve trunk is preserved by itsconnecting or supporting tissues. It is these con-necting structures which act as guides to thedamaged fibres. as they regenerate. The majorityof axonotmeses recover spontaneously.The third is a condition of temporary impairment

of conduction in a nerve which is termed Neura-praxia. It recovers spontaneously at a rate fartoo rapid to be attributed to regeneration (usuallyin two to six weeks, but sometimes much less).More than one of these types of lesion can exist

simultaneously in the same nerve, but the patho-logical and clinical phenomena of such injuries canstill be classified under these three headings.

It must be emphasised that unless the dividedends of the nerve can be seen it is not possible todiagnose with certainty a state of neurotmesisuntil several months after the injury. If, immedi-ately following trauma, there is complete paralysisof all the muscles whose nerve supply arises distalto the lesion and loss of sensation of pin-prick andlight touch in the area supplied exclusively by thenerve concerned, all one can say is that the lesionis probably severe, and usually either a neurotmesisor axonotmesis. Sometimes, however, even if all

these signs are present, it is not possible to estimatethe severity of the lesion at all except after thepassage of time. Slight injuries to the radialnerve, for example, can produce such signs withrelative ease, but rapid recovery soon proves thecondition to have been only one of neurapraxia.This state can often be surmised from the natureof the damaging force which is commonly pressureor stretching of brief duration, or a mild or moderatecontusion.

Since the majority of cases of axonotmesisrecover spontaneously the paralysed muscles mustbe suitably cared for and watched, but one shouldnever wait until a diagnosis of neurotmesis isestablished beyond all doubt before advisingexploration of the lesion. It becomes a highlyprobable diagnosis if at the end of three monthsthere is no recovery of motor function in any ofthe muscles originally paralysed and these showthe characteristic reactions of degeneration onelectrical testing. It is then that exploration isadvisable. Neurotmesis can only be diagnosedwith certainty when the full time necessary forregeneration has elapsed and it is found thatparalysis and tlie reaction of degeneration stillexist. By then the chances of surgery beingbeneficial will have been lessened.Some facts about sensory findings are to be

noted.There is much overlapping of the sensory areas

supplied by adjacent nerves and although it isprobable that such overlap does not fully functionexcept when there is complete nerve section orblock, it is precisely in such cases that sensorytests are most important. So for practical purposesit is best to confine one's tests to those areas notoverlapped by adjacent nerves.But tests even in these areas are only reliable

shortly after total nerve lesions, because ingrowthof fibres from adjacent uninjured nerves occurs.and may give a false impression of recovery.

If immediately following trauma only some ofthe muscles distal to the lesion are paralysed, ifthere is not complete loss of sensation in the skinarea exclusively supplied by the nerve or if not allkinds of sensation are lost in that area, then thelesion is incomplete and must be either an axonot-mesis or a neurapraxia. The rate of recovery inthis group is a cardinal point of distinction betweenthe two varieties. Neurapraxia is also stronglysuggested if normal electrical responses are pre-served in the muscles for more than about eightto ten days following the lesion.The most reliable Signs of Recovery in nerve

lesions again are motor and both the active move-ments and the electrical reactions of the musclesserve as guides. Where regeneration occurs themuscles lose their paralysis in the anatomical

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September, I946 NERVE INJURY OF THE EXTREMITIES 261

order of origin of their nerve supply from thetrunk. The rate of regeneration in motor nervesis about I cm. per week, slowing down as the fibrenears the end of its journey. About forty dayselapses following an injury before this processbegins. The gap is rather longer in cases of nervesection. Thus, if the site of the lesion is known.One can calculate the time at which a particularmuscle should show signs of recovery if regenera-tion is occurring. In cases of neurapraxia, how-ever, there is no particular order of muscularrecovery and all may regain power almost simul-taneously. Only return of sensation in theexclusive area of the nerve concerned is of signifi-cance in estimating recovery and then only if itoccurs too early for ingrowth from adjacent nervesto have taken place. Pain sensibility reappearsbefore tactile, but in cases of neurapraxia tactileand pin-prick sensation may be both absent andreturn together. Sensory and motor recoveryare not necessarily co-eval. In tibial andperoneal nerve lesions, for example, sensoryrecovery is often much earlier and in ulnar andmedian lesions often much later than motorrecovery.The degree of muscular atrophy, the state of

muscle tone, trophic disturbances and the sensa-tions produced by pressure on nerve trunks and.muscles are not reliable guides to the state ofrecovery.

Finally, a few facts ought to be rememberedabout electrical tests. If, thirty or forty daysafter the injury, bearable faradic stimulation causesa response from paralysed muscles, then the nerveis not severed. Faradic current acts through thenerve because the duration of the effective portion

of its wave is *oo of a second which is too short atime of action to evoke a response from muscle.The loss of response to faradism of a muscle-nervecomplex is part of the Reaction of Degeneration.The other parts concern the response to galvanismand they are:-

(I) Hyperirritability of the muscle whichresponds to half or a smaller fraction of the normalminimum current required. Instead of respondingby the normal sudden twitch, however, it respondswith a slow contraction.

(2) The amount of galvanic current required tothrow the severely degenerated muscle into tetanusis only I'5 to 1*2 times the amount which justproduces a contraction. In healthy muscle theratio is 4 or 4-5 to I.

(3) To elicit contraction from denervated musclethe amperage required for cathode-closing stimulihas to be as great or at times even greater thanthat required for anode-closing stimuli. In health,of course, a smaller amperage suffices to elicitcontraction with a cathode-closing stimulus.

This reaction of degeneration requires at veryleast a week to develop after the severance of amuscle from its nerve. It may take from one totwo years for the degeneration of muscle to becomeso complete that all response to galvanism is lost.A rise in the amount of galvanic current necessaryto produce muscular contraction is one of theearliest signs of regeneration of the nerve, providedthat increased local tissue resistance due to suchchanges as inflammatory infiltration can be ex-cluded.

I wish to thank Dr. C. C. Worster-Drought forkindly lending me the photographs.

POST-GRADUATE MEDICAL JOURNAL

CONTENTS FOR OCTOBER 1946

THE PRESENT POSITION OF ETHER ANAESTHESIAby Dr. John Elam

ETHER ANAESTHESIA, I842-I900by Barbara M. Duncum, D.Phil.THE ADMINISTRATION OF ETHER

by J. T. Challis

INTRAVENOUS ANAESTHESIAby Ronald Jarman, D.S.C., D.A.

HYSTERIAby E. A. Bennet, M.C., M.A., M.D., D.Sc., D.P.M.

UROLOGICAL DIAGNOSIS IN GENERAL PRACTICEby A. W. Badenoch, M.D., F.R.C.S.

THE SEPTIC HANDby James C. Gillies, F.R.C.S.E.

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