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SECTION III
NEUROSURGERY
CHAPTER VIII
MOTOR DISTURBANCES IN PERIPHERAL NERVE LESIONS a
One of the functions of a peripheral nerve is the transmission of motor impulses. When a peripheral nerve is injured or severed its function is diminished or destroyed, thus resulting in a loss of motion. If the loss of motion is complete, it is defined as paralysis, if incomplete as paresis. The state of the function of motion is determined by an examination of a muscle at the moment of voluntary or willed movement. Inasmuch as many muscles are deep-seated and others seem to contract when synergistic muscles are shortened, it is impossible, in many instances, to determine paralysis by an examination of the muscle itself; consequently, the preservation of the function of muscles is largely determined by the examination of movement of segments about the joints.
Loss of motion may be the result of conditions other than paralysis of a muscle or muscles. Among these causes may be included local shock, pain, swelling, fractures, dislocations, adhesions, or ankylosis of joints, contracture of opposing uninjured muscles, spasm, sclerosed fibrous tissue, as in isehemic paralysis, tendon and muscle section or loss, and hysteria.
EXAMINATION OF MOTOR FUNCTION
POSTURE
Loss of function of any peripheral nerve produces a position and deformity which is characteristic, such as wrist-drop of musculospiral nerve paralysis, frequently associated with a "tumor of the wrist" due to the distention of the ligaments of the wrist, producing a protrusion of the proximal metacarpal bone. Other deformities include the talipes equinovarus or foot-drop of external popliteal nerve paralysis, the talipes equinus of sciatic nerve paralysis, the ape hand of ulnar and median nerve paralysis, the characteristic position of the thumb in a plane with the palm, in median nerve paralysis, the sagging shoulder of a spinal accessory nerve paralysis, the winged scapula of a long thoracic nerve paralysis.
RANGE OF MOVEMENT
The degree of motility of segments about a joint should be determined by examination of both active and passive motion. In examining for passive motility due consideration must be given to the pain elicited. The range of movement may be determined by a goniometer and measured in degrees of a circle, or by tracings obtained from molds made with a flexible lead tape.
a The subject matter treated herein is general in nature; that is to say, much of it was know prior to the World War: however, its inclusion is believed to be essential to a clear understanding of how nerve lesions were treated during the period of the war.-ED.
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first obtaining a tracing of the movements of the segment in one direction (flexion) then in the other direction (extension).
It is important to note the position of segments of joints adjacent to the ones being examined, for example, in musculospiral paralysis with wrist-drop there may be some interphalangeal joint fibrosis. If the range of flexion of the fingers be obtained with the wrist "dropped" it will be far less than with the wrist in a position between extension and flexion. Similarly in median and ulnar nerve paralysis the range of extension of the finger will be less with the wrist extended than when the wrist is flexed. In popliteal nerve paralysis the dorsal flexion of the foot will be less with the leg extended than when it is flexed.
FIG. 80.- Lead tape and tracings
ACTIVE MOTION
Because of the many factors entering into the movement of segments about the joints, but particularly because of the frequency with which more than one muscle may produce similar movements about the segments of the joints, the necessity for great care in the analysis of all muscle movements is stressed.
The segments about the joints in the body may normally be moved incertain directions to certain degrees, flexion, extension, abduction, adduction, rotation, circumduction, etc. The failure of such movements indicates a loss of function which with certain precautions may be attributed to the motor paralysis.
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Having eliminated such causes as plain, swelling, con tracture, spasm. fibrosis, ankylosis of joint, fracture, etc., one begins to study the loss of function by observation of range of motility in various directions. Here certain precautions are necessary. Each joint must be studied separately. The part of the extremity proximal to the joint tested should be passively immobilized; for example, in testing for extension of the wrist, the forearm should be immobilized. Just as in examining for passive motility so here the muscles moving the segment should be placed in a position which is neutral, so that their function can best be motivated. In a musculospiral paralysis, although the flexors of the fingers are uninjured, the degcree and force of motility is diminished unless the hand is passively extended on the wrist.
The influence of gravity must be properly evaluated and its forces nullified by proper position. Paretic muscles may be capable of contraction and he too enfeebled to move a part or whole of any extremity against gravity. A deltoid muscle may be enfeebled to such a degree that abduction of the arm to a right angle is impossible when the patient is standing, but with the patient in a supine position. abduction of the arm may be possible. At times under this condition it is advisable further to facilitate movement and diminish the force of gravity by placing the paretie extremity on a loard which has been powered with tale.
In a musculospiral lesion, extension at the wrist may be impossible with the forearm unsupported and in a pronated position, yet feeble extension maybe produced with the forearm in a position midway between pronation andsupination and supported on a powdered board. Similarly flexion of the forearm may be impossible against gravity, but possible if the upper extremity issupported in a position of abduction at a right angle. Extension of a paretic quadriceps femoris may be impossible in an erect position with the thigh flexedand quite possible when the lower extremity is supported on its inner or outersurface while the patient lies on his side. Such precautions must be taken aswell in examining the hamstrings, the dorsal and plantar flexors of the feet,in short, of all the muscles of the body.
At times the force of gravity works in the opposite direction and, as will be pointed out under supplementary movements, it often produces a movementwhich is misinterpreted as muscle function. When the triceps is paralyzed.if the arm be abducted, the forearm flexed and then externally rotated, gravitvmiay produce extension at the elbow. Similarly when the quadriceps femorisis paralyzed and the thighs passively flexed on the abdomen and the legs onthe thigh while the patient is in a supine position, gravity may extend the leg.
At times a muscle mav be so enfeebled that it can not change the positionof the segments about a joint but its contraction can be ascertained by palpation. Frequently such examination leads to erroneous conclusions, as in ulnar nerve paralysis the tendon of the flexor carpi ulnaris may seem to contract when the wrist is flexed by the flexor carpi radialis and palmaris longus.
Sometimes if the paretic segment be passively moved in the direction of the action of the paretic muscle the patient may actively increase this movement. For example, in an external popliteal nerve paresis, if the foot he
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passively dorsi-flexed to a degree, the patient may then be able to actively increase the degree of dorsi-flexion of the foot.
Frequently, although the patient may not be able to produce a movement of a segment in a certain position, he may he able to retain this position when it is passively produced, as in a paresis of the extensors of the wrist, when the wrist is passively extended, he may for a brief interval hold it in that position.
The degree of motor deficiency may be measured relatively by the observation of the degree of capability of producing change in position of segment in (a) neutral position, (b) against gravity, and (c) against interposed resistance. In estimating the amount of interposed resistance one may compute it in degrees of one's own strength or as compared with the uninjured corresponding
FIG. 81.- Spring scales dynamometer
segment of the patient. In a paresis of the extensors of the wrist, one may compare the strength of the paretic to the normal side by resisting with one's own hands the extension at the wrist. The degree of motor deficiency may then be described as paralyzed, very weak, moderately weak, weak. Or moderately strong, and so recorded.
The necessity for accuracy in the examination of motor function can not be overemphasized. Careful measurements and precise records are necessary not only for the purpose of diagnosis and prognosis, but also for the determination of the progress of a case. Accurate measurement of motor function is possible only by a dynamometric examination.
A simple and accurate method may be employed by the interposition of a spring scale between the examiner's hand and a segment to be examined. One
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may employ several such scales, some measuring to 500 grams and others as high as 50 pounds. To determine the strength of flexion of the distal phalanx of the thumb the hook of the scale is fastened to the distal phalanx and, holding the scale in one hand, the remaining portion of the thumb is fixed or immobilized with the other hand. The patient is then requested to flex the thumb and the degree of motor function is read in terms of grains or pounds. It is essential that influence of movement of adjacent segments be avoided by passive fixation.
When dealing with more complicated movemnents, such as pronation, or supination, or rotation, a flat piece of wood at one end of which a hole has been drilled may be employed. The hook of the scale is inserted into the hole and the patient grasps the flat piece of wood and, turning it either by pronation or
FIG. 82.- Measuring pronation by spring scales
supination, the results ]fav he read upon the scale. At times it may be necessary to bind the hook of the scale or the piece of wood to a segment about the joint being examined.
The results so obtained may be recorded opposite the name of muscles supposed to move the segment in the direction measured, or, and this is far more accurate, upon a diagrammatic representation of the segment. For example, in examining the movements of the hand and fingers, each result is noted upon the palm or dorsal surface of the part of the hand recorded. Schematic representation of abduction of the fingers, flexion of the proximal phalanges, adduction, opposition and short abduction of the thumb, may be denoted as in the following illustration (fig. 83).
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In lesions of the ulnar and median nerve this type of examination and recording has led to the observation of many phenomena of great diagnostic and prognostic value which have not heretofore been described. These are dealt with under injuries of the several nerves.
SUPPLEMENTARY MUSCLE MOVEMENT
Supplementary muscle movement, supplementary motility, or supplementary motion or trick movement, is frequently responsible for misinterpretations in the examination of cases of peripheral nerve lesions.
The preservation of certain movements, the loss of which is supposed to follow particular nerve lesions, has been observed for many years. Sherren 1 called attention to the fact that Swan,2 in 1824, was astonished at how much a rabbit could move its leg after experimental section of the sciatic nerve. Later Letievant 3 studied this plhenoinenon and termed it supplementary mo-tility. Since that time numerous investigators have observed its presence In peripheral nerve lesions, notably Duchenne4 and Beevor,5 to whom may be credited much of the present knowledge of these movements. Head and Sherren,6 Claude,7 and Athanassio-Benisty 8 are among the recent observers who noted its presence. American workers. Coleman, 9 Woods, 10 and Pollock, 11 among others, have been particulamly interested in these movements and have contributed considerable information as to their occurrence.
These movements may be caused by a number of factors, among which may be included the anastomotic supply of muscles from adjacent nerves, and one must recall the not uncommon existence of an a typical nerve supply--total supply of the flexor brevis pollicis by the ulnar nerve, and the supply of the first dorsal interosseous by the median. Supplementary muscle movements may likewise be produced by muscles other than for primary movements--the flexion of the wrist which is produced by contraction of the abductor longus pollicis and the extensor ossis metacarpi pollicis: by movement occurring as the result of mechanical factors producing a change of direction of leverage by the shortening and lengthening of tendons and muscles passing over several joints--in a lesion of the musculospiral nerve with paralysis of the extensors of the wrist, when the wrist-drop does not exceed an angle of 120 º, complete flexion of the fingers produces extension at the wrist; by slight movement resulting from the recoil of elastic tissue following a minovement in a direction opposite to the one desired--in median nerve paralysis flexion of the distal phalanx of the thumb may be imitated by the recoil occurring following strong extension of the distal phalanx of the thumb:, by utilizing the force of gravity--in paralysis of the median nerve pronation may be produced first by stretching the long wrist and finger extensors and then the forearm resting on the knee the remaining portion of pronation is produced by allowing the force of gravity to carry the forearm through the subsequent action.
RECOVERY OF VOLUNTARY MOTILITY
The order in which movement is restored to muscles paralyzed as the result of peripheral nerve lesions has a sufficient constancy to attribute to each nerve a clinical individuality. 12 Genallyspeaking, with severe lesions of
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the nerve, a certain degree of muscular tonicitv returns before any reappearance of voluntary motion. At first, voluntary movements are awkward and uncertain and frequently the reaction time of a movement is considerably lengthened. One must bear in mind what has been called by André-Thomas 13 "an error in the switching" of the motor fibers which have not taken the proper direction and have not encountered each time the sheaths intended for their reception, as when a patient suffering from an injury to the musculospiral nerve wishes to extend his wrist the supinator longus contracts powerfully and often in excess of the radial muscle.
At times it has been noted that preceding the ability to produce voluntary motion the patient experiences a feeling of being able to produce such motion when he wills it. Thus, in a musculospiral lesion before recovery has taken place, the patient may not have been able to sense the feeling of extension, whereas when recovery is taking place he begins to feel the sense of extending the wrist, although such extension may not be produced.
FURTHER CONSIDERATION OF CERTAIN FACTORS PRODUCING DEFECT IN MOTION
Some of the factors producing defect in motion deserve additional description.
SHOCK
Loss of motion following injuries of war may occur as the result of local shock and not as a result of direct injury to the peripheral nerve. Immediately following the reception of a guinshot wound there may be a complete paralysis of an extremity. This paralysis more or less rapidly disappears and if a peripheral nerve is injured, may leave paralysis of the muscle supplied by that nerve. Return of motor function occurs in from a few hours to a number of days, depending upon the amount of shock and the degree of injury of the soft parts and blood vessels. This loss of motion is far more common in injuries which are the result of shrapnel and high-explosive shells than of bullets. It is a constant accompaniment of wounds associated with fractures of long bones. It is not necessarily an accompaniment of loss of consciousness or surgical shock.
This loss of motion rarely is accompanied by loss of sensation and it is notable that, even when a nerve is injured by local concussion or at times by contusion, frequently motor function is lost whereas sensation is preserved. S. Weir Mitchell 14 observed this during the Civil War.
JOINT HANGES
S. Weir Mitchell called attention likewise to the common affection of joints in lesions of the peripheral nerves and, as in the Civil War so in the World War, these changes produced immobility at times of greater importance than paralysis of muscles themselves. These joint changes may be of a number of varieties and their causes not easily determined. Of the known causes one may enumerate fractures in the joints, dislocations, suppuration of joints, prolonged suppuration of nearby parts, prolonged immobilization, ischemic
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contractures resulting in retraction of muscle tendons, and certain nervous lesions the character of which is unknown.
Although it is supposed generally that prolonged immobilization is the primary cause of most of the joint changes there are many cases in which this is not so. Occasionally one mav see an early arthritic involvement consisting of a painful swelling of the joint, which differs from the early inflammatory swelling of the wound itself. This may last for weeks, and be followed by partial ankylosis. At other times a gradual retraction of muscular tendons and hardening of a joint capsule occurs, sometimes associated with prolonged and particularly improper immobilization, at times associated with prolonged suppuration. Very frequently one sees changes in painful and partial nerve lesions, characteristically present in painful lesions of the internal popliteal and median nerves, perhaps as a part of the picture of causalgia. These partial and painful lesions must consist of more than onlv at direct injury of part of a nerve because there is no more reason why an injury to a part of a nerve should be followed by joint changes or ankylosis than an injury of a whole nerve where, in the absence of a suppurative lesion, no immobilization or joint changes may be present. They are probably associated with a definite low-grade infection which follows the lymphatics of the nerve to the joint.
Injuries of certain nerves produce changes in certain joints peculiar to themselves. For example, injuries to the musculospiral nerves in the middle of the arm are associated with ankylosis of the elbow. When this ankylosis occurs early it is associated with a spasm of the biceps, when late it is the result of prolonged suppuration or fracture of the humerus. In painful lesions of the median nerve the joint changes are notable, widespread, and of severe character: the interphalangeal and metacarpophalangeal joints of all the fingers are affected. At times a partial ankylosis of the metacarpoplalangeal joints of the thumb occurs wherein only abduction and adduction are possible, and as a result attempts at extension produce abduction at right angles to the plane of the palm. The wrist joint and at times the elbow joint may be involved. What is true of the painful partial lesions of the median nerve is likewise true of the ulnar to a far lesser degree. The interphalangeal joints of the foot may he involved in a partial painful lesion of the internal popliteal and limitation of abduction of the foot is often seen in external popliteal lesions.
Shortening of opposing muscles is not so frequently observed since the necessity of proper splinting has been recognized. Occasionally it occurs and offers retardation to recovery of function. Such shortening is seen commonly when deformities occur as the consequence of the force of gravity in addition to overaction of unopposed muscles, as in musculospiral paralysis affecting the flexors of the wrist, in paralysis of the external popliteal affecting the tendo Achillis, and to a lesser degree in circumflex nerve paralysis, affecting the pectoral muscles. Such shortening may occur even when gravity does not contribute to the deformity, as in overaction of the extensor conminunis digitorum in ulnar nerve paralysis, shortening of the abductor pollicis and the extensor ossis metacarpi pollicis in median nerve paralysis, of the lumbricales in radial nerve paralysis, of the extensor coninmunis digitorulm in internal popliteal nerve paralysis, of the tibialis posticus in external popliteal nerve paralysis.
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MUSCLE SHORTENING RESULTING FROM SPASM
Muscle shortening may at times result from a different cause, namely, spasm. This condition is usually observed in partial lesions of the peripheral nerves; in muscles the nerve supply of which may not have been primarily injured. These partial lesions are the result of some irritative agent acting, perhaps, reflexly. Often they are associated with some vascular lesion. At times they occur as an accompaniment of a painful lesion of an adjacent joint or bursa-in arthritis of the shoulder, or in subacromial bursitis, a spasm of the pectoralis major frequently is observed. Such spasms are to be clearly differentiated from the so-called physiopathic reflex nervous disturbances which occur without any lesion of a peripheral nerve and from lesions at a distance from the site of loss of function. Similarly, they must be differentiated from the fibrous shortening of ischemic or Volkmann's paralysis.
ISCHEMIC PARALYSIS
In addition to the compression produced by bony callus, that which is produced by sclerosing fibrous tissue must be considered. In such cases there may be no symptoms suggestive of nerve injury immediately following the trauma, but a few weeks later particularly after the removal of a dressing such as a splint or a plaster-of-Paris cast, symptoms of compression manifesting themselves by partial or complete paralysis will be found. In this group the largest number of cases consists of those due to the formation of sclerosing fibrous tissue. This sclerosing results from the organization of diffused blood or of the products of inflammation. The symptoms, particularly the motor symptoms, are frequently confusing in so far as the diagnosis of a possible peripheral nerve injury is concerned. Characteristically, however, such a lesion is never limited to the distribution of the muscular supply of any one or more peripheral nerves; all muscles in an extremity may be involved to a greater or lesser degree. The sensory changes are not definite and when they occur they too are not limited to the anatomical sensory distribution of the peripheral nerves or a combination of such nerves.
The electrical reactions do not show the changes consistent with a pure peripheral-nerve lesion. One may find that certain parts of muscles supplied by an individual nerve may react to faradism whereas other parts do not. In general, it may be found that, commensurate with the degree of fibrosis, the muscles have a disappearance of both faradic and galvanic response. Interphalangeal fibrosis, with partial or complete ankylosis, is very common. Cold-ness of the extremity and the cyanosis are characteristic signs.
TONE
When a peripheral nerve is severed the spinal reflex is interrupted in the motor arc and loss of tone results. If one could measure loss of tone accurately, and if the degree of hypotonicity were an accurate indication of the severity of peripheral nerve lesions, it would be important that this function be carefully examined. Unfortunately, loss of tone occurs in partial lesions as well as in complete lesions of peripheral nerves. It is measurable only in the
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early stages following a wound to a peripheral nerve, inasmuch as later it maybe complicated by other factors such as swelling, fibrosis, and contracture, as the result of changes consequent to fracture, joint changes, suppuration, and vascular changes. Frequently, after the secondary changes have disappeared. a fibrosis or hardening results which prevents an accurate determination of the tone of an extremity. The position of an extremity is not always an indication of the hypotonicity of the muscles, inasmuch as secondary shortening may prevent wrist-drop or foot-drop. Tone may be measured by some objective method, as the employment of a tonometer which may be rather simply made, as shown in Figure 84.
FIG. 84.- Tonometer
When measured in this manner it is found that soon after an injury of a peripheral nerve, in the absence of any changes, such as swelling and inflammation, there is a marked hypotonia which may be measured in the amount of millimeters of mercury necessary to push the plunger a certain distance into a muscle mass. Whereas, in a normal muscle a pressure of 160 to 180 millimeters of mercury may be required, in a paralyzed muscle a pressure of but 40to 60 millimeters of mercury is sufficient to plunge the indicator 10 millimeters into the mass. Some time after injury this type of examination proved to be quite useless, because the subsequent atrophv frequently vitiated the result
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of the examination. Although one may find frequent references to the return of tone as an indication of the return of function of a muscle, it has been found that the secondary changes prevent the observation of the return of this function. When observed, of course, it is a valuable sign, and if in a given case of musculospiral paralysis with a certain degree of wrist-drop as the result of hypotonicity the wrist is seen to assume an attitude in which it drops to a lesser degree, this may be accepted as a hopeful sign in the absence of secondary shortening.
ATROPHY
What has been said of tone is true also of atrophy. For some time it has been accepted that when a peripheral nerve is severed trophic disturbances occur in the muscles and these disturbances are followed by atrophy of the affected muscles. It has been supposed that this atrophy is commensurate with the degree of injury of the peripheral nerve. Although this is true, one is unable to measure the degree of atrophy so accurately as to make it a valuable sign in differentiating complete from incomplete lesions, and extensive atrophy of a paralyzed muscle may be interpreted, with a number of reservations, as meaning a severe lesion. Ulnar nerve lesions, as a rule, show extensive atrophy whether they are severe or not. As a sign, atrophy is of service in denoting the severity
FIG. 85.- Can with spout for measuring volume of extremity by water displacement
of a lesion only when seen soon after injury; the amount of atrophy observed some months after an injury is not commensurate with the severity of the lesion. Painful lesions of the median nerve and of the ulnar nerve are very frequently associated with rapid and marked atrophy. When observed some months after injury absence of demonstrable atrophy is not an indication of a reparable lesion. Frequently replacement of muscle mass by other tissues is responsible for the seeming lack of atrophy, and no method of examination permits us to determine how much atrophy has been present. Inasmuch as peripheral nerve lesions are associated with destruction of other tissues such as fracture and lacerations of muscles and soft parts with blood vessel lesions, it is apparent that seeming atrophv of long muscles or muscle masses may frequently be the result of disuse and factors other than trophic changes in the nerve supplying that muscle.
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If, for example, one measures the amount of water displaced by an atrophied extremity as compared with the amount displaced by the opposite normal one, some interesting facts are discovered (fig. 85). As compared with the unaffected extremity, the affected one shows in an irrecoverable ulnar nerve lesion an atrophy of 4.5 percent of the total mass; in recovering lesions 4.2 percent; in radial nerve lesions there is an atrophy of 4.3 percent in recovering lesions, 5 percent irrecoverable ones. In lesions of the median nerve those recovering showed 11.2 percent and irrecoverable 50 percent atrophy; in sciatic nerve lesions recovering lesions showed 9.7 percent and those irrecoverable 10 percent; the external popliteal showed in the recovering lesions 6 percent and in the irrecoverable 7.2 percent.
Although the percentage of loss of muscle mass was slightly greater in the severe irrecoverable lesions, the difference was not sufficient to be of diagnostic or prognostic value. In addition to this, some irrecoverable sciatic nerve lesions showed but 1 percent loss when a recovering one showed a 17 percent loss. In a recovering external popliteal nerve lesion 16 percent loss was found and in an irrecoverable one only 1 percent loss. This immediately indicates that the demonstration of atrophy is not an accurate guide to the severity of the lesion, and the absence of atrophy does not indicate a recoverable one. Although some of the discrepancies are probably due to the replacement of muscle fibers by other tissues, it would seem in some instances that those cases wherein exercise and massage, electrical stimulation, and passive movement of the extremity were given that the degree of atrophy seemed less.
Though ulnar nerve lesions show predominantly the greatest degree of atrophy rapidly occurring, radial nerve lesions show the least atrophy.
Graphic methods of recording signs and symptoms in many instances have a greater value than descriptive methods. Frequently it is impossible to have photographic records of the hands and feet in cases of peripheral nerve lesions; under this condition it is found serviceable to record the contour of the palm and sole by making impressions of the hand and foot. The degree of atrophy and resulting deformity of the hand and foot indicate clearly the type of peripheral-nerve lesions with which we are dealing. Not only is the position of the hand determined but the atrophy and the contracture of the muscles are shown as well. Only five of the peripheral nerves showed distinctive changes in a sufficiently large percentage to make it profitable to study lesions by this method. These nerves are the ulnar, median, radial, internal popliteal, and sciatic. The picture produced by a combined lesion of the ulnar and median is likewise distinctive. The imprint of the hand in the case of a lesion of the ulnar nerve shows the following characteristics: The clawing of the inner two fingers is well demonstrated by the absence from the imprint of any part of these fingers except the tip. The hypothenar muscles are seen to be atrophied by the presence of a notch on what normally consists of a rounded contour made by these muscles (fig. 86).
Between the mounds of the ring and middle finger is seen another notch, and when the atrophy is very severe a notch appears between the ring and little fingers as well (fig. 86-c). The fingers can not be spread apart, and the first phalanx of the thumb is in a position of extension. The atrophy of the adductor
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FIG. 86.- Imprint in a case of ulnar nerve lesion: a, Affected: b, affected:c, affected: d, normal; e, affected; f affected. A, Notch indicating atrophy of hypothenar muscle; B. notch between the mounds of ring and middle finger indicating atrophy; C, break in line along the radial border of the base of the index finger indicating atrophy or the adductor pollicis
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pollicis is seen by a break in the line along the radial border of the base of the index finger (fig. 86-d).
Median nerve lesions show very clearly the disturbance of whorl formation on the tips of the index and middle finger (fig. 87-a). When severe clawing is present in these two fingers, it is marked by the imprint of the very tip, frequently including the nail. The atrophy of the thenar eminence is usually well marked, and is shown by the prominence of the base of the thumb and a considerable notch in the normally rounded contour of the radial border of the thenar eminence (fig. 87-b). The distal phalanx of the thumb is in extension. When severe clawing is present, it is made evident by the absence of any imprint of the central portion of the palm. Not only is the atrophy of the thenar eminence noted by the notches proximal to the base of the thumb, but also in many instances loss of tissue is demonstated along the radial border of the first phalanx of the thumb (fig. 87-b). Failure of desquamation and the presence of many new lines is demonstrated over the thenar eminence(fig. 87-c).
Radial nerve lesions are characterized by the cramped appearance of the finger which results from inability to place the palm flatly on the paper because of the flexed position. The most characteristic feature of this imprint is the position of the thumb, which is adducted, the distal phalanx falling within or on the border of the outline of the index finger. The thumb is rotated about its axis inwardly so that the radial border of the distal phalanx is straight and not rounded. The distal phalanx of the thumb is usually flexed. Absence of the signs of atrophy in the thenar and hypothenar eminences is an additional feature of this form of lesion.
In combined lesions of the ulnar and median nerve signs of atrophy of both the thenar and hypothenar eminences are demonstrable by these notches found along their borders (fig. 89-a). Clawing is present in all four fingers; the mounds are often separated (fig. 89-b). The center of the palm shows a larger area in which no imprint is seen. When, in addition to partial lesions of the ulnar and median. the radial nerve is involved, the thumb shows at times the same rotation as was observed in the radial lesions. Frequently in lesions of the external popliteal nerve there is a flattening of the toes, so that the plantar surface or the entire length of the toe will produce an imprint. Lesions of the sciatic nerve show, in addition, a slight pes cavus, and in some cases a clawing of the toes, indicated by the absence of their imprint on the paper.
MUSCULOSPIRAL NERVE
The position of the hand in musculospiral paralysis is characterized by a very marked drop of the hand and fingers; the wrist and first phalanges are flexed: the thumb is abducted and falls within the line ot the outer border of the index finger (fig. 90).
The best method of testing the function of the triceps is to allow the patient's arm to hang over the back of a chair, the arm being horizontal, the forearm hanging loosely at right angles to it. The patient is asked to straighten his arm. The muscle may then be both inspected and palpated during the attempt. Care must be exercised not to misinterpret that extension of the
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forearm which occurs from a flexed position as the result of gravity controlled by the flexors. For this reason it is important to have the patient raise his elbow high enough so that it becomes impossible for him to extend the bended forearm by reason of the weight alone. Another way to test the paralysis of the triceps is to extend the elbow, then to ask the patient to resist any attempt to flex the forearm on the arm. Because the long head of the triceps receive sits motor supply immediately after the nerve leaves the tendon of the teres major, complete loss of extension of the forearm is infrequent in musculospiral paralysis.
The supinator longus is brought into action when flexion of the forearm is attempted with the forearm seripronated. With the extremity in this position the patient is asked to resist extension at the elbow, under which condition an unparalyzed supinator longus will stand out prominently. Contrary to generally accepted statements that the biceps can not aid in supination
FIG. 90.- Musculospiral palsy
unless the elbow is partly flexed, at times the biceps supinates the forearm even when it is completely extended.
Weakness of the extensors of the wrist is observed when the patient attempts to raise the hand against the action of gravity. In eliciting this sign care should be taken to keep the elbow and forearm of the patient motionless and resting on a table with the hand loosely suspended and pronated. When the extensors of the wrist are paralyzed no contraction is felt during the attempt at extension; on the contrary, there is energetic contraction of the flexors of the hands and fingers. Inversely, an attempt at flexion of the fingers does not produce a synergistic extension at the wrist, and it will be found that the patient can neither close his fist nor flex all the phalanges completely; the third phalanx will flex badly or not at all (fig. 91). To verify lateral movements at the wrist, the possibility of error arising from the movement of the elbow should be eliminated
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by resting the forearm on a table but the hand should be raised almost to the horizontal instead of being allowed to drop. A certain amount of abduction is possible in paralysis of the extensor through the action of the flexorulnaris. The abduction, however, is incomplete and faulty, and is accompanied by ulnar deviation.
In a lesion of the musculospiral nerve below the elbow paralysis of the extensors of the fingers may occur without involvement of the extensors of the wrist. Under these conditions the patient can not extend the wrist if, at the same time, he attempts to extend the fingers, but if he flexes the fingers the extension of the wrist may then be accomplished. To explain this we must recall the laws governing the action of the muscles going over several joints.
Beevor 5 states that "when a muscle by passing over two or more joints has two or more different actions, then, if only one of these actions be required,
FIG. 91.- Attempted Sexton of fingers in musculospiral palsy
other muscles are brought into the movement whose actions are antagonistic to those of the muscles not required.11 These synergic muscles place the prime movers (in this instance the extensors of the wrist) in the greatest elongation so as to augment their dynamic power and fix the joint so that the movement may be performed from a secure basis. Still another factor must be considered. Beevor 5 found that if the movement of extending the wrist be performed with the fingers actively and fully extended, the extensors of the fingers have to do all the work themselves and against the contraction of flexors of the wrist until the amount of work is equivalent to 4 or 5 pounds before the extensors of the wrist will join in and help them. In the cited instance of paralysis of the extensors of the fingers with preservation of the extensors of the wrist, the extensors of the fingers can not possibly reach the amount of pull which is necessary before the extensors of the wrist can be made to contract.
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SUPPLEMENTARY MOTILITY
In a lesion of the inusculospiral nerve, with paralysis of the extensors of the wrist, dorsal flexion of the hand may be produced by the action of muscles not innervated by this nerve, as in the energetic contraction of the flexors of the fingers (fig. 92). This occurs under certain conditions and is noted frequently. When the wrist-drop does not exceed an angle of 120 º complete flexion of the fingers produces extension at the wrist. In this condition the extensors of the wrist are shortened by contracture and fibrosis so that the angle between the hand and forearm is such that passive dorsiflexion or dorsal dislocation of the hand occurs. Without this provision the fingers could not be completely closed because of the shortened extensor tendons. The mechanism may be illustrated by using the wrist as a hinge, the hand as the weight, the flexors as the power transmitted through a pulley at the metacarpophalangeal joint to a fixed point at the origin of the extensors of the wrist.
FIG. 92.- Extension of wrist by supplementary movement of flexion of fingers
In some cases strong contraction of the pronator radii teres will produce extension of the hand on the forearm. During this movement the head of the radius is strongly depressed toward the palm, the styloid process at the ulna is pulled dorsally and the hand is deviated to the ulnar side. One may demonstrate readily that the hand can be flexed to a greater degree when the forearm is supinated than pronated, and if flexed to its fullest degree when the forearm is supinated, the hand will be seen to extend when strong pronation is instituted. The extension at the wrist is probably due to two factors: Lengthening of the tensor tendons and muscles; a leverage exerted on the scaphoid by the head of the radius. At times, in addition to the contraction of the pronator, there is seen strong abduction anf apposition of the thumb against the proximal phalanx of the index finger. At the same time resistance to this action is made by the contraction of the lumbrical muscle and the hand is extended on the forearm to a notable degree. During this action the middle, ring, and little finger show flexion at the proximal phalanges and extension of the two distal phalanges(fig. 93). Contrary to the opinion of Duchenne 4 and Benisty, 15 the American material when examined showed, in agreement with Beevor 5 and Mackenzie, 16 that for pure lateral movements of the wrist both the extensors and flexors are
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necessary. Adduction and abduction of the wrist are superseded by pronation and supination of the forearm in the position of wrist-drop of a musculospiral palsy. If, however, the hand be passively extended to the same plane as that of the forearm, abduction accompanied by flexion of the wrist ensues as the result of contraction of the flexor carpi ulnaris, and occasionally abduction has likewise been observed.
FIG. 93.- Extension of wrist by supplementary movement of contraction of pronator radii teres
The extensors of the fingers extend the first phalanges, and only the first phalanges, of the fingers on the metacarpal bones. To demonstrate the immobility of the first phalanges it is necessary to have the wrist passively semi-extended. Under this condition no extension will take place at the first phalanges. It is possible to tense the proximal phalanges of the fingers by extending the terminal ones through the interossei. At the same time flexion of the proximal phalanges occurs as the result of the unopposed action of the lumbricales. Slight passive extension of the proximal phalanges may be produced by
FIG. 94.- Extension of the distal phalanx of the thumb in musculospiral palsy
flexion of the hand at the wrist. Frequently simulation of extension of the first phalanx of the index finger is accomplished by strong adduction and apposition of the thumb against the first phalanx of the index finger, which is thereby passively lifted dorsally.
The extensor longus pollicis extends the two phalanges of the thumb. In addition to it, however, the abductor and adductor pollicis and flexor brevis
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pollicis are prime movers for extension of the distal phalanx of the thumb. Therefore, although never as complete or as strong as when the extensor longus pollicis is spared, the other muscles may produce extension of the distal phalanx of the thumb (fig. 94). Simulation of this movement may be produced by flexion of the distal phalanx of the thumb followed by relaxation. Such a mechanism in frequently observed in slight flexion of the fingers, in ulnar-median lesions and flexion and extension of the toes, in internal and external popliteal lesions, respectively. Abduction of the thumb in the plane of the palm is impossible in musculospiral paralysis and during attempts to abduct the thumb, the tendons of the "anatomical snuffbox" do not stand out in the slightest degree.
MUSCLE ATROPHY
Muscular atrophy is noted two or three months after the injury and may become so marked that it appears as if the skin and subcutaneous tissue were adherent to the posterior aspect of the ulna and radius.
FIG. 95.- Partial lesion of musculospiral nerve
PARTIAL LESIONS
It is significant that in lesions in the arm it is usual to find all of the muscles below the innervation to the supinator longus paralyzed, irrespective of the severity of the lesion. However, it may be noted that at times the extensors of the wrist may be paralyzed and those of the fingers unaffected; again, the extensor of the middle finger may be impaired. Occasionally the extensors of the thumb and fingers were involved, whereas the extensors of the wrist were spared (fig. 95). The constancy of certain partial lesions of various nerves has been attributed to the intraneural localization of fibers supplying certain muscles as pointed out by Stoffel,17 Marie, Meige, Gosset,18 and Dejerine and Mouzon. 19 However, it may be well to remember that Dustin 20 believes that he has conclusively shown that between each branch of a nerve there was a reas-sembling of nerve fibers in the form of an intraneural plexus so that a long intra-neural pathway does not exist.
889
RECOVERY
According to Oppenheim, the muscles recover in direct relation to the length of nerve fibers regenerating. This does not appear to be the case. Benisty 15 states that the order of recovery is nearly always the same. The common extensor is restored only after the radial muscle, the middle, ring, and little fingers begin to extend first, and lastly the index; but sometimes it is the index and middle fingers that first quite recover their movements. The exten-sors of the thumb and the abductor of the thumb regain their power last of all. From the available observations of the United States Army material a marked difference is seen in that the extensors of the thumb recovered before those of the finger. As to the order of recovery of the extensors of the fingers and thumb, those of the thumb showed some recovery in over 50 percent of cases but when this did not occur the thumb was almost the last to recover. The extensor of the middle finger was one of the first to recover in over 50 percent of cases and1 the index finger was last in one-third of the number of cases. Rarely, return of function was seen in the long abductor of the thumb, and in the extensor of the thumb before that in the extensors of the wrist.
SIGNS OF RECOVERY
Simultaneous extension of the wrist and all the fingers seems to be the final stage in recovery of voluntary movement. Pitres 21
FIG. 96.- Sign of complete recovery of musculospiral nerve
suggested two tests for determining the completeness of recovery in musculospiral paralysis. The first, placing the arm in an attitude of a man taking an oath, with wrist and fingers extended, the thumb raised and separated from the finger with the tendons of the extensors and the long abductor of the thumb marking out the anatomical snuffbox. Then he is requested to supinate his hand. The second test consists of the patient placing his little finger on the seam of his trousers with his fingers well extended and with the palm of his hand turned to the front.
MEDIAN NERVE
TOTAL PARALYSIS
When the median nerve has been completely divided or when physiologic function has been lost, the hand inclines slightly to the ulnar side of the arm,
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as shown in Figure 97. The index and middle fingers without being completely extended are more extended than normally. There is considerable atrophy of the muscles of the thenar eminence and the thumb is in the plane of the palm
FIG. 97.- Median nerve palsy
producing the so-called "ape hand." Pronation is incomplete and defective. When the forearm is flexed the patient supplements this defect by holding the elbow out. When it is extended he rotates the arm inward, resulting in passive
FIG. 98.- Inability to completely close the fist in median palsy
pronation of the hand. Paralysis of the palmar muscle may be determined by palpation of the tendons at the bend of the wrist when flexion at the wrist is opposed. Paralysis of the flexor sublimis and outer part of the flexor profundus
891
digitorum is manifested by absence of flexion in the index finger and feeble flexion in the middle finger. This finger is usually influenced by the movement of the ring finger and at times the deep flexor may be supplied by the ulnar. These defects in flexion may be readily seen when the patient is asked to "make
FIG. 99.- Imperfect clasping of fingers in median nerve palsy
a fist" (fig. 98). The index and middle fingers will then be seen to have their phalanges only slightly flexed. The same defects may be observed by clasping the hands together as in prayer when the index finger will remain extended. Flexion of the proximal phalanges of the fingers may be carried out very well in
FIG. 100.- Imperfect opposition of thumb in median nerve palsy
spite of the paralysis of the lumbricales. Paralysis of the flexor longus pollicis makes it impossible for flexion of the second phalanx of the thumb to occur.
Paralysis of the thenar muscle is shown by very defective apposition and abduction of the thumb at right angles to the palm.
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SUPPLEMENTARY MOVEMENTS
In addition to the supplementary movements of pronation which have been mentioned above, they occur commonly in flexion of the proximal phalanges of the two outer fingers. The fact that the flexor profundus digitorum for the middle finger may in some instances receive its supply from the ulnar, explains the frequent presence of flexion of the first phalanx of that finger, inasmuch as the lumbricales have their origin in the tendon of the flexor profundus digitorum. If they are paralyzed, and especially if some contracture and shortening has taken place, contraction of the flexor profundus digitorum will produce a pull on the inert lumbricales and result in flexion of the proximal phalanges. That there is a pull exerted on the lumbricales seems to be shown by the fact that flexion of the proximal phalanx is stronger when combined with flexion of the terminal phalanges than when performed alone. The lumbrical muscles of the middle finger likewise receive their nerve supply from the ulnar. As was seen in paralysis of the extensors of the hand wherein flexion of the fingers produced
FIG. 101.- Opposition of the thumb by the adduetor pollicis and flexor brevis pollicis in median nerve palsy
a passive extension at the wrist, so under certain conditions the interossei may produce movements ordinarily subserved by the lumbricales. The interossei when extended produce a pull on the tendons of the flexor profundus and sublimis digitorum, and when the lumbricales are paralyzed, especially if they are shortened afterwards, passive flexion of the proximal phalanges will occur. This mechanism permits full extension of the terminal phalanges, and in median nerve lesions extension of the terminal phalanges of the middle and index finger. It is to be noted that despite the paralysis of the flexors in a median nerve lesion, the position of the fingers is frequently one of flexion and not of extension. Flexion of the second phalanges of the two inner fingers occurs only a little more weakly than normal as the result of the accompaniment of this movement to the normal flexion of the proximal and distal phalanges of these fingers. Flexion of the second phalanx of the middle finger is frequently present in this general flexor movement; it is influenced by flexion of the ring finger; the flexor sublimis digitorum for this finger in some instances must receive some of its nerve supply from the ulnar. Flexion of the terminal phalanxof the index finger is always absent. Flexion of the terminal phalanx of
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the middle finger may be present in those cases where the flexor profundus digitorum is supplied by the ulnar nerve. Extension of the wrist produces slight passive flexion of the fingers which is better observed in combined lesions of the ulnar and median nerves. Flexion of the terminal phalanx of the thumb may be simulated by a rebound following extension of the phalanx. Apposition of the thumb to the little finger may be simulated by the action of the adductor pollicis combined with the inner head of the flexor brevis pollicis and flexion of the terminal phalanges of the finger being opposed. It should be insisted upon that abduction when tested should occur at right angles to the palm.
When the metacarpophalangeal joint of the thumb is partially ankylosed so that no flexion or extension of the plane of the thumb is possible, traction of the extensor longus pollicis and the extensor ossis metacarpi pollicis produces abduction of the thumb at right angles to the palm,
INCOMPLETE LESIONS
Benisty 15 states that the flexion of the index finger is the most defective movement, though apposition of the thumb is very poor as well. There is frequently imperfect flexion of the middle finger and of the second phalanx of the thumb. The pronators and flexors of the wrist are either not affected at all, or very slightly.
The flexor carpi radialis was found to be rarely involved in the peripheral nerve lesions of the American wounded. This finding is in conformity with that of other observers. Of the small hand muscles the opponens was the most frequently affected.
Careful dynamometric study shows that physiologic interruption cannot be differentiated from anatomic section by the strength of the movement of the phalanges of the fingers, because of supplementary motility. Although in a considerable number of cases the movements of the index finger were stronger, this did not allow one to determine the character of the lesion. Return of function in the opponens pollicis would indicate a partial lesion, but because of supplementary motility it is very difficult to determine.
RECOVERY
Benisty believes that recovery of function of the muscles in lesions of the median nerve takes place in complete and partial lesions in very much the same way. The pronator and palmar muscles regain their function and activity first, then the flexors of the middle finger, and afterwards the flexors of the thumb. Flexion of the index finger and afterwards the flexors of the thumb. Flexion of the index finger and apposition of the thumb are impaired for a very long time. Stopford's 22 statistics show that in 14 cases of suture of the median nerve in the lower third of the forearm the abductor brevis pollicis recovered first in 5 cases; of 10 cases at the bend of the elbow above the motor branches, in 1 case the pronator and flexor carpi radialis recovered first, in 3 cases the abductor brevis pollicis; in 8 cases of suture in the arm the pronator radii teres, flexor carpi radialis, and palmaris longus recovered in 1 case and the abductor brevis pollicis in 3. Among the American injured recovery occurred
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first in the flexor carpi radialis and flexor longus pollicis. Movement seemed to begin to return early in the flexor of the index finger, but from a study of residual paralysis it was evident that flexion of the index finger remained imperfect
FIG. 102.- Closure of fist in recovered median palsy
for a very long time, comparable, therefore, to the opponens pollicis. Where recovery occurs in the small hand muscles, the opponens is the last to recover.
Complete recovery of the median nerve may be demonstrated by the ability to completely flex the thumb and index finger in making a fist or in clasping the hands. Figs. 102, 103.
FIG. 103.- Recovery of median nerve
PAINFUL LESIONS OF THE MEDIAN NERVE
A very large number of lesions of the median nerve are characterized by the predominance of pain. This painful type of lesion was noted during the Civil War by S. Weir Mitchell,14 who, subsequently, described its intensity and character under the name of causalgia.
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The motor disturbances usually are slight, and total paralysis of all the muscles below the level of the wound is of rare occurrence. Some weakness in movement, however, is always present, usually localized in the flexors of the finger but particularly the index finger and of the thenar muscles. Much of the weakness is due to the pain which is increased upon movement. In- voluntary movement, consisting of an irregular tremor of the thumb and index finger, but noticeable in all the fingers, is characteristic of these painful lesions.
FIG. 104.- Causalgia in median nerve lesion combined with ulnar lesion
ULNAR NERVE
In ulnar nerve lesions the appearance of the hand is quite characteristic. There is noticed an atrophy which is at times very marked at the first dorsal interosseous space and to a lesser degree at the other spaces; the hand assumes a claw shape, the result of the unopposed action of the extensor communis digitorum. Sometimes clawing may be plainly seen in the little finger but can hardly be seen in the ring finger; at times the middle finger is clawed as well as the ring and little fingers. The hypotbenar eminence shows considerable atrophy, and palpation gives the impression of a hollow rather than an eminence. Atrophy of the abductor of the thumb may be made out at the inner part of the thenar eminence.
Paralysis of the flexor carpi ulnaris may be made out by inspection and palpation of the flexors of the wrist when the patient flexes the wrist against resistance. Paralysis of the flexor profundus of the little and ring fingers maybe demonstrated by the imperfect flexion of the ring and little fingers in having the patient try to make a fist. The flexion produced at the metacarpophalangeal and second interphalangeal joints results from the influence exerted upon all segments of the finger when the flexor sublimis contra cts. Flexion of the distal phalanges of these fingers often is practically nil. Paralysis of the hypothenar muscles is shown by an inability to flex the proximal phalanx of the little finger the distal phalanges being extended. Paralysis of the interossei and of the inner two lumbricales produces the characteristic claw hand. Although all the interossei may be paralyzed, there is complete clawing only of
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FIG. 105.- Ulnar nerve lesion
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the fourth and fifth fingers and sometimes of the middle finger. The reason for this is clear, inasmuch as the first two lumbricales which are supplied by the median are unparalyzed. Extension of the distal phalanges of the fingers is very feeble in the index and middle and practically impossible without supplementary motility in the ring and little fingers. Aside from supplementary movement, the lateral movements of adduction and abduction are lost in the middle and ring fingers and often in the little finger. They are much diminished in the index finger. Paralysis of the adductor pollicis and of the inner head of the flexor brevis pollicis produces defects in prehensile movements, attention to which has been drawn by Duchenne 4 and recently by J. Froment. 23 If the patient is asked to grasp any object between his thumb and index finger, such as a folded newspaper, and told to hold it tightly he vigorously flexes the second phalanx of the thumb and presses the tip awkwardly against the outer margin of the first phalanx of the index finger. This is Froment's sign of the newspaper.
FIG. 106.- Ulnar "paper sign"
PARTIAL LESIONS
Lesions of partial, incomplete, or dissociated paralysis of the ulnar nerve are very frequent. The commonest type, according to Benisty, is paralysis of the interossei and hypothenar muscles, with simple paresis of the flexor profundus and flexor carpi ulnaris. In our World War cases it was observed that whether we were dealing with a lesion in the arm or the forearm the same orderof frequency of paralyzed or weak muscles existed. Those muscles paralyzed most frequently were, as noted by Benisty, the hypothenar group and the interossei group. The order of frequency of involvement was as follows: (1) All muscles weak; (2) hypothenar interossei paralyzed; (3) all muscles paralyzed;(4) abductor pollicis paralyzed. When the long flexors were involved all the muscles were weak. Careful dynamometric examination showed that physiologic interruption could not be distinguished from anatomic section by strength of movements of the phalanges in the fingers. In partial lesions relatively greater strength in the phalanges was observed, but at times was an inaccurate guide to the severity of the lesions. Relatively greater strength in the first dorsal interosseus or in the abductor of the little finger proved to be anaccurate guide as to the completeness of the lesion.
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SUPPLEMENTARY MOTILITY
Flexion of the distal and proximal phalanges of the ring and little fingers is performed by the two inner tendons of the flexor profundus digitorum and the two inner lumbricales, respectively. Imperfect flexion of these phalanges may result from the influence exerted on all segments when the flexor sublimis digitorum contracts. This is more marked in the little than in the ring finger.
Slight flexion of the proximal phalanx of the ring finger may be obtained from the contraction of the flexor profundus digitorum pulling on the lumbricales muscle, which has part of its origin from the tendon of the profundus. Although the interossei which extend to the second and third phalanges of all fingers are paralyzed, inability to extend these phalanges in the index and middle finger is rare. Benisty15 attributes this to the preservation of the lumbricales, which she states extends the second and third phalanges, and the
FIG. 107.- Extension of the distal phalanges of the index and middle fingers in ulnar palsy
interossei. With this MacKenzie 16 disagrees and he is inclined to believe that the dorsal interossei for the index and middle fingers receive some of their nerve supply from the median. Besides this, he believes that with hyperextension of the proximal phalanx, there is an alteration in the line of pull of the interossei which become angular instead of straight, and that an extended proximal phalanx forms a rigid dorsal support for the sublimis tendon, thus increasing its flexion pull. Therefore, paralysis of the lumbricales alone would produce at one time overaction of flexion of the second phalanx and a poor mechanical principal for extension of the distal phalanges. Other factors, however, enter into the production of extension of the second and third phalanges of the index and middle fingers. Duchenne, 4 Benisty, 15 and MacKenzie 16 contend that the extensor communis digitorum does not produce extension of these phalanges. On the other hand, Beevor 5 points out that although it was true that when the extensor digitorum was paralyzed the second and third
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phalanges could be extended, and when the interossei were paralyzed claw-hand occurred and extension of the second and third phalanges was impossible, yet if in the latter case the third phalanges were passively flexed, the second and third phalanges could be extended. He says it is probable that in claw-hand the inability of the extensor digitorum to extend the terminal phalanges is due to its energy being expended on the first phalanges, which are not pre-vented from over-extension by the lumbricales which are paralyzed.
The following factors enter into preservation of extension of the second and third phalanges: Innervation of the first and second dorsal interossei by the median, passive extension of the second and third phalanges by flexion of the proximal phalanges, thereby shortening the interossei. If the interossei are paralyzed and the lumbricales preserved, the pull on the interossei is straight and not angular; under these conditions, contraction of the extensor communis
FIG. 108.- Abduction of the thumb by the extensor longus pollicis in ulnar palsy
digitorum may exert a pull on the inert interossei and produce extension of the second and third phalanges. Some pull on these interossei may be exerted by the extensor communis digitorum even if these conditions are absent, as may be seen in combined ulnar and median lesions. The fact that the extensor communis digitorum exerts a pull on the inert interossei does not mean that it is at all concerned with the normal extension of the second and third phalanges, which may be the result of an entirely independent contraction of the interossei.
In adduction of the thumb, as pointed out by Duchenne, the extensor longus pollicis is the prime mover, and in ulnar nerve lesions it may supplant the loss of the adductor pollicis.
Abduction of the fingers away from the midline may result from forced extension of the first phalanges. It is very marked in the index and little fingers. Slight adduction results from flexion of the first phalanges. Both of these movements have been known for a long time. The reason for the preservation of lateral movements in the middle and index fingers is given by
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Benisty 15 as the preservation of the lumbricales, as well as the extensor' action of the first phalanges. As MacKenzie16 points out, the lumbricales are not concerned with lateral movements of the fingers. The preservation of lateral
FIG. 109.- Abduction of fingers by forced extension
movements of these two fingers is due, in addition to the extensor movements of the first phalanges, to a dual nerve supply, as it has been noted on a number of occasions that the first dorsal interosseus is partially preserved in complete ulnar section. Besides the abduction observed in forced extension of the first
FIG.. 110.- Adduction of index finger by extensor indicis with hand in ulnar deviation
phalanx, abduction movement of the index finger can be produced by strong contraction of the extensor ossis metacarpi pollicis and extensor brevis pollicis; the first dorsal interosseous having part of its origin on the metacarpal bone of
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the thumb, is pulled outward by extension of this bone and produces abduction of the index finger. When the hand is abducted to the ulnar side, the tendon of the extensor indicis is so deflected that its contraction produces slight adduction of the index finger.
RECOVERY
The order of recovery in ulnar nerve lesions given by Benisty 15 is flexor carpi ulnaris, flexor profundus digitorum, then the small hand muscles, which recover very slowly. The committee upon injuries to the nervous system of the Medical Research Council 24 stated that better functional recovery is to be expected in the flexor carpi ulnaris, flexor profundus digitorum, and in the abductor minimi digiti than in the other muscles. Because of supplementary motility the strength of movement of the phalanges themselves is a misleading sign of recovery. In our cases it was found that recovery occurs more regularly in the flexor carpi ulnaris and late in the small hand muscles, but that the abductor of the thumb recovers more frequently than the abductor of the little finger.
FIG. 111.- Pitres test or recovery from ulnar palsy. a, Normal movement; b, failure of test in ulnar palsy
SIGNS OF RECOVERY
Complete recovery may be shown by the following sign described by Pitres 21: The palm being placed flat upon the table with the fingers abducted, the patient can move the little finger inward and outward and then scratch the top of the table with the nail of his little finger without moving his wrist.
MEDIAN AND ULNAR NERVES COMBINED
TOTAL PARALYSIS
The only movements possible in combined lesions of the median and ulnar nerves in the muscles supplied by these nerves are those occurring as the result of supplementary motility. The appearance of the hand is characteristic. The wrist is slightly hyperextended on the forearm and the hand
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inclines to the radial side, the thumb is in the abduction and on a plane with the palm. The first phalanges of the fingers are moderately extended on the metacarpus, and slight passive flexion of the last two phalanges occurs. The thenar and hypothenar eminences are markedly atrophic.
FIG. 112.- Ulnar and median nerve lesion
SUPPLEMENTARY MOTILITY
Slight passive movement of flexion at the wrist is produced by hyperextension of the hand with sudden relaxation. Active contraction of the abductor longus pollicis assists in carrying out this movement of flexion. At times this muscle is capable of producing flexion in the absence of relaxation
FIG. 113.- Flexion of the wrist by the extensor ossei metacarpi pollicis
following hyperextension. Flexion of the fingers is similarly performed by hyperextension of the hand and extension of the fingers which are then relaxed. Slight abduction of the fingers may be produced by energetic contraction ofthe extensors.
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PARTIAL LESIONS
Partial lesions of the ulnar and median nerves produce many interesting types of dissociated paralysis. A number of these have been described by Benisty: 15 One, in which the small hand muscles and flexors of the fingers alone being paralyzed; another in which there is in addition to the paralysis of the small hand muscles, a paresis of the flexors which produces a very marked clawing. A number of other types have been described but their recognition is of no great importance. Careful dynamometric studies show that when observed some time after injury anatomic section of both ulnar and median nerves produced complete paralysis of all of the phalanges of the fingers and thumb and severe lesions, not anatomic sections, show some movement in some of the phalanges of all of the fingers. In incomplete lesions of either ulnar or median nerves weak movements of the phalanges of the fingers, if interpreted alone, are insufficient guides to whether one of these nerves is severed, and if severed, which one. Because of the widespread supplementary motility, recovery of function is difficult to study and a definite pattern of involvement can not be determined.
MUSCULOCUTANEOUS NERVE
In paralysis of the musculocutaneous nerve satisfactory flexion can be produced by the voluntary action of the brachio radialis supplied to the musculospiral
FIG. 114.- Musculocutaneous paralysis
The pronator radii teres is also a flexor of the forearm, and in some cases has efficiently produced flexion in combined paralysis of the musculocutaneous and musculospiral nerves. Evidence of paralysis of the musculocutaneous nerve may be determined by palpation of the biceps when flexion of the forearm is resisted, with the forearm in position between pronation and supination.
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CIRCUMFLEX NERVE
The muscles supplied by the circumflex nerve are the teres minor and deltoid. When the deltoid muscle is completely paralyzedl abduction of the arm is impossible.
FIG. 115.- Circumflex nerve palsy Greatest adduction
SUPPLEMENTARY MOTILITY
Satisfactory abduction of the arm when the circumflex nerve is completly palralyzed occurs very frequently. The frequency may he seen from the report of Bunts,25 who, in 1903, found that in 19 cases of circumflex nerve paralysis 7 patients recovered function.
Of the seven, four recovered function in the absence of the deltoid muscle. From studies of clinical cases and preparations of anatomic models, it appears that there are two distinct types of suplplementary motility which permit abduction of the humerus in complete paralysis of this deltoid muscle. Of course, the movement of torsion or bending of the spine need not be included, as it only increases the distance between the extended hand and the ground and in no way abducts the humerus. The movement of abduction backward seems never to be supplemented, so that such a movement as is necessary to put one's hand in the hip pocket is impossible.
The first type of supplementary movement is that in which the head of the humerus is firmly fixed in the glenoid cavity, probably by the subscapularis, the infraspinatus, the pectoralis major, and the supraspinatus. During this
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period external rotation of the humerus occurs. The serratus magnus and trapezius, with the rhomboidei and the levator anguli scapulae then produce the rotation of the scapula, elevating the humerus; some actual abduction may likewise occur. Thus the first and second phases of abduction are combined but the second phase overshadows the first. The third phase may be concluded by the supraspinatus, the clavicular head of the pectoralis major, and the coracobrachialis.
The second type is that in which the first phase of abduction of the humerus may occur as the result of combined action of the supraspinatus, the infraspinatus, and probably acting in conjunction with the coracobrachialis and possibly the long head of the biceps; the second phase of abduction occurs as
FIG. 116.- Complete adduction of arm by supplementary movement in circumflex nerve palsy
in the normal individual, by the action of the serratus magnus, the trapezius, the rhomboidei, and the levator anguli scapule; the third phase is completed by the coracobrachialis, the clavicular head of the pectoralis major, and the supraspinatus.
BRACHIAL PLEXUS
Brachial plexus lesions in civil practice have been divided as to type into lesions in the primary cords, the secondary cords, and root lesions. The secondary cords, usually spoken of as the cords of the brachial plexus, have been the most frequent type of lesions observed. Some of the cases have been classified into upper-arm paralysis, the Erb's type of injury involving the fifth and sixth cervical roots, and the lower-arm paralysis, or the Klumpke-Dejerine tvpe, producing a paralysis of the common median and ulnar nerve trunks. Direct lesions of the brachial plexus due to war wounds present no clearly defined classification. Ordinarily, immediately following the injury there is complete paralysis of the whole brachial plexus which, as the effects of the Concussion disappear and the changes due to hemorrhage and infiltration diminish, revolves itself into one or another type of involvement of one or more cords, or an incomplete type of total brachial plexus paralysis.
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As in civil practice, an involvement of the upper primary cords produces a paralysis of the fifth and sixth cervical roots, known as Erb's paralysis. The muscles affected by paralysis resulting from this lesion are the deltoid, biceps, brachialis anticus, supinator longus, as well as the supraspinatus and infraspinatus, the rhomboideus, and subscapularis, the clavicular fibers of the pectoralis major, serratus magnus, and, finally, the latissmus dorsi and teres major.
FIG. 117.- Erb's form of brachial plexus palsy analgesia (black) of fifth and sixth cervical segments
The arm can not be flexed at the elbow on account of the paralysis of the flexors of the forearm, and can not be raised or abducted on account of paralysis of the deltoid. The movements of the wrist and fingers are not interfered with. The arm is weak in adduction and it can be rotated onlv inward or outward or not at all. The rhomboid muscle stands out less prominently in its attempts to oppose the two shoulder blades. The patient is able but feebly to put the affected hand on the buttock of the same side.
FIG. 118.- Brachial plexus lesion affecting common trunk of ulnar and median nerves
The paralysis resulting from a lesion of the common trunk of the median and ulnar nerves need not be described as it differs in no wav from a combined lesion of these nerves. Lesions of the inner cord of the brachial plexus are
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evidenced by paralysis of all the intrinsic muscles of the hand and some or all of the flexors of the wrist and fingers.
Lesions of the posterior cord are evidenced by paralysis of the muscles supplied by the circumflex, musculospiral, and subscapularis nerves. Lesions of the outer cord result in a paralysis of the muscles supplied by the musculocutaneous and median nerve, with the exception of the intrinsic muscles of the hand.
In addition to these clearly defined types of paralysis there may be a more complicated paralysis involving the whole, or nearly the whole, of the brachial plexus. It is to be noted that lesions of the brachial plexus have a general tendency to recover. Often this recovery is only partial and definite paralysis of one or two nerves or some muscles may be permanent. It is necessary, therefore, to continue the observation for several months, both clinically and
FIG. 119.- Partial lesion of whole brachial plexus, affecting chiefly posterior and outer cords
electrically, to estimate the recoverability of certain muscles involved in these partial lesions.
One of the interesting things observed in lesions of the brachial plexus has been the coincidence of lesions of the spinal cord with these injuries. In this type there is almost always injury by projectiles which pass through the neck, either from left to right or right to left. The symptoms which appear at once are that the patient falls forward vithout losing consciousness, and all four extremities are paralyzed. A few days or a week after the accident, according to the gravity of the injury, the lesion subsides in one entire half of the body, opposite the brachial monoplegia. The leg on the affected side then recovers and the brachial monoplegia alone remains, often severe, persisting for a longtime and improving very slowly. At times a paralysis of the opposite arm of a root type may persist for a certain period.
The loss of power as the result of the brachial plexus lesion is most marked in the hands and fingers.
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Frequently the picture is completed by a paralysis of the cervical sympathetic or Horner's syndrome, enophthalmos, narrowing of the palpebral fissure and myosis. This very frequently is intermittent and often disappears early.
SCIATIC NERVE
Although the internal and external popliteal nerves run separately up to the lumbosacral plexus, above the popliteal space they are bound together by connective tissue so closely that lesions above the popliteal space may be considered as lesions of the sciatic nerve.
Motor branches are given off the sciatic nerve trunk from above downward to the semitendonosus, semimembranosus, the long head of the biceps, short head of the biceps, and adductor magnus. The musculocutaneous branch of the external popliteal supplies the peroneus longus and peroneus brevis: the anterior tibial branch supplies the tibialis anticus. extensor longus digitorum, extensor proprius hallucis, peroneus tertius and extensor brevis digitorum. The muscular branches of the internal popliteal go to the gastrocnemius, popliteal, plantaris and soleus, while the posterior tibial innervates the popliteus, the deep part of the soleus,
FIG. 120.- Sciatic nerve palsy
tibialis posticus, flexor longus digitorun and flexor longus hallucis. The internal plantar nerve supplies the abductor hallucis, flexor brevis hallucis, flexor brevis digitorum, flexor accessorius and the two first lumbricales. The external plantar nerve supplies the interossei, the muscles of the little toe, the third and fourth lumbricales, and the adductor obliquus et tranversus hallucis. Because the nerve to the semitendonosus is given off very high rarely is there a complete paralysis of flexionof the leg. As a rule, flexion is only diminished in strength and the diminution of strength is in the biceps, the semitendonosus or the semimembranosus being less affected. In appearance the foot dangles and drops. Frequently there is observed a marked atrophy of all the muscles below the knee. No active movement is possible in the muscles below the knee.
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SUPPLEMENTARY MOTILITY
Interpretation of muscle function in the lower extremity is much simpler than that in the upper, chiefly because of the minor importance of the intrinsic foot muscles as compared with those in the hand. Attention, therefore, centers chiefly in the movements of the larger muscles in the lower extremity. Inasmuch as supplementary movements can occur only when one of the divisions of the sciatic nerve is totally paralyzed and the other partially or not at all involved, description of these movements are made under the heads of the external popliteal nerve and the internal popliteal nerve.
PARTIAL INJURY
Dissociated or partial paralysis may be due to greater damage to either the internal or external popliteal branches or partial injury to both. Operative and clinical experience shows that the external popliteal suffers greater damage, as a rule, than does the internal popliteal. Of a series of 37 cases seen soon after injury the external popliteal was paralyzed and the external popliteal was weak in 12 cases; all the muscles were weak in 10 cases; the internal popliteal was paralyzed and the external popliteal was weak in 4 cases; the external popliteal alone was paralyzed in 2 cases, the internal popliteal alone in 2 cases, and only the extensors of the toes in 2 cases; all muscles were paralyzed in 2 cases.
RECOVERY
According to Benisty,15 the muscles which are the first to recover are usually the tibialis anticus, the peroneus longus, or the gastrocnemius; very much more rarely recovery begins in the tibialis posticus. The flexors and extensors of the toes are always the Inst to recover.
The Medical Research Council of Great Britain 21 reported that, as a rule, the internal popliteal nerve shows signs of return of function earlier than does the external popliteal. Stopford's 22 records of sutured cases show that the order of recovery is the gastrocnemius, tibialis anticus, extensor longus digitorum, extensor proprius hallucis.
The records of the Military Orthopedic Hospital, Shepherd's Bush, gives the order of recovery in eight cases as tibialis posticus, gastrocnemius, tibialis anticus, extensor longus digitorum, extensor longus hallucis, extensor brevis digitorum, and peroneus longus.
In a group of 41 of our recovered cases there was a return of function in the tibialis anticus in 18 in the gastrocnemius in 11, in all muscles in 9, in the tibialis posticus in 8, in the peronei in 4, in all muscles supplied by the external popliteal in 3, in the flexors of the toes in 1, and in all muscles supplied by the internal popliteal in 1 case. In 14 cases following suture, function returned first in the gastrocnemius in 8 cases, in the tibialis posticus in 5 cases, in the peronei in 4 cases, in the flexors of the toes in 3 cases, in the tibialis anticus in 3 cases, and in the extensors of the toes in 1 case. In severe cases, and following suture, return of function in the branches of the internal popliteal occurred earlier than in those of the external popliteal; extension of the toes was very late in appearing, and in spontaneously recovering lesions flexion of the toes occurred very late.
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PAINFUL LESIONS
As was noted above under the median nerve, so in the sciatic nerve some injuries result in a painful type of paralysis. It has been found that only such injuries are painful as show an involvement of the fibers of the internal popliteal nerve.
During the first week after injury complete paralysis is often present. Then motor recovery begins, most often in the region of the internal popliteal. In some cases, however, where the external popliteal branch is less severely injured, movements controlled by this nerve are the first to recover. As with the median nerve, involuntary movements are sometimes observed, consistingof abduction and adduction of the foot or flexion of the toes.
EXTERNAL POPLITEAL NERVE
Somewhat analogous to the musculospiral nerve, the external popliteal nerve, when injured, produces immediate and extensive paralysis of all the muscles supplied by it. As the result of this injury a deformity characterized by foot-drop is observed. In addition to the foot-drop a slight drop of the first phalanx of all the toes may be seen. At times a dorsal tumor of the tarsus is observed. This is usually due to the more or less pronounced projection of the heads of the astragulus and scaphoid bones and to the thickening of the sheaths of the extensor tendons.
When examining voluntary motion it is necessary to immobilize the knee of the patient and to be alert lest twitchings of the aponeurosis of the leg caused by contrac- tion of the muscles of the thigh be mistaken for contraction of muscles supplied by the external popliteal nerve.
FIG. 121.- External popliteal nerve palsy
When carefully observed, no active movement of dorsal flexion of the foot is possible. Abduction of the foot is executed by the tibialis posticus. Extension or dorsal flexion of the proximal phalanges of the toes is impossible. The distal phalanges may be extended by the contraction of the interosseus tendon which in the foot as in the hand extends the last two phalanges. Abduction of the foot can not be performed.
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SUPPLEMENTARY MOVEMENT
Supplementary movements of the ankle joint are fairly frequent. Strong flexion of the toe occasionally results in inversion and slight dorsal flexion of the foot, due to a mechanism similar to that observed in which strong flexion of the fingers produces passive extension of the hand in musculospiral lesions. Movements of the toes are sometimes confusing when the contraction of the antagonists of the paralyzed muscle is followed by a rebound simulating the normal action of the muscles under investigation. If the dorsal flexors of the toes are paralyzed and the patient attempts to contract the paralyzed muscle, plantar flexion of the toes may be the initial movement followed by a rebound of the toes to the original position.
PARTIAL LESIONS
Cases of incomplete and dissociated paralysis are met with infrequently. They generally occur following wounds in the leg in which either the musculocutaneous or the anterior tibial nerve alone has been injured. Dissociated paralysis may occur, however, in lesions above the bifurcation of the nerve. Under this condition we may have a paralysis of the tibialis anticus alone, or of the peronei muscle alone, the extensors of the toes being spared. Occasionally the extensors of the toes may be paralyzed and the other muscles not at all or very slightly involved.
RECOVERY
The order of recovery is given by Benisty 5 as tibialis anticus, peronei, extensor longus digitorum, and extensor proprius hallucis. Stopford 22 agrees with this, whereas the records of the Military Orthopedic Hospital put the extensor longus digitorum first. Among 29 American cases spontaneously recovering, the tibialis anticus recovered in 22 cases, the peronei in 7, the extensor longus digitorum in 3, and the other muscles in 3. In 6 cases showing recovery out of 27 cases sutured, the order was tibialis anticus, extensor longus digitorum, and the peronei.
INTERNAL POPLITEAL NERVE
In lesions above the popliteal space complete isolated injury to the internal popliteal nerve is rare. More frequently, as noted above under lesions of the sciatic nerve, partial or dissociated paralysis of the nerve, accompanied by more or less complete paralysis of the external popliteal nerve occurs. In lesions below the popliteal space the internal popliteal may be completely severed. Motor disturbances which result are paralysis of plantar flexion of the foot. Frank adduction of the foot is impossible; it is always accompanied by elevation of the foot and is then due to contraction of the tibialis anticus. Flexion and separation of the toes are abolished and no muscle or tendon in the sole can move.
POSTERIOR TIBIAL NERVE
Paralysis of this nerve frequently occurs as the result of injury in the calf and produces a paralysis of all the muscles of the sole. This is very frequently a painful paralysis of a causalgic nature.
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FIG. 122. – Anterior crural palsy
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ANTERIOR CRURAL NERVE
All the muscles supplied by the anterior trurtl nerve are parialyzed as the result of injury striking the actual trunk of the anterior erural at the highest part, of the thigh below Poupart's ligament. Usually some of these muscles are preserved and the most frequent nerves to be involved are the nerves to the quadriceps and the internal saphenous nerve. A lesion of the nerve to the quadriceps produces paralysis of this muscle with inability to extend tle leg on the thigh. Some extension of the leg on the thigh has been noted by contraction of the tensor fascia femoris, supplied by the superior gluteal nerve.
LUMBOSACRAL PLEXUS
The lumbosacral plexus is verv rarely injured except in its root in consequence of a projectile having injured the cauda equina in its intraspinal course inside or outside of the dura mater.
CRANIAL NERVES
TRIGEMINAL NERVE
Lesions of the trigeminal nerve are not uncommon. Usually the lesion involves but one of the branches. Occasionally a paralysis of the masseter or of the pterygoid, or both musles may be observed. When this occurs, upon clenching the two jaws together the paralyzed masseter does not con tract: upon opening the mouth the jaw deviates to the paralyzed side. The same observation holds true in attempting to protrude the lower jaw in front of the upper.
FACIAL NERVE
The facial nerve is fairly frequently injured in wounds of the parotid region and of the neck. Moreover, wounds of the cranium, particularly in the temporofrontal region are very often accompanied by paralysis of the motor filaments of the orbicularis palpebrarum, or the frontalis.
FIG. 123.- Facial palsy
Most, frequently some of the branches of the seventh nerve are injured alone. Complete paralysis of the seventh nerve is not uncommon and a dissociated paralysis of the seventh nerve from a lesion of the trunk likewise frequently occurs. Paralysis of
914
the trunk of the seventh nerve is characterized by complete absence of movements of expression on the paralyzed side, with inability to wrinkle the forehead upward or to close the eye, and attempts at closing the eye are associated with movement of the eyeball upward, or Bell's phenomenon. In addition to this, the patient is unable to pucker the lips or to smile or show the teeth on the paralyzed side. The expression of the face is characteristic, the paralyzed side being "washed out" and expressionless, and because of atony the angle of the mouth droops, the nasolabial fold is obliterated, and there is an effacement of wrinkles on the forehead. Frequently because of inability to hold the lips closely together there is drooling. All of the signs are exaggerated during attempted movement of the face or during involuntary movement, as in laughing.
FIG. 124.- Paralysis of trapezius
GLOSSOPHARYNGEAL NERVE
This nerve is rarely injured alone but when injured produces paralysis of the superior constrictor of the pharynx. This is manifested by difficulty in swallowing solids so that the patient is obliged to facilitate this deglutition by the ingestion of fluids. At the same time the soft palate may be involved so that the unparalyzed part of the palate produces deviation to the sound side. When this occurs nasal regurgitation of fluids may be present. When the tongue is held protruded by the examiner, phonation of the broad "a" produces a movement of the posterior wall of the pharynx toward the unaffected side.
PNEUMOGASTRIC NERVE
This is rarelv affected alone, but when paralyzed produces a paralysis of the adductor of the vocal cords.
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SPINAL ACCESSORY NERVE
When injured alone, usually the external branch only, intended for the innervation of the trapezius and the sternocleidomastoid, is involved. The internal branch, which joins the pneumogastric soon after its exit from the cranium, supplies the muscles of the larynx and those of the soft palate. According to some authors, it is this nerve which, running along with the pneumogastric, produces the motor disturbances due to the injuries of the vagus, this nerve itself being purely sensory. When the external branch is paralyzed there ensues a paralysis of the sternocleidomastoid and the trapezium. On turning the head to the side the paralyzed sternocleidomastoid muscle does not become prominent. The shoulder of the affected side droops, the inner angle of the scapula deviates outward, the outer angle droops, and the lower angle approximates the midline and is projected under the skin. The infraspinous portion of the trapezius receives its innervation from the fourth cervical nerve. Frequently this must course with the branches of the external branch of the spinal accessory, inasmuch as when we deal with lesions of the spinal accessory high in the neck the infraspinous portion of the trapezius is involved as well as the supraspinous portion, and under this condition abduction of the arm is impossible because of absence of fixation of the shoulder. Lesions low in the neck produce only a weakness in the supraspinous portion of the trapezius, and abduction of the arm may often be adequately performed, inasmuch as the infraspinous portion of the trapezius serves to adequately fix the shoulder blade during the first stage of abduction of the arm.
FIG. 125.- Hypoglossal nerve palsy
HPYOGLOSSAL NERVE
The hypoglossal nerve supplying the muscles of the tongue, the geniohyoid muscle, and the subhyoid muscle, is rather frequently injured in the suprahyoid region and more frequently in the lateral pharyngeal space. This lesion is shown by a hemiparesis of the tongue, the corresponding half of the tongue is atrophied and shriveled, and within the mouth it is drawn to the unparalyzed side. When protruded, it points to the paralyzed side.
916
SIMULTANEOUS INJURIES OF CRANIAL NERVES
Simultaneous lesions of the ninth, tenth, and eleventh cranial nerves have frequently been observed as the result of war injuries and often injury of one or more additional nerves has been present, most frequently the twelfth, occasionally the cervical sympathetic, and rarely the seventh nerve.
Vernet 26 has described a syndrome due to a combined lesion of the glossopharyngeal, pneumogastric, and spinal accessory nerves, called by him the syndrome of the posterior lacerated forearm. Collet 27 described a combination of symptoms due to a complete lesion of the ninth, tenth, eleventh, and twelfth cranial nerves under the name of glosso-laryngo-scapulo-pharyngeal hemiplegia. The same condition was described by Sicard 28 as the syndrome of condylo-posterior lacerated forearm. Villaret 29 described the syndrome of the posterior retroparotid space, which is characterized by the addition of a lesion of the sympathetic nerve to the syndrome of the last four cranial nerves, producing thereby enophthalmos, narrowing of the palpebral fissure and myosis. One of the notable features of all the cases is that whatever other nerves might be affected, the ninth, tenth, and eleventh are rather con- sistently injured together. Such lesions are produced by wounds in the uppermost part of the latero-pharyngeal space. Simultaneous injury of these nerves usually occurs as the result of a missile passing obliquely from the mastoid region on one side to the malar bone on the other, injuring the three nerves and missing both the carotid and jugular vessels.
FIG. 126.- Syndrome of the posterior retroparotid space, showing paralysis and atrophy of tongue, narrowing of palpebral fissure, myosis, and enophthalmos
The symptomatology of a combined lesion narrowing of palpebral fissure, myosis, and en. of the ninth, tenth, and eleventh cranial nerves is constant and easily recognized. As a characteristic triad of symptoms indicative of a complete lesion of these three nerves. Vernet proposes nasal regurgitation of fluid, dysphagia of solids, and hoarseness. representing, respectively, paralysis of the palate, pharynx, and larynx.
REFERENCES
(1) Sherren, James: The Distribution and Recovery of Peripheral Nerves. Studies from Instances of Division in Man. Lancet, London, March 17, 1906, i, 727.
(2) Swan, Joseph: A Treatise on Diseases and Injuries of the Nerves. Longmans (and others), London, 1824.
(3) Létiévant, É.: Traité des sections nerveuses. J. B. Bailliére et fils, Paris, 1873, 142.
(4) Duchenne, G. B.: Physiologie des mouvements. J. B. Balliére et fils, Paris, 1867.
(5) Beevor, Charles E.: The Croonian Lectures on Muscular Movements and their Representation in the Central Nervous System. Adlard and Son, London, 1904.
(6) Head, Henry, and Shlerre, Janmes: The Consequences of Injury to the Peripheral Nerves in Man. Brain, London, 1905, xxviii, November, pt. 2, 116.
(7) Claude, Henri: Blessures des nerfs. Revue neurologique, Paris, 1916, Nos. 4-5, 492.
(8) Athanassio-Bénisty, Mme.: The Treatment and Repair of Nerve Lesions, Military Medical Manuals, University of London Press, Ltd., London, 1918.
(9) Coleman, C. C.: The Interpretation of Muscle Function in its Relation to Injuries of the Peripheral Nerves. Surgery, Gynecology and Obstetrics, Chicago, 1920, xxxi, No. 2, 246.
(10) Woods, A. H.: Misleading Motor Symptoms in the Diagnosis of Nerve Wounds. Archives of Neurology and Psychiatry, Chicago, 1919, ii, No. 5, 532.
(11) Pollock, Lewis ,J.: Supplementary Muscle Movements in Peripheral Nerve Lesions. Ibid., 518.
(12) Marie, Pierre and Athanassio-Bénisty, Mme.: Du retour de la contratilité faradique avant le rétablissement de la motilité dans les muscles paralysés á la suite des lesions des nerfs peripleriques. Revue neurologique, Paris, April 15, 1915, xxvii, 494.
(13) André -Thomas: Hypertonic misculaire dans la paralysie radiale en voie d'amélioration. Sensations cutanées dans le domaine du nerf radial provoquées par la pression de muscles qui recoivent leur innervation du méme nerf. Séance du 29 Juillet, 1915, Société de neurologie. Revue neurologique, Paris, 1915, xxvii, Nos. 20-21, 771.
(14) Mitchell, S. Weir, Morehouse, George R., and Keen, Wm. W.: Gunshot Wounds and other Injuries of Peripheral Nerves. J. B. Lippincott & Co., Philadelphia, 1864.
(15) Athanassio-Bénisty, Mme.: Formes cliniques des lesions des nerfs. Masson et Cie., Paris, 1916.
(16) Mackenzie, Wm. C.: The Action of Muscles. H. K. Lewis and Co., Ltd., London, 1918, 112.
(17) Stoffel: Deformitäten nach Nervenverletzungen und ibre Behandlung. Verhandungen der deutschen orthopädischen Gesellschaft, Stuttgart, May 28, 1920, xv, 196.
(18) Marie, Pierre, Meige, Henry et Gosset, A.: Les localisations motrices dans les nerfs périphéiriques. Bulletin de l'académie de médecine, Paris, 1915, lxxiv, 3d. s., No. 52, 798.
(19) Dejerine, Mme., and Mouzon, J.; Les lésions des gros troncs nerveaux: des membres par projectiles de guerre. Presse médicale, Paris, 1915, xxiii, No. 40, 321.
(20) Dustin, A. P.: Le service de neurologie á l'ambulance "Ocean." Travaux de l'ambulance "Ocean," Masson et Cie., Paris, 1917.
(21) Pitres, A.: La valcur des signes cliniques permettant de reconnaitre dans les blessures des nerfs periphériques. Revue neurologique, Paris, 1916, xxix, Nos. 4-5, 477.
(22) The British Medical Research Council, Special Report Series No. 54. The Diagnosis and Treatment of Peripheral Nerve Injuries. His Majesty's Stationery Office, London, 1920, 37.
(23) Froment, J.: La préhension dans les paralysies du nerf cubital et le signe du pouce. Presse médicale, Paris, 1915, xxiii, No. 50, 409.
(24) The British Medical Research Council, Special Report Series No. 54. The Diagnosis and Treatment of Peripheral Nerve Injuries. His Majesty's Stationery Office, London, 1920.
(25) Bunts, F. E.: Nerve Injuries about the Shoulder-Joint. Transactions of the American Surgical Association, Philadelphia, 1903, xxi, 520.
(26) Vernet, M.: Syndrome du trou dechiré posterieur. Revue neurologique, Paris, 1918, xxv, Nos. 11-12, 117.
(27) Collet et Petzetakis: Le reflex oculocardiaque dans les lésions traumatiques des pneumogastriques. Comptes rendus des séances de la societé de biologie, Paris, 1916, lxxix, 1147.
(28) Sicard, J. A. et Roger, H.: Paralysie des quatres derniers nerfs craniens. Marseille m?dicale, 1918, Iv, No. 21, 886.
(29) Villaret, M.: Le syndrome de l'espace rétro-parotidien postérieur. Paris médicale, 1917, xxii, No. 2, 246.
