Peripheral Nerve Lesions

When we speak here of the “peripheral nerves,” we are referring to the nerve plexuses formed by the junction and regrouping of fibers derived from the spinal nerve roots, as well as to the more distally lying peripheral nerve trunks and branches. The plexuses always contain mixed fiber types and the peripheral nerve trunks nearly always do, i. e., somatic motor, somatosensory, and often also autonomic (particularly sympathetic) fibers. The individual peripheral nerve trunks bear an anatomically invariant relationship to the muscles and cutaneous zones that they innervate. This pattern of innervation is fundamentally different from that of the spinal nerve roots, because, as we recall, the nerve root fibers undergo reassortment in the plexuses. This fact enables the clinical examiner to distinguish a peripheral nerve lesion from a radicular lesion based on the observed pattern of neurological deficits. The main clinical manifestations of

peripheral nerve lesions are marked paresis, extensive sensory deficits, and diminished sweating in the zone of innervation of the affected nerve or nerve branch. Pain can be produced by either a radicular lesion or a peripheral nerve lesion and is thus not a distinguishing feature of either.

Preliminary anatomical remarks. A peripheral nerve is a cablelike bundle of nerve fibers of different functional types (see p. 3). The nerve fiber is the smallest “building block” of a peripheral nerve; it consists of an axon and an encasing myelin sheath (if present), which is the membrane of a Schwann cell wrapped around the axon numerous times. Individual nerve fibers are surrounded by a delicate connective tissue called endoneurium. The nerve fibers and the endoneurium are then bundled together into larger fascicles, each of which is surrounded by a tough perineurium. Along the length of the nerve, the individual fascicles make many plexus-like intercon-

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1pectoral nn. (med./lat.) C5−T1 pectoralis major & minor mm.

2 lateral cord

3 dorsal (posterior) cord

4 medial cord

5axillary n. C5, 6 deltoid m. C5, 6 teres minor m. C5, 6

6 musculocutaneous n. C5−7 biceps brachii m. C5, 6 coracobrachialis m. C6, 7 brachialis m. C5, 6

7radial n. C5−T1

triceps brachii m. C7−T1 anconeus m. C7, 8 brachioradialis m. C5, 6

extensor carpi rad. long./brev. mm. C6−8 extensor digit. m. C7, 8

extensor indicis m. C7, 8 extensor digiti minimi m. C7, 8

ext. poll. long./brev. mm. C7, 8 abd. poll. long. m. C7, 8

8median n. C5−T1 pronator teres m. C6, 7

flexor carpi radialis m. C6−8 palmaris longus m. C7, 8 flexor digit. superf. m. C7−T1

flexor digit. prof. m. (radial side, II/III) C7−T1

pronator quadratus m. C7−T1 opponens pollicis m. C7, 8 abductor poll. brev. m. C7, 8

superf. head of flex. poll. brev. m. C6−8

lumbrical mm. I & II C8−T1

9ulnar n. (C7) C8−T1 flexor carpi uln. m. C8−T1

flexor digit. prof. m. (ulnar side, IV/V) C8−T1

palm./dors. interossei mm. C8−T1 lumbrical mm. III & IV C8−T1 adductor pollicis m. C8−T1

deep head of flex. poll. brev. m. C8−T1 palmaris brevis m. C8−T1

10medial brachial cutaneous n. C8−T1

11medial antebrachial cutaneous n.

C8−T1

12thoracodorsal n. C6−8 latissimus dorsi m.

13subscapular nn. C5−8 subscapular m. C5−7 teres major m. C5−6

14long thoracic n. C5−7 serratus anterior m.

15nerve to the subclavius m. C5, 6 subclavius m.

16suprascapular n. C4−6 supraspinatus m. C4−6 infraspinatus m. C4−6

17dorsal scapular n. C3−5 levator scapulae m. C4−6 rhomboid mm. C4−6

18phrenic n. C3, 4

Peripheral Nerve Lesions

Fig. 12.16 Anatomical bottlenecks in the shoulder region, at

which nerves and/or blood vessels can be compressed.

anterior scalene m.

middle scalene m.

brachial 1 plexus

subclavian a.

subclavian v.

2

clavicle

1st rib

3

1scalene hiatus costoclavicular

2passage

3subpectoralpassage

Fig. 12.17 Muscles of the upper limb and the nerve roots that innervate them. With the aid of this diagram, brachial plexus lesions can be localized from the pattern of muscle weakness that they cause.

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Fig. 12.18 Upper limb posture and sensory deficit in right upper brachial plexus palsy (diagram). The deltoid, biceps, and supraand infraspinatus mm. are atrophic, the arm is internally rotated, and the palm of the hand points posteriorly.

Fig. 12.19 Upper limb posture and sensory deficit in right lower brachial plexus palsy (diagram). The intrinsic muscles of the hand are atrophic, the sensory deficit corresponds to the C7 and C8 dermatomes, and there is an accompanying Horner syndrome.

sometimes the elbow extensors and the extensors of the hand. A sensory deficit is not necessarily present; if there is one, it is located in the area of the shoulder, on the outer surface of the upper arm, or on the radial edge of the forearm (Fig. 12.18).

Lower brachial plexus lesion (Dejerine−Klumpke palsy). This type of lesion involves the fibers originating in the C8 and T1 roots. Its prominent findings include weakness of the intrinsic muscles of the hand, some-

times also of the long flexors of the fingers, and rarely of the wrist flexors. The triceps brachii m. usually remains intact. The mechanism of the precipitating accident, and the anatomical relationships in this area, often lead to an accompanying dysfunction of the cervical sympathetic supply, resulting in Horner syndrome with impaired sweating. On the basis of these findings, a lesion of the T1 root is presumed to be present, proximal to the origin of its branch to the sympathetic chain. There is always a sensory deficit involving the ulnar edge of the forearm, hand, and fingers (Fig. 12.19).

C7 palsy. In the present context, we are speaking not of a lesion of the C7 root itself, but rather of the fibers derived from it that make up the C7 portion of the brachial plexus. This type of palsy involves deficits in the distribution of the radial n. (p. 226), while the function of the brachioradialis m. is preserved.

Etiologic Classification of Brachial Plexus Lesions

Traumatic Lesions

Traumatic lesions of the brachial plexus are usually due to motor vehicle accidents; rarer causes include occupational injury and direct stab or gunshot wounds. The initial clinical finding is not uncommonly a total upper limb paralysis (Fig. 12.20), which may later improve until it resembles one of the types of localized brachial plexus lesion described above. The prognosis is generally better for upper brachial plexus lesions; bloody CSF obtainable by lumbar puncture and, later, clinical evidence of myelopathy are poor prognostic signs indicating probable nerve root avulsion. In such patients, MRI may reveal empty nerve root pouches (Fig. 12.21). The treatment consists of the fitting of an abduction splint and the performance of passive exercises to prevent freezing of the shoulder joint. Brachial plexus surgery is highly complex and demanding and is occasionally resorted to in cases of upper brachial plexus injury.

Brachial plexus palsy caused by trauma during delivery is the result of obstetrical complications, such as breech delivery. When the damaged axons regenerate, they may reconnect to the “wrong” muscles and/or muscle groups, leading to pathological accessory movements and abnormal motor patterns.

Compressive Lesions of the Brachial Plexus

External compression can injure the brachial plexus in persons who carry heavy loads on their shoulders or wear heavy backpacks. Lesions of this type usually affect the upper brachial plexus and sometimes only individual branches of it. The long thoracic n. is most frequently involved (p. 224).

Compression at anatomical bottlenecks. The collective designation “thoracic outlet syndrome” (TOS) is commonly used for these conditions, usually in nonspecific fashion, and often, unfortunately, as a vague term for brachialgia of as yet undetermined origin, or for other unexplained symptoms relating to the brachial plexus. Scalene syndrome is usually due to the

Fig. 12.20 Complete right brachial plexus palsy. Atrophy of all muscles of the upper limb, internal rotation of the arm.

anomalous presence of a cervical rib, a fibrous band (which may be visible in a CT scan), or some other type of structural anomaly in the scalene hiatus. The typical manifestations of scalene syndrome include: clinical evidence of a lower brachial plexus lesion, worsening of symptoms on lowering of the arm, and fixed or motioninduced circulatory insufficiency of the subclavian a. (as revealed by a vascular bruit, and/or by disappearance of the radial pulse when certain maneuvers are performed, e. g., the Adson maneuver—turning the chin to the side of the lesion, with simultaneous backward bending of the head).

Costoclavicular syndrome. This syndrome, like the scalene syndrome, should be diagnosed only if a causative anatomical anomaly and objectifiable neurological deficits (usually, a lower brachial plexus palsy) can be found. An arteriogram is occasionally helpful in establishing the diagnosis, as it may demonstrate motiondependent compression of the subclavian artery or vein (Fig. 12.22).

Fig. 12.22 Costoclavicular syndrome in a 24-year-old patient with clinical evidence of a lower brachial plexus lesion. An arteriogram of the brachial a. reveals free passage of contrast medium (a) when the arm is dependent. When the arm is elevated, however, (b) the subclavian a. is compressed between the clavicle and the first rib.

a

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b

Treatment of compression syndromes. Both the scalene syndrome and costoclavicular syndrome should be treated conservatively at first, once their diagnosis has been definitively established. Special exercises are used to strengthen the shoulder-elevating muscles. Surgical treatment is reserved for the small minority of patients with objectifiable, severe neurological deficits. A supraor transclavicular approach gives the surgeon optimal access to the anatomical structures.

Neuralgic Shoulder Amyotrophy

Pathogenesis. This disorder is presumed to be due to an inflammatory/allergic affection of the brachial plexus. It usually arises spontaneously, but is sometimes seen in the aftermath of an infectious disease, or after the administration of serum (brachial plexus neuritis).

Clinical manifestations. This disease affects men more often than women and is usually located in the right arm. It always begins with intense local pain in the shoulder, which generally lasts for a few days. Rarely, the pain will persist at a milder intensity for a longer period. Once the pain subsides, motor weakness of the muscles of the shoulder girdle and/or of the arm develops. The weakness can, in principle, affect any muscle group of the upper limb, but it tends to affect the muscles innervated by the upper portion of the brachial plexus. Paresis of the serratus anterior m. is particularly common. There may be no objectifiable sensory deficit.

Treatment. No specific treatment is required beyond analgesic medication in the initial, painful phase.

Prognosis. The prognosis is generally good, but it may take many months for the weakness to resolve completely.

Other Causes of Brachial Plexus Lesions

Radiation-induced brachial plexus lesions usually appear with a latency of one or more years after radiotherapy, usually in women who have been treated with surgery and radiotherapy for breast cancer. In 15 % of patients, pain is the main symptom; it can increase over the course of several years. The differentiation of radia- tion-induced brachial plexopathy from a recurrent malignant tumor is not always easy; a short interval between the completion of radiotherapy and the onset of pain (except when a very high radiation dose was given) and very intense pain, both tend to suggest a recurrent tumor rather than radiation injury as the cause. Imaging studies are helpful, but even these cannot always reliably distinguish scarring from new tumor tissue.

Pancoast tumors of the apex of the lung usually cause a lower brachial plexus palsy accompanied by severe pain. The sympathetic chain is usually involved as well; thus, Horner syndrome and diminished sweating in the upper body on the affected side are typical findings (Fig. 12.23).

a

b

c

Fig. 12.23 Right-sided Pancoast tumor in a 68-year-old man. There is clinical evidence of compression of the lower brachial plexus and of the sympathetic chain. a Right Horner syndrome. b Atrophy of the intrinsic muscles of the right hand, especially the thenar muscles. c Weakness of the wrist and finger extensors on the right.

Other causes of brachial plexus palsy , some of which are very rare, are usually diagnosable only by the specialist: acute palsy due to occlusion of a small artery supplying the plexus, after medical procedures, in heroin addicts, in familial brachial plexus neuritis, parainfectious and serogenic forms, etc.

Diseases of the Peripheral Nerves

of the Upper Limbs

Suprascapular N. (C4−C6)

Anatomy. This nerve innervates the supraspinatus and infraspinatus mm. It reaches them after passing through the scapular notch and then running dorsally. It receives sensory branches from the shoulder joint, but not from the skin.

Typical deficits. A lesion of the suprascapular n. produces weakness and atrophy of the two muscles on the dorsal surface of the scapula (Fig. 12.24). The first 15° of lateral elevation of the arm are weak (supraspinatus m.), as is external rotation of the arm at the shoulder joint (infraspinatus m.) (Fig. 12.25).

Causes. Overuse of the arm can lead to mechanical compromise of the nerve in the scapular notch. Other causes include trauma and a ganglion lying in the notch.

Axillary N. (C5−C6)

Anatomy. This nerve provides motor innervation to the deltoid and teres minor mm. and sensory innervation to a palm-sized patch of skin on the proximal, lateral surface of the upper arm (superior lateral brachial cutaneous n.) (Fig. 12.26).

Typical deficits. Axillary nerve palsy manifests itself as marked weakness of lateral abduction and forward elevation of the arm. The normal roundness of the shoulder is flattened. External rotation of the arm at the shoulder joint is lessened at rest, so that the dependent arm is held in mild internal rotation (Fig. 12.27).

Causes. The most common cause of axillary n. palsy is dislocation of the shoulder (forward and downward). The prognosis in such patients is favorable.

Fig. 12.25 Testing of the muscles innervated by the suprascapular n. a Weakness of the supraspinatus m. is most evident in the first 15° of lateral elevation of the arm. b Weakness of the infraspinatus m. is evident when the arm is externally rotated at the shoulder joint.

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Fig. 12.24 Atrophy of the supra and infraspinatus muscles due to a lesion of the left suprascapular n. in a 25-year old man. The etiology remained unclear in this case.

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Fig. 12.27 Left axillary nerve lesion in a 26-year-old man. Atrophy of the left deltoid m. with “pointed” shoulder contour. The sensory deficit in the territory of the superior lateral brachial cutaneous n. is indicated.

Differential diagnosis of axillary nerve palsy includes complex brachial plexus lesions affecting the upper portion of the plexus, rotator cuff lesions, and restriction of movement by pain in humeroscapular periarthropathy.

Long Thoracic N. (C5−C7)

Anatomy. This nerve is the longest branch of the brachial plexus. It is a purely motor nerve supplying the serratus anterior m.

Typical deficits. A long thoracic nerve palsy causes winging of the scapula, which is particularly evident when the arms are held high, or when the patient extends the arms and presses with the palms of the hands against a wall (Fig. 12.28).

Causes. Lesions of the long thoracic n. are usually due to excessive mechanical strain on the shoulder (carrying heavy loads) or to neuralgic shoulder amyotrophy

(p. 222). Cryptogenic cases also occur.

Musculocutaneous N. (C5−C7)

Anatomy. This nerve innervates the biceps brachii and coracobrachialis mm. and a portion of the brachialis m.

Its sensory terminal branch, the lateral antebrachial cutaneous n., innervates the skin on the radial side of the forearm (Fig. 12.29).

Typical deficits. Lesions of the musculocutaneous n. cause marked weakness of elbow flexion. This must be tested with the forearm in the supinated position, because, if the forearm is pronated or in neutral position, the elbow can still be flexed by the powerful brachioradialis m., which is innervated by the radial n.

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radial n. lat. brach. cut. n. deltoid m.

medial head of triceps brachii m.

lateral head of triceps brachii m.

muscular branch of musculocutaneous n.

posterior antebrachial cutaneous n.

brachialis m. extensor carpi radialis longus m.

brachioradialis m. extensor carpi radialis brevis m.

superficial branch of radial n.

posterior antebrachial cutaneous branch

tendon of extensor carpi radialis longus m.

tendon of extensor carpi radialis brevis m.

communicating branch to ulnar n.

Peripheral Nerve Lesions

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dorsal branch of ulnar n.

communicating branch to radial n.

dorsal digital nn.

dorsal branch

palmar cutaneous branch

superficial branch

palmaris brevis m.

communicating branch to median n. palmar

digital nn.

the absence of characteristic symptoms, is not an indication for surgery.

Treatment. Keeping the hand in the neutral position at night with a well-padded volar splint often brings relief. If it does not, or if objectifiable neurological deficits are already present, there should be no hesitation in proceeding to surgery. Operative carpal tunnel release involves splitting of the flexor retinaculum with an open or endoscopic technique (generally performed either by a neurosurgeon or by a hand surgeon).

Ulnar N. (C8−T1)

Anatomy. The anatomy of the ulnar n. is shown in Fig. 12.38. Among the muscles innervated by this nerve, the ulnar flexors of the wrist and fingers (the flexor carpi ulnaris m. and the ulnar portion of the flexor digitorum profundus m.) are functionally much less important than the ulnar-innervated intrinsic muscles of the hand. The ulnar n. is, indeed, the most important nerve for finger function: it innervates not only the hypothenar mm., but also all of the interossei, the 3rd and 4th lumbrical mm., and, in the thenar region, the adductor pollicis m. and the deep head of the flexor pollicis brevis m. It provides sensory innervation to the ulnar edge of the hand, the volar surface of the fifth finger, and ulnar half of the fourth finger. A sensory branch arising from the ulnar n. in the distal third of the forearm innervates the skin on the ulnar side of the dorsum of the hand, as well as on the dorsal surface of the fifth finger and the ulnar half of the fourth finger.

Typical deficits. The typical clinical picture of ulnar nerve palsy is a claw hand (Fig. 12.39): because the interossei and lumbrical muscles cannot contract, the ulnar digits are hyperextended at the metacarpophalangeal joints, while the remaining digits are flexed at these joints. The long fingers can no longer be fully adducted against one another, the fingers cannot be strongly spread apart, and the patient cannot flick the middle finger against the examiner’s palm with full, normal strength. A key finding is that, when the patient grasps a flat object (such as a piece of paper) between the thumb and the index finger, weakness of the adductor pollicis m. (ulnar n.) leads to functional substitution by the flexor pollicis longus m. (median n.), and therefore to flexion of the thumb on the affected side at the interphalangeal joint. This finding, called Froment sign, is highly characteristic of ulnar nerve palsy (Fig. 12.40).

Fig. 12.40 Froment sign in right ulnar nerve palsy. Flexion of the interphalangeal joint of the thumb when the patient pulls on a flat object (piece of paper).

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In addition to these general clinical manifestations of ulnar nerve palsy, there are other specific findings that depend on the level of the lesion:

If the lesion is proximal (at the elbow or higher), it will also affect the ulnar portion of the flexor digitorum profundus m., thereby impairing flexion of the distal phalanx of the fourth and fifth digits (Fig. 12.41).

Fig. 12.39 Claw hand due to a right ulnar nerve lesion at the elbow. Typical features include hyperextension at the metacarpophalangeal joints and hyperflexion at the interphalangeal joints, particularly on the ulnar side of the hand. There is marked atrophy of the interossei and of the hypothenar muscles.

Fig. 12.41 A test for the function of the flexor digitorum profundus m. of the little finger (ulnar n.). Flexion of the little finger at the distal interphalangeal joint.

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