Fig. 12.42 Typical appearance of the hand in a lesion of the deep branch of the ulnar nerve at the wrist. Marked muscle atrophy in the first interosseous space, with preservation of the hypothenar musculature. Sensation was intact in this case.

Causes. Ulnar nerve palsy is often of traumatic origin. The nerve can be chronically dislocated at the elbow, where it can slip out of the ulnar groove on the medial epicondyle of the humerus; it is also vulnerable to external compression at this point (the “funny bone”), as well as to compression due to anatomical variations of the ulnar groove (sulcus ulnaris syndrome, cubital tunnel syndrome). Similarly, the ulnar n. can be damaged in the palm of the hand (e. g., by occupational tools), or by anatomical variations at the wrist (syndrome of the “loge de Guyon”).

Treatment. The treatment depends on the cause and location of the lesion. Chronic compression of the nerve is treated by removal of the source of compression. This may involve splinting or padding of the elbow, or even operative relocation of the nerve from a more dorsal to a more volar position.

Fig. 12.43 Weakness of the abdominal wall musculature, worse on the left side, due to neuroborreliosis affecting the caudal thoracic nerve roots.

If the lesion is at the wrist, it can be precisely localized by the involvement or noninvolvement of the palmaris brevis m. and the spatial configuration of the sensory deficit. The flexor muscles of the forearm that are innervated by the ulnar n. remain intact.

An isolated lesion of the purely motor terminal branch of the ulnar n. (its deep branch) causes weakness of the interossei, while the hypothenar and lumbrical mm. and the muscles of the forearm innervated by the ulnar n. are spared. There is usually no sensory deficit (Fig. 12.42).

Diseases of the Nerves of the Trunk

Anatomy. The peripheral nerves supplying the thoracic and abdominal wall are derived from nerve roots T2 through T12. Each peripheral nerve in this region contains fibers that are (nearly) exclusively derived from a single nerve root. We recall that this is not the case in the limbs, where there is an intervening plexus between the nerve roots and the peripheral nerves, in which the nerve fibers are reassorted. The clinical manifestations of a peripheral nerve lesion in the trunk are thus very similar to those of a nerve root lesion.

Typical deficits. The most characteristic neurological syndrome due to nerve dysfunction in this area is intercostal neuralgia, i. e., bandlike, usually burning pain radiating around the trunk from back to front, at a single dermatomal level.

Causes. The nerves of the trunk can be damaged by viral infection (e. g., herpes zoster), by mass lesions, or by a diabetic or infectious mononeuritis (e. g., borreliosis). Mononeuritis can produce unilateral weakness of the musculature of the abdominal wall; the corresponding segment of the abdominal wall becomes flaccid and pouches visibly outward (Fig. 12.43). Sensation in this area is diminished, too, and the abdominal skin reflex is absent at the corresponding level.

Rarely, painful entrapment neuropathy may affect individual sensory terminal branches of the nerves of the trunk. Notalgia paraesthetica is a neuropathy of this kind causing pain in the back: one of the dorsal rami of the thoracic spinal nerve roots becomes stuck in a small gap in the fascia, producing hypesthesia in a coin-sized, paravertebral area of skin, as well as pain. There are comparable entrapment syndromes of the ventral rami, causing, e. g., the so-called rectus abdominis syndrome.

Diseases of the Lumbosacral Plexus

Anatomy. The structure of the lumbosacral plexus is illustrated in Fig. 12.44. It lies in a well-protected location in the posterior wall of the pelvis. Its cranial portion (the

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1

1

2

Fig. 12.44 Anatomy of the lumbosacral plexus.

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3

4

Fig. 12.45 Anatomical course of the iliohypogastric and ilioinguinal nn. 1 Psoas major m. 2 Iliacus m. 3 Iliohypogastric n. 4 Ilioinguinal n.

L2

L3

2

Fig. 12.46 Anatomical course and distribution of the lateral femoral cutaneous n. The nerve turns from a nearly horizontal to a nearly vertical course (in the standing patient) at the point where it traverses the inguinal ligament. 1 Psoas major m. 2 Iliacus m.

lumbar plexus, L1−L4) gives off, as its main branches, the ilioinguinal, iliohypogastric, femoral, and obturator nn.

These nerves innervate most of the hip flexors and knee extensors. The caudal portion of the lumbosacral plexus (the sacral plexus, L5−S3) gives off the superior and inferior gluteal nn. for the gluteal muscles, as well as the sciatic n., which supplies the knee flexors and all muscles of the lower leg and foot.

Typical deficits. The clinical manifestations of a lumbosacral plexus lesion depend on its location; in general, one finds a combination of the deficits seen in lesions of the individual peripheral nerve trunks lying distal to the plexus lesion.

Causes. Lumbosacral plexus palsy is usually due to a local mass, but it may also be due to prior radiation therapy or to an autoimmune disorder known as chronic, progressive lumbosacral plexopathy.

Diagnostic evaluation. Ancillary testing, primarily with CT or MRI, is generally needed to identify the etiology of a lumbosacral plexopathy. These imaging studies can demonstrate the presence of a mass.

Diseases of the Peripheral Nerves

of the Lower Limbs

Genitofemoral and Ilioinguinal Nn. (L1−L2)

Anatomy. The course of these two (almost) monoradicular, mixed nerves is depicted in Fig. 12.45.

Typical deficits. Lesions of these nerves cause local pain in the groin (ilioinguinal nerve syndrome), a sensory deficit in the corresponding zone(s) of cutaneous innervation, and sometimes, in men, loss of the cremaster reflex (because the afferent arm of the reflex loop is interrupted). The associated motor deficit only affects oblique muscles of the abdominal wall and is hardly noticeable.

Lateral Femoral Cutaneous N. (L2−L3)

Anatomy. This purely sensory nerve passes through the three layers of the abdominal wall and then penetrates the inguinal ligament, usually at a point three finger breadths medial to the anterior superior iliac spine, to emerge onto the anterior fascia of the thigh. It provides sensory innervation to a palm-sized area of skin on the anterolateral surface of the thigh (Fig. 12.46).

Typical deficits. The lateral femoral cutaneous n. is vulnerable to injury at the point where it penetrates the inguinal ligament. The resulting clinical disturbance is an entrapment neuropathy called meralgia paresthetica, characterized by burning pain in the cutaneous distribution of the nerve. The pain is better when the hip is flexed, e. g., when the patient raises the ipsilateral foot onto a low stool; it is worse on hyperextension of the leg (reverse Lasègue sign). The site where the nerve passes through the inguinal ligament is often tender to light pressure. Most patients find the symptoms bearable and

need only be reassured that the condition is benign. Differential diagnosis. Meralgia paresthetica must be

saphenous n.

infrapatellar branch of saphenous n.

saphenous n.

Fig. 12.47 Anatomical course and distribution of the femoral n.

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Peripheral Nerve Lesions

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237

Diseases of the Spinal Nerve Roots and Peripheral Nerves

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Fig. 12.52 Weakness of the left gluteus maximus m. The left buttock, on active contraction, is less voluminous than the right, and the left gluteal fold hangs lower.

L4

L5

S1

S2

superior gluteal n.

S3

inferior gluteal n. (to the gluteus maximus m.)

weakness of the gluteus minimus and gluteus medius mm. can be caused by an L5 nerve root lesion. Bilateral weakness of the hip abductors is found, for example, in muscular dystrophy.

Sciatic N. (L4−S3)

Anatomy. The sciatic n. is the common trunk of the fibular (= peroneal or common peroneal) and tibial nn. It is the longest and thickest nerve in the human body. Its anatomy is shown in Fig. 12.53. The portions of the sciatic n. that are destined to become the fibular and tibial nn. are already clearly distinct from one another in the sciatic n. just distal to its exit from the pelvis, but they are usually ensheathed in a common epineurium nearly all the way down to the level of the popliteal fossa. The sciatic nerve trunk, in its proximal portion, gives off cu-

Fig. 12.53 Anatomical course and distribution of the sciatic n.

gluteus medius m. gluteus minimus m. tensor fasciae latae m. piriformis m.

gemellus superior m.

obturator internus m. gemellus inferior m.

inferior cluneal nn.

posterior femoral cutaneous n.

adductor magnus m.

semimembranosus m.

semitendinosus m.

sciatic n.

quadratus femoris m.

gluteus maximus m.

muscular branch of obturator n. adductor magnus m.

short head of biceps femoris m.

long head of biceps femoris m.

inferior cluneal nn.

posterior femoral cutaneous n.

taneous branches to the buttock and the posterior surface of the thigh (the inferior cluneal nn. and the posterior femoral cutaneous n.). Along its further course, it gives off motor branches to the knee flexors (the semimembranosus, semitendinosus and biceps femoris mm., which may be collectively termed the ischiocrural muscles or hamstrings).

Typical deficits. The clinical manifestations of a sciatic nerve lesion depend on the level of the lesion and the extent to which it involves the fibular and tibial portions of the nerve. Proximal lesions (but not distal ones) produce hypesthesia on the buttock and the posterior surface of the thigh and impair knee flexion. The strength and reflexes of the knee flexors are best tested in the prone patient (Fig. 12.54). For the clinical manifestations of fibular and tibial nerve lesions, see below.

Causes. The sciatic nerve trunk can be injured by fractures of the pelvic ring or proximal portion of the femur, by surgical procedures in the region of the hip, or by faultily delivered injections. Tumors are a less common cause of sciatic nerve palsy.

Fibular N. (L4−S2)

Anatomy. The fibular (peroneal or common peroneal) n., after it separates from the tibial portion of the sciatic n., travels to the lateral margin of the popliteal fossa, winds around the fibular neck, and then enters into the body of the fibularis longus (peroneus longus) muscle, where it divides into the superficial and deep fibular (peroneal) nn. The superficial fibular (peroneal) n. provides motor innervation to the fibular (peroneal) muscles and sensory innervation to the lateral surface of the lower leg and the dorsum of the foot, with the exception of the space between the first and second toes (the first interosseous space). The latter is supplied by the deep fibular (peroneal) n., which also innervates the dorsiflexors of the foot and toes and the intrinsic muscles of the dorsum of the foot.

The anatomy of the fibular n. is shown in Fig. 12.55.

Typical deficits. The clinical manifestations of a lesion of the deep fibular n. include foot drop and steppage gait (Fig. 3.2, p. 15). Sensation is impaired on the dorsum of the foot and completely abolished in the first interosseous space. A lesion of the superficial fibular n. causes weakness of pronation of the foot (i. e., inability to elevate the lateral edge of the foot); when the patient walks, the lateral edge of the foot hangs downward. Sensation is impaired in the lower leg and on the dorsum of the foot. If the trunk of the fibular n. (= the common peroneal n.) is affected, all of the above deficits are seen.

Causes. The trunk of the fibular n. can be injured by penetrating or blunt trauma, e. g., by knee fractures. Injection palsies of the sciatic n. usually affect its fibular portion. The most common cause of fibular nerve palsy, however, is compression of the nerve at the fibular neck by local, external pressure (faulty surgical positioning, a cast, etc.). This type of palsy is spontaneously reversible. The site of the lesion can be precisely localized with the aid of electroneurography (Fig. 4.24, p. 61).

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Fig. 12.54 Functional testing of the knee flexors. The patient is prone. This is mainly a test of the semimembranosus, semitendinosus, and biceps femoris mm.

Differential diagnosis. A foot drop combined with loss of sensation on the dorsum of the foot can be seen in combined lesions of the L4 and L5 nerve roots, but such lesions will additionally impair abduction of the hip and inversion of the foot. Bilateral foot drop caused either by

Steinert myotonic dystrophy or by peroneal muscle atrophy in the setting of HMSN type I can mimic a bilateral fibular nerve palsy. An initially isolated, progressive, unilateral foot drop without any associated sensory deficit may be the first symptom of spinal muscular atrophy or ALS.

Tibialis anterior syndrome. This syndrome often causes difficulties in differential diagnosis. It is caused by infarction (due to compression) of the muscles in the anterior compartment of the lower leg, because of overuse, trauma, or a hematoma. Steadily rising local pressure within the anterior compartment, which is tightly encased in fascia, leads first to intense local pain, and then to muscle swelling. The pain increases on passive extension of the muscles by plantar flexion of the foot. The muscles become necrotic in 12 to 24 hours and are later replaced by connective tissue. The resulting contracture prevents the appearance of the flaccid foot drop that is otherwise characteristic of fibular nerve palsy. In the acute phase of the tibialis anterior syndrome, the deep fibular n. can be damaged, because its course passes through the anterior compartment of the lower leg. The resulting sensory deficit may be diagnostically misleading, because it may be taken to imply a peripheral nerve lesion as the primary causative event.

Tibial N. (L4−S3)

Anatomy. This nerve, derived from the medial portion of the sciatic n., innervates the plantar flexors of the foot and toes in the lower leg, as well as all of the intrinsic muscles of the foot, except those on the dorsum. It provides sensory innervation to the heel and sole (Fig. 12.56).

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articular branch to the knee

superficial fibular (peroneal) n.

deep fibular (peroneal) n.

common fibular (peroneal) n.

lateral sural cutaneous n.

superficial fibular (peroneal) n.

deep fibular (peroneal) n.

Typical deficits. Weakness of plantar flexion makes tiptoe walking impossible, while weakness of the intrinsic muscles of the foot makes the patient unable to fan the toes. The sensory deficit on the sole of the foot is particularly troublesome because of the important protective function of sensation in this area.

Tarsal tunnel syndrome is an entrapment neuropathy affecting the terminal branch of the tibial n. as it passes under the medial malleolus. It is seen almost exclusively after fractures or sprains of the upper ankle joint. Its typical feature is local pain behind the medial malleolus or on the sole of the foot, which increases when the patient walks. The nerve trunk is tender to palpation be-

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hind the medial malleolus. Sensation is diminished on the sole of the foot and the plantar skin is abnormally smooth and dry. The patient can no longer fan the toes (Fig. 12.57).

Morton metatarsalgia. A painful neuroma can develop on a digital nerve (a sensory terminal branch of the tibial n.) if the nerve is chronically injured by being compressed between two adjacent metatarsal heads. This condition, called Morton metatarsalgia, causes pain in the forefoot, which is initially felt only on walking, but later also at rest. The pain can be induced by the examiner by laterally compressing the anterior arch of the foot or by squeezing the metatarsal heads against each

Fig. 12.57 Weakness of the intrinsic muscles of the foot in tarsal tunnel syndrome (lesion of the tibial n. behind the medial malleolus).

Fig. 12.58 Excised neuroma of an interdigital nerve. The neuroma was found at the branch point of the nerve. The patient had suffered from Morton metatarsalgia.

other. An injection of local anesthetic along the course of the nerve, applied from the dorsal surface of the foot proximal to the site of the neuroma, will bring complete, though transient, relief. Specially padded shoe inserts may be therapeutically useful. If the pain persists, the neuroma should be surgically excised through a plantar approach (Fig. 12.58).