Down the Garden Path
The patient, a 52-year-old office worker, had been receiving intramuscular vitamin B12 injections every month for the past 3 years because of vitamin B12 deficiency. A few days after a physician’s assistant in a specialized outpatient clinic gave her such an injection in the right gluteal region, she complained to her family physician of a “fuzzy” feeling over the right shin and dorsum of the foot, as well as occasional pain, “like an electric shock,” going down the leg. The doctor suspected an iatrogenic peripheral nerve injury. His physical examination revealed marked dorsiflexor weakness of the right big toe and also, to a lesser extent, of the other toes of the right foot, but foot dorsiflexion was of normal strength. There was diminished sensation to touch, and even more so to noxious stimulation, in the anterolateral quadrant of the right leg below the knee, and on the dorsum of the foot. The knee- and ankle-jerk reflexes were symmetrically elicitable; the tibialis posterior reflex was bilaterally absent. The doctor concluded that the patient had an iatrogenic right sciatic nerve lesion mainly affecting the peroneal nerve fibers.
Lesions of the peripheral nervous system (nerve roots, nerve plexuses, and peripheral nerves) are associated with flaccid weakness, diminution or loss of intrinsic muscle reflexes, and sensory deficits. Autonomic and trophic disturbances may be present as well (but not in nerve root lesions affecting the limbs). Each nerve root and each peripheral nerve have their own highly characteristic pattern of sensory and motor deficits; thus, the clinical findings generally enable the examiner to determine which root or nerve is affected. Sometimes, however, the differential diagnosis is harder. In the case described, the physician was too quick to conclude that the sciatic nerve was damaged in its peroneal component, on the basis of the history, the pattern of the sensory deficit, and the intact reflexes. All of these findings would, indeed, have been consistent with a peroneal nerve lesion, but not the motor findings. Peroneal nerve lesions markedly impair not just toe dorsiflexion, but foot dorsiflexion as well, because this nerve innervates all the dorsiflexor muscles, including the tibialis anterior muscle—yet this patient could still dorsiflex her foot. Nor did her shock-like pain shooting down the leg conform to the classic picture of a peroneal nerve lesion. The physician should have considered an L5 nerve root lesion in the differential diagnosis.
The family physician sent the patient to a neurologist for a consultation. She told the neurologist that she had, in fact, suffered from severe back pain a few days earlier. The neurologist confirmed the weakness of toe dorsiflexion, also noting weakness of hip abduction and foot inversion. These findings suggested an L5 nerve root lesion. A magnetic resonance imaging (MRI) of the lumbosacral spine revealed a centrolateral intervertebral disk herniation at L4/L5 compressing the right L5 root. Electromyography revealed marked denervation potentials in the right extensor hallucis longus muscle, which is innervated almost exclusively by the L5 root, while there was none in the tibialis anterior muscle (innervated mainly by the L4 root). To confirm the diagnosis, the neurologist studied the gluteus medius muscle, a muscle innervated by the L5 root (via the superior gluteal nerve) but remote from the distribution of the peroneal nerve; here, too, there were typical signs of denervation. The patient’s sensory disturbance thus had nothing to do with the intramuscular injection but was, rather, due to the disk herniation.
Lesions of the peripheral nervous system cause flaccid weakness, sensory deficits, and autonomic disturbances in variable distributions and combinations, depending on their site and extent. They can be classified as follows:
Lesions of the anterior horn cells in the spinal cord (see section ▶ 7.7).
Lesions of the spinal nerve roots (radicular lesions).
Lesions of individual peripheral nerve trunks or branches.
13.1 Radicular Syndromes
Radicular lesions are usually due to mechanical compression; less commonly, they may be infectious/inflammatory or traumatic. Their main clinical manifestation is pain, usually accompanied by a sensory deficit in the dermatome of the affected nerve root. Depending on the severity of the lesion, there may also be flaccid weakness and areflexia in the muscle(s) innervated by the nerve root.
The spinal nerve roots constitute the initial segment of the peripheral nervous system. The anterior (ventral) nerve roots contain efferent fibers, while the posterior (dorsal) nerve roots contain afferent fibers. The motor roots from T2 to L2 or L3 also contain the efferent fibers of the sympathetic nervous system. The anterior and posterior roots at a single level of the spinal cord on one side join to form the spinal nerve at that level, which then passes out of the spinal canal through the corresponding intervertebral foramen. At this point, the nerve roots are in close proximity to the intervertebral disk and the intervertebral (facet) joint ( ▶ Fig. 13.1).
Fig. 13.1 View of a cervical vertebra and intervertebral disk. The normal anatomy of the intervertebral (neural) foramen is shown on the right side of the figure; narrowing of the foramen by uncarthrosis is shown on the left. 1 Facets of the intervertebral joint; 2 root with spinal ganglion; 3 lateral/medial intervertebral disk herniation; 4 vertebral artery; 5 uncarthrosis; 6 dorsal spondylosis; 7 ventral spondylosis; 8 spinal dura mater. (Reproduced from Mumenthaler M. Der Schulter–Arm-Schmerz. 2nd ed. Bern: Huber; 1982.)
In their further course, the fibers of the spinal nerve roots of multiple segments form plexuses, from which they are then distributed to the peripheral nerves. The areas innervated by the nerve roots thus differ from those innervated by the peripheral nerves.
Dermatomes and myotomes The sensory component of a spinal nerve root innervates a characteristic segmental area of skin, which is called a dermatome. The efferent fibers of a spinal nerve root, after redistribution into various peripheral nerves, innervate multiple muscles (the myotome of the nerve root at that level). Each muscle, therefore, obtains motor impulses from more than one nerve root, even if it is only innervated by a single peripheral nerve.
Root segments and root-indicating muscles ▶ Table 13.1 is a list of the muscles that are often affected by radicular lesions and are accessible to clinical neurologic examination. The muscles that derive most of their innervation from a single nerve root are called root-indicating muscles.
Pain and hypalgesia in shoulder region
Diaphragmatic paresis or plegia
Partial diaphragmatic paresis is more ventral in C3 lesions, more dorsal in C4 lesions
Pain and hypalgesia on lateral aspect of shoulder over deltoid muscle
Deltoid and biceps paresis
Diminished biceps reflex
Radial side of arm and forearm down to thumb
Biceps and brachioradialis paresis
Diminished or absent biceps reflex
Dorsolateral to C6 dermatome down to second, third, and fourth fingers
Triceps, pronator teres, and (occasionally) finger flexor paresis; thenar eminence often visibly atrophic
Diminished or absent triceps reflex
Triceps reflex key to differential diagnosis versus carpal tunnel syndrome
Dorsal to C7 dermatome, i.e., ulnar side of arm and forearm, down to little finger
Intrinsic hand muscles visibly atrophic, particularly on hypothenar eminence
Diminished or absent triceps reflex
Triceps reflex key to differential diagnosis versus ulnar nerve palsy
From greater trochanter crossing over the anterior aspect to the medial aspect of the thigh and knee
Weakness of quadriceps (knee-jerk) reflex
Differential diagnosis versus femoral nerve palsy: intact sensation in distribution of saphenous nerve
From lateral thigh across patella to upper inner quadrant of calf and down to medial edge of foot
Quadriceps and tibialis anterior paresis
Weakness of quadriceps reflex
Differential diagnosis versus femoral nerve palsy: involvement of tibialis anterior muscle
From lateral condyle above knee across the upper outer quadrant of the calf to the big toe
Paresis and atrophy of extensor hallucis longus muscle, often also of extensor digitorum brevis muscle; paresis of tibialis posterior muscle and of hip abduction
Absent tibialis posterior reflex (of diagnostic value only when clearly elicitable on opposite, unaffected side)
Differential diagnosis versus peroneal nerve palsy: in the latter, tibialis posterior muscle and hip abduction are preserved
From posterior thigh over posterior upper quadrant of calf and lateral malleolus to little toe
Paresis of the peronei muscles, often also of the gastrocnemius and soleus muscles
Absent gastrocnemius reflex (ankle-jerk or Achilles reflex)
Combined L4, L5
Combination of L4 and L5 dermatomes
Paresis of all foot and toe extensors and of quadriceps muscle
Diminished quadriceps reflex, absent tibialis posterior reflex
Differential diagnosis versus peroneal nerve palsy: peronei muscles spared. Note reflex findings
Combined L5, S1
Combination of L5 and S1 dermatomes
Paresis of toe extensors, peronei muscles, sometimes also gastrocnemius and soleus muscles
Absent tibialis posterior and gastrocnemius reflexes
Differential diagnosis versus peroneal nerve palsy: tibialis anterior muscle spared. Note reflex findings
Causes of radicular syndromes In most patients, the cause is compression of the nerve root from outside by a space-occupying lesion, most often a herniated intervertebral disk (“slipped disk”), but sometimes a tumor, abscess, or other type of mass. In the cervical segments, spondylotic narrowing of the intervertebral foramina is a further common cause of radicular pain and brachialgia ( ▶ Fig. 13.2). Infectious and inflammatory processes can also cause monoradicular deficits, for example, herpes zoster and borreliosis (Lyme disease; see section ▶ 6.7.5 and ▶ Fig. 13.50). Diabetes mellitus, too, can cause monoradiculopathy with pain and weakness. Finally, individual nerve roots can be affected by traumatic lesions, for example, root avulsion (see ▶ Fig. 13.23) or root compression due to a fracture.
Fig. 13.2 Stenosis of the left C3/C4 intervertebral foramen (arrow); 3D CT reconstruction.
Radiculopathy is often due to a mechanical injury or irritation of a nerve root by degenerative disease of the spine, particularly intervertebral disk herniation. A radicular deficit, however, should never simply be assumed to be due to disk herniation. Other causes must always be considered.
General Clinical Features and Differential Diagnosis of Radicular Lesions
See also Section ▶ 7.1.2.
Regardless of the etiology, a disease process affecting any particular nerve root evokes a characteristic pattern of symptoms and neurologic findings:
Pain in the distribution of the affected nerve root.
A sensory deficit and irritative sensory phenomena (paresthesia, dysesthesia) in the dermatome of the affected nerve root.
Paresis of the muscle(s) supplied by the affected nerve root, generally less marked than the paresis caused by a peripheral nerve lesion (no plegia!), but possibly severe in the root-indicating muscles.
Muscle atrophy is common, but usually less severe than in peripheral nerve lesions. Chronic radicular lesions can, rarely, cause fasciculations.
Impaired reflexes in the segment corresponding to the affected nerve root.
The characteristic syndromes of the individual nerve roots supplying the upper and lower limbs are summarized in ▶ Table 13.1. The table also provides information on the differential diagnosis of radicular and peripheral nerve lesions in certain common situations.
Radicular syndromes are to be differentiated from lesions in more distal components of the peripheral nervous system (plexuses, peripheral nerves), as well as from lesions of the anterior horn of the spinal cord. This can usually be done by careful clinical examination alone, but electromyography may be required for unambiguous confirmation.
The lack of an autonomic deficit may be a useful clinical criterion in the differential diagnosis of radicular lesions that affect the limbs, because sympathetic fibers travel in the spinal nerve roots only at levels T2 through L2 (see earlier); therefore, an autonomic deficit in a limb always indicates a lesion distal to the nerve root.
When there is a purely motor deficit, unaccompanied by a sensory deficit or pain, a lesion of the spinal motor neurons (e.g., spinal muscular atrophy or amyotrophic lateral sclerosis [ALS]) should be suspected, rather than a radicular lesion.
If the patient complains only of pain radiating into the periphery, in the absence of any demonstrable sensory deficit or weakness, the clinician should think of pseudoradicular pain (see section ▶ 14.7) due to mechanical overuse or another abnormality of the musculoskeletal apparatus.
13.1.2 Radicular Syndromes due to Intervertebral Disk Herniation
The proximity of the spinal nerve root to the intervertebral disk at the level of the intervertebral foramen carries with it the danger of root compression by disk herniation. The nerve root can be compressed either by a merely bulging disk or by a disk herniation in the strict sense, that is, a prolapse of nucleus pulposus material (which is usually soft) through a hole in the annulus fibrosus.
Definitions In a disk protrusion (“bulging disk”), the annulus fibrosus is intact, but bulges outward. This situation is sometimes (misleadingly) called “incomplete disk herniation.” Disk herniation (alternatively, disk prolapse or “complete” disk herniation) is defined as the emergence of disk tissue through a hole in the annulus fibrosus. In a subligamentous disk herniation, the herniated disk tissue is still contained beneath the posterior longitudinal ligament; in a transligamentous herniation, the ligament, too, has been perforated and there is disk tissue in the spinal canal.
General clinical features The typical manifestations of acute radiculopathy due to intervertebral disk herniation are the following:
Local pain in the corresponding area of the spine, with painful restriction of movement and a compensatory, abnormal posture of the spine (scoliosis, flattening of lordosis).
Usually, after a few hours or days, radiation of pain into the cutaneous distribution (dermatome) of the affected nerve root.
Pain on stretching of the nerve root (e.g., in the lower limb, a positive Lasègue sign).
Exacerbation of pain by coughing, abdominal pressing (Valsalva maneuvers), and sneezing.
Objectifiable neurologic deficits (hyporeflexia or areflexia, paresis, sensory deficit, atrophy in the late stage) depending on the severity of the root lesion.
Cervical Disk Herniation
Cervical disk herniation is a common cause of acute torticollis and of (cervico)brachialgia.
Etiology Cervical disk herniation may occur as the result of cervical trauma, a twisting injury of the cervical spine, an excessively rapid movement, or mechanical overload.
Clinical features The most commonly affected segments are C6, C7, and C8. Subjectively, patients usually complain of pain in the neck and upper limb, and sometimes of a sensory deficit, which does not necessarily cover the entire zone of innervation of the affected root.
Diagnostic evaluation The clinical history and physical examination should enable identification of the affected nerve root. The objectively observable neurologic deficits are listed in ▶ Table 13.1 and shown schematically (independently of etiology) in ▶ Fig. 13.3.
Fig. 13.3 Cervical radicular syndromes. Synopsis of pain radiation, somatomotor deficits, and reflex deficits in the common cervical nerve root compression syndromes. (Adapted from Stöhr M, Riffel B. Nerven- und Nervenwurzelläsionen. Weinheim: Edition Medizin VHC; 1988.)
The Spurling test can provide additional evidence of cervical nerve root irritation: the head is leaned backward and the face is turned to the side of the lesion. Carefully titrated axial compression by the examiner’s hand may induce pain radiating in a radicular distribution ( ▶ Fig. 13.4).
Fig. 13.4 Spurling cervical compression test for the provocation of radicular pain in cervical disk herniation. Pain can often be elicited by reclination and rotation of the head toward the affected side even without axial compression. (Adapted from Mumenthaler M. Der Schulter-Arm-Schmerz. 2nd ed. Bern: Huber; 1982.)
Imaging studies (CT and/or MRI) are indispensable for the demonstration of nerve root compression by a herniated intervertebral disk. These are sometimes supplemented by neurography (i.e., measurement of nerve conduction velocities) and electromyography.
One should not forget, however, that a mere disk protrusion without any detectable nerve root compression is a common incidental radiologic finding and is of no pathologic significance without clearly correlated symptoms.
Treatment Temporary rest and physical therapy, with the addition of appropriate exercises as soon as the patient can tolerate them, usually suffice as treatment. Sufficient analgesic medication must also be provided, to prevent the chronification of the pain syndrome through the maintenance of an abnormal, antalgic posture (persistent fixation of the affected spinal segments by muscle spasm) and through nonphysiologic stress on other muscle groups.
Surgical treatment may be needed because of intractable pain, persistent, severe, or progressive paresis, or signs of spinal cord compression. The operation generally involves fenestration of the intervertebral space at the appropriate level to expose the affected nerve root and disk, widening of the bony intervertebral foramen (foraminotomy), then discectomy, and, under some circumstances, spondylodesis (fusion) if there is thought to be a risk of spinal instability afterward. Fusion should be performed in such a way as to distract the vertebrae above and below and thereby maintain the patency of the intervertebral foramen. Disk prostheses (artificial intervertebral disks) have also become available in recent years.
Lumbar Disk Herniation
Lumbar disk herniation is one of the more common causes of acute low back pain and sciatica.
The anatomic relationship of the lumbar roots to the intervertebral disks (both normal and herniated) is shown schematically in ▶ Fig. 13.5.
Fig. 13.5 Anatomic relationships of the lumbar intervertebral disks to the exiting nerve roots.
Pathogenesis and clinical features A first episode of lumbar disk herniation (and often the first or second recurrence as well) may present with no more than acute low back pain (lumbago), a sudden “charley horse.” The event may be precipitated by a relatively banal movement in the wrong direction; in particular, the lumbar spine may suddenly freeze in a twisted position if the individual incautiously tries to lift a heavy load with the upper body turned to one side. Any further movement of the lumbar spine is blocked by muscle spasm, a reflex response to the pain. Even the smallest movement is painful, as are coughing and abdominal pressing (Valsalva maneuvers). The pain usually resolves after a few days of bed rest. It is usually only when the herniation recurs later that the patient experiences pain radiating into the leg, that is, sciatica, possibly in combination with typical radicular neurologic deficits.
In our experience, motor deficits generally arise only later in the course of this syndrome. The patient must be examined carefully to determine whether a deficit is present. The L5 root is most commonly affected, usually by an L4–L5 disk herniation, and the S1 root is the next most commonly affected after that, usually by an L5–S1 disk herniation. The corresponding clinical findings are listed in ▶ Table 13.1 and are depicted schematically, independently of etiology, in ▶ Fig. 13.6.
Fig. 13.6 Lumbar radicular syndromes. Synopsis of pain radiation, somatomotor deficits, and reflex deficits in the common lumbar and sacral nerve root compression syndromes. (Adapted from Stöhr M. Riffel B. Nerven- und Nervenwurzelläsionen. Weinheim: Edition Medizin VHC; 1988.)
For the following special clinical entities that can be caused by lumbar disk herniation, see also section ▶ 7.1.2:
Epiconus syndrome (damage to the segment of the spinal cord just above the conus medullaris, at spinal levels T11 and T12).
Conus medullaris syndrome (damage to the conus medullaris at level L1).
Cauda equina syndrome (compression of the nerve roots in the lumbar spinal canal below the L1 level).
Diagnostic evaluation Often, the posture of the standing patient already displays the typical appearance of a lumbar disk herniation ( ▶ Fig. 13.7). As in cervical disk herniation, the level of the affected nerve root can generally be determined from the pattern of referred pain and any motor, sensory, and reflex deficits that may be present. The peripheral nerve trunk containing the axons derived from the affected root is often sensitive to pressure (at the Valleix’s pressure points), and stretching of the nerve is often painful. The latter can be tested by passive raising of the supine patient’s extended leg (the Lasègue test). Pain caused by elevation of the leg on the side opposite the sciatica (the crossed Lasègue sign) usually indicates a large, sequestrated disk herniation. If a higher lumbar root (L3 or L4) is affected, one should look for the reverse Lasègue sign, that is, test for pain on extension of the leg in the prone patient, which stretches the femoral nerve rather than the sciatic nerve. If the herniation is lateral or extraforaminal, pain may also be inducible by lateral bending of the trunk.
Fig. 13.7 A patient with lumbar disk herniation. The normal lumbar lordosis is no longer present, and scoliosis is seen.
Imaging studies (CT, ▶ Fig. 13.8 and ▶ Fig. 13.9; MRI, ▶ Fig. 13.10) are not absolutely essential if the clinical picture is sufficiently characteristic, but they should be performed if there is any doubt as to the etiology of radiculopathy or if surgery is needed. In evaluating diagnostic images, one should pay attention not only to potentially herniated disks, but also to the foraminal and extraforaminal structures ( ▶ Fig. 13.8).
Fig. 13.8 Lateral L3/L4 disk herniation (arrowheads), CT image. The normal spinal ganglion on the right side is visible in the intervertebral foramen (arrow).
Fig. 13.9 Left S1 radicular compression in a 40-year-old man. a Myelography reveals a broadened and shortened left S1 nerve root (arrowhead) and an indentation of the dural sack from the right at this level. b CT reveals high-grade spondylarthrosis and bilateral stenosis of the lateral recesses.
Fig. 13.10 Disk herniation as seen on an MRI scan. Left L4–L5 disk herniation with a caudally displaced free fragment. Clinical examination revealed left L5 and S1 radiculopathy. a Sagittal T2-weighted image. b Axial T2-weighted image. The free fragment lies behind the L5 vertebral body in the left lateral recess and displaces the dural sac the right.
Diagnostic images should always be interpreted critically and in the light of the clinical findings.
Neurography, electromyography, myelography, and postmyelographic CT can sometimes yield additional useful information if the situation is unclear.
Treatment The initial treatment is almost always conservative and follows the same lines as described earlier for cervical disk herniation: bed rest with adequate analgesia usually suffices. The latter is important to prevent nonphysiologic stress on musculoskeletal structures because of an abnormal, antalgic posture.
Surgery should be considered only if conservative treatment fails. An incipient cauda equina syndrome (bladder and bowel dysfunction, saddle hypesthesia, bilateral pareses, and impairment of the anal reflex, cf. section ▶ 7.1.2) is an absolute indication for urgent surgery.
Cauda equina syndrome is an indication for an emergency neurosurgical procedure.
At surgery, the intervertebral space at the appropriate level is opened to expose the affected nerve root and disk (fenestration), the bony intervertebral foramen is widened (foraminotomy), and the herniated disk tissue is removed (discectomy). In rare cases, fusion (spondylodesis) is performed as well if there is thought to be a risk of postoperative spinal instability. General rules regarding surgery for intervertebral disk herniation are summarized in the flowchart of ▶ Fig. 13.11.
Fig. 13.11 Diagnostic and therapeutic flowchart for lumbar disk herniation.
Decompressive surgery is urgently indicated if the radicular pain suddenly disappears while the weakness stays the same or worsens. This is considered to be a sign of the impending death of the nerve root.
13.1.3 Radicular Syndromes due to Spinal Stenosis
Slowly progressive mechanical compression of the intraspinal neural structures usually affects elderly patients in whom congenital narrowness of spinal canal has been accentuated by further, progressive, degenerative osteochondrotic and reactive-spondylogenic changes. Lumbar spinal stenosis causes (possibly bilateral) radicular pain and neurologic deficits that arise while the patient is walking (spinal claudication, also called intermittent claudication of the cauda equina). Cervical spinal stenosis causes paresthesiae of the hands and signs of cervical spinal cord compression.
Cervical Spinal Stenosis
A narrow cervical spinal canal can compress not only the cervical nerve roots, but also the spinal cord itself, producing a myelopathy. Cervical spondylogenic myelopathy is discussed in detail in section ▶ 7.3.2.
Lumbar Spinal Stenosis
For anatomic reasons, a narrow lumbar spinal canal causes an entirely different clinical syndrome than cervical spinal stenosis:
Clinical features In addition to low back pain, which is usually chronic, intermittent claudication is the most characteristic symptom: as the patient walks, sciatica-like pain arises on the posterior aspect of one or, usually, both lower limbs and then becomes progressively severe. The pain appears earlier if the patient is walking downhill, because of the additional lumbar lordosis that downhill walking induces. This historical feature differentiates neurogenic from vasogenic intermittent claudication, in which the pain tends to be more severe when the patient walks uphill. A further differentiating feature of neurogenic, as opposed to vasogenic, intermittent claudication is that standing still generally does not, by itself, make the pain go away. The patient must additionally bend forward, sit down, or crouch—these maneuvers induce kyphosis of the lumbar spine and thereby decompress its neural contents.
Diagnostic evaluation Nowadays, the definitive diagnostic study is MRI, though radiculography and myelographic CT are still sometimes needed ( ▶ Fig. 13.12).
Fig. 13.12 Lumbar spinal stenosis. The myelogram (a) and postmyelographic CT (b) reveal spinal canal stenosis at the level of the L3–L4 disk. In the myelogram, no contrast medium is seen at this level. In the postmyelographic CT, there is no contrast medium in the dural sac and only a little in the nerve root sleeves. The dural sac is compressed by degenerative changes in the intervertebral disk (note the gas inclusions) and of the facet joints (note the hypertrophic osteophytes).
Treatment Surgery is indicated if the symptoms are very severe and the neurologic deficits are progressive. Decompression of the affected segments is performed by opening the narrowed lateral recesses, possibly in combination with a stabilizing spondylodesis (fusion).
13.1.4 Radicular Syndromes due to Space-Occupying Lesions
Tumors and other space-occupying lesions can mechanically compress nerve roots and thereby cause radicular deficits and, often, pain.
Tumors: neurinoma in the lumbar ( ▶ Fig. 13.13) or cervical region ( ▶ Fig. 13.14) and meningioma are the most common types of primary intraspinal tumor, while ependymoma ( ▶ Fig. 13.15), glioma (usually astrocytoma), and vascular tumors are rarer.
Radiculopathy can also be caused by a primary destructive process affecting a spinal vertebra ( ▶ Fig. 13.16), particularly metastatic carcinoma.
Finally, infectious and inflammatory processes of the vertebrae and intervertebral disks (e.g., spondylodiscitis), as well as spinal abscesses and empyema, can cause radicular or spinal cord compression.
Fig. 13.13 Neurinoma of the left L2 nerve root (MRI). The neurinoma completely fills the L2–L3 intervertebral foramen. a Normal, nonthickened roots can be seen in the foramina immediately above and below. b The transverse image reveals the hourglass-shaped neurinoma on the left side, with both intraspinal and extraspinal extension.
Fig. 13.14 Neurinoma filling of the right C8 nerve root in a 26-year-old woman with progressive sensory loss in the C8 dermatome, of one year’s duration. a T1-weighted spin-echo image: the neurinoma is seen as a thickening of the right C8 nerve root. b Neurinomas take up contrast medium. The lesion appears bright in this contrast-enhanced image.
Fig. 13.15 Sausage-shaped cystic ependymoma filling the spinal canal from L1 to L3 and compressing the cauda equina (MR image).
Fig. 13.16 Metastatic melanoma in the lumbosacral spinal canal, 8 years after resection of the primary tumor. The patient presented with cauda equina syndrome. a Sagittal MR image. b Axial MR image. The nerve roots of the cauda equina are displaced dorsally and to the left by the compressive lesion.
Clinical features The patient usually complains of pain radiating into the periphery; if the lesion is at a thoracic level, the pain tends to be in a band-like distribution around the chest. Motor or sensory deficits may also be clinically detectable, depending on the level of the lesion. A space-occupying lesion within the lower lumbar canal can produce cauda equina syndrome of greater or lesser severity (see section ▶ 7.1.2).
Diagnostic evaluation Imaging studies are essential; MRI is the study of first choice, though CT can also be informative for bony processes. Plain X-rays are not sensitive enough to be useful in most cases. They can, at most, yield clues to pathologic findings that require further investigation (e.g., a widened intervertebral foramen due to a neurofibroma, or a pedicle that has been destroyed by a metastasis).
Treatment Surgery (resection of the compressive lesion) is usually needed. Further treatment may also be needed depending on the underlying illness (radiotherapy and/or chemotherapy for neoplastic lesions, antibiotics after the removal of an abscess or empyema).
13.2 Peripheral Nerve Lesions
The typical clinical features of a peripheral nerve lesion are high-grade flaccid paresis, a marked sensory deficit, and diminished sweating in the dermatome of the damaged nerve or nerve segment. Pain may be present, as in radicular lesions. Peripheral nerve lesions are usually due to trauma or nerve compression.
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 so, that is, 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 differs from that of the spinal nerve roots because of the reassortment of the nerve root fibers in the plexuses. This fact enables the clinician to distinguish a peripheral nerve lesion from a radicular lesion on the basis of the observed pattern of neurologic deficits.
A peripheral nerve is a cable-like bundle of nerve fibers. 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 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 interconnections with one another; they are held together as a single peripheral nerve by an encompassing layer of epineurium. This is not a tough husk around the nerve, but rather a loose, lipid-rich layer of connective tissue, reinforced by transversely and longitudinally oriented collagen fibers. It contains not only the nerve fascicles, but also the vasa nervorum. The nerve trunks are fixed to the adjacent connective tissue at only a few points, at which they are especially vulnerable to mechanical damage. Larger nerve trunks are often found together with arteries and veins in so-called neurovascular bundles surrounded by a common connective tissue sheath. These bundles form an anatomic unit that is clearly demarcated from the surrounding structures.
Causes of Peripheral Nerve Lesions
Most lesions of the nerve plexuses or the peripheral nerve trunks are either traumatic (caused by excessive traction, stab wounds, cuts, bony fractures, etc.) or due to prolonged compression, that is,
Compression from outside the body.
Compression at anatomic bottlenecks.
Space-occupying lesions within the body in the vicinity of the nerve (especially tumors and hematomas).
Less commonly, plexus and nerve lesions can be caused by infection and/or inflammation, for example, neuralgic shoulder amyotrophy, which is probably an autoimmune disorder affecting the brachial plexus (see later in section ▶ 13.2.2).