Physical Address
304 North Cardinal St.
Dorchester Center, MA 02124
Cervical disk disease is a common disorder, accounting for 1% to 2% of all hospital admissions in the United States. Unlike lumbar disk disease, which is approximately six times more common, cervical disk disease is rarely caused by trauma. In fact, severe degenerative cervical disk disease often develops in indolent patients.
Etiology. Cervical disk disease is likely multifactorial, with contributing factors ranging from advancing age to neck trauma to heavy lifting to smoking. The nucleus pulposus in the middle of the disk dehydrates with age, placing more stress on the circumferential annulus fibrosus. Tears in the annulus may permit a sudden herniation of the nucleus—a ruptured disk. Alternatively, chronic annular bulging or nuclear herniation may incite a bony reparative process (spondylosis), leading to the formation of extensive bony spurs (osteophytes). These spurs are generally located along the anterior portion of the disk interspace or posteriorly, within the intervertebral foramen.
Osteophytes or ruptured disks produce neurologic symptoms when they compress the spinal cord or adjacent spinal nerve roots. The cervical nerve roots are most susceptible to injury at the point where they enter the intervertebral foramen (neuroforamen), a space delineated by the uncovertebral joint (anteromedially), the facet joint (posterolaterally), intervertebral disks and the vertebral end plates (medially), and by the pedicles of the vertebral bodies (above and below).
Symptoms. The first manifestation of cervical disk disease is often cervical radiculopathy, with symptoms and signs referable to compression of a cervical nerve root. The cervical nerve roots exit above the vertebral body of the same number, with the exception of the C8 root, which emerges at the C7-T1 interspace. Thus a lesion of the C5-6 disk produces C6 radiculopathy. Spondylosis is implicated in cervical nerve root compression about three times more often than acute disk rupture and most frequently involves the C6 or C7 nerve root. The C5 and C8 nerve roots are involved less often and the T1 root only rarely.
Cervical and unilateral arm pain is the most common symptom of cervical disk disease, and patients often complain of numbness or weakness in the involved arm. Occasionally, pain also involves the shoulder, occiput, or anterior chest. Cervical tenderness is present, and range of motion in the neck is decreased. Hyperextension and rotation of the neck toward the painful side (Spurling's maneuver) decrease the diameter of the neural foramen and may exacerbate radicular symptoms.
Clinical Diagnosis. Neurologic examination, with careful attention to motor, reflex, and sensory findings in the upper extremities, often reveals a diagnostic constellation of signs. C5 radiculopathy usually causes weakness of shoulder external rotation (infraspinatus muscle) and shoulder abduction (supraspinatus and deltoid muscles), with decreased biceps and brachioradialis reflexes and hypalgesia over the lateral shoulder. C6 radiculopathy is characterized by diminished sensation over the thumb and index finger; however, the pattern of weakness and abnormal reflexes may be difficult to distinguish from C5 radiculopathy due to overlap between the C5 and C6 myotomes. Of note, forearm pronation (pronator teres muscle) is more likely to be involved with injury to the C6 root. In C7 radiculopathy, weakness is noted in the triceps brachii and extensor muscles of the wrist. The triceps reflex is usually decreased or absent, and sensation over the index and middle fingers is often decreased. C8 radiculopathy causes intrinsic hand muscle weakness affecting the finger abductors, adductors, and flexors. The triceps reflex may also be decreased, and sensation may be diminished over the ring and little fingers. The rare T1 radiculopathy may be associated with weakness of the intrinsic hand muscles, particularly abduction of the thumb (abductor pollicis brevis muscle), and Horner syndrome (ptosis, miosis, and anhidrosis), which results from disruption of the sympathetic outflow to the face and eye via the root of C8 or T1, or both.
Treatment. The majority of patients who have symptoms and signs of cervical radiculopathy respond to conservative treatment , including activity modification, use of a soft cervical collar to immobilize the neck for a brief period, mild analgesics, anti-inflammatory medications, and muscle relaxants as required. In some cases, cervical traction and epidural steroid injections may also be considered. If symptoms persist beyond 2 to 4 weeks, further testing, including cervical magnetic resonance imaging (MRI) and electromyography (EMG) may be indicated. If the findings suggest significant nerve root compression in the setting of progressive neurologic deficits or intractable pain, surgical therapy may be considered. Cervical root decompression may be accomplished by an anterior or posterior approach through the neck. However, epidemiologic data suggest that up to 90% of patients improve with conservative treatment alone.
Herniation of an intervertebral disk, alone or in combination with spondylosis, is the most common cause of surgically remediable lumbar and cervical radiculopathy. In patients with signs and symptoms of radiculopathy, the clinician can often localize the problem to within one or two spinal segments. However, when conservative management has failed or when excruciating, unrelenting pain or severe weakness with or without loss of sphincter control forces consideration of surgery, precise anatomic localization of the disk herniation is necessary. Magnetic resonance imaging (MRI) is the most reliable diagnostic procedure in most cases.
MRI effectively demonstrates the bony architecture of the spine, the contours of the intervertebral disk, the paraspinal soft tissues, and the contents of the spinal canal. Various MRI sequences can be used to confirm disk herniation and visualize degenerative or traumatic changes, such as annular tears and end-plate edema. Changes that would suggest the presence of a radiculopathy include foraminal narrowing as well as a decreased amount of adipose tissue surrounding neuroforaminal nerve roots and dorsal root ganglia.
Computed tomography (CT) myelography, a fluoroscopic procedure in which a water-soluble contrast medium is injected into the spinal canal, followed by CT imaging of the spine, may also help with localization in that it can further delineate the extradural, bony and paraspinal tissues, especially in patients who have undergone previous spine surgery, resulting in technical artifacts that can obscure the MRI.
The cervical region has little, if any, epidural fat, and frequently only a small fragment of disk is enough to cause severe nerve root compression. Because of the lack of epidural fat and the small size of disk herniations, CT is less effective than myelography for diagnosing cervical radiculopathy. In disk herniation, myelography commonly demonstrates displacement of the dural sac, impaired filling or displacement of an axillary sleeve, or nerve root swelling.
When either MRI or CT myelography fails to suggest a clear-cut diagnosis, the other procedure should be considered. CT myelography may be more effective in patients with a prior history of spine surgery and metal hardware placement or when MRI is contraindicated, as when the patient has an internal cardiac pacemaker.
In the cervical region, CT and myelography are complementary. The combination of both studies clearly shows the nature and degree of spinal cord distortion, which is valuable in determining the proper treatment. The diagnosis of cervical spinal nerve root avulsion from traction injury of the arm is best visualized with a combination of CT and myelography; imaging identifies the diagnostic leakage of cerebrospinal fluid (CSF) into the neuroforaminal and extraspinal space.
Clinical localization of cauda equina compression may be difficult. In this case, MRI of the lumbosacral spine (LS) is helpful in localizing the compressive lesion. In the majority of patients with cauda equina compression related to disk disease, the MRI will demonstrate extensive disk material occupying over one third of the intraspinal canal space. CT myelogram may also demonstrate a myelographic block, the degree of which can help quantitate the severity of neural compression and be monitored in several different patient positions.
However, MRI is the test of choice because it is more rapidly performed with minimal risk of complications; characterization of the LS spine with MRI in conjunction with the clinical picture may be sufficient for planning surgery.
Lumbar disk disease causing low back and nerve root pain is a common problem that relates to the five lumbar vertebrae and the sacrum. The adjacent vertebrae are joined by strong ligaments at the articular facets and the vertebral bodies. Cartilage lines the articular surfaces of the vertebral bodies. The disk fills the space between the cartilaginous end plates and is normally a tough fibrocartilaginous structure. The dural sac contains the nerve roots of the cauda equina and extends through the spinal canal. As they exit the spinal canal at each segment, the nerve roots course caudad to the facet before passing through the intervertebral foramen. With aging, the disk degenerates, fragments, and loses its adherent properties. Thus appropriate mechanical forces can cause the fragment to move, usually posterolateral at the point of least ligamentous resistance, where the nerve root exits the spine. Pressure on the nerve root may produce pain and neurologic deficit.
As a result of abnormal movement at the facet joint, a hypertrophic, osteoarthritic process known as spondylosis develops. Enlargement of the facet joints by this spondylotic process narrows the intervertebral foramen, which may cause mechanical pressure on the exiting nerve root. In some persons, the anteroposterior diameter of the spinal canal is narrow, with deep lateral recesses. Thus the spondylotic process produces spinal stenosis, which causes pressure on the dural sac and cauda equina.
Lumbar spine disease may be manifested by pain in the low back, a monoradicular syndrome, a cauda equina syndrome, or spinal stenosis. As an isolated symptom, low back pain is usually self-limited and responds to conservative measures.
Initially, only a detailed history and physical examination may be necessary (see Plate 4-3 ). However, increasing pain with or without neurologic symptoms in a person who has systemic symptoms raises the question of a destructive lesion and merits further investigation, especially if the response to treatment has been limited. Back pain that is not helped by lying down is non-specific but occurs with cancer or infections.
The monoradicular syndromes are the classic syndromes of a ruptured disk. Most disk ruptures occur at L5-S1 and L4-5. The herniated disk at L5-S1 usually compresses the S1 root as it passes the interspace on its way beneath the S1 facet. In the same manner, the L4-5 disk compresses the L5 root, and the L3-4 disk compresses the L4 root. Rarely, the disk extrudes laterally into the intervertebral foramen, and then the L5-S1 disk produces an L5 root syndrome; the L4-5 disk, an L4 root syndrome; and the L3-4 disk, an L3 root syndrome. Failure to diagnose these problems accurately results in inadequate treatment.
The S1 root syndrome includes sciatic pain (“sciatica”) from the buttock to the posterior thigh, to the posterior or lateral calf, and into the foot. When due to disk herniation, it often increases with coughing or sneezing. Numbness and paresthesias commonly occur on the lateral aspect of the foot, the sole, and the heel. Weakness, if present, is in plantar flexion of the ankle and foot. The ankle jerk is absent.
The sciatic pain of the L5 root syndrome is indistinguishable from that of the S1 root syndrome. Dorsiflexion of the foot and eversion and inversion of the ankle may be weak. The ankle and knee jerk are normal, but the internal hamstring reflex may be diminished or absent. Sensory change develops in the dorsal and medial aspects of the foot and great toe. In the less common L4 root syndrome , pain radiates to the lateral and anterior thigh. The quadriceps muscle is weak and atrophied, and the knee jerk is lost. Sensory change occurs in the anterior thigh and pretibial regions. The clinical manifestations of herniation at L4-5 and L5-S1 are summarized in Plate 4-4 .
Compression of the cauda equina by a midline disk herniation or tumor may lead to bladder or bowel dysfunction, often with bilateral sciatica, saddle anesthesia, and leg weakness. This is a surgical emergency because deficits may become irreversible if treatment is delayed,
In lumbar spinal stenosis , congenital or acquired narrowing of the spinal canal or intervertebral foramina is caused by disk bulging or protrusion, bony hypertrophic changes, or thickening of the ligamentum flavum. In addition to back pain that is relieved by sitting or bending forward, symptoms include pain or other sensory disturbances occurring in one or both legs with exercise, occasionally in a radicular distribution, and resolving with rest. Such “neurogenic claudication” is distinguished from vascular claudication by the lack of any circulatory abnormality in the legs; the arterial pulses are normal.
Most of the monoradicular syndromes, even those with mild neurologic deficit, respond to conservative care for several weeks; this involves a short period of bed rest (generally not more than 2 or 3 days), followed by mobilization and an exercise program. For patients with a definite diagnosis of radiculopathy secondary to a herniated disk who do not improve, options are limited. Some choose more prolonged rest, whereas some with mild symptoms may choose to return to activities of daily living despite the pain.
In patients in whom further treatment is necessary because of pain or neurologic deficit, surgery must be considered and must be preceded by imaging of the lumbosacral spine to rule out a destructive lesion or an anomaly such as spondylolisthesis. The important tests are spinal magnetic resonance imaging (MRI) or, less often, computed tomography (CT) myelography.
If no destructive lesion is present and test results show that the pain and neurologic deficit are caused by the herniated disk, surgery is indicated. The surgeon must keep in mind that the important structure is the nerve root. Adequate exposure is essential to expose the root cephalad and caudad to the extruded fragment and to the lateral margin of the spinal canal. This allows maximal exposure of the disk and nerve root, which can be minimally manipulated. The extruded disk is removed and foraminotomy is done. The root is then retracted medially, the annulus is exposed, and the disk is removed from the interspace to reduce the chance of recurrence. The patient is discharged 1 to 3 days postoperatively and can return to a sedentary job in 2 weeks. Diskectomy, with use of the operating microscope, is also a satisfactory procedure if done at the correct level to adequately expose the root.
The midline disk herniation is a much more serious problem. The entire cauda equina can be compressed at the level of the rupture. Because of the danger of irreversible neurologic damage, bilateral sciatica demands more urgent evaluation than unilateral sciatica. Any suggestion of sphincter disturbance should lead to urgent spinal MRI or CT myelography, and, if necessary, to decompressive laminectomy with disk removal.
Conservative treatment for lumbar spinal stenosis includes weight loss, physical therapy (to improve posture, strengthen abdominal muscles, and increase lumbar flexion) and nonsteroidal anti-inflammatory agents. Surgery may be required to relieve symptoms or prevent further deterioration and usually involves single or multilevel decompressive laminectomy, sometimes with lumbar fusion.
The patient who does not improve after surgery should be reevaluated to rule out a recurrent disk fragment and to establish that surgery was done at the correct level. If no surgical lesion is found, the patient should be encouraged to exercise and to return to work and attempt to live with the symptoms. Analgesic drugs, especially narcotics and tranquilizing medications, should be avoided. Pain clinics have been helpful in rehabilitating some of these patients. Those with persistent lumbar disk signs but no clinical or radiographic findings should not have any type of surgery. Rehabilitation should be attempted.
Become a Clinical Tree membership for Full access and enjoy Unlimited articles
If you are a member. Log in here