Degenerative Disc Disease

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Pathogenesis and Pathophysiology. The vertebral disc is composed of the inner gelatinous nucleus pulposus and the surrounding annulus fibrosus. Vertebral disc herniation refers to rupture of the annulus with displacement of the central nucleus. In youth, the disc is highly elastic. With the passage of time, the direct vascular supply to the vertebrae and discs decreases, and they undergo the accumulated effects of axial loading. The resulting decreases in water and oxygen content, and metabolic efficiency lead to a disc that is more compressible, less elastic, and more prone to tear and rupture. Disc rupture and herniation can cause pain by several mechanisms. The periosteum of the bony spine, the ligaments, the outer fibrous annulus of the vertebral discs, and the dura are all innervated by nociceptive afferents from the spinal nerves. A ruptured or torn fibrous disc may generate local pain owing to mechanical stress on these pain-sensitive structures. Also, the exposed disc material has a direct toxic effect and elicits a local inflammatory response, both of which may promote increased pain sensitivity. In addition to these local effects, the mass of the herniated disc material may compress the spinal roots by protruding into the lateral recess or the neural foramen, or it may protrude into the spinal canal, compressing the spinal cord in the cervical or thoracic region or the cauda equina in the lumbosacral region. Details of the mechanisms by which compression causes neurological dysfunction are complex and probably include mechanical alteration of axonal membranes, impaired axonal flow, and ischemia due to compromise of the microcirculation with resultant edema and eventual demyelination. Finally, regional muscle spasm may accompany other effects, adding to the pain and disability.

The accumulation of degenerative lesions in the lumbosacral spine may compromise the area of the central canal available to the cauda equina enough to cause symptomatic lumbar spinal stenosis with or without discrete disc herniation. Most commonly, these lesions include degenerative discs that bulge posteriorly, a hypertrophied ligamentum flavum that bulges anteriorly, and hypertrophied facet joints that crowd into the bony canal posterolaterally ( ...Fig 29-1 ). Less common lesions may contribute to the problem, hastening significant stenosis: congenitally short pedicles, spondylolisthesis without spondylolysis, or abnormal angulation of the bony spine.

Epidemiology and Risk Factors. Vertebral disc degenerative changes are a universal accompaniment of aging.

Figure 29-1 Lumbosacral spinal stenosis. L4 vertebra in cross section. Posterior bulging of the intervertebral disc, hypertrophy of degenerated facet joints, and hypertrophy of the ligamentum flavum crowd into the central canal to cause lumbar spinal stenosis.

Teenagers rarely develop symptomatic disc herniation. The peak incidence of symptoms occurs between the ages of 30 and 50. Patients often describe the onset of low back pain, usually remittent and without specific features, in their twenties, perhaps after identifiable trauma, and the onset of more specific symptoms that leads to the diagnosis of disc herniation is often not preceded by further trauma. Probably the accumulation of degenerative changes to the annulus and the preservation of the expansile gelatinous nucleus, overlapping with a period of life when job and sports-related activities increase the amount of mechanical stress on the body, account for this peak in the incidence of disease. The incidence then falls off in the older population, probably due to the lack of mobility of the desiccated disc and the relative lack of physical activity. Women and men are affected approximately equally.

There is a tendency toward disc herniation in some families, such as those with congenital spinal anomalies, including fused and malformed vertebrae and lumbar spinal stenosis due to short pedicles. Patients with increased weight and tall stature are at increased risk for this condition. Also, acquired spinal disorders, such as common degenerative arthritis and ankylosing spondylitis, predispose to disc degeneration. Various behaviors that increase risk include sedentary occupations, physical inactivity, motor vehicle use, vibration, and smoking. In younger women, pregnancy and delivery are associated with lumbosacral herniation, and new symptoms of cervical disc herniation may occur in part because of the bending and lifting involved in child rearing.

Clinical Features and Associated Disorders. The most common site of disc herniation in the cervical region is the C6-C7 level, followed by C5-C6, C7-T1, and C4-C5. Patients typically develop some local pain in the neck that radiates to the shoulders or the interscapular region. In the most common lateral herniations, radicular symptoms ensue. These symptoms include pain in the shoulder and arm, which may follow a dermatomal pattern but more typically is deep and aching and only roughly corresponds to the involved dermatome. At the cervical levels, the roots emerge laterally to exit through the neural foramina above the correspondingly numbered vertebral bodies. Because the spinal cord and bony vertebral levels are roughly aligned in the neck, the level of herniation corresponds to the level of root irritation. Hence, C6-C7 herniation affects the C7 root (...Fig, 2.9Z2.). Pain may be exacerbated by coughing or straining. Numbness is more likely to supply reliable localizing information than pain. Compression of the C6 root typically causes numbness in the thumb and index finger, and compression of the C7 root typically involves the index and middle fingers. When compression is severe, myotomal weakness, reflex loss, and, with time, fasciculations and atrophy may ensue. With C6 compression, the biceps, brachioradialis, pronator teres, and radial wrist extensors may be weak, and the brachioradialis and biceps reflexes may be diminished or lost. With C7 weakness, the wrist and finger extensors and the triceps are typically weak. The triceps reflex may also be diminished or lost. With C8 compression, there is often interscapular pain and pain in the medial aspect of the arm and hand with weakness of the hand intrinsic muscles. The finger flexor reflex may be lost. Lesions above C6 are less common and are associated with correspondingly more proximal sensory symptoms and weakness. Lesions of the C5 root may cause shoulder pain and pain and numbness in the lateral aspect of the upper arm. Many muscles can be used to test the C5 root, including the infraspinatus, supraspinatus, deltoid, biceps, and supinator. Lesions above this level may cause neck pain and sensory loss in the neck, supraclavicular area (C3), and acromioclavicular area (C4) of the shoulder. Lesions involving the spinal cord or roots above C4 may paralyze the diaphragm and cause respiratory compromise ( Table. 29-1 ).

In the lumbosacral region, the most common site of

Figure 29-2 Cervical disc herniation. At the cervical levels, roots emerge from the spinal cord near their level of exit. Each root emerges above its corresponding vertebra, with C8 emerging between C7 and T1. Posterolateral herniation at this level causes compression of the exiting roo(horizontalhatching). Hence, C6-7 herniation causes C7 compression, and so on. A large central herniation in this region can compress the spinal cord and cause a cervical myelopathy (vertical hatching).





Muscle Weakness


Location of Pain

Reflex Change



Shoulder abduetion (15-90 degrees)

Lateral shoulder



Elbow flexion

Lateral upper arm


Shoulder abduction (0-15 degrees)

Lateral epicondyle


Humerus external rotation


Brachioradialis (C5-C6)

Elbow flexion in semipronation

Posterior shoulder


Pronator teres (C6-C7)


Lateral forearm

ECR (C6-C7)

Radial wrist extension

Thumb and index finger


Triceps (C6-C8)

Elbow extension

Posterior shoulder


ECR (C6-C7)

Radial wrist extension

Medial forearm

ED (C7-C8)

Finger extension

Index and middle fingers


Flexor pollieis longus

Thumb flexion

Interscapular medial forearm

Finger flexors


Finger flexion

Little finger

Abductor digiti minimi

Finger abduction Little finger abduction

ECR, Extensor carpi radialis; ED, extensor digitorum; FDS, Flexor digitorum superficialis; FDP Flexor digitorum profundus Actual motor innervation is multisegmental. Most of the myotomal overlap is disregarded here to emphasize clinically useful localization.

Medial forearm Medial epicondyle

None herniation is the L5-S1 level, followed by the L4-L5 level and then higher levels. Symptoms of lumbosacral herniation often follow lifting or twisting injuries, or they may result from accumulated low-level trauma. Pain typically occurs in the parasacral area and radiates to the buttocks. Below C8, the roots exit through the neural foramina below the correspondingly numbered vertebral bodies. In patients with the most common posterolateral herniation, dermatomal radicular pain typically occurs at the level below the emerging root, which usually escapes entrapment above the protruding disc. Hence, L4-L5 herniation affects the L5 root ( ...Fig 29-3 ).

With posterolateral L5-S1 herniations and S1 root entrapment, the pain radiates to the posterior aspect of the thigh and, especially when the root is stretched, into the posterolateral lower leg, lateral heel, and sole. This pattern can be demonstrated by straight-leg raising, in which the smaller the angle of elevation required to elicit pain, the greater the suggestion that root compression is responsible. '1 Characteristic pain on elevation of the opposite leg may be even stronger evidence of root compression.^' Some patients with symptoms that are exacerbated by root traction avoid full weight bearing on the heel of the involved side, standing with the knee flexed and the heel off the floor. When pain is less severe, symptoms may be elicited by having the patient walk on the heels. Numbness is felt in the posterolateral leg, lateral aspect of the heel, and the sole of the foot. The gastrocnemius and hamstrings may be weak, and the ankle jerk may be diminished or lost. More lateral herniation of the L5- S1 disc or herniation of the L4-L5 disc may entrap the L5 root. Here the pain may be similar, with adjustment of the findings to fit the L5 dermatome and myotome. Numbness is most marked on the dorsum of the foot. Weak muscles include the foot elevators (tibialis anterior group), everters (peronei), and invertors (tibialis posterior), and the toe extensors (extensor hallucis longus). Herniations at higher levels in the lumbosacral region cause pain and deficits that correspond to the roots involved (..Table.29.-2. ).

In addition to these radicular syndromes, patients with central herniations in the cervical or thoracic region may develop pain and acute myelopathic symptoms with spasticity and quadriparesis or paraparesis, sensory loss at or below the segmental dermatome of the lesion, hyperactive reflexes, and Babinski's signs. Soon after an acute lesion develops, the reflexes may diminish because of spinal

Figure 29-3 Lumbosacral disc herniation. The most common posterolateral herniation compresses the nerve root traveling downward to emerge one level below the level of the exiting root. Hence, L5-S1 herniation most commonly compresses the descending S1 root (horizontalhatching). More lateral herniation may compress the root exiting at the level of hernia1(c/iagonal hatching). A large central herniation may compress multiple bilateral descending roots of the cauda equ(nerticalhatching).



Muscle Weakness


Location of Pain

Reflex Change


Iliopsoas (sometimes, but mainly L2-L3)

Hip flexion (mainly L2-L3)

Inguinal crease



Iliopsoas (L2-L3)

Hip flexion

Anterior and lateral thigh



Adductor group

Hip adduction

Medial thigh and knee



Knee extension



Knee extension

Medial lower leg


Tibialis anterior

Foot dorsiflexion

Medial malleolus



Great toe extension

Anterolateml lower leg

Tibialis posterior


Toe extension

Dorsum of foot

Internal hamstrings

Tibialis anterior

Foot dorsiflexion


Foot eversion

Tibialis posterior

Foot inversion

Gluteus medius

Hip abduction

Internal hamstrings

Knee flexion


Biceps femoris

Knee flexion

Lateral heel


Gastrocnemius soleus

Foot plantar fiexion

Sole of foot


Toe flexion

Gluteus maximus

Hip extension

EHL, Extensor hallucis longus; EHB, extensor hallucis brevis; EDL, extensor digitorum longus; EDB, extensor digitorum brevis; FDB, flexor digitorum brevis Actual motor innervation is multisegmental. Most of the myotomal overlap is disregarded here to emphasize clinically useful localization.

EHL, Extensor hallucis longus; EHB, extensor hallucis brevis; EDL, extensor digitorum longus; EDB, extensor digitorum brevis; FDB, flexor digitorum brevis Actual motor innervation is multisegmental. Most of the myotomal overlap is disregarded here to emphasize clinically useful localization.

shock. Patients with lumbosacral central herniation may develop acute compression of the cauda equina. This causes radicular pain, paresthesias, and sensory loss referable to multiple bilateral roots, bilateral leg weakness, and loss of the lower extremity reflexes. Bowel and bladder dysfunction may occur early. When subtle, this dysfunction may be limited to asymptomatic bladder retention noted only on postvoid catheterization. When dysfunction is more severe, there may be perianal and perineal sensory loss, loss of anal tone and reflexes (the reflex anal sphincter constriction due to perianal skin stimulation or anal wink and the bulbocavernosus reflex), and fecal and urinary retention and incontinence.

Degenerative herniations in the thoracic region are uncommon, and symptoms and findings at these levels should raise a suspicion of other underlying lesions, such as tumor or abscess. Disc herniations at this level may cause radiating dermatomal pain resulting from root compression; more frequently, they progress to spinal cord compression.

The symptom most suggestive of lumbar spinal stenosis is neurogenic claudication. Low back pain radiates to the buttocks and thighs and may extend more distally along the lumbosacral dermatomes. This pain is brought on by walking. Unlike vascular claudication, rest in the upright position does not relieve the pain, but rest while seated or forward bending, such as leaning on a shopping cart, may provide relief. Pain is exacerbated by spinal extension, such as downhill walking. When spinal stenosis is severe, patients bend forward while walking. Symptoms and signs may be either mechanical, due to bone, ligament, and joint involvement, or radicular, due to compromise of the lateral recesses or neural foramina.

Proximal compression resulting from root entrapment may increase the vulnerability of nerves to dysfunction due to distal entrapment. This double crush phenomenon is presumed to be a result of disturbed axoplasmic flow and disrupted architecture of the neurofilaments. Therefore, when surgical repair of a distal entrapment fails to provide the expected relief, a contributing radiculopathy resulting from degenerative disc disease should be considered.

Differential Diagnosis. Disc herniations must be differentiated from other causes of acute and chronic neck, back, and extremity pain, radiculopathy, and myelopathy. Malignant and benign tumors affecting the spine, infection, epidural hematoma, various arthritides, including rheumatoid arthritis, ankylosing spondylitis, and Reiter's syndrome, and other spondyloarthropathies may present with similar early symptoms and signs. Various anomalies, such as conjoined spinal roots and multiple roots emerging through a single foramen, may also be confused with disc disease. Degenerative arthritis of the spine can cause symptoms by many mechanisms, including disc herniation, and the various lesions that are causing symptoms in a particular person should be differentiated as clearly as possible to allow directed therapy.

Evaluation. A careful history and physical examination are critical in the evaluation of disc herniation. It has been well established with all imaging modalities that asymptomatic patients have a high incidence of anatomical lesions. To properly detect clinically relevant illness, it is therefore essential to establish the closest possible clinical correlation of the symptoms and signs with the anatomical findings of the various imaging studies. The initial history should screen for problems that raise a suspicion of severe underlying disease. All patients should be questioned about trauma, cancer, infections, recent fever, and the use of anticoagulant medications. The underlying family history and risk factors for tumor, infection, hematoma, and various disorders that predispose to disc disease should be sought. The physical examination, likewise, is undertaken to seek evidence of other severe underlying disease and to localize and classify the pain and any deficits as mechanical, radicular, or myelopathic. It is most important immediately to establish the presence of major deficits that demand rapid diagnosis and treatment. These include the cauda equina or conus syndrome, acute or progressive myelopathy, and severe radicular motor deficits. If, on the other hand, the findings are consistent with a ruptured disc and either no deficit or a mild to moderate one, it is reasonable to temporize before pursuing a workup to fully evaluate the

cause. If plain radiographs of the affected area reveal no evidence of unexpected lesions, conservative therapy for disc herniation may be tried before further imaging is performed. This approach is justified by the good prognosis for spontaneous recovery of patients with acute radiculopathy with mild to moderate deficits. When the clinical examination leaves doubt about the localization of the lesion, electromyography (EMG) can supplement the diagnosis of radiculopathies and suggest other localizations, such as plexopathies and neuropathies. Electromyography is more sensitive if it is delayed until at least 10 to 14 days after the onset of a new deficit.

The tests available for imaging include plain radiographs, computed tomography (CT), myelography with or without CT, and magnetic resonance imaging (MRI). X-ray studies can be used to screen for unexpected infection, tumor, or deformity of the bony spine. Radiographs cannot show the neural tissues or the disc itself, but loss of disc space height and other degenerative changes may provide some indirect diagnostic information. Interpretation of plain radiographs must be tempered by an awareness of the high frequency of degenerative findings in asymptomatic populations. Plain radiographs taken under conditions of flexion and extension can also be used to assess spinal stability. Myelography is invasive, indirect, and nonspecific; however, it retains certain advantages in the era of MRI. It can visualize the entire length of the spine and best defines the root sleeves. Although myelography alone cannot distinguish between osteophytes and a herniated disc compromising a foramen, when combined with CT, it provides the best visualization of lateral pathology and small osteophytes. It is now most commonly used to answer specific questions that remain after the MRI examination. CT is superior to MRI in distinguishing soft tissue from bone. MRI has emerged as the preferred imaging choice in most cases. It demonstrates bone and soft tissues directly, easily allows multiplanar visualization, and is suited to the visualization of multiple levels. The high contrast of epidural fat and the cerebrospinal fluid (CSF)-filled thecal sac allows accurate assessment of subtle compression in most cases.

Lumbar spinal stenosis is evaluated by CT or MRI. MRI best demonstrates the relationship of the bony and neural structures. CT best demonstrates lateral recess stenosis. Although the dimensions of the bony canal can be used as guidelines, diagnosis must ultimately be based on the correlation of stenosis with the clinical findings. The transverse interfacet dimension should be greater than 16 mm. A dimension of less than 10 mm indicates severe stenosis. An anteroposterior dimension of less than 12 mm suggests stenosis; however, this finding is less sensitive in patients with symptomatic disease. A lateral recess of 3 mm or less suggests stenosis.

Management. The crucial initial step in management of patients with disc herniation syndrome is to identify those lesions that merit further evaluation and immediate therapy. In the remaining cases, the good prognosis for early recovery justifies a trial of conservative therapy before definitive imaging is done. Conservative therapy includes rest in a position of comfort followed by early remobilization, gentle exercises, and analgesics for pain as needed. Nonsteroidal anti-inflammatory agents probably provide little relief in most cases. For severe pain, judicious time- limited use of narcotics should be considered. Oral and epidural corticosteroids can be helpful. Many other modalities are available, but there are few reliable data about their effectiveness in populations: medical and physical measures (e.g., ice, heat, massage, and ultrasound) that address secondary muscle spasm, transcutaneous electrical nerve stimulation (TENS), acupuncture, exercise, and traction. '3! If improvement within the initial 4 to 6 weeks is not satisfactory, it is helpful to confirm the diagnosis by imaging. This may provide a diagnosis of an unsuspected condition, localization for epidural steroid injection, or information about suitability for eventual surgery.

Clear indications for surgery include the presence of acute myelopathy, cauda equina syndrome, severe or progressive motor deficits, and intractable pain. When conservative measures fail to provide a satisfactory response within 6 to 12 weeks, surgery should also be considered. Studies comparing the outcome of surgical therapy with conservative care suggest that early recovery occurs more often with surgery. Although the benefits of surgery are lost with prolonged follow-up periods, it is important to point out that in an often cited study, patients in the conservative therapy group who had not responded to this therapy received surgery. '4 Newer microsurgical techniques allow shorter hospitalization and rehabilitation periods but have not been shown to improve long-term outcome. The success rate of chymopapain chemonucleolysis has not reached that of surgery in most hands, and this treatment carries significant risks. Percutaneous nucleotomy has also been disappointing and should not be pursued given the current level of experience.

For patients with lumbar spinal stenosis, initial therapy is symptomatic, with analgesics, pain-modulating medications, and physical and occupational therapy. When significant disability and pain remain despite conservative measures, referral for surgical decompression should be considered.

Prognosis and Future Perspectives. The prognosis for the relief of pain and a full functional recovery is good. With bed rest alone, Weber found that 70 percent of patients experienced decreased pain and improved function within 4 weeks, and 60 percent had returned to work. '5! Seventy percent were functionally unrestricted at 1 year. With selective surgery, 90 percent of patients should have a good functional recovery within a year. Patients with psychosocial problems tend to do worse with either therapy, but those with appropriate indications respond better to surgery. Sensory dysfunction does not recover as fully as motor function, and a large proportion of patients retain some sensory deficits. Patients in whom relapse occurs should be re-evaluated for new lesions that are potentially addressable by surgery; however, the success rate of surgery declines with follow-up procedures, and a significant proportion of patients with disc herniation experience relapse with chronic low back pain.

Research into the mediators and biomechanics of pain may further elucidate the mechanisms of pain in disc disease and provide other conservative therapies. Improved imaging techniques may further refine the selection of patients for surgery. It is hoped that improved surgical

selection and further refinements in surgical technique may continue to improve outcome and shorten the period of disability. Cervical Spondylosis

Pathogenesis and Pathophysiology. Degenerative changes of the spine universally accompany aging, and the accumulation of such degenerative changes in the cervical spine constitutes cervical spondylosis. These spondylotic changes become clinically important when they cause pain or neurological dysfunction. Aging leads to desiccation and shrinkage of the intervertebral discs. The resultant loss of vertebral height narrows the intervertebral foramina. The weakening of the containing fibrous annulus allows bulging of the desiccated discs, which may then form transverse bars that protrude posteriorly, compromising the spinal canal. Their protrusion more laterally into the foramina may further compromise this space. Osteophytes and hypertrophic osteoarthritic changes of the facet and uncovertebral joints may further impinge on the spinal canal and foramina. Hypertrophy of the ligamentum flavum, which runs longitudinally along the posterior wall of the spinal canal, may compromise this space even more ( ...Fig ^-.^ ). Intuition suggests that compression of the cervical spinal cord and nerve roots by the stenosis of the spinal canal and foramina is responsible for the myelopathy and radiculopathies characteristic of cervical spondylosis. However, a finer understanding of the pathogenesis of this disorder has been elusive. Proposed explanations of the neurological deficit include (1) direct compression by stenosis adequate to compromise the cord and roots, (2) rubbing of the spinal cord and roots on protruding skeletal structures that may not themselves be severely compressive, and (3) arterial or venous compromise. All of these factors may play a role. Pathological study shows the presence of distorted and flattened spinal cords that correspond to spondylitic bars. Demyelination of the lateral columns

Figure 29-4 Cervical spondylosis. C5 vertebra in cross section. Posterior osteophytes of the vertebral endplate and hypertophy of the ligamentum flavum compromise the cervical spinal canal and cause flattening of the spinal cord.

occurs at the stenotic site and caudally and of the posterior columns rostrally. This demyelination corresponds to the sites of rubbing: anteriorly and inferiorly with neck flexion and posteriorly and superiorly with extension. In the central gray matter ischemic changes with neuronal loss are seen. Sometimes syringomyelia can be found. Root sleeves may be thickened and rootlets adherent.

Epidemiology and Risk Factors. The major risk factor for cervical spondylosis is aging. Although trauma may contribute, there is usually no history of significant trauma. Screening of asymptomatic patients shows a high frequency of spondylotic changes that increases with advancing age. By age 59, 70 percent of women and 85 percent of men have changes on radiographs, and by age 70, the number increases to 93 percent of women and 97 percent of men. [aJ Up to 75 percent of these patients have abnormal neurological findings by age 65, but fewer have symptoms of spondylosis. M Heavy labor and especially occupations that expose the patient to vibration probably increase the risk of spondylosis.

Clinical Features and Associated Disorders. The major clinical features are the symptoms and signs referable to cervical myelopathy and radiculopathy. Patients may complain of neck pain and pain radiating into the arms. There may be weakness of the legs and sensory loss, especially of position sense. The weakness or sensory loss may be discovered when an elderly patient presents for gait problems or falls rather than as a direct complaint. Bowel and bladder dysfunction are uncommon complaints accompanying advanced cervical myelopathy. Most commonly, the onset of symptoms is insidious; however, occasionally an elderly patient with spondylosis presents with catastrophic onset of quadriparesis or paraparesis after a fall.

Typically, there is some limitation of neck mobility. Examination of the cranial nerves should be normal, although the jaw jerk may be increased in some cases. Weakness is common in the lower extremities, especially in the iliopsoas, hamstrings, and extensors of the feet and toes. Tone in the lower extremities is spastic, and Babinski's sign may be present. Sensory loss to light touch, vibration, and joint position is sometimes found. The major deficits in lower extremity function are determined by the degree of myelopathy. Findings in the upper extremities vary depending on the level of central canal stenosis and the degree of cervical root involvement. Patients may have mild weakness with brisk reflexes. When roots are compromised, especially in the lower cervical myotomes, atrophy, weakness, and fasciculations may be found, at times mimicking the signs of amyotrophic lateral sclerosis. Sensory loss in the upper extremities may also be seen, following a simple radicular pattern or, more commonly, a patchy distribution, presumably due to multiple root and cord involvement.

The main associated features are those of disorders that compromise the cervical spine and predispose to osteoarthritis. These include prior trauma, prior disc herniation, various congenital anomalies of the cervical spine, and underlying systemic arthritic disorders.

Differential Diagnosis. The issue of differential diagnosis is particularly important when one is dealing with a condition that is commonly present as an asymptomatic radiological finding. When a patient presents with a combination of radicular signs and symptoms accompanied by

cervical myelopathy, the diagnosis of spondylotic disease is not difficult. However, this clinical presentation is not common, and most patients have either myelopathy resulting from central protrusions or radiculopathy resulting from lateral protrusions, but not both. The differential diagnosis must therefore cover conditions that cause pure myelopathy, motor neuron disease, and combined myelopathy and radicular or neuropathic lesions.

The syndrome of slowly progressive spastic weakness of the extremities, worse in the lower than in the upper extremities, may be produced by a variety of pathological causes. Some of these are listed here along with clues that may help to distinguish them from spondylotic myelopathy.

Multiple Sclerosis (see Ch.apte.L48 ). Age of onset, gender, and types of neurological findings do not reliably distinguish chronic spinal multiple sclerosis. Early onset of bladder symptoms, visual complaints, and mental status changes should be sought. Cranial MRI may demonstrate periventricular bright lesions on T2-weighted images in the majority of patients with multiple sclerosis. Visual evoked responses and oligoclonal bands in the CSF, if abnormal, are helpful.

Amyotrophic Lateral Sclerosis (see Chapter^ ). 'n most patients with amyotrophic lateral sclerosis, lower motor neuron signs are evident from the beginning, but spasticity predominates in a few. The finding of atrophy of muscle and increased reflexes in the same myotome strongly suggests amyotrophic lateral sclerosis. Bulbar symptoms or signs should be carefully sought on examination and should be evaluated with EMG. The sensory loss from radicular or long tract involvement, common in cervical spondylosis, should be absent. In one recent series, 5 percent of patients with amyotrophic lateral sclerosis underwent a cervical laminectomy in the hope of arresting progressive spasticity, emphasizing how commonly the two conditions coexist.

Primary Lateral Sclerosis. A few patients with a slowly progressive, purely spastic condition are found to have a degenerative disease allied to amyotrophic lateral sclerosis, but without lower motor neuron features.

Subacute Combined Degeneration of the Spinal Cord (see Chapter JO ). Vitamin B12 deficiency should never be overlooked. A low serum B12 level, hypersegmented polymorphonuclear leukocytes, and macrocytic anemia are some of the abnormalities found in early cases. The lesions of B 12 deficiency begin in the cervical or thoracic cord, and deficits are often primarily sensory, which is quite uncommon in patients with cervical spondylosis.

Dural Arteriovenous Fistula. Several decades ago it was believed that spinal arteriovenous malformations presented either as subarachnoid hemorrhage or as the lumbar syndrome of painful cauda equina deficit. It is now known that small arteriovenous fistulas in the spinal dura can cause myelopathy with either a stepwise progression or abrupt onset. Most malformations are seen on MR' or myelography; however, some require selective angiography of the segmental arteries that supply the cord for definitive diagnosis.

Myelopathy Associated with AIDS (see Chapter 44 ). A subacute vacuolar change in the spinal cord may develop in patients with human immunodeficiency virus (HIV) infection, usually in those with frank acquired immune deficiency syndrome (AIDS) and a history of multiple opportunistic infections. Most patients are younger than the average patient with spondylosis. The clinical findings often emphasize an ascending sensory disorder.

HTLV-I Myelopathy (see ChapieL41 ). A slowly progressive spastic paraparesis with early bladder involvement in a patient from a region endemic for human T-cell leukemia-lymphoma virus (HTLV)-I infection should prompt suspicion of this infectious cause. Patients typically have milder spasticity of the upper extremities. Diagnosis can be made by identifying the presence of antibodies to HTLV-I in serum.

Familial Spastic Paraplegia. These patients can be recognized by their family history, usually that of an autosomal dominant disorder. No direct DNA testing is available.

Syringomyelia. Cervical syringomyelia may occur in isolation or in association with the Chiari malformation, trauma, or tumor. Patients typically have lower motor neuron signs in the upper extremities due to involvement of the central gray matter and upper motor neuron signs in the upper and lower extremities due to involvement of the descending corticospinal tracts. The segmental loss of spinothalamic modalities of sensation and the neuropathic quality of the accompanying neck, back, and extremity pain as well as the context of an associated underlying problem suggest the diagnosis. MRI demonstrates the syrinx.

Compressive Lesions at the Craniocervical Junction. The Chiari malformation may cause myelopathy, vertigo, and ataxia. There may be an associated syringomyelia. Basilar impression due to instability of the atlanto-occipital joint or atlantoaxial instability, as in rheumatoid arthritis, may cause slowly progressive myelopathy. These lesions often occur in the context of spondylotic lesions, and it is very important to clarify the source of progressive findings. Certain tumors, such as meningiomas and schwannomas, at the craniocervical junction may also mimic the signs of cervical spondylosis. Often the history suggests a loss of function on one side followed by progression of signs to all four extremities. Down-beating nystagmus suggests the localization. Imaging high enough to demonstrate the craniocervical junction is crucial before cervical myelopathy is attributed to spondylotic lesions.

Evaluation. Evaluation begins with a careful history and examination. This is especially important because of the known high rate of radiological spondylotic abnormalities in asymptomatic populations. It is very important to establish the best possible correlations between the clinical findings and the imaging abnormalities. Available imaging modalities include plain radiographs, CT myelography, and MRI. Plain films can show many of the degenerative changes of bony elements; however, they do not reveal the relationship of these to the neural structures. Simple flexion and extension films performed with care can also demonstrate spinal instabilities that are not apparent on MRI or CT myelography. MRI is the easiest noninvasive means of diagnosis. MRI can demonstrate the dimensions of the spinal canal and foramina and distortion of the spinal cord and roots caused by the impingement of bony structures. Gadolinium enhancement can demonstrate the presence of various alternative lesions that may be under consideration. CT myelography can be used to answer any questions that remain after MRI. The myelogram may fail to show complete block even when significant spondylotic myelopathy is present.

Management. Conservative management of cervical spondylosis includes immobilization with a cervical collar and the use of non-narcotic, nonsteroidal medications for pain. The symptoms and signs in most patients stabilize with this therapy; that is, the myelopathy does not progress, and in some patients it improves. Yet controlled studies evaluating the benefit of immobilization have not been done. When radicular pain is the major problem demanding further intervention, epidural steroid injections can be effective. We refer patients for neurosurgical evaluation and surgical therapy when their myelopathy progresses despite these conservative measures, after careful consideration of other diagnostic possibilities as listed earlier. There has been no documentation of long-term benefit from surgery, although many series have shown evidence of benefit in the short term. [8] Posterior decompressive laminectomy is the procedure that has the longest history. However, unless it is performed over many levels, it will not relieve multilevel compression. Wide decompression performed over a number of segments may be complicated in later years by a swan neck deformity owing to the loss of posterior supporting elements. The anterior approach with interbody fusion is especially suitable for patients with single level nerve root compression. Its benefits for cord compression are less well defined. When radicular symptoms are due to bony osteophytes, foraminotomy may relieve the symptoms and signs of root compression. Although the benefit of surgery has not been systematically validated, and many patients improve spontaneously or with immobilization by a collar, clinical experience with individual cases suggests that selected patients do benefit and show marked improvement shortly after decompressive surgery.

Prognosis and Future Perspectives. The natural history of cervical spondylosis is not known. Although the course of the disease is progressive and most patients have chronic symptoms, the large majority remain stable for many years and do not require surgical intervention.

MRI has greatly advanced the precision of diagnosis while sparing most patients the discomfort and risk of myelography. Future advances in imaging may further facilitate diagnosis. Rowland has pointed out our great lack of knowledge of the natural history of cervical spondylosis as well as the need for controlled trials to demonstrate the effects of surgery and clarify surgical indications. [8] Such studies, if they are done, will require a cooperative effort and careful definition of clinically relevant questions.

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  • Danait
    Can b12 deficiency dessicated disk?
    3 years ago

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