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Degenerative Disorders of the Cervical Spine
Overview of Disc Degeneration and Herniation in the Cervical Spine
Cervical degenerative disc disease (DDD) is not a specific diagnosis but a pathophysiologic process that incorporates a spectrum of disease states. Manifestations of cervical DDD can range from neck pain and headache to cervical radiculopathy and/or myelopathy. Fortunately, most of these pathologies can be managed nonoperatively; they may require surgical intervention if the symptoms and signs are found to be persistent or progressive. The clinician’s job is to determine the most specific diagnosis that explains the symptoms so that the optimal treatment can be applied.
Axial spine pain, which should be distinguished from disc degeneration, is the most frequent musculoskeletal complaint. Axial spine pain—whether cervical, thoracic, or lumbar—often is attributed to disc degeneration. Disc degeneration does not always cause pain, but it can lead to internal disc derangement or disc herniation. Each of these diagnoses has unique clinical findings and treatments.
The genetic influence on disc degeneration may be attributed to a small effect from each of multiple genes or possibly a relatively large effect of a smaller number of genes. To date, several specific gene loci have been identified that are associated with disc degeneration. This association of a specific gene with degenerative disc changes has been confirmed. Other variations in the aggrecan gene, metalloproteinase-3 gene, collagen type IX, and alpha 2 and 3 gene forms also have been associated with disc pathology and symptoms.
Nonspecific axial pain is an international health issue of major significance and should be discriminated from pain associated with a disc herniation. Approximately 80% of individuals are affected by this symptom at some time in their lives. Impairments of the back and spine are ranked as the most frequent cause of limitation of activity in individuals younger than 45 years old by the National Center for Health Statistics ( www.cdc.gov/nchs ). Axial pain typically described as discogenic pain may not even arise from the disc itself.
Nonanatomic factors, specifically work perception and psychosocial factors, are intimately intertwined with physical complaints. Compounding the diagnostic and treatment difficulties is the high incidence of significant abnormalities shown by imaging studies, which in asymptomatic matched controls is 76%. Optimal outcome primarily depends on “proper patient selection”; such patients can be difficult to identify. Until the pathologic process is better described and reliable criteria for the diagnosis are determined, improvement in treatment outcomes will change slowly.
Disc and Spine Anatomy
The intervertebral disc has a complex structure; the nucleus pulposus has an organized matrix, which is laid down by relatively few cells. The central gelatinous nucleus is contained around the periphery by the collagenous anulus, the cartilaginous anulus, and the cartilage endplates cephalad and caudad. Collagen fibers continue from the anulus to the surrounding tissues, tying into the vertebral body along its rim and into the anterior and posterior longitudinal ligaments and the hyaline cartilage endplates superiorly and inferiorly. The cartilage endplates are secured to the osseous endplate by the calcified cartilage. Few, if any, collagen fibers cross this boundary. The anulus has a lamellar structure with interconnections between adjacent layers of collagen fibrils ( Fig. 38.1 ).
At birth, the disc has some direct blood supply contained within the cartilaginous endplates and the anulus. These vessels recede in the first years of life, and by adulthood there is no appreciable blood supply to the disc. Over time, for reasons not well understood, the water content of the gelatinous nucleus matrix decreases, with a decreased and altered proteoglycan composition. These changes lead to a more fibrous consistency of the nucleus, which ultimately fissures. Blood vessels grow into the disc through these outer fissures, with an increase in cellular proliferation and formation of cell clusters. Also, there is an increase in cell death, the mechanism of which is unknown. The cartilage endplates become thinned, with fissuring occurring with subsequent sclerosis of the subchondral endplates. The above-enumerated changes are quite similar if not identical to the changes of disc degeneration. Herniated discs have a greater number of senescent cells than nonherniated discs and have higher concentrations of matrix metalloproteinases.
The normal adult disc has a large amount of extracellular matrix and a few cells that account for about 1% by volume. These cells are of two phenotypes: anulus cells and nucleus cells. The anulus cells are more elongated and appear more like fibroblasts, whereas nucleus cells are oval and resemble chondrocytes. These two cell types behave differently and may be able to sense mechanical stresses. In culture, they respond differently to loads and produce different matrix proteins. The anulus cells produce predominantly type I collagen, whereas nucleus cells synthesize type II collagen. The characteristics of these cell types under normal and abnormal circumstances are beginning to be determined, and much is known, but this is beyond the scope of this chapter; however, this information is necessary to understand and subsequently treat disc disorders.
The cells within the disc are sustained by diffusion of nutrients into the disc through the porous central concavity of the vertebral endplate. Histologic studies have shown regions where the marrow spaces are in direct contact with the cartilage and that the central portion of the endplate is permeable to dye. Motion and weight bearing are believed to be helpful in maintaining this diffusion. The metabolic turnover of the disc is relatively high when its avascularity is considered but slow compared with other tissues. The glycosaminoglycan turnover in the disc is quite slow, requiring 500 days.
Neural Elements
The organization of the neural elements is strictly maintained throughout the entire neural system, even within the conus medullaris and cauda equina distally. The orientation of the nerve roots in the dural sac and at the conus medullaris follows a highly organized pattern, with the most cephalad roots lying lateral and the most caudad lying centrally. The motor roots are ventral to the sensory roots at all levels. The arachnoid mater holds the roots in these positions.
The pedicle is the key to understanding surgical spinal anatomy. The relation of the pedicle to the neural elements varies by region within the spinal column. In the cervical region, there are seven vertebrae but eight cervical roots. Accepted nomenclature allows each cervical root to exit cephalad to the pedicle of the vertebra for which it is named (e.g., the C6 nerve root exits above, or cephalad to, the C6 pedicle). This relationship changes in the thoracic spine because the C8 root exits between the C7 and T1 pedicles, requiring the T1 root to exit caudal (or below) the pedicle for which it is named. This relationship is maintained throughout the remaining more caudal segments. The naming of the disc levels is different, in that all levels where discs are present are named for the vertebral level immediately cephalad (i.e., the C6 disc is immediately caudal to the C6 vertebra, and disc pathology at that level typically would involve the C7 nerve root).
Natural History of Disc Disease
One theory of spinal degeneration assumes that all spines degenerate and that current methods of treatment are for symptomatic relief, not for a cure. The degenerative process has been divided into three separate stages with relatively distinct findings. The first stage is dysfunction, which is seen in individuals 15 to 45 years old. It is characterized by circumferential and radial tears in the disc anulus and localized synovitis of the facet joints. The next stage is instability. This stage, found in 35- to 70-year-old patients, is characterized by internal disruption of the disc, progressive disc resorption, degeneration of the facet joints with capsular laxity, subluxation, and joint erosion. The final stage, present in patients older than 60 years, is stabilization. In this stage, the progressive development of hypertrophic bone around the disc and facet joints leads to segmental stiffening or frank ankylosis ( Table 38.1 ).
TABLE 38.1
Spectrum of Pathologic Changes in Facet Joints and Discs and Interaction of These Changes
Modified from Kirkaldy-Willis WH, editor: Managing low back pain , New York, 1983, Churchill Livingstone.
| Phases of Spinal Degeneration | Facet Joints | Pathologic Result | Intervertebral Disc | |||
|---|---|---|---|---|---|---|
| Dysfunction | Synovitis | → | Dysfunction | ← | Circumferential tears | |
| Hypermobility | ↓ | ↖ | ||||
| Continuing degeneration | ↗ | Herniation | ← | Radial tears | ||
| Instability | Capsular laxity | → | Instability | ← | Internal disruption | |
| Subluxation | → | Lateral nerve entrapment | ← | Disc resorption | ||
| Stabilization | Enlargement of articular processes | → | One-level stenosis | ← | Osteophytes | |
| ↘ | Multilevel spondylosis and stenosis | ↙ | ||||
Each spinal segment degenerates at a different rate. As one level is in the dysfunction stage, another may be entering the stabilization stage. Disc herniation in this scheme is considered a complication of disc degeneration in the dysfunction and instability stages. Spinal stenosis from degenerative arthritis in this scheme is a complication of bony overgrowth compromising neural tissue in the late instability and early stabilization stages.
In general, the literature supports an active care approach, minimizing centrally acting medications. The judicious use of epidural steroids also is supported for short-term relief but does not have effect on long-term outcomes. Nonprogressive neurologic deficits can be treated nonoperatively with expected improvement clinically. If surgery is necessary, it usually can be delayed 6 to 12 weeks to allow adequate opportunity for improvement. The important exceptions are patients with cervical myelopathy or progressive neurologic deficits, who are best treated surgically.
The natural history of DDD is one of recurrent episodes of pain followed by periods of significant or complete relief. The frequency and intensity of symptoms helps determine the aggressiveness of intervention.
Before a discussion of diagnostic studies, axial spine pain with radiation of radicular pain to one or more extremities must be considered. Understanding certain symptoms must be juxtaposed to a rudimentary understanding of certain pathophysiologic entities. It is doubtful if there is any other area of orthopaedics in which accurate diagnosis is as difficult or the proper treatment as challenging as in patients with persistent neck and arm or low back and leg pain. Although many patients have a clear diagnosis properly arrived at by careful history and physical examination with confirmatory imaging studies, more patients with pain have absent neurologic findings other than sensory changes and have normal imaging studies or studies that do not support the clinical complaints and findings. Inability to easily determine an appropriate diagnosis in a patient does not relieve the physician of the obligation to recommend treatment or to direct the patient to a setting where such treatment is available. Careful assessment of these patients to determine if they have problems that can be successfully treated (operatively or nonoperatively) is imperative to avoid overtreatment and undertreatment.
Operative treatment can benefit a patient if it corrects a deformity, corrects instability, relieves neural compression, or treats a combination of these problems. Obtaining a history and completing a physical examination to determine a diagnosis that should be supported by other diagnostic studies is a useful approach; conversely, matching the diagnosis and treatment to the results of diagnostic studies, as can often be done in other subspecialties of orthopaedics (e.g., treating extremity pain based on a radiograph that shows a fracture), is risky because numerous studies have documented abnormal imaging in asymptomatic populations.
Diagnostic Studies
Radiography
The simplest and most readily available diagnostic tests for cervical pain are anteroposterior and lateral radiographs of the involved spinal region. On lateral radiographs bony abnormalities, such as subluxation, congenital narrowing, or fracture, can be identified. Soft-tissue swelling may be visible. Anteroposterior radiographs can reveal uncovertebral arthritis; potential abnormalities can be identified by looking at the relationships between pedicles and the spinous processes. Obtaining other views, such as flexion and extension radiographs, can reveal if instability is present. Oblique views show the foramen. These simple radiographs show a relatively high incidence of abnormal findings.
Myelography
The value of myelography is the ability to check all spinal regions for abnormality and to define intraspinal lesions; it may be unnecessary if clinical and CT or MRI findings are in complete agreement. The primary indications for myelography are inability to get an MRI, suspicion of an intraspinal lesion, patients with spinal instrumentation causing artifact, or questionable diagnosis resulting from conflicting clinical findings and other studies ( Fig. 38.2 ). In addition, myelography is valuable in a previously operated spine and in patients with marked bony degenerative change that may be underestimated on MRI. Myelography is improved by the use of postmyelography CT, in this setting and in evaluating spinal stenosis.
Several contrast agents have been used for myelography: air, oil contrast, and water-soluble (absorbable) contrast agents, including metrizamide (Amipaque), iohexol (Omnipaque), and iopamidol (Isovue-M). Because these nonionic agents are absorbable, the discomforts of removing them and the severity of the postmyelography headache have decreased.
Computed Tomography
Most clinicians now agree that CT is an extremely useful diagnostic tool in the evaluation of spinal disease. The current technology and computer software have made possible the ability to reformat the standard axial cuts in almost any direction and magnify the images so that exact measurements of various structures can be made. Software is available to evaluate the density of a selected vertebra and compare it with vertebrae of the normal population to give a numerically reproducible estimate of vertebral density to quantitate osteopenia.
Numerous types of CT studies for the spine are available. One must be careful in ordering the study to ensure that the areas of clinical concern are included. Sagittal, axial, and coronal cuts allow a three-dimensional view of the cervical spine. Location markers allow finer scrutiny of the area of pathology.
Magnetic Resonance Imaging
MRI is currently the standard for advanced imaging of the spine and is superior to CT in most circumstances, in particular, identification of infections, tumors, and degenerative changes within the discs. More importantly, MRI is superior for imaging the disc and directly imaging neural structures. Also, MRI typically shows the entire region of study (i.e., cervical, thoracic, or lumbar). Of particular value is the ability to image the nerve root in the foramen (especially with foramen specific oblique cuts), which is difficult even with postmyelography CT because the subarachnoid space and the contrast agent do not extend fully through the foramen. Despite this superiority, there are circumstances in which MRI and CT, with or without myelography, can be used in a complementary fashion.
One of the difficulties with MRI is showing anatomy that is abnormal but which may be asymptomatic. MRI evidence of disc degeneration has been reported in the cervical spine in 25% of patients younger than 40 years and in 60% of patients 60 years and older. The demonstrated findings must be carefully correlated with the clinical impression. The importance of this concept cannot be overstated. The best way to obtain meaningful clinical information from MRI of the spine is to have a specific question before the study. This question is derived from a patient’s history and a careful physical examination, and is posed using the parameters of (1) neural compression, (2) instability, and (3) deformity. In each case, the specific location of the abnormality should be suspected before MRI and confirmed with the study. Ideally an advanced imaging study should be used for confirmation, not reevaluation. Only abnormalities in one or a combination of these categories are important, because operative techniques can treat only these problems. Failure to interpret an imaging study in this way, especially MRI, which is sensitive to anatomic abnormalities, would inevitably lead to poor clinical choices and outcomes.
A newer MRI imaging technique—diffusion tensor imaging—is based on the diffusion rate of water in tissue and has been reported to demonstrate spinal cord impairment in patients with early stage cervical spondylosis before it is visible on plain MRI scans (see discussion of cervical spondylotic myelopathy). The information it provides can be helpful in early identification of patients in whom operative treatment is indicated.
Other Diagnostic Tests
Numerous diagnostic tests, in addition to radiography, myelography, CT, and MRI, have been used in the diagnosis of intervertebral disc disease. The primary advantage of these tests is to rule out diseases other than primary disc herniation, spinal stenosis, and spinal arthritis.
Electromyography and nerve conduction velocity can be helpful if a patient has a history and physical examination suggestive of radiculopathy at either the cervical or the lumbar level with inconclusive imaging studies. One advantage of electromyography is in the identification of peripheral nerve dysfunction and diffuse neurologic involvement indicating higher or lower lesions. Paraspinal muscles in a patient with a previous posterior open surgical approach usually are abnormal and are not a reliable diagnostic finding.
Bone scans are another procedure in which positive findings usually are not indicative of intervertebral disc disease—but they can confirm neoplastic, traumatic, and arthritic problems in the spine. Various laboratory tests, such as a complete blood cell count, differential white blood cell count, C-reactive protein, biochemical profile, urinalysis, serum protein electrophoresis, and erythrocyte sedimentation rate, are extremely good screening procedures for other causes of pain in the spine. Rheumatoid screening studies, such as rheumatoid arthritis, antinuclear antibody, lupus erythematosus cell preparation, and HLA-B27, also are useful when indicated by the clinical picture.
Injection Studies
Whenever a diagnosis is in doubt, and the complaints seem real or the pathologic condition is diffuse, identification of the source of pain is problematic. The use of local anesthetics or contrast media in various specific anatomic areas can be helpful. These agents are relatively simple, safe, and minimally painful. Contrast media such as diatrizoate meglumine (Hypaque), iothalamate meglumine (Conray), iohexol (Omnipaque), iopamidol, and metrizamide (Amipaque) have been used for discography and blocks with no reported ill effects. Reports of neurologic complications with contrast media used for discography and subsequent chymopapain injection are well documented. The best choice of a contrast medium for documenting structures outside the subarachnoid space is an absorbable medium with low reactivity because it might be injected inadvertently into the subarachnoid space. Iohexol and metrizamide are the least reactive, most widely accepted, and best tolerated of the currently available contrast media. Local anesthetics, such as lidocaine (Xylocaine), tetracaine (Pontocaine), and bupivacaine (Marcaine), are used frequently epidurally and intradurally. The use of bupivacaine should be limited to low concentrations and low volumes because of reports of death after epidural anesthesia using concentrations of 0.75% or higher.
Spinal arachnoiditis was associated in past years with the use of epidural methylprednisolone acetate (Depo-Medrol). This complication was thought to be caused by the use of the suspending agent, polyethylene glycol, which has since been eliminated from the Depo-Medrol preparation. For epidural injections, we prefer the use of Celestone Soluspan, which is a mixture of betamethasone sodium phosphate and betamethasone acetate. Celestone Soluspan provides immediate and long-term duration of action, is highly soluble, and contains no harmful preservatives. Celestone should not be mixed with local anesthetics containing preservatives such as parabens or phenol because flocculation and clogging of the suspension can occur. If Celestone is not available, other commonly used preparations for spinal injections include methylprednisolone (Depo-Medrol) and triamcinolone acetonide (Kenalog), all of which are particulate corticosteroids ( Table 38.2 ). Isotonic saline is the only other injectable medium used frequently around the spine with no reported adverse reactions.
TABLE 38.2
Common Corticosteroids Used in Spinal Interventions Compared With Hydrocortisone
From el Abd O: Steroids in spine interventions. In Slipman CW, Derby D, Simeone FA, Mayer TG, editors: Interventional spine: an algorithmic approach , Philadelphia, 2008, Elsevier.
| Hydrocortisone | Methylprednisolone (Depo-Medrol) | Triamcinolone Acetonide (Kenalog) | Betamethasone Sodium Phosphate and Acetate (Celestone Soluspan) | |
|---|---|---|---|---|
| Relative antiinflammatory potency | 1 | 5 | 5 | 25 |
| pH | 5.0-7.0 | 7.0-8.0 | 4.5-6.5 | 6.8-7.2 |
| Onset | Fast | Slow | Moderate | Fast |
| Duration of action | Short | Intermediate | Intermediate | Long |
| Concentration (mg/mL) | 50 | 40-80 | 20 | 6 |
| Relative mineralocorticoid activity | 2+ | 0 | 0 | 0 |
When discrete, well-controlled injection techniques directed at specific targets in and around the spine are used, grading the degree of pain before and after a spinal injection is helpful in determining the location of the pain generator. The patient is asked to grade the degree of pain on a 0-to-10 scale before and at various intervals after the spinal injection ( Box 38.1 ). If a spinal injection done under fluoroscopic control results in an 80% or more decrease in the level of pain, which corresponds to the duration of action of the anesthetic agent used, we presume the target area injected to be the pain generator. Less pain reduction, 50% to 65%, does not constitute a positive response.
Box 38.1
Pain Scale and Diary
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0 No pain
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1 Mild pain that you are aware of but not bothered by
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2 Moderate pain that you can tolerate without medication
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3 Moderate pain that is discomforting and requires medication
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4-5 More severe pain and you begin to feel antisocial
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6 Severe pain
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7-9 Intensely severe pain
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10 Most severe pain (you might contemplate suicide because of it)
| Activity | Comments | Location of Pain | Time | Severity of Pain (0-10) |
|---|---|---|---|---|
Epidural Steroid Injections
Epidural injections in the spine were developed to diagnose and treat spinal pain. Information obtained from epidural injections can be helpful in confirming pain generators that are responsible for a patient’s discomfort. Structural abnormalities do not always cause pain, and diagnostic injections can help to correlate abnormalities seen on imaging studies with associated pain complaints. In addition, epidural injections can provide pain relief during the recovery of disc or nerve root injuries and allow patients to increase their level of physical activity. Epidural steroid injections in the treatment of disc herniation and radiculitis are performed based on the pathophysiologic mechanism of reducing inflammation; however, the evidence suggests that local anesthetics with or without steroids are equally as effective as steroids alone in many settings. Because severe pain from an acute disc injury with or without radiculopathy often is time limited, therapeutic injections help to manage pain and may alleviate or decrease the need for oral analgesics.
Steroids prepared for intramuscular injection also have been used frequently in the epidural space with few and usually transient complications. There are conflicting reports on the short- and long-term quality-of-life outcomes and the cost-effectiveness of cervical epidural steroid injections. A cost-effectiveness analysis of steroid injection compared to conservative management for patients with radiculopathy or neck pain found that at short-term follow-up (3 months) steroid injections produced greater improvement in quality-of-life scores at a lower cost. Epstein, however, warned against cervical epidural steroid injections, citing several serious complications, including epidural hematomas, infection, inadvertent intramedullary cord injections, and cord, brainstem, and cerebellar strokes. Other cited adverse reactions include procedural-related pain, steroid side effects, and vasovagal reactions, which are relatively minor and self-limited. We have found these complications and reactions to be rare.
The most adverse immediate reaction during an epidural injection is a vasovagal reaction. Dural puncture has been estimated to occur in 0.5% to 5% of patients having cervical or lumbar epidural steroid injections. The anesthesiology literature reported a 7.5% to 75% incidence of postdural puncture (positional) headaches, with the highest estimates associated with the use of 16- and 18-gauge needles. Headache without dural puncture has been estimated to occur in 2% of patients and is attributed to air injected into the epidural space, increased intrathecal pressure from fluid around the dural sac, and possibly an undetected dural puncture. Some minor common complaints caused by corticosteroids injected into the epidural space include nonpositional headaches, facial flushing, insomnia, low-grade fever, and transient increased back or lower extremity pain. Epidural corticosteroid injections are contraindicated in the presence of infection at the injection site, systemic infection, bleeding diathesis, uncontrolled diabetes mellitus, and congestive heart failure.
We perform epidural corticosteroid injections in a fluoroscopy suite equipped with resuscitative and monitoring equipment. Intravenous access is established in all patients with a minimum of a 20-gauge angiocatheter placed in the upper extremity. Mild sedation is achieved through intravenous access with the patient remaining alert and responsive. We recommend the use of fluoroscopy for diagnostic and therapeutic epidural injections for several reasons. Epidural injections performed without fluoroscopic guidance are not always made into the epidural space or the intended interspace. Even in experienced hands, needle misplacement occurs in 40% of epidural injections when done without fluoroscopic guidance. Accidental intravascular injections also can occur, and the absence of blood return with needle aspiration before injection is an unreliable indicator of this complication. In the presence of anatomic anomalies, such as a midline epidural septum or multiple separate epidural compartments, the desired flow of epidural injectants to the presumed pain generator is restricted and remains undetected without fluoroscopy. In addition, if an injection fails to relieve pain, it would be impossible without fluoroscopy to determine whether the failure was caused by a genuine poor response or by improper needle placement.
Cervical Epidural Injection
Cervical epidural steroid injections have been used with some success to treat cervical spondylosis associated with acute disc disruption and radiculopathies, cervical strain syndromes with associated myofascial pain, postlaminectomy cervical pain, reflex sympathetic dystrophy, postherpetic neuralgia, acute viral brachial plexitis, and muscle contraction headaches. The best results with cervical epidural steroid injections have been in patients with acute disc herniations or well-defined radicular symptoms and in patients with limited myofascial pain. In a group of 70 patients with herniated cervical discs without myelopathy for which conservative management failed to relieve symptoms, cervical epidural steroid injections provided significant pain relief and avoided surgery in 63%. Better outcomes were noted in patients older than 50 years and those who received the injections earlier (<100 days from diagnosis). Preoperative opioid use has been suggested to be associated with worse patient-reported outcomes. Wei et al. found that pre-injection opioid use was associated with slightly higher odds of worse disability and leg/arm pain; however, increased pre-injection opioid use did not affect long-term outcomes.
At this time, extreme caution is needed when performing cervical transforaminal injections because of the increasing number of reports of catastrophic neurologic complications involving injury to the spinal cord and brainstem after such injections. These injuries are the result of intraarterial injection into either a reinforcing radicular artery or the vertebral artery, as well as intra-arterial corticosteroid injection with distal embolization. Injection into a radicular artery is an unavoidable complication but one that can be recognized by using real-time monitoring of a test dose of contrast medium. In the case of intraarterial injection, the procedure should be aborted to avoid injury to the spinal cord.
Interlaminar Cervical Epidural Injection
Technique 38.1
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Place the patient prone on a pain management table. We use a low-attenuated carbon fiber tabletop that allows better imaging and permits unobstructed C-arm viewing. For optimal placement and comfort, place the patient’s face in a cervical prone cutout cushion.
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Cervical epidural injections using a paramedian approach should be done routinely at the C7-T1 interspace unless previous surgery of the posterior cervical spine has been done at that level, in which case the C6-7 or T1-2 level is injected. Aseptically prepare the skin area with isopropyl alcohol and povidone-iodine several segments above and below the laminar interspace to be injected. If the patient is allergic to povidone-iodine, use chlorhexidine gluconate (Hibiclens).
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Drape the area in sterile fashion.
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Using anteroposterior fluoroscopic imaging, identify the target laminar interspace. With the use of a 27-gauge, ¼-inch needle, anesthetize the skin so that a skin wheal is raised over the target interspace on the side of the patient’s pain with 1 to 2 mL of 1% preservative-free lidocaine without epinephrine. To diminish the burning discomfort of the anesthetic, mix 3 mL of 8.4% sodium bicarbonate in a 30-mL bottle of 1% preservative-free lidocaine without epinephrine. Nick the skin with an 18-gauge hypodermic needle. Under fluoroscopic control, insert and advance a 22-gauge, 3½-inch spinal needle in a vertical fashion until contact is made with the upper edge of the T1 lamina 1 to 2 mm lateral to the midline.
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Anesthetize the lamina with 1 to 2 mL of 1% preservative-free lidocaine without epinephrine. Anesthetize the soft tissues with 2 mL of 1% preservative-free lidocaine without epinephrine as the spinal needle is withdrawn.
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Insert an 18-gauge, 3½-inch Tuohy epidural needle and advance it vertically within the anesthetized soft-tissue track until contact is made with the T1 lamina under fluoroscopy.
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“Walk off” the lamina with the Tuohy needle onto the ligamentum flavum. Remove the stylet from the Tuohy needle, and attach a 10-mL syringe filled halfway with air and sterile saline. Advance the Tuohy needle into the epidural space using the loss-of-resistance technique. When loss of resistance has been achieved, aspirate to check for blood or cerebrospinal fluid (CSF). If neither blood nor CSF is evident, remove the syringe from the Tuohy needle and attach a 5-mL syringe containing 1.5 mL of nonionic contrast dye.
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Confirm epidural placement by producing an epidurogram with the nonionic contrast agent ( Fig. 38.3 ). To confirm proper placement further, adjust the C-arm to view the area from a lateral perspective. A spot radiograph can be obtained to document placement.
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Inject a test dose of 1 to 2 mL of 1% preservative-free lidocaine without epinephrine and wait 3 minutes. If the patient does not complain of warmth, burning, or significant paresthesias or show signs of apnea, place a 10-mL syringe on the Tuohy needle and slowly inject 2 mL of 1% preservative-free lidocaine without epinephrine and 2 mL of 6 mg/mL Celestone Soluspan slowly into the epidural space. If Celestone Soluspan cannot be obtained, 40 mg/mL of triamcinolone is a good substitute.
Zygapophyseal (Facet) Joint Injections
The facet joint can be a source of back or neck pain; the exact cause of the pain is unknown. Theories include meniscoid entrapment and extrapment, synovial impingement, chondromalacia facetae, capsular and synovial inflammation, and mechanical injury to the joint capsule. Osteoarthritis is another cause of facet joint pain; however, the incidence of facet joint arthropathy is equal in symptomatic and asymptomatic patients. As with other osteoarthritic joints, radiographic changes correlate poorly with pain.
Although the history and physical examination may suggest that the facet joint is the cause of spine pain, no noninvasive pathognomonic findings distinguish facet joint–mediated pain from other sources of spine pain. Fluoroscopically guided facet joint injections are commonly considered the “gold standard” for isolating or excluding the facet joint as a source of spine or extremity pain.
Clinical suspicion of facet joint pain by a spine specialist remains the major indicator for diagnostic injection, which should be done only in patients who have had pain for more than 4 weeks and only after appropriate conservative measures have failed to provide relief. Facet joint injection procedures may help to focus treatment on a specific spinal segment and provide adequate pain relief to allow progression in therapy. Either intraarticular or medial branch blocks can be used for diagnostic purposes. Although injection of cortisone into the facet joint was a popular procedure through most of the 1970s and 1980s, many investigators have found no evidence that this effectively treats low back pain caused by a facet joint. The only controlled study on the use of intraarticular corticosteroids in the cervical spine found no added benefit from intraarticular betamethasone over bupivacaine.
Cervical Medial Branch Block Injection
Technique 38.2
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Place the patient prone on the pain management table. Rotate the patient’s neck so that the symptomatic side is down. This allows the vertebral artery to be positioned further beneath the articular pillar, creates greater accentuation of the cervical waists, and prevents the jaw from being superimposed. Aseptically prepare and drape the side to be injected.
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Identify the target location using anteroposteriorly directed fluoroscopy. Each cervical facet joint from C3-4 to C7-T1 is supplied from the medial nerve branch above and below the joint that curves consistently around the “waist” of the articular pillar of the same numbered vertebrae ( Fig. 38.4 ). To block the C6 facet joint nerve supply, anesthetize the C6 and C7 medial branches.
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Insert a 22- or 25-gauge, 3½-inch spinal needle perpendicular to the pain management table and advance it under fluoroscopic control ventrally and medially until contact is made with periosteum. Direct the spinal needle laterally until the needle tip reaches the lateral margin of the waist of the articular pillar and then direct the needle until it rests at the deepest point of the articular pillar’s concavity under fluoroscopy.
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Remove the stylet. If there is a negative aspirate, inject 0.5 mL of 0.75% preservative-free bupivacaine.
Cervical Discography
The approach to the cervical spine differs from the approaches used for discography of the lumbar and thoracic spine. The cervical spine is approached anteriorly rather than posteriorly. Complications associated with cervical discography because of the surrounding anatomy include injury to the trachea, esophagus, carotid artery, and jugular veins and spinal cord injury and pneumothorax. Discitis is a concern in the cervical spine; disc infection often originates from the gram-negative and anaerobic flora of the esophagus.
Traditionally, the approach to the cervical intervertebral discs has been via a paralaryngeal route that requires displacement of the trachea and esophagus away from the site of entry. A more lateral approach that is gaining popularity bypasses these structures and does not require such displacement.
Cervical Discography
Technique 38.3
(FALCO)
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Place the patient supine on the procedure table.
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Insert an angiocatheter into the upper extremity and begin intravenous antibiotic infusion. Alternatively, intradiscal antibiotics can be given during surgery.
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Sedate the patient, and prepare and drape the skin sterilely, including the anterolateral aspect of the neck.
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Under fluoroscopic imaging, identify the intervertebral discs with aligned endplates and sharp margins of the intervertebral discs. Approach the paralaryngeal area from the right, using a finger to displace the esophagus and trachea to the left and the carotid artery to the right. With the other hand, insert a 2- or 3½-inch spinal needle over the finger through the skin and into the outer anulus of the disc. Advance the needle into the center of the disc, using anteroposterior and lateral fluoroscopic guidance.
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An alternative method is a more lateral approach to the cervical spine using a single needle. This approach may reduce the incidence of infection by passing the needle posterior to the trachea and esophagus en route to the disc space. Position the patient or the C-arm to place the cervical spine in an oblique position for optimal foraminal exposure and continue adjusting until the endplates, disc space, and uncovertebral process are in sharp focus ( Fig. 38.5 ).
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Insert a 2- or 3½-inch needle into the skin and advance it until the tip makes contact with the subjacent uncovertebral process. “Walk off” the needle just anterior to the uncovertebral process. Advance the needle into the center of the disc, using anteroposterior and lateral fluoroscopic guidance.
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After needle placement with either technique, the rest of the procedure is essentially the same as that described for thoracic or lumbar discography ( Chapter 39 ).
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Inject either saline or a nonionic contrast dye into each disc.
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Record any pain response as none, dissimilar, similar, or exact in relationship to the patient’s typical pain. Record intradiscal pressures to assist in determining if the disc is the cause of the pain.
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Perform radiography and CT of the cervical spine on completion of the study.
Cervical Disc Disease
Herniation of the cervical intervertebral disc with spinal cord compression has been identified since Key detailed the pathologic findings of two cases of cord compression by “intervertebral substance” in 1838. Cervical disc disease is slightly more common in men. Factors associated with the injury are frequent heavy lifting on the job, cigarette smoking, and frequent diving from a board. Patients with cervical disc disease also are likely to have lumbar disc disease. MRI has shown increasing cervical disc degeneration with age.
The pathophysiology of cervical disc disease is the same as DDD in other areas of the spine as described by Kirkaldy-Willis. Physiologic changes in the nucleus are followed by progressive annular degeneration. Frank extrusion of nuclear material can occur as a complication of this normal degenerative process. As the disc degeneration proceeds, hypermobility of the segment can result in instability or degenerative arthritic changes or both. In contrast to those in the lumbar spine, these hypertrophic changes are predominantly at the uncovertebral joint (uncinate process) ( Fig. 38.6 ). Hypertrophic changes eventually develop around the facet joints and vertebral bodies. Progressive stiffening of the cervical spine and loss of motion are the usual result in the end stages. Hypertrophic spurring anteriorly occasionally results in dysphagia. Increased amounts of matrix metalloproteinases, nitric oxide, prostaglandin E 2 , and interleukin-6 have been identified in disc material removed from cervical disc hernias, suggesting that these products are involved in the biochemistry of disc degeneration. These substances also are implicated in pain production.
The classic approach to discs in this region has been posteriorly with laminectomy. Anterior cervical discectomy with fusion is still the most commonly performed procedure when the disc is removed anteriorly to avoid disc space collapse, but the reported results of disc arthroplasty have it challenging the gold standard of ACDF. Foraminotomy is the classic procedure of choice when the disc fragment is lateral and can be removed posteriorly but fully endoscopic foraminotomy is showing promise to be the procedure that provides the least immediate morbidity and quickest recovery.
Signs and Symptoms
The signs and symptoms of cervical intervertebral disc disease are best separated into symptoms related to the spine itself, symptoms related to nerve root compression, and symptoms of myelopathy. Several authors reported that when the disc is punctured anteriorly for the purpose of discography, pain is noted in the neck and shoulder. Complaints of neck pain, medial scapular pain, and shoulder pain are probably related to primary pain around the disc and spine. Anatomic studies have indicated cervical disc and ligamentous innervations. This has been inferred to be similar in the cervical spine to that of the lumbar spine, with its sinuvertebral nerve.
Symptoms of root compression usually are associated with pain radiating into the arm or chest with numbness in the fingers and motor weakness. Cervical disc disease also can mimic cardiac disease with chest and arm pain. Usually the radicular symptoms are intermittent and combined with more frequent neck and shoulder pain.
The signs of midline cervical spinal cord compression (myelopathy) are unique and varied. The pain is poorly localized and aching and may be only a minor complaint. Occasional sharp pain or generalized tingling may be described with neck extension. This is similar to the Lhermitte sign in multiple sclerosis. The pain can be in the shoulder and pelvic girdles; it is occasionally associated with a generalized feeling of weakness in the lower extremities and a feeling of instability. Global numbness in the upper extremities and difficulty with fine motor coordination are common findings. Gait disturbances and difficulty with tandem gait may be the first symptoms.
In patients with predominant cervical spondylosis, symptoms of vertebral artery compression also may be found, including dizziness, tinnitus, intermittent blurring of vision, and occasional episodes of retroocular pain. The signs of lateral root pressure from a disc or osteophytes are predominantly neurologic ( Boxes 38.2 to 38.6 ). By evaluating multiple motor groups, multiple levels of deep tendon reflexes, and sensory abnormalities, the level of the lesion can be localized as accurately as any other lesion in the nervous system. The multiple innervation of muscles sometimes can lead to confusion in determining the exact root involved. For this reason, MRI or other studies done for imaging confirmation of the clinical impression usually are helpful.
Box 38.2
C5 Nerve Root Compression
Indicative of C4-5 disc rupture or other pathologic condition at that level.
Box 38.3
C6 Nerve Root Compression
Indicative of C5-6 disc herniation or other local pathologic condition at that level.
Box 38.4
C7 Nerve Root Compression
Indicative of C6-7 disc rupture or other pathologic condition at that level.
Box 38.5
C8 Nerve Root Compression
Indicative of C7-T1 disc rupture or other pathologic condition at that level.
Sensory Deficit
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Ring finger, little finger, and ulnar border of palm
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