Cervical Disc Herniation

Definition: MRI studies of asymptomatic individuals indicate that 40% of patients studied have disc abnormalities. Cervical disc herniations present with symptoms that are analogous to those produced in the lumbar spine. Pain radiating down the arm is a hallmark of an acute disc herniation in the cervical spine. Because of the presence of the spinal cord, severe disc herniations can cause spinal cord dysfunction, which include weakness in the legs and balance problems. Generally speaking though, the presentation and duration of symptoms in the cervical spine is similar to that of the lumbar spine. 60-80% of acute symptoms will resolve in 46 weeks with rest and other conservative measures. During this time, the spine should not be manipulated in any way. Muscle and sensory weakness or abnormality can be increased with any manipulation except longitudinal traction applied gently on the neck bones. Medications such as anti-inflammatories or a short course of low dose steroids can reduce the inflammation until the natural history of the problem until complete resolution occurs. For patients who remain symptomatic beyond 6-8 weeks of conservative care a decision about interventional treatment should be discussed between the patient and the physician. Increasing pain is a relative indication for surgery on the cervical spine. Muscle weakness or sensory

changes which continue for 8-12 weeks or progressive neurological deficit are strong indications for surgical intervention. Signs of spinal cord compression such as balance or bowel and bladder problems are another strong indication for aggressive intervention. Prevalence: United States HNP may be observed with magnetic resonance imaging (MRI) in 10% of asymptomatic individuals aged younger than 40 years and 5% of those older than 40 years. Degenerative disc disease (DDD) may be observed with MRI in 25% of asymptomatic individuals aged less than 40 years and 60% of those aged more than 40 years. The true incidence and prevalence of cervical radiculopathy is uncertain; however, 51% of adults experience neck and arm pain at some time. In a population-based study in Rochester, Minn, the annual incidence of documented cervical radiculopathy for men and women from all causes was 107.3 and 63.5 cases per 100,000 population, respectively.7 International A study from Italy in 1996 reported a prevalence of cervical spondylotic radiculopathy as 3.5 cases per 1000 people.8 Mortality/Morbidity Occasionally, an acute HNP can herniate centrally and cause a myelopathy. This can manifest as hyperreflexia, positive pathologic reflexes (such as Babinski and Hoffman signs), and sphincter disturbances. If left untreated, the effects can be irreversible.

Sex Kelley suggests that the male-to-female incidence of cervical disc herniation is approximately 1:1.9 Marchiori and Henderson cite women as reporting higher disability with increasing levels of DDD than men.10 Age HNP typically affects younger patients (ie, <40 y). DDD, part of natural aging, typically affects older patients (ie, >40 y). History

Pertinent history should include the following information: o Information about pain onset (eg, abrupt onset suggests acute injury) o Time since injury o Mechanism of injury o Percentage of axial versus peripheral pain (eg, 90% neck pain vs 10% upper limb) o Review of systems to uncover possible systemic illness (eg, fever suggests infection, weight loss suggests malignancy). Discogenic pain without nerve root involvement typically is vague, diffuse, and distributed axially. o Pain referred from disc to upper limb usually is nondermatomal. o Activities that increase intradiscal pressure (eg, lifting, Valsalva maneuver) intensify symptoms. Conversely, lying supine provides relief by decreasing intradiscal pressure.

Vibrational stress from driving also exacerbates discogenic pain. Depending on whether primarily motor or sensory involvement is present, radicular pain is deep, dull, and achy or sharp, burning, and electric. o Such radicular pain follows a dermatomal or myotomal pattern into the upper limb. o Cervical radicular pain most commonly radiates to the interscapular region, although pain can be referred to the occiput, shoulder, or arm as well. o Neck pain does not necessarily accompany radiculopathy and frequently is absent. o Patients may present with distal limb numbness and proximal weakness in addition to pain. Atrophy may be present. o A study has demonstrated cervical HNP-induced thermal changes (ie, thermatomes) in specific upper extremity distributions. o Mechanical stimulation of cervical nerve roots has shown that the distribution of referred radicular symptoms (ie, dynatome) may be different from sensory deficits outlined by traditional dermatomal maps.

Risk Factors:

HNP results from repetitive cervical stress or, rarely, from a single traumatic incident. Increased risk may accrue because of vibrational stress, heavy lifting, prolonged sedentary position, whiplash accidents, and frequent acceleration/deceleration. DDD is part of natural aging, but it is also a consequence of poor nutrition, smoking, atherosclerosis, job-related activities, and genetics.

IDD can result from cervical trauma, including whiplash, cervical flexion/rotation injury, and repetitive use. Cervical radiculopathy results from nerve root compression secondary to herniated disc material, stenosis, or proteoglycan-mediated chemical inflammation released from discs. Smoking and certain occupational activities also predispose patients to cervical radiculopathy.

Mechanisms: Manifestations of HNP are divided into subcategories by type (ie, disc bulge, protrusion, extrusion, sequestration). Disc bulge describes generalized symmetrical extension of the disc margin beyond the margins of the adjacent vertebral endplates. Disc protrusion describes herniation of nuclear material through a defect in the annulus, producing a focal extension of the disc margin. Extrusion applies to herniation of nuclear material resulting in an anterior extradural mass attached to the nucleus of origin, often via a pedicle. Disc sequestration refers to separation of material from the disc, which ultimately comes to lie in the spinal canal. Examples of disc herniation are seen in the images below. Herniation typically occurs secondary to posterolateral annular stress. Herniation rarely results from a single traumatic incident. Acute traumatic cervical HNP serves as a major etiology of central cord syndrome. The C6-C7 disc herniates more frequently than discs at other levels. Acute disc herniation causes radicular pain through chemical radiculitis in which proteoglycans and phospholipases released from the nucleus pulposus mediate chemical inflammation and/or direct nerve root

compression. Interleukin 6 and nitric oxide are also released from the disc and play a role in the inflammatory cascade. The chemical radiculitis is a key element in the pain caused by HNP as nerve root compression alone is not always painful unless the dorsal root ganglion is also involved. Herniation may induce nerve demyelination with resulting neurologic symptoms. Cervical HNP may be resorbed during the acute phase. Indeed, studies documenting frequent herniation resorption and correlating herniation regression with symptom resolution support conservative treatment of cervical radicular pain. A rare trauma-induced high cervical (C2-C3) HNP syndrome manifests as nonspecific neck and shoulder pain, perioral hypesthesia, more radiculopathy than myelopathy, and more upper limb motor and sensory dysfunction than lower limb symptomology. Decreased middle and/or lower cervical spine mobility from spondylosis, with consequent overload at higher segments, may precipitate high cervical disc lesions in older patients. A retro-odontoid disc may result from an upwardly migrating C2-C3 HNP. Some case reports describe cervical HNPs causing Brown-Squard syndrome, as well as atypical nonradicular symptoms in patients with congenital insensitivity to pain. Cervical radiculopathy results from mechanical nerve root compression or intense inflammation (ie, chemical radiculitis). Specifically, nerve root compression may occur at the intervertebral foraminal entrance zone at the narrowest segment of the root sleeve anteriorly by disc protrusion and uncovertebral osteophytes and posteriorly by superior articulating process, ligamentum flavum, and periradicular fibrous tissue.5 Decreased disc height, as well as age-related foraminal width decrease from inferior Z-

joint hypertrophy, may impinge subsequently on nerve roots. The cervical region accounts for 5-36% of all radiculopathies encountered. Incidence of cervical radiculopathies by nerve root level is as follows: C7 (70%), C6 (19-25%), C8 (4-10%), and C5 (2%). The most common cause of cervical radiculopathy is foraminal encroachment (70-75%). The cause is multifactorial, including degeneration of the discs and the uncovertebral joints of Luschka and the zygapophyseal joints. In contrast to lumbar spine disorders, HNP in the cervical spine is responsible for only 20-25% of radiculopathies. Cervical DDD most commonly is due to age-related changes, but the condition also is affected by lifestyle, genetics, smoking, nutrition, and physical activity. Degenerative disc changes observed on radiographs may reflect simple aging and do not necessarily indicate a symptomatic process. The disc begins to degenerate in the second decade of life. Circumferential tears form in the posterolateral annulus after repetitive use. Several circumferential tears coalesce into radial tears, which progress into radial fissures. The disc then disrupts with tears passing throughout the disc. Loss of disc height occurs with subsequent peripheral annular bulging. Proteoglycans and water escape through fissures formed from nuclear degradation, resulting in further thinning of the disc space. Vertebral sclerosis and osteophytic formation ultimately follow.6 IDD describes pathologic annular fissuring within the disc without external disc deformation. This disorder results from trauma-related nuclear degradation, cervical

flexion/rotation-induced annular injury, or whiplash. The innervated outer disc annulus serves as a major pain generator. DDD ultimately may progress to IDD. Clinical Manifestations: A cervical herniated disc will typically cause pain patterns and neurological deficits as follows: C4 - C5 (C5 nerve root) - Can cause weakness in the deltoid muscle in the upper arm. Does not usually cause numbness or tingling. Can cause shoulder pain. C5 - C6 (C6 nerve root) - Can cause weakness in the biceps (muscles in the front of the upper arms) and wrist extensor muscles. Numbness and tingling along with pain can radiate to the thumb side of the hand. This is one of the most common levels for a cervical disc herniation to occur. C6 - C7 (C7 nerve root) - Can cause weakness in the triceps (muscles in the back of the upper arm and extending to the forearm) and the finger extensor muscles. Numbness and tingling along with pain can radiate down the triceps and into the middle finger. This is also one of the most common levels for a cervical disc herniation C7 - T1 (C8 nerve root) - Can cause weakness with handgrip. Numbness and tingling and pain can radiate down the arm to the little finger side of hand.

Clinical management: The majority of herniated discs will heal themselves in about six weeks and do not require surgery. One study

found that "After 12 weeks, 73% of patients showed reasonable to major improvement without surgery." If pain due to disc herniation, protrusion, bulge, or disc tear is due to chemical radiculitis pain, then prior to surgery it may make sense to try an anti-inflammatory approach. Often this is first attempted with non-steroidal anti-inflammatory medications (NSAIDs), but the long-term use of NSAIDs for patients with persistent back pain is complicated by their possible cardiovascular and gastrointestinal toxicity; and NSAIDs have limited value to intervene in tumor necrosis factor-alpha (TNF)-mediated processes. An alternative often employed is the injection of cortisone into the spine adjacent to the suspected pain generator, a technique known as epidural steroid injection[ Although this technique began more than a decade ago for pain due to disc herniation, the efficacy of epidural steroid injections is now generally thought to be limited to short term pain relief in selected patients only. In addition, epidural steroid injections, in certain settings, may result in serious complications. Fortunately there are now emerging new methods that directly target TNF. These TNF-targeted methods represent a highly promising new approach for patients with chronic severe spinal pain, such as those with failed back surgery syndrome. Ancillary approaches, such as rehabilitation, physical therapy, anti-depressants, and, in particular, graduated exercise programs, may all be useful adjuncts to anti-inflammatory approaches. Conservative Non-surgical methods of treatment are usually attempted first, leaving surgery as a last resort. Pain medications are often prescribed as the first attempt to alleviate the acute

pain and allow the patient to begin exercising and stretching. There are a variety of other non-surgical methods used in attempts to relieve the condition after it has occurred, often in combination with pain killers. They are either consideredindicated, contraindicated, relatively contraindicated, or inconclusive based on the safety profile of their risk-benefit ratio and on whether they may or may not help: Indicated 1. Patient education on proper body mechanics 2. Physical therapy, to address mechanical factors, and may include modalities to temporarily relieve pain (i.e. traction, electrical stimulation, massage) 3. Non-steroidal anti-inflammatory drugs (NSAIDs) 4. Oral steroids (e.g. prednisone or methylprednisolone) 5. Epidural (cortisone) injection 6. Intravenous sedation, analgesia-assisted traction therapy (IVSAAT) 7. Weight control 8. Tobacco cessation 9. Lumbosacral back support Contraindicated Spinal manipulation: A 2006 review of published research stated: "Contradictions in the literature exist in terms of the use of spinal manipulation in the management of disc herniation, with some authors advocating its usefulness, and others suggesting it is contraindicated." According to the WHO, in their guidelines on chiropractic practice, when there is a
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"frank disc herniation with accompanying signs of progressive neurological deficit", it is absolutely contraindicated. Inconclusive Non-surgical spinal decompression: A 2007 review of published research on this treatment method found shortcomings in most published studies and concluded that there was only "very limited evidence in the scientific literature to support the effectiveness of non-surgical spinal decompression therapy." Its use and marketing have been very controversial.
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Surgery Surgery should only be considered as a last resort after all conservative treatments (non-surgical therapy) have been tried, that did not alleviate the pain and heal the disc herniation. Surgery is indicated if a patient has a significant neurological deficit.The presence of cauda equina syndrome (in which there is incontinence, weakness and genital numbness) is considered a medical emergency requiring immediate attention and possibly surgical decompression. Regarding the role of surgery for failed medical therapy in patients without a significant neurological deficit, a metaanalysis of randomized controlled trials by the Cochrane Collaborationconcluded that "limited evidence is now available to support some aspects of surgical practice". More recent randomized controlled trials refine indications for surgery as follows:

The Spine Patient Outcomes Research Trial (SPORT) Patients studied "intervertebral disk herniation and persistent symptoms despite some nonoperative treatment for at least 6 weeks...radicular pain (below the knee for lower lumbar herniations, into the anterior thigh for upper lumbar herniations) and evidence of nerve-root irritation with a positive nerveroot tension sign (straight leg raisepositive between 30 and 70 or positive femoral tension sign) or a corresponding neurologic deficit (asymmetrical depressed reflex, decreased sensation in a dermatomal distribution, or weakness in a myotomal distribution) Conclusions. "Patients in both the surgery and the nonoperative treatment groups improved substantially over a 2-year period. Because of the large numbers of patients who crossed over in both directions, conclusions about the superiority or equivalence of the treatments are not warranted based on the intentto-treat analysis" The Hague Spine Intervention Prognostic Study Group Patients studied "had a radiologically confirmed disk herniation...incapacitating lumbosacral radicular syndrome that had lasted for 6 to 12 weeks...Patients presenting with cauda equina syndrome, muscle paralysis, or insufficient strength to move against gravity were excluded." Conclusions. "The 1-year outcomes were similar for patients assigned to early surgery and those assigned to conservative treatment with eventual surgery if needed, but the rates of pain relief and of perceived recovery were faster for those assigned to early surgery."

Surgical options include: Chemonucleolysis - dissolves the protruding disc[ IDET (a minimally invasive surgery for disc pain) Discectomy/Microdiscectomy - to relieve nerve compression Laminectomy - to relieve spinal stenosis or nerve compression Hemilaminectomy - to relieve spinal stenosis or nerve compression Lumbar fusion (lumbar fusion is only indicated for recurrent lumbar disc herniations, not primary herniations) Anterior cervical discectomy and fusion (for cervical disc herniation) Disc arthroplasty (experimental for cases of cervical disc herniation) Dynamic stabilization Artificial disc replacement, a relatively new form of surgery in the U.S. but has been in use in Europe for decades, primarily used to treat low back pain from a degenerated disc. Nucleoplast

Surgical goals include relief of nerve compression, allowing the nerve to recover, as well as the relief of associated back pain and restoration of normal function.