CHAPTER SYNOPSIS:

Cervical disc degeneration is a condition that can be a part of normal aging but is also associated with disease states such as neck pain and deformity. Disc degeneration can occur in a wide age-group, but it becomes more common with increasing age. Of the large group of people who have disc degeneration, only a subset has clinically meaningful symptoms. Disc degeneration can lead to axial neck pain, radiculopathy, and myelopathy, and may require surgical intervention. Clinical examination is the key to evaluating and determining surgical candidates. Ever more reliance on imaging modalities to show disc degeneration cannot substitute for good clinical assessment and judgment. Furthermore, the choice of surgical technique has grown significantly in recent years. This creates more need for better decision making and excellent technical skills.

IMPORTANT POINTS:

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  Disc degeneration by itself is not a disease state.

  
  
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  Disc degeneration that causes axial neck pain is usually treated without surgery.

  
  
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  Surgical treatment of axial neck pain secondary to disc degeneration has resulted in suboptimal success rates.

  
  
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  Disc degeneration can be the cause of radiculopathy or myelopathy and may present clinically with the combination of axial neck pain and neurologic compressive pathology.

  
  
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  Surgical treatment should decompress any neurologic stenosis and stabilize motion segments as necessary by either anterior, posterior, or combined approaches.

CLINICAL/SURGICAL PEARLS:

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  Spurling maneuver is an excellent examination for a physical sign of neuroforaminal stenosis.

  
  
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  Abduction relief sign often indicates a soft disc herniation placing tension on the affected nerve root.

  
  
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  Transverse skin incision can be used to access three disc levels just as easily as a longitudinal incision and yet be much more cosmetically appealing.

  
  
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  Good exposure results from good mobilization along the medial border of the sternocleidomastoid muscle.

  
  
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  The patient’s social and occupational situation can have a significant impact on the decision when choosing a surgical approach.

  
  
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  Whether anterior or posterior fusion surgery is chosen, multilevel segmental instrumentation leads to the most rigid construct and better fusion rates.

CLINICAL/SURGICAL PITFALLS:

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  Multilevel cervical corpectomy represents a significant biomechanical challenge. Attempts at stand-alone anterior instrumentation after multilevel corpectomy have a significant failure rate. Anterior cervical discectomy combined with fewer contiguous corpectomies can allow for additional fixation to avoid this issue. If multilevel corpectomy is necessary, concomitant posterior instrumentation should be considered.

  
  
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  Multilevel cervical laminectomy is now rarely performed because of concerns about postlaminectomy kyphosis. In the juvenile patient, postlaminectomy kyphosis is a serious concern and, therefore, is a contraindication to multilevel cervical laminectomy.

  
  
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  In multilevel posterior instrumented fusions, the screws at the most cephalad levels are most likely to lose bony purchase. Bicortical lateral mass screw fixation or extending the fusion should be considered.

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PATHOANATOMY

The cervical disc is mostly composed of collagen, proteoglycans, and water. The collagen network provides the structure, whereas the proteoglycans, with theirs hydrophilic properties, attract and maintain the water within the disc. Under normal conditions, the water holds the disc taut and assists in evenly distributing the forces applied to the annulus fibrosis and vertebral end plates. However, with age and degeneration, the proteoglycan content within the nucleus pulposus decreases, thereby losing its natural attraction to hold water and subsequently causing a loss of height and integrity of the disc. In addition, the outer part of the disc, the annulus fibrosis, also begins to change its composition. It is normally made up of concentric collagen sheaths, mostly type I and II collagen. With degeneration and time, the type II collagen is increasingly replaced with type I collagen, making it weaker and increasing the potential for microtrauma and ultimately tears.

Degenerative arthritis of the cervical spine has long been known to increase with advancing years. The severity of changes, even in asymptomatic individuals, has been shown to progress in a roughly linear pattern with advancing age. The pathophysiology of degenerative cervical disc disease involves a multitude of complex issues. Anatomically, it involves the disc, zygapophyseal facet joints, uncovertebral joints of Luschka, posterior longitudinal ligament, and ligamentum flavum. However, the underlying principle seems to stem from the loss of water content within the disc. This causes the loss of height of the disc and the loss of the natural cervical lordosis. In turn, the distribution of load is transferred to the facet and uncovertebral joints, resulting in inevitable arthritis. In addition, the vertebral end plates become sclerotic in response to the abnormal stresses it now experiences.

In the cervical spine, intervertebral discs are present between C2 and T1. The discs provide stability that helps to protect neural elements and maintain the normal alignment but also serves to provide motion. The viscoelastic property of the disc matrix acts as a shock absorber and spreads the forces applied to the motion segment more uniformly to the vertebral body end plates. Disc degeneration is characterized by the loss of this viscoelastic property, and the formation of end plate sclerosis and osteophytes that results from the increased load on the vertebral body. The height of the normal disc keeps the intervertebral (neural) foramen patent; therefore, loss of height is associated with foraminal stenosis. With disc degeneration, the disc loses its structural integrity, and bulges or herniates past its natural borders and impinges onto surrounding neural elements to cause either radiculopathy or myelopathy.

Although disc degeneration is clearly associated with disease, its presence does not directly correlate with disease. In fact, a large percentage of the normal asymptomatic population has degenerated discs. Disc degeneration, however, is more common with increasing age. Although the pathophysiology of disc degeneration is still poorly understood, genetic contributions are thought to be important. The genetics is not a simple Mendelian scenario; therefore, the presence of significant disc degeneration in a family member is not predictive.

HISTORY AND PHYSICAL FINDINGS

Degenerative disc disease of the cervical spine can present in a variety of ways including axial neck pain, radicular symptoms, or myelopathic symptoms. Axial pain can arise from either the disc itself or correlate with facet joint disease. The disc is innervated by the sinuvertebral nerve that extends nerve fibers to the annulus and longitudinal ligaments of the spine. Nerve fibers are not normally found in the nucleus pulposus. The localization of axial pain can be vague, and identifying the painful disc can be difficult even with advanced imaging. Axial pain can arise from arthritic changes within the five joints of the cervical spine: the anterior disc, the two posterolateral joints of Luschka, and the two posterior facet joints. In addition, the end plates can become sclerotic and cause pain. Biochemical signals that activate the inflammatory cascade and pain pathway may be important in pain generation. Axial pathology may also present as muscle spasms, stiffness, or even referred pain, such as headaches. Facet pain can produce a radiating pattern that can sometimes be mistaken for radicular symptoms. Typically, facet pain is worse with extension and loading the facet.

Radicular pain stems from the neck but presents with pain or paresthesias in the arms and hands. Radiculopathy is a disorder of the nerve root that can arise from mechanical or chemical irritation. The pain travels through the afferent pathways by activation of sensory fibers as they travel through the dorsal root. Compression or irritation of the nerve root may cause motor, sensory, or reflex deficits. The most commonly affected nerve roots are C5, C6, and C7. It is thought that this is due to higher degree of motion at the corresponding motion segments (C4-5, C5-6, and C6-7) and the fact that statistically these are the levels that are most commonly involved in spondylosis. Objective findings suggestive of radiculopathy include hyporeflexia in the biceps (C5), brachioradialis (C6), or triceps (C7); weakness or atrophy of the innervated muscle group; or pain or paresthesias along a dermatomal fashion. Provocative tests such as the Spurling maneuver, which induces root stretch and foraminal stenosis compression, are used to assist in the confirmation of the diagnosis. The Spurling maneuver is performed by axial compression of the head. It is considered positive if pain radiates into the ipsilateral limb in which the head is turned. This test is not sensitive (30%), but it is specific (93%) for cervical radiculopathy and, therefore, should not be used as a screening tool, but instead as a confirmation of the diagnosis. Another maneuver that can be used is the shoulder abduction relief test. In this maneuver, the radicular symptoms are relieved when the ipsilateral arm is elevated through abduction, so that the hand or forearm rests on top of the head. Relief of symptoms indicates that the problem stems from a cervical extradural compression of the nerve root.

Myelopathy arises from central canal narrowing that causes spinal cord compression. This must be differentiated from radiculopathy that is related to root compression and foraminal stenosis. Myelopathy can present in many different ways, but can manifest with symptoms of hand numbness and clumsiness, gait disturbance, and spasticity. Typical complaints from patients are that their hands do not work as well as they used to (difficulty with buttons and picking up coins), or that others have commented that their gait seems that of a drunk. Bowel and bladder disturbance is usually not a presenting complaint in early or mild myelopathy but can become important in the more severely affected individual. In the extreme, the patient can be wheelchair bound because of their poor gait. Myelopathy can be caused by disc herniation, end plate osteophytes, ossification of the posterior longitudinal ligament, and/or ligamentum flavum hypertrophy/redundancy, which occurs with loss of disc height.

Physical findings of myelopathy include hyperreflexia below the level of cord compression, the presence of Hoffman sign, inverted radial reflex, difficulty with tandem gait, and in some patients, intrinsic muscle wasting in the hands (myelopathy hand). The Hoffman reflex/sign is elicited by tapping or flicking the terminal phalanx of the third or fourth finger, and a positive response is seen with flexion of the terminal phalanx of the thumb. The Hoffman sign is not specific because a significant percentage of the normal population is positive for this test. The Babinski reflex, also known as plantar reflex, is a primitive reflex in infants. However, if seen in adults, it is referred to as the Babinski sign and is considered pathologic. It is elicited by using a blunt object to rub the lateral aspect of the plantar surface of the foot. If, in turn, the hallux extends upward and the other toes fan out, it is considered positive. The presence of this reflex represents a problem within the corticospinal tract. Although these physical findings are helpful in making the diagnosis, they are not diagnostic by themselves but have to be taken into context with the history and imaging findings.