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Thursday, September 24, 2020




Of all the pathologic processes found in the cervical spine, cervical spondylosis is the most common (see Plates 1-12 and 1-13). It can be found to some extent in all humans as we age. Spondylosis starts with the normal degeneration of the intervertebral disc. As this occurs, the disc progressively loses the ability to maintain its water content. Disc dehydration and other molecular changes to the disc composition result in a decrease in disc height. With loss of disc height, its normal biomechanical characteristics change. As spondylosis progresses, osteophytes form ventrally and posteriorly and the uncovertebral and facet joints hypertrophy. This process occurs to some degree at every spinal functional unit, and it may result in neural compression. It is important to remember, however, that most people remain clinically asymptomatic during this process.

The initial pathologic process in the progression of cervical spondylosis is intervertebral disc desiccation. As is the case in other parts of the spine, when the anulus pulposus loses its hydration, the anulus fibrosis plays a larger role in the weight bearing of the disc. This results in several pathologic processes, all of which are interconnected. First, there is an increased frequency of disc herniations into the canal or foramen. Second, the ventral aspect of the spinal canal must bear an increased amount of force; and this may lead to loss of cervical lordosis and sometimes to kyphotic deformity. With continued loss of disc integrity, there is communication between the dorsal aspects of the vertebral body, which results in the formation of bone spurs (osteophytes), which then may decrease the space available for the spinal cord and cause myelopathic symptoms or may extend into the cervical foramina, causing radiculopathic symptoms (or a combination of the two myeloradiculopathy). The pathology of these entities is discussed next.



Cervical myelopathy is a result of encroachment on the spinal cord (see Plate 1-13). As just described, the process of cervical spondylosis results in a loss of spinal canal space by several processes. The first is the propensity for cervical disc herniation, which is caused by disc degeneration but can be aggravated by thickening, or hypertrophy, of the posterior longitudinal ligament. The other cause is encroachment by osteophytic processes that result from the communication of vertebral bodies or uncinate joints that lack cervical disc buffering. Osteophyte formation is postulated to be a protective mechanism of the spine to increase the surface area of each vertebral body to better distribute the normal forces of daily activity. Cervical myelopathy may result from one or both of these processes. It is a relatively common clinical entity and has significant effects on a patient’s quality of life. Additionally, preexisting myelopathy can significantly predispose a patient to serious spinal cord injury after only minor trauma.

Cervical myelopathy is a constellation of signs and symptoms resulting from spinal cord dysfunction. Patients with cervical myelopathy present a classic picture of “upper motor neuron” signs. They have difficulty with gait, balance, and fine motor coordination in the upper extremities, particularly in movements such as buttoning a shirt or tying one’s shoes. Weakness and stiffness of the legs is common, and urinary symptoms of urgency or retention are also possible in later stages. On examination, patients frequently have hyperactive reflexes below the level of the spinal cord compression (generally exacerbated in the lower extremities) and also may demonstrate pathologic Hoffman and Babinski signs. Motor testing may demonstrate weakness in any of the upper extremity muscle groups, depending on the severity and level of spinal cord compression. In advanced disease, the intrinsic muscles of the hand demonstrate impressive wasting (“myelopathy hand”). Lower extremity strength is variable, with proximal muscle weakness being more common than distal muscle weakness. Examination of gait is a valuable clinical tool, because patients with myelopathy often exhibit a stiff, spastic, or wide-based gait. The clinical phenomenon of “central cord syndrome” generally occurs when a patient with preexisting myelopathy sustains a hyperextension injury. These patients present acutely with upper greater than lower extremity weakness and sensory changes below the level of their injury. Urinary or fecal incontinence may also be present. The prognosis for central cord syndrome is favorable.

Observation of these signs and symptoms warrants MRI of the cervical spine and referral to a spine surgeon. A thorough imaging evaluation with radiographs and MRI provides adequate assessment of spinal alignment and the location(s), pattern, and degree of neural compression. Cervical myelopathy is a surgical disease in the majority of patients because it is usually progressive and, as such, neurologic deterioration may be permanent. The natural history of cervical myelopathy is periods of disease stability with intermittent, stepwise decreases in function. The goal of surgery is to halt disease progression, although some degree of functional recovery is often observed postoperatively.



When a cervical nerve root is inflamed or impinged at the level of the cervical foramen, cervical radiculopathy may occur. It most commonly occurs as a result of disc herniation in the younger patient or as a result of nerve root compression due to cervical spondylotic changes. Compression of the nerve root can result in pain, weakness, or sensory deficits that correspond to the dermatomal and myotomal distribution of the nerve itself.

Patients may present with acute or chronic cervical radiculopathy due to isolated nerve root compression. Patients with existing cervical myelopathy may also have a radicular pain component, termed cervical myeloradiculopathy. More than 90% of patients with cervical radiculopathy improve with nonoperative care. Examination of a patient with cervical radiculopathy includes a typical motor and sensory examination but also maneuvers intended to compress the nerve root or to relieve tension on the root and exacerbate or alleviate symptoms. This may include the shoulder abduction sign, in which the examiner holds the patient’s hand over the head to alleviate symptoms. The Spurling maneuver is a provocative test in which the head of the patient is turned to the side of the symptoms and axial pressure is then applied by the examiner (see Plate 1-14). This is thought to narrow the intervertebral foramen and exacerbate the patient’s symptoms. A “positive” Spurling sign is exacerbation of arm pain. It has been found to be very sensitive, although not specific for radiculopathy. Observation of the patient in late stages of the disease may demonstrate wasting of the intrinsic hand muscles if one of the lower cervical nerves is involved, but, unlike in cervical spondylotic myelopathy, the findings are unilateral.

Diagnosis of cervical radiculopathy is aided by a thorough review of plain radiographs (including oblique views), MR images, or a CT myelogram of the cervical spine. It allows appropriate visualization of the cervical discs and nerve roots and aids the clinician in preoperative decision making.


The decision to employ surgery for cervical myelopathy or radiculopathy requires a high degree of consideration of its risks, benefits, and preference of the patient. Surgical treatment of cervical myelopathy is less controversial given its positive effect on a patient’s quality of life and the well-known benefits of spinal cord decompression. The treatment of cervical radiculopathy depends on the etiology (disc herniation or foraminal narrowing) and on the number of affected nerve roots. Complicating the surgical approach is that these conditions often occur together, so surgery may be aimed at alleviating both myelopathy and radiculopathy in a single operation. An important distinction to remember between radiculopathy and myelopathy is the former is typically a nonoperative disease whereas the latter is a surgical one. That is, a radiculopathy usually responds very favorably to nonoperative care.

Anterior Approach to the Cervical Spine

One of the most common spine surgeries performed is the anterior cervical discectomy and fusion. Patients who have degenerative changes of the spine involving mainly the ventral aspect of the spinal cord or nerve root(s) are likely to benefit from this procedure. The surgery involves an incision just lateral to the midline of the neck, and a dissection lateral to the trachea and medial to the carotid sheath of the neck to approach the anterior cervical spine. From there, the prevertebral fascia is incised and the intervertebral disc is exposed and removed, as is the posterior longitudinal ligament. This exposes the ventral dura and exiting roots. This may be performed at one or multiple levels in the spine. An intervertebral graft (tricortical iliac crest autograft, cadaveric allograft, or synthetic cage) is used to replace the intervertebral disc to facilitate fusion of the adjacent vertebrae. The addition of an anterior cervical plate improves fusion rates and prevents graft dislodgment. Another option for ventral treatment of both radiculopathy and myelopathy is cervical disc replacement, which utilizes the same approach to the spinal column. Cervical corpectomy (removal of the central vertebral body) is indicated for spinal cord compression occurring behind the vertebral body or in cases of osteomyelitis or tumor.

Posterior Approaches to the Cervical Spine

For select patients with myelopathy or myeloradiculopathy, decompressive posterior surgery may be appropriate. Two common procedures are laminectomy with instrumented fusion and laminoplasty of the cervical spine. In both procedures, a midline incision is made in the neck and the overlying muscles are dissected from bone to expose the spinous processes and laminae. The laminae and spinous processes are either removed (laminectomy) or are altered to expand the cervical spinal canal (laminoplasty). There are multiple laminoplasty techniques.

Radiculopathy can be often treated posteriorly via a decompression of the foramen and lamina (laminoforaminotomy). These procedures are typically attempted at one or two levels, are performed unilaterally, and may offer significant symptomatic improvement to the appropriately selected patient.



Like all arteries, the vertebral artery consists of an intima, media, and adventitia. Whereas the term dissection is often applied to any vertebral artery injury, there exists a gradient of damage that is observed. A small intimal tear, for example, may have minimal, if any, clinical consequences. A true dissection of the vertebral artery refers to the creation of a tear through the intima allowing blood to enter into the arterial wall. The arterial pulsations result in a growing amount of blood in the arterial wall and lead to thrombosis. If blood ruptures through the wall entirely, a hematoma is created. This is known as a pseudoaneurysm, which may also be catastrophic if the lumen becomes occluded. The furthest end of the spectrum is vertebral artery transection, which is frequently fatal regardless of which vertebral artery is affected.

The vertebral artery is well protected by the transverse foramina between C6 and C1. This bony protection comes at a cost: whereas the bony ring of the transverse foramen prevents injury of the artery during low-energy trauma, fracture of the transverse foramen from a high-energy mechanism places the vertebral artery at risk of injury from bony impingement. The majority of patients found to have a vertebral artery dissection after blunt trauma have associated cervical spine trauma. Nontraumatic dissections are often spontaneous.

Much attention is paid to rare, but nonetheless important, causes of vertebral artery injury. These include chiropractic manipulation, contact sports, and yoga. There are several anatomic considerations that make these events more likely to occur. First, the vertebral artery is relatively susceptible to different forces at two points during its course. The first is between the atlas and the axis, where high rotary potential allows for the possibility that a forced, high-energy, high-velocity rotation may cause damage. This is what may occur during certain chiropractic manipulations. The other site is at the extraosseous (V3) segment where the vertebral artery lies in the sulcus arteriosus prior to piercing the dura on its course to the brain. At this level, the vertebral artery is truly unprotected by major bony landmarks, and activities causing prolonged hyperextension may result in vertebral artery damage. The effects of vertebral artery dissection are related to the neurologic structures that it sustains, and damage can occur via several mechanisms. Dissection or embolism can cause occlusion or diminished flow to the posterior circulation, creating vertebrobasilar insufficiency. Clinically, dizziness, ataxia, altered level of conscious- ness, and visual changes may be observed. Rarely, blood supply to the anterior spinal cord may be compromised if the anterior spinal artery (which arises from the vertebral artery) is affected. If the damaged vertebral artery is anomalous and feeds the posterior inferior cerebellar artery without joining to form the basilar artery, then lateral medullary syndrome (Wallenberg syndrome) can result. A constellation of symptoms results, including an ipsilateral Horner syndrome, facial numbness, and cerebellar deficits, as well as contralateral numbness below the neck.

If a vertebral artery dissection is suspected, the gold standard diagnostic tool is the angiogram. If angiography is unavailable or not clinically advisable, a CT- angiogram may be obtained. The treatment of a dissection ranges from medical treatment alone with anticoagulation and blood pressure support to endovascular stenting or surgical intervention depending on the type and severity of the pathologic process.



Locked facets (also known as “jumped facets”) are the result of spinal trauma and can occur unilaterally or bilaterally. The consequences of this distinction are significant because the resultant differences in treatment and outcomes diverge greatly. Bilateral locked facets are the result of traumatic hyperflexion injuries, and a majority of those patients presenting with bilateral locked facets are quadriplegic. Those with incomplete spinal cord injury have some potential for recovery, but the prognosis remains poor. There exists debate as to whether reduction should be undertaken closed (with traction) or open (using pins to distract the spine intraoperatively before surgical fixation). Unilateral locked facets are also the result of hyperflexion, but a component of rotational subluxation is implied (the rotation is thought to cause only a single locked facet). These patients tend to present with less severe findings of a neurologic examination and may be neurologically intact. Depending on the concurrent fractures present in the spine, these patients may ndergo closed reduction with a high rate of success.

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