Cervical Stenosis: Myelopathy

Published on 11/04/2015 by admin

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Last modified 22/04/2025

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25 Cervical StenosisMyelopathy

Introduction

Cervical spondylotic stenosis is the number one cause of myelopathy in patients over the age of 55.1 For this reason, the spine surgeon focusing on the care of the aging population must be adept in understanding the clinical presentation of cervical myelopathy and correlating these changes to the radiographic studies available. After this careful review, the appropriate management can be discussed with the patient as it relates to his or her overall medical health.

Axial neck pain and symptoms related to cervical stenosis are among the most common complaints of the elderly patient to the spinal surgeon. The cervical spine holds the formidable task of transferring the structural load of the fixed occiput to the relatively fixed thoracic spine. It does so while concurrently allowing a significant degree of motion in all three planes. This delicate balance between structural integrity and flexibility accounts for the significant degree of degenerative changes that occur as the spine ages.

Degenerative changes that begin in the cervical disk lead to a cascade of changes in the bony and soft tissue anatomy of the cervical spine. The disk height is diminished, and intrinsic changes in the disk prevent the natural distribution of axial and rotational forces.2 These unnatural increased forces at the vertebral endplates, uncovertebral joints, and facet complexes lead to the formation of peripheral osteophytes that can diminish the diameter of the canal. Through repeated cycles of flexion and extension, the spinal cord can be stressed against these osteophytes. Posterior to the spinal cord, degenerative changes can lead to reactive hypertrophy of the ligamentum flavum as well as facet arthropathy.2 Extension of the cervical spine can lead to buckling of the posterior ligaments and further compression on the spinal cord.3 The situation is further exacerbated in individuals with a congenitally narrowed spinal canal.3 The average cervical spinal canal diameter on plain x-ray is 17 mm.4 The diameter of the spinal cord itself, on average, is measured at 9 mm, while the CSF space and ligaments that surround the spinal cord are averaged at 4 mm. Patients are often thought to become symptomatic from cervical stenosis with diameters less than 13 mm.5

The pathophysiology of cervical myelopathy is still under investigation. Pathologic analysis of the injured cervical spinal cord reveals a flattening and indentation of the cord. These changes are most directly seen in the dorsal and lateral columns.1 There is evidence to suggest that ischemic changes are the direct cause of the injury seen in the cervical spinal cord.3 In severe cases of myelopathy, necrosis and cavitations are seen in the central spinal gray matter as well. Demyelination changes are also evident in the lateral columns at the level of compression, with further demyelination changes in the caudal corticospinal tract.1 Furthermore, the cervical spinal cord between C5 and C7 is a watershed region and is acutely sensitive to any changes in vascular flow. Compressive forces that affect the delicate radicular arteries, anterior spinal artery, and dorsal spinal artery at these levels can lead to the central necrosis of the gray matter that is seen with myelopathy.1

The symptoms of cervical spondylotic myelopathy can be varied and subtle. A thorough history and a sensitive physical examination are as essential as the radiographic data. Initial signs of spinal cord injury often manifest in the lower extremities.4 These symptoms include fatigue and subjective weakness in the legs as well as a worsening sense of imbalance and gait difficulties. Symptoms often progress to the upper extremities and manifest as difficulty manipulating objects with the fingers and loss of manual dexterity. Bowel and bladder dysfunction is a variable symptom, and its prognostic indication remains unclear. Pathologic reflexes and other symptoms of upper motor neuron injury are common, including increased tone in the extremities with associated hyperreflexia, clonus, and positive Hoffman and Babinski signs. In severe cases, abnormal sensory changes can also be appreciated.

Cervical spondylosis is considered the most common progressive degenerative disease of the cervical spine. It is seen in 10% of patients by the age of 25 years and 95% of patients by the age of 65.1 Cervical spondylosis remains the most common cause of myelopathy in the aging individual, but there are numerous other causes that must be considered. Other causes of myelopathy include: ossification of the posterior longitudinal ligament, ossification of the ligamentum flavum, trauma, intrinsic/extrinsic tumors, compressive abscesses, or inflammatory disease processes including rheumatoid arthritis.3

Anterior and posterior decompressive procedures have been shown to be effective treatments in halting the progressive course of cervical myelopathy.2 A prospective multicenter nonrandomized comparison of operative and nonoperative treatment for cervical myelopathy with a mean follow up of 11 months revealed that patients treated with operative management had significant improvement in functional status and neurologic symptoms.6 Even with this information, patient selection for operative treatment of myelopathy remains key, as the natural history of the disease remains unpredictable.

Anterior approaches are often successful in treating focal anterior pathology such as a discrete cervical disk herniation. Although the anterior approach is safe and effective, there exist many potential risks that must be carefully understood. These risks include possible injury to the vascular structures (carotid and vertebral artery, jugular vein), neurologic structures (recurrent laryngeal nerve), and soft tissue structures (esophagus, trachea, lymphatic duct).4 Furthermore, the fusion that is performed after an anterior cervical discectomy/corpectomy will limit cervical mobility and can lead to accelerated degenerative changes at the end of the fusion construct.

Posterior cervical decompression for cervical stenosis is a safe and effective treatment option, but can also have increased risks in the elderly population. The procedure requires a significant degree of muscle division and reflection off the cervical spine. These muscles can have the propensity to become denervated or devascularized when retracted for the long procedure. This can lead to postoperative pain and spasm that can be persistently disabling in 18% to 60% of patients.7 The complete removal of the laminae, spinous process, interspinous ligaments, and a portion of the facets can have long-term negative effects on cervical sagittal balance.2 Iatrogenic destabilization of the cervical spine and postoperative kyphosis can be limited by lateral mass fusion of the cervical segments, but this procedure leads to extended operative time, increased blood loss, and restrictive motion.2 Furthermore, as discussed earlier, fusion can lead to adjacent segment degenerative changes.

By utilizing techniques developed for the posterior decompression of the lumbar spine, minimal access surgery can be performed in the cervical spine. The cervical microendoscopic decompression of stenosis (CMEDS) is a procedure that allows for bilateral posterior decompression of one to three cervical levels through a single 1.8 cm incision.8 By utilizing a unilateral approach, the contralateral musculature and ligaments are preserved, leading to less perioperative pain and increased stability of the posterior “tension band.” The limited studies in the use of this procedure have shown the potential for decreased blood loss, decreased length of stay, decreased use of pain medications, and preservation of normal cervical lordosis.7

Indications/Contraindications

The muscle-sparing techniques to decompress symptomatic cervical myelopathy hold key advantages in the elderly population. As with any surgery, the appropriate indications and patient selection are vital to favorable surgical outcomes. Most patients who are candidates for an open cervical decompression are candidates for a cervical microendoscopic decompression of stenosis (CMEDS). The primary indication for the CMEDS is clear radiographic evidence of cervical spondylosis with clinical evidence of myelopathy. Patients with a primary posterior pathology, hypertrophied ligamentum flavum, severe facet arthropathy, and hypertrophied cervical laminae are especially favorable candidates for surgery. Symptomatic anterior pathology at multiple levels due to moderate disk protrusion and disk osteophtye complexes are appropriate indications for surgery as well.

As described earlier, the natural course of cervical myelopathy remains unclear, but there appears to be a clear consensus that new onset of myelopathic symptoms or gradual worsening of myelopathic symptoms are indications for operative management. In regards to myelopathy of unknown duration, it is important to have a clear discussion with the patient regarding the uncertain nature of the natural history of the disease. Furthermore, it is important to discuss the effects of further worsening of myelopathic symptoms as well as the risks for any possible operative intervention. It is our opinion that surgical intervention should be strongly considered in these patients due to the devastating consequences of exacerbation of symptoms of cervical spondylotic myelopathy (CSM) and the low morbidity of the muscle-sparing posterior decompression.

Contraindications to the CMED would be similar to the contraindications for a posterior open cervical decompression of CSM. These contraindications would include primary anterior pathology with little evidence of posterior spondylotic changes. This would include patients with evidence of central disk herniation that may or not be calcified. Other disease processes that fit in this category include multilevel OPLL. Furthermore, clear preoperative evidence of cervical subluxation on flexion/extension plain films, or a significant degree of cervical kyphosis would be other contraindications for a muscle-sparing posterior cervical decompression. In both these disease processes, the need for surgical fusion of the cervical spine should be considered.

Operative Techniques

The patient is seen in the preoperative area and his symptoms and physical exam are reviewed to evaluate for any clinical changes. His incision is marked and he is brought to the operating room. At the discretion of the anesthesiologist, a fiberoptic intubation is often employed to minimize any risk to the stenotic cervical spinal canal. Prophylactic antibiotics are administered prior to beginning the procedure. The use of preoperative corticosteroids is an option. The patient is then prepared for neurophysiologic monitoring throughout the procedure with somatosensory evoked potentials, motor evoked potentials, and electromyography of the appropriate cervical roots. Neuromuscular relaxants are used sparingly to prevent any iatrogenic changes in the neuromonitoring through the procedure. A urinary catheter is usually not placed. The patient is maintained at normotensive systolic pressures throughout the procedure. If the patient has a history of hypertension or other significant cardiac risk factors, an arterial line is placed for continuous monitoring. The patient will ultimately be placed in a sitting position. Measures to detect and treat air embolism are options, including a central venous access line or a precordial Doppler.

After the airway and lines are secured, the patient is rotated 180 degrees away from the anesthesiologist. The patient is placed in a Mayfield fixation device and is positioned in the seated position. The head is slightly flexed to straighten the cervical spine, with the ultimate goal of having the spine directly perpendicular to the floor. We have found this positioning to be very effective in decreasing epidural bleeding and minimizing pooling of blood in the operative field. In patients with large shoulders or thin necks, the ability to visualize the entire cervical spine with fluoroscopy is improved in this position as well. All pressure points are padded, and the arms are draped over the patient’s lap. The neck is checked to prevent any hyperflexion, which can lead to obstruction of the airway or compromised venous drainage. In general, there should be at least two fingerbreadths distance from the chin to the chest. The C-arm is then positioned to achieve a true lateral image, with the arc swung either under the table or directly in front of the patient. The base of the C-arm is often placed ipsilateral to the side of the incision. The operative levels are identified and the skin incision is marked. The endoscope and monitor are checked to be in working condition. The monitor is placed above the patient or next to the patient’s head contralateral to the incision site. The monitor is placed directly in the line of sight for the surgeon so that he or she can comfortably manipulate the instruments while observing the monitor.

The patient’s posterior neck is shaved, scrubbed, and draped in the usual manner. Adhesive-lined drapes and an antibacterial adhesive layer (Ioban – 3M Health Care, St. Paul, MN) are used, as staples or metal stays will interfere with the fluoroscopy. The suction tubing, electrocautery, camera cables, and light source are passed and secured over the patient away from the field.

The operative level is rechecked by lateral fluoroscopic imaging with a sterile K-wire placed against the neck of the patient to approximate the level. The incision is 1.8 cm long running rostral to caudal and is 1.5 cm lateral to the midline. Local anesthetic is injected and the incision is made. The incision is opened to the cervicodorsal fascia under direct visualization, and the fascia is incised as well under direct visualization, to the size of the skin incision. The smallest tubular dilator is then introduced past the fascia and slowly docked against the rostral cervical lamina under fluoroscopic guidance. As the interlaminar space can be variable from individual to individual in the cervical spine, and as the ligamentum flavum is thinned out laterally, it is imperative to have precise control of the dilator as it spreads the dorsal cervical musculature. The dilator is carefully docked at the inferomedial edge of the lateral mass at the border of the lamina, and the positioning is reconfirmed with lateral fluoroscopy.

The tubular muscle dilators are serially inserted and the final 16-mm tubular METRx retractor is inserted and fixed in place to the table-mounted flexible retractor arm. The serial dilators are removed and the position of the retractor is confirmed by fluoroscopy. The 25-degree angled endoscope is then attached to the camera, white-balanced, and attached to the retraction tube via a cylindrical plastic friction-couple.

Upon initial view with the endoscope, there will be a layer of soft tissue and musculature over the lamina and lateral mass. A curette is used to carefully assess the bony anatomy under the soft tissue. The soft tissue is cleared away via monopolar cautery, bipolar cautery, and pituitary rongeurs over solid bone of the lamina. A small up-angled curette is placed under the inferior lip of the lamina, and the ligamentum flavum is carefully detached. A 1 or 2-mm bayoneted Kerrison punch with a small footplate is then placed under the lamina to begin the laminotomy.

The laminotomy is continued with the use of the Kerrison punch, or a drill with a fine cutting bit can be utilized medially where the ligamentum flavum is thickest. It is important not to dissect or detach the ligamentum flavum and to allow it to cover and protect the dura during the bony decompression. There should never be any ventral manipulation or pressure placed against the ligamentum flavum or the dura underneath. After the ipsilateral laminotomy is completed, the tubular retractor is “wanded” and angled 45 degrees off the midline to visualize the contralateral side. The up-angled curettes are once again used to carefully dissect the ligamentum flavum off the spinous process and contralateral lamina. At this point, we use a drill with a fine cutting tip with a guarded sleeve extended to protect the vulnerable soft tissue on the opposite side of bony drilling. The undersurface of the spinous process and the contralateral lamina are carefully and methodically drilled away to decompress the spinal canal. The drilling is continued up to the contralateral facet to provide for adequate bilateral decompression.

After the bony decompression is completed, attention is then turned to carefully dissecting a plane between the hypertrophied ligamentum flavum and the dura. Angled curettes are used to carefully dissect away the ligament from the dura, and 2-mm Kerrison punches are used to dissect off the ligament. The decompression continues until a pulsatile decompressed dura is visualized (Figure 25-2 ). Any further bony compression from facet hypertrophy or osteophytes off the adjacent lamina are carefully drilled or resected with the Kerrison rongeurs. A fine probe is used to assess the contralateral foramen to reassure that there is no compression of the exiting nerve root. The tube is then returned to its original position. Once again, through the use of angled curettes and Kerrison rongeurs, the hypertrophied ligament is carefully dissected away from the ipsilateral field. Any further bony compression from osteophytes or facets that are visible after removal of the ligamentum flavum is drilled away. The ipsilateral foramen is also tested to assure that no foraminal stenosis remains. The cleared dura should be pulsatile and fully decompressed. The field is then irrigated with antibiotic saline and hemostasis is achieved. The tubular retractor is detached from the retractor arm and is slowly removed. The removal is carefully observed on the monitor to confirm no arterial bleeding in the musculature that must be addressed while removing the retractor system. If a second rostral or caudal level is to be decompressed, the smallest tubular dilator is reinserted through the same cervicodorsal fascial incision and similarly docked to the level of interest, and the decompression is repeated.

For wound closure, the fascia is closed with absorbable sutures. Inverted absorbable sutures are used for the subcutaneous layer. A running subcuticular stitch is placed, and then Dermabond is applied. There is no dressing placed over the wound. The patient is returned to the supine position and is awoken and extubated. The patient is observed for 2 to 3 hours in the recovery area prior to being discharged home. If the patient has significant medical comorbidities, we elect to admit the patient and observe overnight prior to discharge. The patients are discharged with a prescription for an opioid/acetaminophen pain reliever as well as a prescription for a muscle relaxant as needed.

Complications and Avoidance

The major risk to any anterior or posterior surgery of the cervical spinal cord is injury to the spinal cord itself. There are two steps in the procedure where the risk of injury is highest. Careful attention must be paid during the initial serial dilation of the tubular retractors. Migration of the dilators between the interlaminar space would have disastrous consequences. For this reason, we do not recommend the use of the K-wire in this procedure. The fascia itself is incised under direct visualization and the smallest dilator is then used to localize the surface of the lamina/facet joint interface. The dilator must be advanced very carefully without any medial angulation to dock directly upon the border of the lamina and lateral mass.

The second high-risk step occurs during the decompression. Unlike in muscle-sparing lumbar decompression of stenosis, there can be no ventral compression of the ligamentum flavum or dura. It is important to use a curette to create a dissection plane between the ligaments and the ventral cervical laminae. After this is completed, the cervical lamina is drilled away to create more working room for the complete decompression.

Dural tears and CSF leak are a rare complication in cervical decompressive surgery. The ability to place a stitch into a small tear in the space provided through the tubular retractor can be very challenging. Treatment of a dural tear can be completed with a small piece of Duragen (Integra Lifesciences Corporation, Plainsboro, NJ) and a small drop of Duraseal (Confluent Surgical). With the removal of the Metrix retractor system at the end of the case, the muscles quickly return to their original position, leaving virtually no dead space for a pseudomeningocele to form.