Cervical Laminectomy 

Updated: Dec 10, 2018
Author: Lawrence S Chin, MD, FACS, FAANS; Chief Editor: Cristian Gragnaniello, MD 



Cervical spondylotic myelopathy (CSM) is caused by reduction of the sagittal diameter of the cervical spinal canal. Normally, the canal diameter in the subaxial cervical spine is approximately 17-18 mm in adults.

CSM may result from congenital or degenerative changes in the cervical spine. It is the most common cause of spinal cord dysfunction in adults older than 55 years, as well as acquired spastic paraparesis or quadriparesis in adults.[1, 2] Risk factors for CSM include cigarette smoking, frequent lifting, and diving.

The degenerative changes occur in the 5 articulations that comprise the cervical motion segment: the intervertebral disc, the two facet joints, and two false uncovertebral joints of Luschka. Normal aging of the spine results in loss of disc height, which in turns brings the uncovertebral joints into contact, thereby distorting the normal biomechanics. Consequently, osteophyte formation, ligamentum flavum hypertrophy, and facet/uncovertebral joint eburnation occur. Disc space collapse also causes a rostral-caudal translation, which in turn magnifies laxity of the joint capsules and ligamentum flavum with further degeneration.

Degenerative changes occur most commonly at C5-6 and C6-7. White and Punjabi classified these changes as “static” factors, a category that also includes congenital spinal canal stenosis (< 13 mm anterior-posterior diameter) and disc herniation. Dynamic factors, on the other hand, are those that exert abnormal forces (translation and/or angulation) on the spinal column during flexion and extension under normal physiological conditions.

Flexion can increase spinal cord compression in the presence of disc protrusions or vertebral osteophytes, which in turn causes stretching of the spinal cord. Extension can increase spinal cord compression by infolding of ligamentum flavum or facet joint capsules, which causes shortening and thickening of the spinal cord. The infolding may be exaggerated if there is simultaneous occurrence of loss of disc space height.

The natural history of CSM is one of progressive disability. Clark and Robertson asserted that, once the disorder was recognized, neurological function did not return to normal. CSM may also result from spinal cord ischemia caused by compression spinal arteries, arterial feeders, or obstruction to venous outflow.

A subset of pathologies may also lead to reduction of the diameter of the cervical spinal canal. These include spinal cord contusions secondary to trauma, intracanal (intradural, extradural, or intramedullary) neoplasia, syringomyelia, and hemorrhage (epidural or subdural). Spinal cord contusions, intramedullary neoplasia, and syringomyelia produce symptoms owing to their intrinsic nature within the spinal cord, frequently resulting in expansion of the spinal cord.


In general, posterior cervical laminectomy is reserved for patients with predominantly dorsal or circumferential compression, multilevel involvement, and a straight or lordotic spine.[3, 4, 5] Also, the standard cervical laminectomy does not require fusion, thus preserving motion segments that would be lost in an anterior cervical discectomy and fusion.

Patients who are unwilling to experience potential limitation to range of motion should be considered candidates for cervical laminectomy or foraminotomy.


Cervical laminectomy has no absolute contraindications. However, because of the risk of kyphosis due to loss of the posterior tension band, cervical laminectomy should be avoided in patients with a preexisting kyphosis, in children, and in those with significant ventral masses that may cause cord compression if kyphotic deformity develops. In children and those with kyphosis, strong consideration should be given to the addition of instrumentation and fusion.[6] Likewise, those with ventral masses should undergo a ventral decompressive technique with or without concomitant laminectomy.

Technical Considerations

Procedure Planning

Imaging aids in the diagnosis and treatment plan. It may include plain radiography, MRI, and CT scanning with or without myelography.[7]

Plain radiography includes anteroposterior (AP), lateral, flexion/extension, and oblique views. AP and lateral views allow for evaluation of alignment (scoliosis, kyphosis, lordosis). In addition, lateral views demonstrate the amount of disc space narrowing, osteophyte formation, reduction in AP canal diameter, and possibly ossification of the posterior longitudinal ligament. Flexion/extension views are used to evaluate for translation and angulation abnormalities, which can aid in deciding between surgical approaches. Oblique views provide information about foraminal narrowing, especially in the setting of uncovertebral joint spurring.

MRI aids in evaluating the soft tissues, intervertebral disc, and spinal cord itself. Parenchymal changes such as myelomalacia and syrinx formation are easily identified.

CT imaging assists in evaluating the bony anatomy, especially if surgical instrumentation is required for stabilization. CT myelography is largely reserved for patients who cannot undergo MRI because of anxiety or concomitant presence of non-MRI–compatible metallic implants.

T2-weighted sagittal (left) and axial (right) MRI T2-weighted sagittal (left) and axial (right) MRI of the cervical spine demonstrating intervetebral disc herniations at the C5-6 and C6-7 levels, associated with posterior ligamentum flavum hypertrophy and bilateral neural foraminal narrowing secondary to facet hypertrophy
T2-weighted sagittal (left) and axial (right) MRI T2-weighted sagittal (left) and axial (right) MRI of the cervical spine demonstrating bilateral neural foraminal narrowing secondary to facet hypertrophy at the C5-6 level without significant central canal compromise


Aside from direct spinal cord or nerve root injury, the most common neurological deficit following laminectomy is C5 (most commonly) or C6 nerve root irritation causing motor weakness, which has been reported in up to 13% of cases.[8, 9] The exact cause is unknown but may relate to indirect tension on these nerve roots after a generous decompression. The mean recovery for these patients was 5.4 months and involves physical and occupational therapy.

Delayed kyphosis following laminectomy may occur in up to 21% of cases.[10, 11] Careful patient selection and surgical techniques reduce this complication. Proponents of laminoplasty or laminectomy with posterior instrumentation and fusion believe kyphosis can be reduced using these techniques.[12]

Infection and wound breakdown may be more common with laminectomy than with ventral procedures, primarily because of reduced mobilization, poor wound care and personal hygiene, and pressure on the incision while lying supine. Its incidence can be reduced by perioperative antibiotic use, sterile surgical site preparation, and technique, as well as appropriate wound care and hygiene.

Other complications include epidural hematoma formation, unintended durotomy, and possible pseudomeningocele formation. About 1.3% of patients develop postoperative epidural hematomas, which may be large enough to cause spinal cord compression and neurological deficits.[13] The risk can be reduced by meticulous hemostasis and leaving an epidural drain, when required.

Cerebrospinal fluid (CSF) leaks result from dural adherence to the ligamentum flavum or lamina or trapping of the dura inside the rongeur jaws. Careful surgical technique can minimize its occurrence, but, when present, it is preferable to close the durotomy with primary suture with or without graft material. Patients may be postoperatively placed on absolute be rest for 48 hours or more and then allowed to gradually mobilize.

Pseudomeningoceles are delayed sequelae of having a durotomy with resulting continuous CSF drainage. The management of these can be difficult, especially when the patient has delayed wound healing secondary to comorbid conditions. While some can spontaneously resolve, in others, its treatment may require re-exploration of the surgical site with duraplasty and placement of a lumbar drain to divert CSF flow. In this scenario, the patient may be placed on extended absolute bedrest that may last up to 5 days postoperatively or longer.


Periprocedural Care

Patient Education & Consent

Patient Instructions

After surgery, patients should avoid strenuous physical activity and lifting more than 10-15 lbs (4-7 kg) for 4-6 weeks. Light aerobic activities and walking are strongly encouraged, as is normal mobilization of the neck to reduce cervical muscle spasm.


Standard cervical laminectomy equipment includes self-retaining retractors, osteotomes, high-speed handheld drills, rongeurs, and punches. Although not always required, surgical loupes and microscopes can be used to aid in visualization and improved illumination.

Patient Preparation


The principal danger from an anesthesiologist’s standpoint is injury to the spinal cord due to either ischemia caused by blood pressure changes or direct compression of the cord during manipulation, such as intubation. Consequently, the severity of spinal cord compression should be determined preoperatively. This is especially true in patients who have a severe spinal cord injury and loss of spinal cord blood flow autoregulation. In this situation, any drop in blood pressure will cause a corresponding loss of spinal cord perfusion pressure and possible spinal cord infarction.

Patients with significant pathology may require awake tracheal intubation. In this setting, the patient can be tested for motor function before and after intubation. For others, careful manipulation during intubation is still important, and video laryngoscopes may be used. A useful adjunct to cervical spine surgery is electrophysiology neurological monitoring (EPS), which can include somatosensory evoked potentials (SSEP), motor evoked potentials (MEP), intraoperative electromyographic responses (EMG), nerve action potential monitoring, and direct spinal cord stimulation.

Although false-positive and false-negative results are well known with EPS, they can provide useful information in selected cases. In these patients, baseline SSEPs should be documented prior to positioning the patient, and choice of induction agents and muscle relaxants is critical to allow for recording of reliable signals. Clear communication between the surgeons, anesthesiologist, and EPS technicians is critical.

Succinylcholine should be avoided in patients with denervation injury, as it can cause acute hyperkalemia. Newer muscle relaxants such as vecuronium and rocuronium are suitable alternatives.


Posterior cervical laminectomies are most frequently performed in the prone position and less frequently in the sitting position.

Prone position

After the patient is anesthetized in the supine position, the head is secured with a skeletal head holder before turning into the prone position. Alternatively, a horseshoe or soft head rest can be used, but rigid fixation is preferred in most cases. The endotracheal tube must be firmly secured and the eyes appropriately lubricated, with the eyelids closed and protected. If used, electrophysiology neurological monitoring is placed and baseline potentials are obtained.

The patient is then turned into the prone position onto chest rolls or a chest frame. It is important that the longitudinal axis of the spine is maintained throughout this process. Hyperextension or hyperflexion must be avoided. The patient’s chin is inspected to ensure it is free from compression, and the breasts are medially displaced to prevent pressure on the nipples. The groin, anterior superior iliac spine, and knees are appropriately padded, with the abdomen resting as free as possible to prevent venous compression, which can lead to worsened intraoperative bleeding.

Lower-extremity pulses should be checked to ensure that the abdominal aorta and femoral arteries are not compressed. A padded roll is placed under the ankles so the knees are bent and feet suspended. The upper extremities are placed by the patient’s side in the neutral position (hands facing the patient and the thumbs down), with the elbows and hands padded. The shoulders may be taped to afford adequate spinal visualization, especially during radiographic confirmation of the operative level. The head is then firmly immobilized via attachment to the bed frame.

The most common complications in the prone position are nerve palsies and compression injuries due to inappropriate positioning, exaggerated limb stretch, and inadequate padding. Simple padding with cushions, sheets, blankets, or egg-crate padding will prevent their occurrence. Brachial plexus injuries can result from excessive downward traction of the shoulders for radiographic visualization. In this case, judicious traction and removal of the tape after radiographic visualization will reduce the risk of injury.

Sitting position

Owing to the higher incidence of venous air embolism (VAE), hypotension, and the discomfort experienced by the surgeon due to maintaining an extended position, the sitting position is less frequently used today.

After the patient is anesthetized in the supine position, a right central venous or atrial catheter and precordial Doppler ultrasonic system are placed. If used, electrophysiology neurological monitoring is placed and baseline potentials obtained. The head is then secured with a skeletal head. The endotracheal tube is firmly secured and the eyes appropriately lubricated, with the eyelids closed and protected.

The surgical table is then gradually brought into the sitting position, with the knees slightly flexed to prevent nerve stretch injury. The heels and gluteal areas should be appropriately padded. The upper extremities are placed in front of the patient’s body and secured with padding at the elbows and hands. The head is then firmly immobilized via attachment to the bed frame.

The most dangerous complication in the sitting position is that of a VAE. Dehydration or blood loss leads to decreased central venous pressures, increasing the risk. Patients with a patent foramen ovale or right-to-left shunt are at an increased risk. VAEs are thought to arise from air that enters noncollapsible veins, dural sinuses, or diploid veins.

VAE causes pulmonary constriction and hypertension with reduction in peripheral resistance, a gradual fall in cardiac output, and subsequent arrest. The use of precordial Doppler ultrasonic systems, right central venous or atrial catheters, and transesophageal echocardiography (TEE) can help early detection of VAEs. TEE and Doppler are the most sensitive in detection, while treatment includes aspiration of the air through the right atrial catheter, discontinuation of nitrous oxide, and administration of pure oxygen. Bone wax, electrocautery, and full-field irrigation should be used to seal possible portals of air entry. Repositioning the patient in the left lateral decubitus position may further facilitate air removal.

Monitoring & Follow-up

Postoperatively, patients are evaluated for adequate wound healing and improvement in preoperative function. At this time, it is important to observe for the redevelopment or worsening of symptoms or neurological function, as well as to monitor for the delayed development of kyphosis.

Owing to paraspinous muscle stripping, patients experience more pain in the immediate postoperative period than preoperatively. For this reason, patients are usually advised preoperatively regarding the likelihood of increased immediate postoperative incisional pain and muscle spasm. Postoperative pain control usually involves a combination of narcotic analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), and muscle relaxants.

A cervical collar is usually not prescribed, although some patients report that a soft cervical collar helps with maintaining support and decreasing pain.



Cervical Laminectomy

After the patient is positioned, the operative site is radiographically localized. The proposed midline incision site is marked and the surgical field prepared and draped. The incision site is infiltrated with 1% lidocaine mixed with 1:100,000 epinephrine.

A midline incision is made with a No. 10 scalpel and the dorsal spine approached through the subcutaneous tissue along the avascular ligamentum nuchae using monopolar cautery. Self-retaining retractors are used throughout to ensure adequate visualization. The paraspinal muscles are stripped from the spinous processes using a subperiosteal technique down along the laminar to the edge of the facets either bluntly or with monopolar cautery. This may be performed either bilaterally (laminectomy) for circumferential disease or unilaterally (hemilaminectomy) for unilateral compression or foraminal narrowing. If C2 is not included in the decompression, it is recommended that its muscle attachments remain to provide upper cervical stability.

Following adequate exposure and hemostasis, the levels to be decompressed are accurately radiographically localized. Many techniques can be used to perform a laminectomy, and surgical loupes or a microscope may be used at any time during the procedure. The conventional approach involves rongeurs (Leksell, Adson, Kerrison) to remove the spinous process and laminae, although this process requires that a portion of the rongeur (footplate) be placed between the laminae and dura. This should be carefully monitored, particularly in patients with severe stenosis.

An alternative method involves incising the interspinous ligament and using a high-speed drill to create a trough bilaterally at the facet-lamina junction. The trough is carried down to the inner cortical margin of the lamina. Care should be taken to prevent accidental damage to the dura with the drill. The thin inner cortical margin is then removed with a 1- or 2-mm Kerrison rongeur. The laminae with the spinous process attached are then removed en bloc. It is important to perform this process delicately, as the dura may be inadvertently attached to the ligamentum flavum and laminae. For a hemilaminectomy, this process is carried out ipsilateral to the pathology.

Any remaining ligamentum flavum is removed. Lateral decompression of the nerve roots may then be performed with a Kerrison rongeur. Not more than 50% of the facet should be removed to prevent joint instability. A more extensive foraminotomy to laterally decompress the exiting nerve root will require additional removal of the superior and inferior facet complex.

Bleeding points from bone are most effectively controlled with bone wax. Epidural venous bleeding may be difficult to control because access is often limited by the thecal sac, nerve root, and facet complex. Bipolar coagulation can be used when there is clear visualization, and it may be helpful to judiciously remove bone to see the bleeding vein. Otherwise, the bleeding must be controlled with cottonoid patties followed by placement of a topical hemostatic agent.

Surgicel (oxidized cellulose) and Gelfoam (Gelatin) act through chemical and direct contact activation of the clotting cascade. Other useful materials include Avitene (collagen fibers) and preparations of gelatin mixed with thrombin such as Floseal and Surgiflo. With any topical agent, the potential for swelling and spinal cord or nerve root compression must be considered.

After adequate decompression and hemostasis is achieved, the operative site is generously irrigated with saline or lactated ringers solution, with or without antibiotics. When the dura is opened, antibiotics are avoided. The incision is then closed in layers and the skin secured with sutures, staples, or skin adhesive.