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.  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. [2, 3] 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.  Likewise, those with ventral masses should undergo a ventral decompressive technique with or without concomitant laminectomy.
Imaging aids in the diagnosis and treatment plan. It may include plain radiography, MRI, and CT scanning with or without myelography.
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.
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.  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. [6, 7] 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. 
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.  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.