Abstract
Spinal stenosis of the cervical spine refers to pathologic narrowing of the central spinal canal that can lead to symptoms of cervical myelopathy. The most common causes are congenital stenosis and spondyloarthritic stenosis (degenerative). In advanced cases of cord involvement, patients can present with myelopathic symptoms of unsteady gait, leg heaviness, lower and upper extremity weakness (i.e., loss in hand dexterity), limb numbness, urinary incontinence, and sexual dysfunction.
Keywords
Cervical myelopathy, cervical spinal stenosis, cervical spondylotic myelopathy
| Synonyms | |
| |
| ICD-10 Code | |
| M47.12 | Other spondylosis with myelopathy, cervical region |
| M47.812 | Spondylosis without myelopathy or radiculopathy, cervical region |
| M48.02 | Spinal stenosis, cervical region |
| M48.03 | Spinal stenosis, cervicothoracic region |
Definition
Spinal stenosis of the cervical spine refers to pathologic narrowing of the central spinal canal that can lead to symptoms of cervical myelopathy. The most common causes are congenital stenosis and spondyloarthritic stenosis (degenerative). The most prevalent type of congenital spinal stenosis is due to presence of short vertebral pedicles that produces an abnormally narrow spinal canal. Congenital stenosis may also be associated with developmental disorders such as achondroplasia, Arnold-Chiari malformation, Klippel-Feil syndrome, Morquio syndrome, or trisomy 21 (i.e., Down syndrome). The main contributing factors in development of the acquired type are the degenerative, hypertrophic, age-related changes that affect the intervertebral discs, facet (zygapophyseal) joints, and uncovertebral joints, as well as the ligamentum flavum ( Fig. 7.1 ). On radiologic imaging, these degenerative changes are present in 25% to 50% of the population by the age of 50 years and in 75% to 85% by 65 years. Some of the other factors that may contribute to pathologic narrowing of the spinal canal include degenerative spondylolisthesis, ossification of posterior longitudinal ligament (OPLL), large disc protrusion or extrusion, and atlantoaxial subluxation, or atlantodens pannus formation as seen in rheumatoid arthritis. Rarely, it may be secondary to such extramedullary pathologic processes as primary spinal neoplasm, metastatic disease, abscess, and trauma. Aside from age, other demographic factors do not contribute significantly to the development of cervical stenosis ; although OPLL was once considered specific to Asians, it has since been well documented in white and other non-Asian populations.
Symptomatic spinal cord compression, or cervical myelopathy, commonly occurs at the cervical levels C5–C7, given the relatively increased biomechanical segmental mobility of these segments and its resultant degenerative “wear and tear.” Concomitant compression of the exiting cervical nerve root(s) is typically observed in cervical spondylotic disease due to associated narrowing of neural foramena. Symptom production can occur by continuous, physical compression of the neural elements or be of an intermittent, dynamic nature as seen with extremes of cervical flexion and extension. Chronic pathologic spinal cord insult can lead to local cord ischemia with subsequent development of cervical myelopathy. Patients with congenital spinal stenosis will tend to present earlier in life because there is less room for accommodation of spondylotic hypertrophy.
Symptoms
Symptomatic presentation of cervical spinal stenosis can be variable and nonspecific, depending on the extent and type of pathologic process and the cervical levels involved. Axial neck pain can develop secondary to degenerative disc disease and zygapophyseal joint arthritis. Patients with cervical foraminal stenosis may complain of radicular arm pain, as well as of paresthesias, dysesthesias, numbness, and weakness of the upper extremity. In advanced cases of cord involvement, patients can present with myelopathic symptoms of unsteady gait, leg heaviness, lower and upper extremity weakness (i.e., loss in hand dexterity), limb numbness, urinary incontinence, and sexual dysfunction. Lower extremity pain is not a typical patient complaint unless concomitant lumbar spinal pathology is present.
Physical Examination
Patients with symptomatic cervical spinal stenosis present with upper or lower motor neuron signs on neurologic examination. Myelopathic gait is ataxic, wide-based, and stiff with a shortened stride. Lower motor neuron findings are seen in the upper extremities and can be bilateral or unilateral; these include muscle atrophy, diminished sensation, decreased reflexes, diminished muscle tone, and weakness. Upper extremity myelopathic findings, such as hyperactive reflexes, increased tone, and present Hoffmann sign, can also be observed in cases of upper and mid cervical spinal cord involvement. A Spurling sign (ipsilateral radicular pain on axial loading of an extended head rotated toward the involved extremity) can also be present. A well-documented feature of cervical spondylotic myelopathy is so called “myelopathy hand,” characterized by wasting of intrinsic and extrinsic hand muscles, loss of power of adduction and extension of the ulnar two to three digits, and inability to rapidly grip and release. Myelopathy hand is demonstrated by the hand grip-and-release test, which measures alternating closed-fist and full finger extension movements (normal result is 20 times in 10 seconds); the finger escape sign is tested with fingers fully extended and adducted, noting a tendency for ulnar digit spread. Lhermitte sign, an electric-like sensation that the patient reports radiating down the back and often into the limbs when the neck is flexed, can sometimes be elicited.
Lower extremity examination is more consistent with upper motor neuron findings in the presence of cervical myelopathy. Exaggerated reflexes, Babinski sign, sustained or unsustained clonus, spasticity, leg weakness, decreased tactile and vibratory sensation, impaired proprioception, and neurogenic bowel or bladder can be seen.
Functional Limitations
The functional limitations depend on the extent of neurologic involvement. A person with mild symptoms can still be completely independent with activities of daily living, mobility, household chores, and work duties. In some cases, pain and weakness can produce various degrees of disability in self-care, such as grooming, bathing, and dressing, as well as in more physically demanding functions, especially in the community setting, such as lifting, carrying, and ambulation. Bowel and bladder incontinence, as well as abnormalities of mood and sleep, can further lead to social isolation and an increased level of actual and self-perceived disability. In extreme cases, paraplegia and quadriplegia can limit nearly all functional activities.
Diagnostic Studies
The initial modality of choice are cervical spine x-rays that can assess the extent of disc space narrowing, facet and uncovertebral joint arthropathy, neuroforaminal osseous stenosis, atlantodens anatomy, and presence of spondylolisthesis. Standard x-ray request should consist of anteroposterior, lateral, oblique, and open mouth views. If dynamic instability is suspected, flexion-extension views are also advised. Cervical myelography can provide additional information on the behavior of neural elements during flexion and extension but has been largely supplanted by less invasive techniques. Magnetic resonance imaging (MRI) has become the modality of choice in assessing the extent of central and neuroforaminal stenosis due to both osseous and soft tissue pathologies ( Fig. 7.2 ). An upright dynamic MRI is able to provide the same functional information as myelography during neck flexion and extension without the need of intrathecal contrast injection; however, this imaging option is not widely available ( Fig. 7.3 ). Somatosensory evoked potentials can confirm the presence of myelopathy, and electromyography can confirm peripheral nerve root involvement.
Several radiologic criteria exist to define what constitutes significant stenosis of the cervical spine. The normal anterior-posterior dimension of the spinal canal at C3 through C7 is 16 to 18 mm. Neck flexion reduces canal diameter by 2 to 3 mm, whereas extension may decrease it up to 3.5 mm at 45 degrees due to ligamentum flavum infolding. According to some sources, an absolute cervical spinal stenosis is present when the sagittal spinal canal diameter is less than 10 mm, and relative spinal stenosis is present when this measurement is 10 to 13 mm. A Torg ratio of less than 0.8, which is measured on cervical x-rays by dividing the sagittal diameter of the spinal canal by the sagittal diameter of the respective vertebral body, has been used to predict the presence of significant spinal stenosis and tries to eliminate any inherent radiographic measurement errors. However, MRI allows more precise assessment of the spinal cord itself and the functional capacity of the surrounding subarachnoid space. Several studies have demonstrated a poor correlation between Torg ratio and extent of stenosis identified on MRI.
Diffusion-weighted sequences, in particular a technique known as diffusion tensor imaging, allow for the visualization of specific nerve tract bundles and may detect early damage to the myelin sheath. Although its utility in imaging the spinal cord is currently limited, diffusion tensor imaging has demonstrated enhanced sensitivity for detecting early cervical spondylotic myelopathy and intramedullary lesions. The presence of intramedullary signal abnormalities warrants further investigation and a more aggressive treatment approach (see Fig. 7.3 ). Computed tomographic myelography continues to offer some advantages over MRI, including superior spatial resolution, ability to distinguish bone from soft tissue intrusion into the cervical foramina, and dynamic visualization of contrast flow.
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