Spinal stenosis is a condition in which the spinal cord and the nerve roots are compressed by a number of pathologic factors, leading to symptoms such as pain, numbness, and weakness. The upper neck (cervical) and lower back (lumbar) areas most frequently are affected, although the thoracic spine also can be compressed most frequently by a disk herniation. Three different anatomic sites in the spine can be affected by spinal stenosis. First, the central canal, which houses the spinal cord, can be narrowed in an anterior-posterior dimension, leading to compression of neural elements and reduction of blood supply to the spinal cord in the cervical area and the cauda equina in the lumbar area. Secondly, the neural foramen, which are openings through which the nerve roots exit the spinal cord, can be compressed as a result of disk herniation, hypertrophy of the facet joints and ligaments, or unstable slippage of one vertebral body relative to the level below. Lastly, the lateral recess, which is seen in the lumbar spine only and is defined as the area long the pedicle that a nerve root enters just before its exit through the neural foramen, can be compressed from a facet joint hypertrophy.  Depending on the level of the spine affected, each type of compression can lead to different symptoms that warrant a particular treatment modality.
In the cervical spine, stenosis can be caused by a combination of factors. Some individuals can have a congenitally narrowed spinal canal that is exacerbated by pathologic factors. Disk herniation together with the formation of osteophytic spurs, hypertrophy of the articular facets and ligamentum flavum, and ossification of posterior longitudinal ligaments can lead to central and foraminal stenosis. Structural factors such as subluxation from disk and facet joint degeneration and changes in the normal lordotic curvatures of the spine can lead to spinal compression. In the thoracic spine, disk herniation either from degenerative causes or trauma can lead to stenosis at specific levels. In the lumbar spine, hypertrophy of the facet joints and ligamentum flavum in the setting of disk herniation or spondylolisthesis can lead to worsening stenosis. Spondylolisthesis in the lumbar spine, defined as anterior subluxation of one vertebral body on top of another, is seen most commonly at L5 on S1 and L4 on L5. This can lead to compression of the nerve that exits below the pedicle of the anteriorly subluxed vertebra and results in neurogenic claudication.
Risk factors that lead to the development of spinal stenosis are multifactorial. There is a genetic influence as demonstrated in the study of twins. Cumulative trauma can lead to the progression of the disease. Osteoporosis can be a contributing factor. Cigarette smoking in several epidemiological studies has been shown to lead to back pain and degenerative spinal diseases. In the lumbar spine, obesity and loss of muscle tone can lead to stresses and dependence on the bony and ligamentous structures of the spine for structural support.
Many theories regarding the pathophysiology of spinal stenosis suggest a number of confluent mechanisms. The spinal cord can be directly compressed by osteophytic bones and ligamentous hypertrophy. Compression of local vascular structures can lead to ischemia of the spinal cord from arterial insufficiency and venous stasis. A herniated disk can exert repeated local trauma to the spinal cord or nerve root during repetitive flexion and extension movements, especially in the unstable spine with multiple levels of subluxations.
Initial evaluation of a patient with spinal stenosis often begins with a detailed history of symptoms and physical exam, with a focus on sensation, motor strength, reflexes, and gait. Stenosis in the cervical spinal can lead to radicular symptoms due to nerve root compression and myelopathy due to spinal cord compression. Radicular symptoms are dependent on the level affected, with the nerve root affected being the one that exists at that level. For example, a C5-6 disk herniation leads to a C6 radiculopathy. C6-7 disk herniation is the most common, leading to a wrist drop and paresthesia in the 2 and three fingers. C5-6 disk herniation is the next common, resulting in weakness in forearm flexion and paresthesia in the thumb and radial forearm. C7-T1 disk herniation can lead to weakness in the hand intrinsics muscles and numbness in the 4 and five digits. Lastly, a C4-5 disk herniation can lead to deltoid weakness and shoulder paresthesia. Patients also can experience pain and paresthesia in the head, neck, and shoulder. Cervical spondylotic myelopathy can be seen in patients with greater than 30% spinal narrowing, leading to gait disturbance, lower extremity weakness, and ataxia. Stenosis in the lumbar spine can lead to neurogenic claudication, myeloradiculopathic symptoms, sensory disturbances, motor weakness, and pathologic reflexes. Disk herniation is most common at the L4-5 and L5-S1 levels. A herniated disk at L5-S1 can lead to plantarflexion weakness, decrease sensation in the lateral foot, and cause pain in the posterior leg. A disk herniation at L4-5 can lead to a foot drop and numbness in the large toe web and dorsal aspect of the foot. Lastly, an L3-4 disk herniation can lead to knee extension weakness, numbness in the medial foot, and pain in the anterior thigh.
Diagnosis can be made through imaging with extended release x-ray, CT, and MRI. With the availability of MRI, a plain radiograph is of limited value although dynamic views in flexion and extension modes can demonstrate dynamic instability or spondylolisthesis. CT can help differentiate calcified disks or bone osteophytes from “soft disks,” differentiate ossification of the posterior longitudinal ligament from a thickened posterior longitudinal ligament and detect bone fractures or lytic lesions. MRI is the gold standard; it is able to show intrinsic cord abnormalities, the degree of spinal stenosis, and differentiate other conditions such as tumors, hematoma, or infection. If a patient has a pacemaker and cannot obtain an MRI, a CT myelogram can be performed to identify the level and degree of stenosis.
In patients who suffer from cervical stenosis without myelopathy, conservative management with bracing, rest, or anti-inflammatory medications initially can be employed. For those with myelopathy, surgical decompression can provide some relief from pain and sensory loss and can prevent the exacerbation of myelopathy. Depending on the levels involved and the pathology, an anterior or posterior decompression and fusion can be employed to relieve the compression and stabilize the spine. In the lumbar spine, initial management of back pain can be done with NSAIDs and physical therapy followed by interventional pain management strategies for persistent back pain. When conservative management is inadequate, or the patient develops progressive myelopathy, neurologic deficits, or spinal instability, surgical decompression and fusion are recommended. Depending on the nature of the pathology, a variety of approaches, including anterior, lateral, or posterior can be employed to restore lumbar lordosis, decompress the stenosis, and promote fusion.
Patients with spinal stenosis are often first encountered by the nurse practitioner, primary care physician, emergency department physician and internist. If the patients are asymptomatic, there is usually no treatment necessary. Patients with pain should be encouraged to participate in an exercise program, discontinue smoking and maintain a healthy weight. The few patients with nerve compression should be referred to an orthopedic or neurosurgeon. However, the primary care providers should educate the patient on potential complications of surgery, which can be disabling. For those who maintain a sedentary lifestyle, the quality of life is poor. (Level V)
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