Lumbar spinal stenosis is a condition that involves narrowing of the spinal canal, nerve root canals, or tunnels of the intervertebral foramina. This narrowing can cause pressure on, or compression of, the neural elements. Patients may be symptomatic despite minimal compression and conversely those with high degrees of compression may be asymptomatic.
Spinal stenosis represents a degenerative condition of the spine resulting in back pain and leg pain. Most cases of spinal stenosis can be managed conservatively, though some cases may need interventional treatments including injections and surgery for improvement in pain and preservation or restoration of neurological function.
The symptoms of spinal stenosis can be divided into two main categories: neurogenic intermittent claudication, and radiculopathy with or without radicular pain. Neurogenic intermittent claudication is a clinical diagnosis. Symptoms include buttock pain, pain radiating into the thighs or legs numbness, tingling, or cramping of the legs, difficulty standing or walking and low back pain. Unlike vascular claudication, the symptoms of neurogenic claudication improve with leaning forward, crouching, or sitting down. Bowel and bladder problems occur rarely.
Radiculopathy is defined as a neurological condition due to nerve root injury sufficient enough to cause objective signs such as weakness, sensation loss and loss of reflexes. Radiculopathy may or may not cause typical radicular pain. Radicular pain is often described as a sharp, burning pain that radiates in a dermatomal distribution. Radiculopathy and radicular pain can occur unilaterally or bilaterally.
Lumbar spinal stenosis can be inherited and acquired. Inherited causes are relatively rare compared to those that are acquired, presenting usually between the ages of 30 and 40. They include congenital lumbar stenosis, scoliosis, and achondroplasia, a condition that results in short, thick pedicles and a smaller spinal canal. The acquired conditions include degenerative, spondylolysis, spondylolisthesis, posttraumatic and iatrogenic causes.They usually present one to two decades later in life, compared to inherited spinal stenosis.
The degenerative process continues to affect all of us as we age. Despite this, not all individuals that develop canal stenosis are symptomatic. It has been postulated that either microvascular compromise of the cauda equina and/or an inflammatory response is required for the symptoms of lumbar spinal stenosis. Both venous congestion and/or arterial insufficiency are thought to lead to nerve root injury and play an important role in the development of intermittent claudication.
Along with mechanical compression, it is postulated that an inflammatory response plays a role in symptomatic patients. The presence of multiple biochemical mediators are hypothesized to lead to nerve root symptoms by way of excitation of the nociceptors, direct neural injury, nerve inflammation, and increased sensitization to pain producing substances.
Degenerative disc disease, facet arthropathy, spondylolisthesis, spondylolysis, herniated disc and discogenic pain should all be considered on the differential for lumbar spinal stenosis. Interestingly many of these diagnoses are contributors to the clinical picture of lumbar spinal stenosis. Other conditions, including sacroiliac joint dysfunction, myofascial pain, hip arthropathy, polyneuropathy, and vascular claudication should be considered and ruled out.
Lumbar spinal stenosis occurs in the low back, but despite the fact, low back pain typically is not the presenting complaint. The major complaint of these individuals is usually leg pain. To make the diagnosis of lumbar spinal stenosis, both clinical history of intermittent neurogenic claudication, and radiographic evidence of neural element compression, are necessary. Caution is advised when interpreting these imaging studies. It has been demonstrated that abnormal findings may be found in a large percentage of asymptomatic individuals.
Initially, standing AP/lateral X-rays may be taken to evaluate alignment of the spine and other bony defects, including fracture, tumor, inherited abnormalities, or degenerative changes. Flexion/extension films add a dynamic component that may show a spondylolisthesis that may not be seen with standing or supine imaging.
MRI is the modality of choice when evaluating the spine. It is noninvasive and can give bone and soft tissue detail, including disc, ligament problems, and nerve root impingement. CT scans can also provide good visualization of the central canal, lateral recess, neuroforamen, and other bony elements. CT scan with lumbar myelography, which is when a contrast medium is injected into the thecal space, can provide excellent imaging of the neural elements.
Electromyography (EMG) and nerve conduction studies (NCS) are helpful tools in the evaluation of spinal stenosis. They are felt to be complementary to MRI by increasing the overall specificity for lumbar spinal stenosis.
Nonsurgical treatments of spinal stenosis do not correct canal narrowing or revert the degenerative process. They can, however, provide long lasting pain relief and improve life function and overall quality of life. Studies have shown that nonoperative treatment of lumbar spinal stenosis is successful in a large percentage of patients.
Nonoperative treatment includes nonpharmacologic and pharmacologic interventions. Strict bed rest should be avoided as stiffness and deconditioning can occur. The use of a brace or corset may be helpful in improving walking distance and overall function, while decreasing pain scores.
Physical therapy can be helpful, with goals of managing the pain while improving overall function. Modalities including heat, cold and transcutaneous electric nerve stimulation and to decrease pain and increase soft tissue mobility. Physical therapy programs should be individualized to persons’ specific needs and address their deficiencies.
Epidural steroid injections should be considered if there is a limited response to noninvasive treatment. Unfortunately there is still a paucity of controlled studies evaluating the effectiveness of epidural injections. Overall there appears to be a favorable response in the treatment of radicular pain more so than axial low back pain. Corticosteroids are felt to inhibit inflammation and decrease edema or vascular congestion.
The goals of surgical intervention include improvement of pain and preservation or restoration of neurological function. The major indications for surgery include intolerable pain in activities of daily living, despite adequate nonoperative treatment, progressively limited walking distances or standing endurance and major neural deficits or an evolving or progressive neural change. There appears to be consensus that decompressive surgery is warranted to optimize the chance of recovery in individuals with cauda equina syndrome or progressive neurological deficit.