Lumbar Spinal Stenosis: Diagnosis and Treatment OptionsJoseph T. Alexander, M.D. IntroductionLumbar spinal stenosis is one manifestation of the general process of spinal degeneration that occurs with aging, and often becomes symptomatic in the seventh and eighth decades of life. Due to the increasing life expectancy of the population, more people are living to an age where this condition is likely to be symptomatic, so this problem is likely to become more common in years to come. Unfortunately, lumbar spinal stenosis continues to be misunderstood and under-diagnosed, and many patients are never offered effective treatment for their symptoms. The symptoms of lumbar stenosis are of two types, and both can be present in the same patient: neurogenic claudication due to central canal narrowing and radicular symptoms due to narrowing of the vertebral foramen. The diagnosis can be more difficult due to the frequent coexistence of other disease processes in this age group, such as degenerative arthritis of the spine, hip or knee, vascular claudication, peripheral neuropathy, and deconditioning of spinal musculature and ligaments. Although the diagnosis can be strongly suspected from the history and physical findings alone in many cases, non-contrast MRI now provides a confirmation in many cases, and routine myelography is no longer necessary. For patients who are persistently symptomatic despite adequate conservative care, surgery can offer an effective and lasting improvement in quality of life. AnatomyAn understanding of the relevant spinal anatomy is important in considering the pathophysiology, presentation and treatment of lumbar spinal stenosis. The intervertebral disc is composed of two parts. The nucleus pulposis forms the inner portion of the disc, and performs a role in cushioning as well as allowing for movement of the adjacent vertebral bodies in multiple planes. The annulus fibrosus forms the outer portion of the disc, and is composed of multiple layers of fibrous tissue arranged on a bias with one another. The annulus both contains the inner discal material as well as connecting and limiting the motion between adjacent vertebral segments. The outer fibers of the annulus blend with the fibers of the anterior and posterior longitudinal ligaments of the spine, and also are strongly attached to the bone at the margins of the disc through Sharpey's fibers. The central canal of the spinal column conveys the spinal cord in the cervical, thoracic and upper lumbar levels. In most individuals, the spinal cord ends by the L2 level; below this level the remaining lumbar and sacral nerve roots travel as the cauda equina. As a general statement, the nerve roots are more tolerant of chronic pressure than the spinal cord, which is why an individual may tolerate a higher degree of stenosis in the lower lumbar spine than in the cervical or thoracic region. The boundaries of the central canal vary with the level of the vertebral body. At the upper level of a vertebral body, the canal is bordered by the body itself anteriorly, the pedicles laterally, and the laminae posteriorly. This is the site that is affected in cases of congenital stenosis, where the pedicles are typically shortened. At the level of the intervertebral disc, the anterior border is formed by the annulus, the posteriolateral borders by the facet joints and capsules, and the posterior border by the ligamentum flavum. These are the structures that are most affected by degenerative processes. The spinal nerve exits the canal via the neural foramen. The nerve actually begins to divide from the thecal sac at the level of the intervertebral disc one segment higher than it exits. The nerve then traverses caudally in close proximity to the medial aspect of the facet joint and then the pedicle before turning laterally to enter the foramen. This space is referred to as the lateral recess. The foramen is bounded superiorly and inferiorly by the pedicles of the adjacent vertebral bodies, anteriorly by the annulus and posteriorly by the facet joint and its capsule. The nucleus pulposis has no vascular supply, and the cells that maintain the proteoglycan matrix are nourished by diffusion from the endplates of the adjacent vertebral bodies. The nucleus likewise has no innervation, so the disc proper does not cause pain. All of the surrounding structures are richly innervated, however, including the annulus, the facet joint and capsule, the periosteum, the interspinal ligaments, the dura and the epidural blood vessels. Degeneration or irritation of these structures causes inflammation and pain characteristic of osteoarthritis of the spine. PathophysiologyAlthough many details remain to be worked out, the basic processes of spinal deterioration are well understood. The intervertebral disc gradually degenerates throughout life, with a resulting loss of intervertebral height and bulging of the annulus. The biomechanical properties of the disc are compromised, which causes local (or "segmental") instability. In many patients there is a concomitant loss of tone in the abdominal and paraspinal musculature, both of which are important in the maintenance of spinal stability. These processes in turn cause increased loads on the facet joints, resulting in hypertrophy of the bone and capsular ligaments. Chronic stresses on the attachment of the annulus to the bone results in the deposition of calcium, which appears on plain radiographs as a "bone spur." There is often significant thickening of the interspinal ligaments, in particular the ligamentum flavum. The processes of annular bulging, bone spur formation, facet joint enlargement and ligamentous hypertrophy result in narrowing of the central spinal canal and the intervertebral foramen. In individual patients, these processes may occur in different proportions, so either the central canal, the foramen, or both can be affected. Although any lumbar spinal segment can be significantly affected by these processes, the L4-L5 segment is the most common, followed by the L3-L4 segment. Since the degenerative changes and narrowing are concentrated at the level of the disc, and the canal diameter is maintained at the level of the pedicles, a characteristic "wasp waist" appearance of the thecal sac develops which can be appreciated on imaging studies. (See Figure 1.)
Several different processes can narrow the intervertebral foramen. Bulging of the annulus and/or formation of bone spurs encroaches on the nerve anteriorly. Hypertrophy of the facet joint limits the foramen posteriorly. Narrowing of the interpeduncular distance and thus loss of the vertical dimension of the foramen can occur in the concave side of a scoliotic curvature or by loss of the intervertebral disc height. The dimensions of the spinal canal and foramen are not constant; rather, they are influenced by dynamic and postural factors. For example, when a person rises from recumbency to standing, the resulting axial load on the intervertebral disc causes further bulging of the annulus, which in turn further compromises the central canal and the foramen. There can also be overriding of the bony processes that make up the degenerated facet joint, which can impinge on the nerve in the lateral recess or the foramen. Finally, excessive lumbar curvature to compensate for thoracic, pelvic or leg length discrepancies can influence canal or foramenal dimensions. PresentationSpinal degeneration is ubiquitous in the human aging process. The resulting local inflammatory effects of osteoarthritis are largely responsible for the high prevalence of low back pain in the population. Spinal stenosis is not in and of itself responsible for low back pain. Virtually all individuals in their seventies have at least some degree of spinal stenosis on imaging studies, yet only a fraction of those individuals manifest the true symptoms of central and/or foramenal stenosis. It is important in the evaluation of patients with symptoms of back or leg pain to determine the contribution of the various forms of spinal degeneration to that patient's unique situation, so that an optimal treatment plan can be formulated. The first major symptom complex of spinal stenosis is that of neurogenic claudication. Patients characteristically have minimal symptoms while seated or lying down, even in advanced cases. Significant pain at night is not typically a part of simple spinal stenosis, and may point to other problems. Initially patients begin to notice a sense of heaviness or aching in the calves with extended walking or prolonged standing, which rapidly improves with sitting down. The distance of walking or time of standing to produce these symptoms gets progressively shorter, with a time course that is quite variable from patient to patient. Eventually, even standing for a very short time or walking a few steps produces intolerable discomfort. If allowed to progress to this stage, patients may report numbness and a sense that the legs will give way, although falls are relatively unusual. Rarely if ever do patients become "paralyzed;" instead they give up standing and walking due to pain than because of muscular weakness. Patients often report increased unsteadiness or loss of balance, and may have begun to use a cane for security. Patients universally report feeling better if they walk stooped forward, and will stereotypically describe increased walking tolerance in stores if they lean on a shopping cart. Bowel, bladder and sexual functions are generally preserved except in very advanced cases. The second major symptom complex relates to narrowing of the lateral recess or the neural foramen. Patients typically complain of severe radiating pain to the dermatomal area of the affected nerve. This pain can either begin suddenly after a physical event such as a fall or an accident, or can evolve gradually over a longer period of time with no clear inciting process. Since the lower lumbar nerves are most commonly affected, this pain generally extends into the thigh, calf or ankle, and is often described as an "electric current," a "hot wire," or a "toothache." If an upper lumbar root such as L1 or L2 is affected, the pain may be perceived in the groin crease, and can be confused with true hip pathology. In a manner analogous to central stenosis, this pain is often highly positional and/or exertional in nature. Patients will report a highly reproducible, excruciating pain pattern with standing or walking; however, sitting down may not as rapidly relieve this pain. This pain tends to be least in the mornings on arising, and tends to build during the day in proportion to the patient's activity level. Once again, patients often report relative pain relief with forward leaning, and many have a significant exacerbation of symptoms with extension of the back or side bending toward the affected nerve, due to further compression of the nerve with this maneuver. (See Figure 2)
Differential DiagnosisProbably the greatest challenge in the evaluation of this patient population is the high prevalence of other disease processes with symptoms that can overlay those of spinal stenosis, not to mention the fact that two or more of these processes often coexist in the same patient. Inaccurate or incomplete diagnosis will certainly confound the success of treatment efforts. Vascular disease can produce true claudication and formal testing of vascular reserve may be necessary if indicated by the history or the findings on physical examination. Osteoarthritis of the spine can be responsible for significant back pain, but etiologies such as metastatic tumors and osteomyelitis need to be considered in appropriate patients, particularly those with pain at night or at rest. Pain due to osteoarthritis of the hip, knee or ankle can be confused with the exertional radiculopathy of foramenal stenosis, but can often be distinguished by provocative testing or diagnostic injections of the suspected joint. A generalized peripheral neuropathy can present with distal numbness; weakness and instability that can suggest central stenosis, while a painful mononeuropathy such as can be seen in diabetes can suggest foramenal stenosis. The neuropathies typically lack the exertional or positional components of stenosis, and are often in fact most symptomatic at night. Electrophysiological testing can help sort out this picture in some cases. Up to ten percent of patients with symptomatic lumbar stenosis will have co-existing symptomatic cervical stenosis, which can add an overlay of myelopathic symptoms such as spasticity, clumsiness, weakness and urinary urgency to the presentation, but this can generally be suspected by the presence of upper extremity complaints and findings. Lastly, many patients do not maintain a healthy lifestyle, and obesity, smoking, physical inactivity and deconditioning can contribute to exercise intolerance and general physical discomfort. Physical ExaminationPhysical examination can be unimpressive in patients with central stenosis. Formal muscle strength testing is often normal, and sensory loss is unusual. Distal reflexes are often diminished or absent. Straight leg raising and provocative maneuvers are often negative. When observed on the way towards the exam room, patients will often ambulate with a forward-leaning posture and a moderately broad-based gait. Care should be taken to check distal pulses to screen for vascular causes of claudication. The findings in foramenal stenosis are often more impressive. There can be dermatomal patterns of sensory loss, and reflex asymmetries are often seen. In more advanced cases, muscle weakness or wasting may be present. Straight leg raising may be positive. Lumbar extension and side bending toward the affected side will characteristically reproduce or exacerbate the patient's typical radicular pain pattern. DiagnosisDue to the nearly universal prevalence of degenerative spinal changes in the population, lumbar spinal radiographs will almost always be "positive" for bone spurs, decreased disc height and facet hypertrophy in older patients. Radiographs, particularly with flexion and extension views, can be helpful in excluding other etiologies or contributing features such as gross spinal instability or spondylolithesis. MRI (without gadolinium) currently represents the "gold standard" in the evaluation of central stenosis. This modality allows the visualization of the disc, neural elements, ligaments and thecal sac in a non-invasive manner. CT scanning does give a more accurate and detailed picture of the bony anatomy, but is less accurate in estimating the degree of compromise of the soft tissue elements, and is not usually adequate as a stand-alone imaging modality. Myelography is no longer routinely necessary, although it can be useful in selected cases, such as where MRI is contraindicated. Electrophysiologic testing is rarely contributory, unless a contributory diagnosis such as peripheral neuropathy is being considered. Modalities such as discography and epiduroscopy have not been useful in my practice for the evaluation of central stenosis. MRI also remains the mainstay of screening in the evaluation of lateral recess or foramenal stenosis, although it can over- or under-estimate the degree of narrowing due to the signal characteristics of bone in standard MRI imaging sequences. In some cases, myelography with postmyelo-graphic CT scanning may give a more accurate picture of the relationship between the bony and neural elements in this clinical setting. MRI with gadolinium may be helpful in evaluating cases of residual or recurrent stenosis after previous lumbar surgery, because of the ability to differentiate between epidural scar and other tissue types. Electrophysiologic testing can be confirmatory if adequate time has passes from the onset of symptoms, or can help to exclude neuropathies in unclear cases. Selective injection of an individual nerve root with local anesthetic under fluoroscopic control can be performed as a diagnostic test, and can be useful in cases of widespread degeneration when multiple levels reveal stenotic changes. In these cases, significant, temporary relief of the patient's characteristic symptoms following injection of the nerve at the suspected spinal level provides confirmation of the clinical impression, while lack of relief indicates a need for further diagnostic testing prior to undertaking surgical intervention. Conservative Treatment OptionsSince the symptoms of stenosis are not life threatening and often progress slowly, there is generally adequate time to pursue conservative management strategies prior to contemplating surgical intervention. If the stenosis was detected incidentally on an imaging test ordered for other reasons, or if the patient is not limited in lifestyle or bothered by symptoms, reassurance and watchful waiting are appropriate. It is also beneficial to diagnose and treat any other contributory conditions. In particular, non-steroidal anti-inflammatory drugs (NSAID's) can provide considerable relief of the pains of spinal osteoarthritis, and certainly represent the foundation of the pharmacologic management of this problem. The introduction of the selective cyclooxygenase-2 inhibitors offers hope to the large group of patients that have been intolerant of NSAID's in the past, if the results of the early clinical trials are applicable to general clinical practice. As far as symptomatic central stenosis is concerned, NSAID's, narcotic and non-narcotic painkillers, muscle relaxants, anti-depressant agents and anti-anxiety medications offer relatively little benefit in reducing the symptoms of neurogenic claudication. As long as patients sit or lay about, they tend to be relatively asymptomatic, but many patients report persistent symptoms with ambulation despite heavy pharmacologic regimens. Steroids taken orally or injected epidurally tend to be effective, but the side effects prevent long term usage and the relief provided is often of short duration. NSAID's can be more effective in the management of the radicular symptoms of foramenal stenosis, and can be supplemented with painkillers if necessary in more severe cases. Once again, however, patients with severe positional and/or exertional radiculopathies may be symptomatic despite these techniques. I have not found much use from adding muscle relaxants in this condition, and patients report a high rate of cognitive side effects. Antidepressants and medications such as Neurontin can be helpful in the management of chronic radicular pain syndromes that have not responded to other techniques. A course of epidural or oral steroids seems to offer a greater chance of long-term relief in patients with foramenal or lateral recess stenosis, perhaps indicative of a greater role of inflammation in this condition compared to that of central stenosis. Physical interventions such as massage, ultrasound, TENS, braces or supports, acupuncture, biofeedback, hot or cold packs, traction, or chiropractic manipulation can offer symptomatic relief of radicular or low back pain. Unfortunately, many patients with claudication from central stenosis or exertional radicular pain from foramenal compromise will gain no benefit from these interventions. Physical therapy can be useful, but must be tailored to the anatomical considerations of these diseases. In particular, movements in extension and side bending can significantly increase patient's symptoms, and should be avoided in this patient population. General reconditioning of the spinal and abdominal musculature and ligaments is helpful in managing the symptoms of spinal degeneration, and body mechanics and proper lifting techniques are useful in preventing exacerbations. "Walking" as a fitness prescription in this patient population is obviously of little value. However, as opposed to the case with vascular claudication, some patients with neurogenic claudication may be able to exercise in a pool, or on a stationary or recumbent bicycle. Many patients are experimenting with alternative or nutritional remedies, but credible studies showing efficacy of these techniques are lacking. Some patients are referred for surgical consideration despite severe medical conditions that would contraindicate surgical intervention (such as severe pulmonary disease or unstable cardiac conditions), extremely advanced age, or conditions such as morbid obesity or severe osteoporosis that would markedly increase surgical risks. Despite the surgeon's desire to help such individuals, it must be remembered that patients with lumbar stenosis are generally minimally symptomatic while seated or recumbent, and that few individuals become "paralyzed" by this condition. Thought must be given to adaptive techniques such as the use of a motorized scooter to restore independence and mobility in such cases, and referral to a rehabilitation specialist for evaluation and treatment may be more useful than a risky surgical intervention. Surgical OptionsFor patients who are persistently or increasingly symptomatic from spinal stenosis, surgical intervention can be highly effective. Because these conditions involve compression by bony and ligamentous compression in extremely intimate juxtaposition with the nerve, there has been little reported clinical success with the use of "percutaneous," "minimally invasive," or "laser" surgical techniques, which do not allow adequate decompression of the neural elements in most cases. In the case of simple central stenosis, patients are treated by laminectomy of the affected lumbar segments, which decompresses the spinal canal and thus the neural elements. It is generally unnecessary to remove the ventral bone spurs or to decompress a bulging annulus to achieve adequate decompression. This procedure is highly effective in the relief of the symptoms of neurogenic claudication, and many patients are able to regain an unlimited tolerance of walking or standing. In the few long-term studies of laminectomy for stenosis that have been performed, the benefits of the procedure seem to be long lasting, although stenosis can develop at adjacent, non-operated levels. Laminectomy does NOT, however, generally relieve the symptoms of low back pain due to spinal osteoarthritis or instability. In fact, laminectomy can often worsen these problems, particularly if the integrity of the facet joints or disc spaces is compromised during the procedure. The controversy over the optimum surgical management of central stenosis centers on the role of and indications for spinal fusion. Given the significant morbidity of spinal fusion in this often elderly population, not to mention the marked prolongation of the recovery period, fusion should be avoided whenever possible. As noted above, if the laminectomy is carefully performed with attention to sparing the facet joints and discal anatomy, few patients will go on to develop symptomatic spinal instability or spondylolithesis. In most published series, approximately five percent of patients that underwent laminectomy for stenosis needed a subsequent spinal fusion operation. On the other hand, patients with preexisting instability, spondylolithesis, back pain out of proportion to claudicatory symptoms, or operations that compromise spinal integrity may be candidates for fusion procedures at the time of their laminectomy. There is no universal rule that will determine the need for fusion; rather, the unique mix of structural and symptomatic concerns must be evaluated for each individual patient to allow optimization of surgical intervention and thus outcome. In the case of lateral recess stenosis, many patients can also benefit from a simple decompression procedure directed at unroofing the affected nerve. Unfortunately, the complex anatomy of the foramen makes the treatment of foramenal stenosis more challenging. Patients with large, degenerated facet joints, broad-based bulging of the annulus and/or shortened interpeduncular distance may not be effectively treated by a facet-sparing decompression alone, due to residual nerve compression in the lateral aspect of the foramen. Even attempts to "undercut" the facet may not reach this site of nerve compression. In my experience one of the most common causes of residual or recurrent leg pain following laminectomy is the failure to adequately decompress the nerve in the lateral foramen. Patients with this type of stenosis may need a procedure that restores the height of the disc space and thus the foramen, such as an interbody fusion procedure. Conversely, patients that require the sacrifice of the facet joint for adequate neural decompression may need restoration of spinal stability through a posterior fusion with instrumentation ("pedicle screws.") Once again, careful attention to patient selection and meticulous operative planning are important in optimizing surgical outcome. Other Types Of Spinal StenosisOne manifestation of spinal degenerative disease is the "synovial" or juxtafacet cyst. It is not uncommon on MRI to see small fluid collections adjacent to the medial aspect of the lumbar facet joint. These seem to be analogous to the fluid collections seen elsewhere in the body adjacent to degenerating joints, such as the ganglion of the dorsum of the hand. Pathological analysis rarely shows a true synovial lining, instead consisting of chronic inflammatory tissue. In rare cases, these cystic collections of fluid can enlarge, compressing the adjacent nerve or even the entire thecal sac. The symptoms are quite similar to those of central or foramenal stenosis, with a striking positional component. The appearance on MRI is pathognomonic, and simple excision of the cyst is generally curative. (See Figure 3)
Spinal stenosis can be present in an idiopathic, congenital form, and can also be associated with some skeletal problems such as achondroplasia. Typically the patients present at a much younger age than in degenerative forms of stenosis. The overall treatment algorithm is similar to that for the degenerative forms, as noted above. However, the risks of development of instability may be greater following laminectomy in these younger patients, requiring greater thought about the utility of spinal fusion in these cases. Paget's disease can be associated with spinal stenosis. Surgical intervention when necessary in these cases is more challenging due to the widespread nature of the problem and the increased vascularity of the bone. Patients may have persistent symptoms following operative intervention for lumbar stenosis. This can be due to inadequate decompression of the affected neural elements at the initial surgery, or can indicate a need for further diagnostic efforts if imaging studies show no evidence of neural compression. If residual stenosis is detected, patients may benefit from additional surgical intervention. In distinction, patients that develop recurrent symptoms can show evidence of stenosis at previously normal levels, can have developed instability and/or spondylolithesis at previously operated levels with associated neural compression, can have a process such as a true herniated disc, or may show evidence of epidural scarring. The treatment in these cases depends on the specific anatomic situation. There seems to be an appreciable rate of development of stenosis adjacent to the level of a previous spinal fusion. (See Figure 4.) Whether this represents a progression of the patient's underlying spinal degeneration or is a process that develops in response to the increased biomechanical stresses on a mobile segment adjacent to a fusion is not fully understood at this time. With increasing numbers of patients undergoing spinal fusion procedures in recent years, this is an important problem in long-term management. Treatment of this problem often requires decompression of the neural elements as well as extension of the fusion to the affected level.
ConclusionSpinal stenosis is one component of the broader process of spinal degeneration, and can affect the neural elements through narrowing of the central spinal canal, the lateral recess or the neural foramen. Although these conditions can be asymptomatic, patients often present with patterns of symptoms of neurogenic claudication, exertional radiculopathy, or both. Diagnosis has been simplified in many cases through the use of MRI. Conservative treatments may be effective in the management of symptoms, but often are of short-term benefit in these conditions. Surgical interventions have to be tailored to the unique pathoanatomical situation in the persistently symptomatic patient, but most individuals will benefit from a straightforward decompressive procedure such as a laminectomy. References: There is a vast literature relating to the pathophysiology and anatomical considerations of spinal degeneration, the presentation and diagnosis of lumbar stenosis and the conservative and operative treatment of symptomatic patients. These topics are covered in much greater detail in several recently published textbooks of spinal disorders, as well as a monograph on spinal stenosis.
Jacksonville Medicine / June, 1999 [dcms-footer.htm] |
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