Spinal stenosis. A common cause of podiatric symptoms

Abstract

Spinal stenosis, involving pressure on either the central spinal cord or nerve root exiting the spinal canal, can cause a variety of symptoms in the lower extremities. A classic symptom is that of neurogenic claudication, involving leg pain and weakness brought on by walking. The pain is relieved by sitting or lying down, not by standing and resting as would be seen in arterial insufficiency-induced claudication. Other symptoms of spinal stenosis can involve paresthesia, weakness or cramping in one or both extremities, rest pain, or burning pain, and are commonly misdiagnosed as peripheral neuropathy, especially in patients with diabetes. Symptoms are often chronic, frequently missed, or misdiagnosed in the medical community, and may cause severe disability or reduction in the quality of life. Spinal stenosis is in some patients the unidentified cause of failure of treatment of foot and leg pain. Podiatric physicians, who focus on the patient’s lower extremities, are in a unique position to be able to identify spinal stenosis and facilitate appropriate treatment. The authors provide current information regarding symptoms of spinal stenosis, a guide to diagnosis including the anatomical etiologies, and a basic understanding of treatment.

Spinal stenosis is a narrowing of the central spinal canal or the nerve root pathways, causing compression of the neural tissue, resulting in symptoms in the back or along the course of the involved nerve roots. It is more common in the lumbosacral spine than in the cervical spine and rarely reported in the thoracic spine [1]. Spinal stenosis can be localized, affecting only one segment, or can affect more than one vertebral level. The most common area of central canal stenosis involves the L4/L5 region of the lumbosacral spine. Etiology of these symptoms is unclear: Some authors believe the symptoms are caused by vascular insufficiency at the nerve roots caused by pressure, others consider it to be secondary to mechanical pressure of the spinal cord and nerve roots [2].

Epidemiology

The prevalence of spinal stenosis in the general population is unknown, but has been reported in literature to be between 1.5% and 6% of those patients undergoing myelograms [3]. The wide variation in reported frequency has been ascribed to varied definitions of spinal stenosis, focusing just on central canal stenosis. These numbers do not reflect the incidence of lateral stenosis. Congenital spinal stenosis often presents symptoms initially in the third and fourth decade. Developmental stenosis, with a variety of degenerative joint disease manifestations, often presents initially in the fifth or sixth decade. Spondylolisthesis rarely occurs before age 50. Most studies show spinal stenosis to be more frequent in men than women, with the exception of there being a greater likelihood of spondylolisthesis in women than in men. Race, occupation, and somatotype do not appear to correlate with the frequency of development of symptomatic spinal stenosis [3].

Symptoms

Neurogenic-induced claudication is the classic presenting symptom of central canal stenosis, and may also be present with lateral stenosis. Patients have cramping, aching, or weakness of the muscles involving the hips, thighs, or calves. The area of symptomatology is dependent on the level at which the stenosis occurs. Calf claudication is usually seen with L4/L5 stenosis.

Symptoms of neurogenic-induced claudication are similar to those of vascular-induced claudication, but a few essential differences occur. The nearly pathognomonic difference is that the patient with neurogenic- induced claudication must usually sit, lie down, or flex the lumbosacral spine to get relief, while the patient suffering arterial insufficiencyinduced claudication may usually stand and rest to get relief. Patients with neurogenic-induced claudication may walk better going uphill, as this may flex the lumbosacral spine. Riding a bicycle may not result in any discomfort, because of lumbosacral spine flexion. Patients are able to walk better while using a walker or a cart. Differences are summarized in

Table 1. Comparison of Vascular-induced and Neurogenic-induced Claudication. 

.

Symptoms of spinal stenosis may be exacerbated by extending the lumbosacral spine. There may be paresthesia, cramping, or a feeling of weakness. Pain may be worse at night, and may be exacerbated by coughing [4].

Lateral stenosis causes symptoms that may overlap with those of central canal stenosis, but may also be more consistent with classic radiculopathy [5]. It may be caused by spodylolisthesis. There may be neurogenic-induced claudication of one or both legs, or there may be burning, aching, or sharp pain following a specific nerve root distribution. Constriction of the L5 or S1 nerve roots can cause symptoms localized to the foot, mimicking extenser tendinitis or plantar fasciitis. This can cause hypersensitivity to any deformity of the foot.

Patients with spinal stenosis may or may not have significant back pain. Often, there is a history of low grade arthritic back pain, aggravated by activity or weather changes. However, back pain may not be nearly as significant or disabling as pain in the extremities. Absence of back pain does not preclude a diagnosis of spinal stenosis.

Diagnosis

The diagnosis must be proceeded by a high index of clinical suspicion, followed by subjective evaluation, physical examination, and confirmed by available diagnostic modalities. Often, central canal stenosis symptoms are not the initial chief complaint of the patient. These symptoms are often chronic, which the patient has accepted as untreatable because of the failure of previous physicians to diagnose the condition. Therefore, description of symptoms must often be solicited by the treating physician. Questioning patients routinely about the distance that they are able to walk can elicit symptoms of neurogenic- induced claudication. Asking patients if they have any other problems with their feet or legs allows them to present the variety of symptoms often associated with stenosis. Any description of symptoms including unilateral or bilateral leg weakness, numbness, legs falling asleep, coldness, tingling, burning, or a tendency of the legs to give way should alert the clinician to the possibility of primary spinal pathology.

Physical findings are often minimal and nonspecific, the most common being decreased lumbosacral motion [2]. In performing range of motion maneuvers, patients can often flex forward without difficulty, but extension of the lumbosacral spine is significantly limited. Anatomically, it has been shown that when the spine moves from flexion to extension, compression of the spinal cord and nerve roots occurs contributing to the precipitation of neurogenic-induced claudication symptoms. Extension shortens the spinal canal, broadens both nerve tissue and the ligamentum flavum, and causes posterior protrusion of offending discs [4].

The straight-leg raising test usually does not cause pain with central canal stenosis, but often does in cases with disk herniation or foraminal stenosis [4]. Abnormal reflexes of individual nerve roots may or may not be seen [2]. Pain and sensitivity may or may not be seen on palpation of the involved area of the lumbosacral spine or course of the involved nerve roots. It is the experience of one of the authors (SMG) that patients with L4/L5 central canal stenosis usually have significant sensitivity along the course of the tibial nerve in the leg on deep palpation.

Currently, the standard test for confirming the presence of spinal stenosis is magnetic resonance imaging [1,6]. It is essential that the physician ordering the magnetic resonance imaging of the lumbosacral spine to rule out stenosis as etiology of peripheral symptoms be aware of the different physical pathologies that can cause the stenosis symptoms, to ensure appropriate care and follow-up treatment. Also, there are false positives, in which the pathology identified is not the cause of the extremity symptom. Final diagnosis must be made by a specialist who can treat this condition.

The presence of any of the following pathologic situations in the anatomically appropriate area should stimulate appropriate referral and treatment:

(1) Congenital Spinal Stenosis. This involves either bony or soft tissue hypertrophy causing narrowing of the spinal canal or intervertebral foramen. This would also be seen in a wide variety of systemic diseases affecting bony development [2].

(2) Acquired Spinal Stenosis. This stenosis is the most common presentation with a wide variety of anatomical etiologies.

(3) Central Canal Stenosis. This is associated with hypertrophy or calcification of surrounding soft tissues, bulging of intervertebral disks, or bony narrowing.

(4) Lateral Stenosis. Lateral recess or foraminal stenosis occurs causing compression of individual nerve roots after they branch off of the spinal cord.

(5) Isolated Intervertebral Disk Resorption. It can cause central or lateral recess stenosis with possible intervertebral canal narrowing. Symptoms are usually bilateral, although unilateral symptoms can result [2].

(6) Spondylolisthesis. Shifting of one vertebrae on another occurs, which may or may not change the neural arch.

(7) Isthemic Spondylolisthesis (spondylolysis). Defect of the pars interarticularis commonly causes hypertrophy of the articular process of the subluxed vertebrae.

(8) Scoliosis. With or without significant degenerative changes, this can cause neural compression.

(9) Spondylosis. Degenerative changes of the bony structure occur, i.e., static hypertrophy or spurring.

(10) Tumor. Neoplastic growth causing compression of spinal cord or nerve root.

Lack of the term “spinal stenosis” in the radiology report does not preclude a form of stenosis as being the etiology of the patient’s symptoms.

It is strongly recommended that physicians exploring the possibility of stenosis causing problems for their patients have communication with the neuroradiologist reading the magnetic resonance imaging scans if the report does not seem definitive. Discussing pathology identified with the neuroradiologist and with specialists who treat the condition will help the physician take the appropriate steps of referral with confidence.

Standard lumbosacral radiographs can identify intervertebral disk-space narrowing, facet joint hypertrophy, and osteopenic appearance. These xrays do not identify well central canal stenosis or foraminal stenosis. Lateral flexion and extension xrays can be used to show instability between vertebrae. However, lumbosacral radiographs alone are insufficient for confirmation or exclusion of spinal stenosis. Computed axial tomography is also used at times, and with contrast is suggested to have equal sensitivity to magnetic resonance imaging [7]. Magnetic resonance imaging with gadolinium contrast is the most accurate test in postoperative evaluation of patients with failed back surgery [8].

Neurologic testing through nerve conduction velocity testing and electromyogram may or may not demonstrate changes associated with spinal stenosis. Some studies suggest that up to 80% of patients with canal stenosis test positive for nerve conduction velocity testing and electromyogram changes in presence of severe canal stenosis. Other studies suggest that changes are more likely to be identified if testing is done following the patient being active enough to bring upon the neurogenic-induced claudication symptoms [6]. A functional test for neurogenic-induced claudication is described by Jensen [9] as being highly accurate. This involves downhill walking in which to maintain a vertical position, the patient must increase the extension of his or her low back causing “symptom march.” This can be facilitated by using a treadmill elevated to create a 10° downhill slope. This activity significantly increases subjective symptoms of spinal stenosis and also increases the likelihood of developing nerve conduction velocity testing and electromyogram changes [2].

Between 1992 and 1995, one of the authors (SMG) ordered 110 magnetic resonance imaging examinations of the lumbosacral spine. All tests were ordered because of suspicion of lumbosacral spinal pathology being the etiology of foot and leg symptoms, not for back symptoms. Seventy tests were positive, 40 were reported as negative (

Table 2. Summation of 70 Positive Results of the Lumbosacral Examinations Performed from 1992 to 1995. 

). Repeat examinations on two of the negative patients, done more than 1 year after initial examinations, were positive. The patients were referred to physicians specializing in physiatry, orthopedic surgery, neurosurgery, or anesthesiology, based on the judgment of the author and desires of the patient.

Treatment

Treatment for spinal stenosis can be conservative or surgical, depending on the response to conservative care, severity or progression of symptoms, or the presence of neurologic deficit. While providing definitive treatment for this condition is outside the scope of podiatric medicine, it is essential to understand the different treatment options in order to best guide the patient in confidence toward appropriate treatment.

Included in the treatment considerations should be the understanding that the natural course of spinal stenosis often does not involve worsening of the condition. Johnsson et al [10] reported that 70% of their cases of spinal stenosis did not change through a 4-year follow-up period. Fifteen percent showed improvement and 15% worsened. Treatment should therefore be based on symptoms and restrictions that the patient has, rather than fear of worsening of the condition. Nonoperative conservative treatment is therefore usually the initial management, unless symptoms are disabling or neurologic deficit is significant.

Conservative treatment often consists of a combination of anti-inflammatory nonsteroidal drugs, narcotics, tricyclic antidepressants, steroid injections, along with physical therapy [5,11,20]. Abdominal strengthening exercises to reduce extension of the lumbosacral spine, lumbosacral corset, use of a cane, and patient education can be used along with physical therapy modalities [12].

Another physical medicine program is reported by Onel et al [13] in which they use a combination of diathermy, exercise, infrared heat, and salmon calcitonin. They noted that 89% of their patients improved in neurogenic claudication symptoms with 29% achieving the ability to walk without limitations.

The use of tricyclic antidepressant medications in the management of musculoskeletal pain and neuritic pain is well documented. Amitriptyline (Elavil^® (Zeneca Pharmeceuticals, Wilmington, DE)) is more effective in relieving back pain than other antidepressants, but also has more adverse effects [11]. Less likely to have problematic side effects are Desyrel^® (Apothecan, Princeton, NJ) and Tofranil^® (CibaGeneva, Summit, NJ). The analgesic effect of antidepressants is distinct from the antidepressant effect and occurs at lower levels. Typical dosage regimen for amitriptyline would be to begin at 10 mg at night, gradually increasing up to 100 or even 150 mg, until a positive effect is seen or adverse effects occur [11] The prescribing physician must be well aware of associated anticholinergic effects, such as dry mouth, urinary retention, drowsiness, blurred vision, and cardiac concerns. Sleep disturbances are a major complication of chronic pain syndromes, and improvement of sleep by tricyclic antidepressant medications is often in itself helpful [14].

People using tricyclic antidepressant medications often report significant improvement in pain after only a few days of use, whereas improvement in depression often requires 1 to 4 weeks of regular use. Some patients who fail to tolerate one tricyclic antidepressant medication often tolerate or respond to another, so that it may be necessary to try different tricyclic antidepressant medications in turn, until satisfactory therapeutic response without intolerable side effects is achieved [14]. It is the experience of one of the authors (SMG) that tricyclic antidepressants are often helpful in relieving discomfort seen with spinal stenosis, but not helpful in improving the walking distance.

Steroid injections, epidural or selective, have been shown to be helpful in both low-back pain and extremity pain. Epidural injections involve injection of a combination of local anesthetic and corticosteroid into the epidural space. Studies report a high likelihood of temporary improvement with accurately placed epidural injections in patients with spinal stenosis [15]. In more severe cases, definitive improvement is much more likely in patients more than 70 years old than in young patients [9]. A series of injections given 1 week apart is common, although other protocols are also used [16]. These injections can be given by anesthesiologists, physiatrists, orthopedic surgeons, or neurosurgeons.

Selective spinal injections, targeting a single nerve root or joint, can also be used. This is often used in cases of lateral stenosis or postoperative scarring, and may be done under fluoroscopic guidance [16].

Steroid injections have been studied as a predictor of the likelihood of success with surgical treatment. Derby et al [17] found that 85% of patients with various spinal conditions who got good temporary relief of symptoms with injection also did very well with surgical treatment. Conversely, they found that 95% who did not temporarily respond well to injection did poorly with surgery, averaging only 25% long-term relief.

Unfortunately, there is a certain percentage of inaccurate placement of epidural steroid injections. A study by Renfrew [18] demonstrated a failure of accurate placement of injection by experienced physicians of more than 35% of the attempts. For this reason, one of the authors considers that at least two epidural injections must be given before rejection of this approach in treatment of spinal stenosis.

There are many considerations in deciding to proceed with surgical treatment in patients with spinal stenosis [1]. Many people still have minor complaints following surgery. Surgery is often more successful in relieving extremity symptoms than relieving back pain. Surgical failure is reported at various percentages in the literature. Patients undergoing surgery must understand the possibility of lack of improvement and the extensive risks involved with spinal surgery. Age alone does not rule out surgical treatment, as it has been shown that lumbar spine surgery can be performed effectively in the elderly [19]. Jonsson and Stromquist [8] also demonstrate that repeated spinal surgery on those patients who had failed first attempts can be very successful, excepting patients who have problematic postoperative fibrosis.

Podiatric physicians may choose to refer their patients to a physiatrist, anesthesiologist trained in pain management, orthopedic back specialist, or neurosurgeon. Discussion regarding the various types of surgical decompression, indications, postoperative course, and likelihood of success is beyond the scope of this article.

Case 1

A 67-year-old insulin-dependent male with diabetes was referred by his endocrinologist for treatment of painful hammer toes, corns, and diabetes management. He reported having increased problems with “diabetic neuropathy” throughout the previous several years. Arterial testing revealed a mild-to-moderate arteriosclerosis obliterans, with ankle and arm indexes between 70 and 80. Discussion revealed that he had claudication symptoms after fewer than 100 yards of walking. He had to sit to get relief from these symptoms. He noted some weakness and numbness, worse on his left leg than his right. He had a severe limitation from his desired lifestyle. A magnetic resonance imaging scan was ordered on the initial visit, and showed central canal stenosis at the L4/L5 level. The patient was not comfortable with the new diagnosis, as he had been confident of the problem being untreatable diabetic neuropathy for many years. A trial of epidural injections provided dramatic relief of pain, but only for 2 months. The patient then became comfortable with the new diagnosis of neurogenicinduced claudication, became willing to undergo surgery, and had spinal decompression of the canal stenosis.

He had complete elimination of claudication symptoms, numbness, and weakness of his lower extremities. He reported that the quality of his life improved dramatically, and his improvement has been maintained following surgery in 1992.

Case 2

A 65-year-old female who had noninsulin-dependent diabetes presented with a painful great toe. The discussion revealed limitation of the ability to walk for the prior 20 years with the patient having claudication distance of one to two blocks, requiring sitting or even lying down. Suspicion of neurogenic-induced claudication resulted in the ordering of a magnetic resonance imaging scan of the lumbosacral spine. This showed a grade I spondylolisthesis with associated L4/L5 central canal stenosis and foraminal stenosis. Because of the severe long-term disability, the patient refused conservative care. Spinal decompression was performed with elimination of all claudication symptoms of the legs. She had recurrence of severe symptoms 1 year later, and required spinal fusion.

Case 3

This 64-year-old female presented in 1986 with a chief complaint of numbness and burning of her feet for approximately 5 years. She also complained of calluses that were only mild, but hypersensitive. She had been in an automobile accident 15 years before. She had no other significant medical problems. Initial examination showed hypersensitivity throughout the foot including sensitivity in all intermetatarsal spaces, and the posterior tibial and tibial nerves bilaterally. A nerve conduction velocity testing and electromyogram showed peripheral neuropathy. She had extensive workup by neurology, repeated twice in the following 5 years, with no identification as to the cause of her symptoms. She was placed on Elavil, which provided mild improvement of pain and marked improvement of her sleep pattern.

The patient was not seen by the treating physician (SMG) between 1990 and 1992. She returned at that time for reexamination and symptoms consistent with spinal stenosis were then recognized. A magnetic resonance imaging scan was performed, and showed spinal stenosis at the L4/L5 level, consistent with the distribution of leg cramps she had, and foraminal stenosis in the L5-S1 level. She had epidural injections. The first epidural injection provided elimination of all leg pain. The second epidural injection, done through a caudal approach directed to the L5-S1 area, eliminated all residual foot pain. She had relief for approximately 1 year. Since that time, she has required injections every 9 to 12 months, each providing excellent relief. She refuses surgical treatment as long as she gets temporary improvement with the injections.

Case 4

A 49-year-old male presented to the office with a chief complaint of chronic pain in his feet and legs. His feet hurt constantly and were aggravated by activity. He had leg cramps with activity and cramping in his legs at night. He noted a long-term history of back pain that was annoying, but did not limit his activity level. Physical examination showed that he had moderately severe gastrocnemius equinus with -10° dorsiflexion with the knee extended, +5° dorsiflexion with the knees flexed. A mild metatarsus adductus was present with mild pronation syndrome. No pain on palpation of the posterior tibial nerve, but he did have pain on palpation of the tibial nerve area in the midcalf and a positive straight-leg raising test bilaterally. He was initially placed on gastrocnemius stretching exercises, heel cups, and anti-inflammatory medications. This eliminated the equinus, and provided mild-to-moderate relief of leg cramps, but significant leg cramps persisted. Modified low die straps were placed on his foot bilaterally to attempt to control pronation symptoms. This provided no relief at all. He had a magnetic resonance imaging scan of the lumbosacral spine that identified central canal soft tissue stenosis in the L3/L4 and L4/L5 level. A herniated nucleus pulposus was also identified in the L5-S1 area. Two lumbar epidural injections relieved all remaining leg cramps and claudication symptoms. He received a caudal injection in the L5-S1 area, which eliminated the majority of his foot pain. Twenty months after his last injection, he still has only mild symptoms in his feet and legs. He is pleased with the present reduction in symptoms.

Case 5

A 68-year-old female presented with a chief complaint of disabling right foot and leg pain present for 16 months. She had seen two podiatric physicians and one orthopedist and had been aggressively treated for heel spur syndrome. Previous treatments included multiple steroid injections, orthoses, physical therapy, night splints, cast immobilization, and nonsteroidal inflammatory drugs. Treatments provided mild (10% to 20%) temporary improvement. She now required a cane for ambulation. Previously, she had had poststatic dyskinesia that had resolved long ago, but disabling pain aggravated by activity, and night pain persisted. The pain was felt primarily in the heel, but soreness and tenderness were present up to the hip. Physical examination showed moderate tenderness on palpation at the medial calcaneal tubercle, also on lateral and posterior compression of the calcaneous. Significant sensitivity was present along the course of the posterior tibial nerve, the tibial nerve, the femoral nerve, and in the sciatic notch. She had mild tenderness on palpation of the lumbosacral spine, but denied any back pain. Lumbosacral magnetic resonance imaging was ordered at the initial visit. Degenerative bulge with loss of disc height and facet hypertrophy resulting in L4-S1 right side foraminal stenosis was identified. A trial of epidural injections was recommended. The patient returned to the treating orthopedic surgeon who concurred with this recommendation. One injection provided 80% relief of pain. Subsequent physical therapy and injections provided moderate long-term relief.

Case 6

A 76-year-old female presented with constant burning pain, worse at night, on the top of the foot and anteromedial ankle bilaterally. Symptoms were present for 1 year with gradual onset. She had no claudication symptoms. Medical history was not contributory. She had had extensive conservative care for “extensor tendinitis” including anti-inflammatories, multiple injections, physical therapy, and cast immobilization: None proved helpful. The authors’ initial evaluation showed moderate tenderness along the tibial nerve, a positive straight-leg raise test, and mild low back pain and sensitivity. She had no pain on palpation or manipulation of the structures of the foot or anterior ankle. Magnetic resonance imaging of the lumbosacral spine was ordered at the initial visit and showed central canal stenosis at the L4-L5 level and foraminal stenosis at the L5-S1 level. A single epidural injection provided 95% relief of pain. She was referred to physiatry for further treatment.

Conclusion

Spinal stenosis is a common disorder causing symptoms in the foot and leg that are often disabling, causing severe limitations in lifestyles of patients. People are often misdiagnosed, especially those with diabetes. A classic symptom is that of neurogenicinduced claudication involving cramping and aching in the legs, thighs, or buttocks that is relieved by sitting or flexion of the spine, not relieved by standing. Vague muscular aches, muscle weakness, pain while nonweightbearing, burning pain, and night pain can also be present in lateral stenosis, involving exiting nerve roots.

Diagnosis is strongly suggested by description of the patient’s symptoms, and is confirmed by a magnetic resonance imaging scan. At times, patients do not believe the diagnosis even after having a positive magnetic resonance imaging scan. Epidural injections, if successful, can convince them they have a treatable condition. It is also thought to be a good prognostic indicator for surgical success.

The presence of other pathology should not eliminate consideration of spinal stenosis. Many of the authors’ spinal stenosis patients have had either vascular, mechanical, or systemic problems that had led to previous misdiagnosis. Patients with pain out of proportion to physical presentation, or who do not respond as expected to treatment, or with unknown cause of foot or leg pain should be considered for spinal stenosis etiology.

Patients with spinal stenosis may deny having pain on initial questioning, as they limit their walking to eliminate claudication symptoms. It is only when questioned as to how far they can walk that they will bring up the fact that they have limitation. This question of walking distance is thus essential in uncovering this condition.

Treatment depends on the severity of symptoms, neurologic deficit, disability, and progression of the disorder. This condition may be self-limiting, may improve, or stay static on its own without treatment. Conservative treatment, including physical therapy to reduce inflammation and strengthening exercises for the abdomen, is often helpful. Anti-inflammatory and tricyclic antidepressants can be helpful in relieving symptoms. Epidural injections or selective spinal injections may provide temporary or long-term relief and are thought to be a good prognostic indicator for success of surgical treatment in patients. Surgical treatment is reported to have a high degree of success in improving the quality of life and can be done safely for older patients. Repeat surgery can often be done in case of failure of previous back surgery.

A high index of suspicion among podiatric physicians will result in identifying this condition and providing help for many patients.