Approximately half a century after Charcot described ischemic pain in the lower extremities, Dejerine in 1911 described a syndrome he called intermittent claudication of the spinal cord (72-74). This neurogenic intermittent claudication is known as pseudoclaudication. In 1954, Verbiest reported in detail symptoms caused by the developmental narrowing of the lumbar vertebral canal (72). Later, a number of cases of neurospinal compression were reported (73-75). Pseudoclaudication or neurogenic claudication is bilateral or unilateral and consists of discomfort or pain in the buttocks, thighs, legs, and calves precipitated by walking uphill, on a straight level, or worse by walking downhill. Standing can also cause symptoms in neurogenic claudication. The discomfort or weakness or frank pain is relieved by sitting or by lying down (76). Bending forward or adopting a flexed position can alleviate the symptoms of neurogenic claudication (75). Leaning against a wall or bending forward can also improve the symptoms of pseudoclaudication. Prolonged standing has been associated with severe discomfort in neurogenic claudication, but not in vascular claudication. Walking downhill can precipitate pain in neurogenic claudication, but not in vascular claudication (77). In advanced cases of neurogenic claudication there is pain both in the standing and in the supine positions. Physical examination of the peripheral pulses is usually normal. By contrast in vascular claudication, the peripheral pulses are diminished or absent, there are bruits and physical findings of peripheral ischemia. The electromyogram is abnormal in neurogenic claudication and normal in vascular claudication. Patients with neurogenic claudication often complain of leg weak ness and may actually fall down (76). This weakness is best evoked by attempts to walk on the heels or on the toes. Any position that tends to cause the canal to become narrower will aggravate pseudoclaudication. Bending forward opens up the canal and relieves the symptoms (76,77). A lordotic position hyperextends the spine and produces radicular pain. Probably the best finding on physical examination is to provoke the symptoms by having the patient stand up or walk for a few minutes and notice if they adopt a flexed position. Standing up for several minutes will cause the patient to bend forward and lean on the nearest back support. Continued walking for several minutes induces leg distress. In about 43% of patients with neurogenic claudication, the deep tendon reflexes are reduced at the ankle level and in 18% of patients there is a reduction at the knee level. In neurogenic claudication rechecking the deep tendon reflexes of the lower extremities after walking for several minutes or standing for several minutes will show a reduction as compared with sitting (76).
Neurogenic claudication and vascular claudication are not mutually exclusive and can co-exist in about 9% of patients with either diagnosis. Vascular changes in the lower extremities may co-exist, because of the older age group in which vascular and neurogenic claudication occur. In one study (72), up to 42% of patients with pseudoclaudication were found to have absent pedal pulses. The etiology of neurogenic claudication is lumbar stenosis (78,79). In the nineteenth century, medical reports were published describing a narrow spinal canal syndrome in achondro-plastic dwarfs. Other rare congenital causes of pseudoclaudication are Morquio's syndrome dysplasia, hypochondroplasia, and Down's syndrome. Apart from discogenic disease acquired causes are Paget' s disease, systemic amyloidosis (80), hypertrophied ligamentum flavum, and calcium pyrophosphate crystal deposition (81). Syphilitic arteritis of the cord (Dejerius syndrome) in years past and the Foix Alajouanine syndrome are two very rare causes of neurogenic intermittent claudication (90). Degenerative joint and ligament hypertrophy is the leading cause of lumbar stenosis. The ligamentum flavum which normally does not exceed 4 mm in thickness may measure 7-8 mm. Spinal stenosis, which is the anatomic cause of neurogenic claudication, can be either congenital with a congenitally narrow spinal canal or more frequently acquired. The diameter of the canal is narrowed by the hypertrophic skeletal changes. In the middle-aged or the elderly patient who can have both neurogenic and vascular complications, the correct diagnosis, because of the variance in the presenting symptomatology and physical signs, has to be confirmed by basic laboratory evaluation. The plain radiographs of the lumbar spine show dense bony structures and the presence of degenerative disease. Further evaluation consists of co-axial tomography and preterably magnetic resonance imaging (MRI) (82,83). Myelography is an important test (82), but is less frequently indicated even when laminectomy is being considered by the consulting surgeon. Computed tomography and MRI are complementary tests for the preoperative elevation (82,83). Plain X-ray films are of far less value in evaluating the lumbar spine; they are more useful for the cervical spine. Pseudoclaudication, which was not widely appreciated in the past (84,85), is now part of the differential diagnosis of intermittent claudication.
Wilson (87) divided patients with this condition into two groups: (1) In the larger group, symptoms occurred during any activity or position involving extension of the lumbar spine that he termed postural cauda equina claudication, and (2) a smaller group of patients, with symptoms of the affected extremities after exercise that he described as ischemic cauda equine claudication.
According to Blau et al. (88,89), the vascular factor is more important. In exercised animals, vessels inside the canal are dilated and if the canal is narrow increased blood supply is prevented, thus leading to ischemia of the cord and the nerve roots. However, this explanation is not shared by others (90). It does not explain why neurogenic claudication occurs in the lordotic position at rest. Pseudoclaudication can be caused by other orthopedic conditions of the hips, knees, and other joints.
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