American Journal of Physical Medicine & Rehabilitation:
LaBan, Myron M. MD, MMSc, FACP
William Beaumont Hospital
Royal Oak, Michigan
To the “Chief,” (EWJ) whose example continues to inspire.
Errors, like straws, upon the surface flow,
He who would search for pearls must dive below.
Academic Vision, John Dryden, 1631–1700
Clinical pearls emerge by repeated observation rather than as a product of the unyielding rigid requirements of the scientific method. In this regard, the physiatric examination by the clinical recognition of the patient’s residual abilities is able to identify neuromusculoskeletal dysfunction. Although not pathognomonic of lumbar spinal stenosis (LSS), iliopsoas weakness, when recognized at the bedside, may be the earliest clinical sign of a stenotic lumbar spine (Fig. 1). Iliopsoas weakness can be elicited with the patient in a supine position, resisting the examiner’s maximal effort to extend the flexed thigh on the pelvis by an eccentric, downward force applied just proximal to the knee.
The symptoms of LSS are highly variable. 1 However, most patients with central spinal stenosis have a primary complaint of low back pain, often with alternating sciatica or neurogenic claudication (claudicatio intermittens spinalis) aggravated by lumbar extension and relieved by spinal flexion. 2 Paradoxically, increased nocturnal low back pain at rest may arouse the patient from a sound sleep, particularly when associated with the presence of a cardiomyopathy or with a reduction in pulmonary compliance (chronic obstructive pulmonary disease), especially when accompanied by pulmonary hypertension (vesper’s curse). 3
The presenting signs of LSS may also be quite disparate as the deep tendon reflexes or lower limb muscle strength may be normal, with sensory responses appropriate and straight-leg raising tolerance unrestricted, despite “severe” lumbar radicular complaints. With a relative paucity of physical signs, the clinical diagnosis of LSS may initially rely only on the history. 4
Described by Portal in 1803, 5 the exact pathogenesis of neurogenic claudication in association with LSS remains in dispute. Blau and Logue 6 espoused a theory of root-level ischemia, whereas Verbiest 7 attributed it to direct mechanical compression. However, a current consensus would suggest that a combination of both theories play key roles in the promulgation of neurogenic claudication. 8 Affecting slightly more men than women, the prevalence of LSS in general increases with age, although 9% at diagnosis are <50 yrs of age. 9 LSS occurs most frequently at the L4-L5 and then L3-L4 levels, less often at L5-S1 (Fig. 2). The psoas major muscle is directly innervated by the lumbar spinal roots L1–L4, the iliacus by the femoral nerve L2-L4. 10 Together, the combination of both a short iliopsoas muscle and the relatively long lever of the femur facilitates the identification of even subtle iliopsoas weakness. Clinically, this weakness rarely calls attention to itself, with the occasional exception of when ascending stairs, in which increased difficulty may be experienced in elevating the thigh sufficiently to clear the next step.
The concomitant presence of an ipsilateral degenerative hip can be confusing because it, too, can be associated with a weak iliopsoas, in this instance, usually accompanied by a loss of joint internal rotation. With this major clinical exception, iliopsoas weakness may be the earliest sign of LSS.
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5. Portal A: Cours d’anatomie medical ou elemens de l’anatomie de l’homme. Paris, Baudoin, 1803, p 299
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8. Hall S, Bartleson J, Onofrio B, et al: Lumbar spinal stenosis: Clinical features, diagnostic procedures, and results in surgical treatment in 68 patients. Ann Intern Med 1985; 103: 271–5
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10. Alvarez A, Hardy HR: Lumbar spine stenosis: A common cause of back and leg pain. Am Fam Physician 1998; 57: 1825–34
© 2004 Lippincott Williams & Wilkins, Inc.