Management of lumbar spinal stenosis

The thorough review of lumbar spinal stenosis (LSS) by Lurie and Tomkins-Lane1 reiterates the dilemma noted in other reviews2,3 and interventional trials4 over the past 20 years. “There is no single objective standard for identifying LSS and diagnosis relies on complex judgments that integrate symptoms, signs, imaging findings, and comorbid conditions” and there is a “lack of standard criteria for diagnosis and for inclusion in studies.” Thus, criteria for patient care or for entry into a randomized clinical trial of a surgical, drug or physical therapy compared to a control intervention begins with medical uncertainty about what is being treated, as well as uncertainty in defining the most clinically important primary outcome. The authors quote Verbiest for the first modern description of LSS. He included among other symptoms and signs of episodic cauda equina disturbance, “On walking and standing” there was “impairment of motor power in the legs.” But, he wrote, “When the patient was recumbent, the symptoms immediately disappeared and neurological examination during rest revealed nothing abnormal.” Could onset of leg weakness during activity, followed by recovery at rest, be detectable and perhaps serve as a sine qua non for the diagnosis of disabling LSS?

We have found that diagnostic acumen about LSS improves using the standard manual muscle test (MMT) and British Medical Council Scale at the time symptoms are evoked, i.e., test the patient when the patient has symptoms. This procedure has obvious face validity, yet somehow has been ignored, even in the case studies of Verbiest and in all clinical trials of treatments for LSS.

First, test lower extremity strength with the patient seated at rest for a few minutes at the hip flexors, the knee extensors starting from 45° in partial extension, and the ankle dorsiflexors. Next, in the supine position, test the hip flexors again starting from 20° elevation of the heel off the table. Finally, while prone, test the hip extensors starting from as high as the leg can be elevated off the table and hamstring knee flexors starting from about 45° in flexion. These are very powerful muscles compared to the examiner’s shoulder and arm, so this positioning allows isolation of each muscle group and greater leverage for the examiner’s effort to overcome resistance, if any weakness is present. Strength should be normal, graded 5/5, unless a radiculopathy, lateral stenosis or other non-LSS entity is present. Then, have the patient walk without leaning forward, until the bilateral discomfort begins or for at least 300 feet. Immediately retest the same muscle groups seated, supine and prone within 30-45 seconds. In the presence of LSS-induced weakness, a decline in strength to offering fair but breakable resistance (graded 4/5) will be found in affected groups. After remaining supine for another 1-2 minutes, the same MMT will reveal no paresis. When we have detected these motor signs in the presence of a moderate to severe LSS by neuroimaging and in the absence of another central or peripheral cause of motor fatigability, decompressive surgery has relieved pain and paraparesis. Based on years of observations, we have come not to recommend surgery unless transient paraparesis occurs. When typical bilateral multi-root distribution pain or dysesthesia occurs in the presence of LSS by imaging, weakness has always been present. Of interest, in those for whom the gait pattern declined pre-op (wider base, imbalance, modest waddle), the gluteal and hamstring muscles were most affected in the immediate post-walking MMT.

With multilevel compression, the MMT cannot reliably detect a second lower level of involvement. Thus, if the hip flexors tested supine become weak after a walk, it is likely that a canal stenosis affects L2/3 roots, but weakness related to an associated L4-5 level of stenosis may not be appreciable – the upper compression may affect the lower cauda equina fibers as well.

As the authors note, the specific pathology may be compressive ischemia or venous congestion. At a neurophysiological level, however, this paresis most likely results from a partial conduction block in some fascicles of myelinated nerve fibers, followed by failure to activate their innervated muscle fibers and abnormal muscle co-activation and torque coupling.5 To develop mild bilateral weakness, as little as 30% of each affected cauda equina segmental nerve needs to be compromised, perhaps like episodic mechanical compression of the median nerve at the wrist with reversible tingling and paresis due to a carpal tunnel syndrome.

Sources of pain with standing and movement in patients suspected to suffer LSS may have other etiologies,2 but the transient bilateral paresis as described is a manifestation of a pathoanatomical compromise of intraspinal canal nerve conduction. Thus, a timely motor exam may lessen the heterogeneity of the present criteria that suggest a diagnosis of LSS, as well as provide a clinically meaningful and measurable change after a successful therapeutic intervention.

References

1. Lurie J, Tomkins-Lane C. Management of lumbar spinal stenosis. BMJ 2016;352:h6234.
2. Siebert E, Pruss H, Klingebiel R, Failli V, Einhaupl K, Schwab J. Lumbar spinal stenosis: syndrome, diagnostics, and treatment. Nat Rev Neurol 2009;5:392-403.
3. Suri P, Rainville J, Kalichman L, Katz J. Does this older adult with lower extremity pain have the clinical syndrome of lumbar spinal stenosis? JAMA 2010;304:2628-36.
4. Delitto A, Piva S, Moore C, et al. Surgery versus nonsurgical treatment of lumbar spinal stenosis: A randomized trial. Ann Intern Med 2015;162:465-73.
5. Dobkin BH. Fatigue versus activity-dependent fatigability in patients with central or peripheral motor impairments. Neurorehabil Neural Repair 2008;22:105-10.