Spinal Stenosis: Neurogenic Claudication Mechanism
The pathogenesis of neurogenic claudication is thought to be caused by ischemia of the cauda equina nerve roots that are involved during exercise1. This is thought to be at the site of anastomosis of two vascular systems that supply blood to the nerve roots which are the vasocorona proximally and the intermediate segmental artery distally. This two systems connect at two-thirds length distal to the spinal cord1. This area is considered to be hypovascularized and easily results in ischemia due to compression.
A 1999 study1 looked to see if these ischemic compressions in patients with neurogenic claudication due to lumbar spinal stenosis could cause motor conduction alterations. Motor conduction alterations to the lower limb would affect motor control and therefore walking ability. Thirty patients with Lumbar Spinal Stenosis (LSS) and 19 healthy volunteers were included in the study. All of the LSS patients had neurogenic claudication in their history and LSS was confirmed with a CT myelogram. Both groups had electrophysiological testing performed on them including the motor evoked potential latency time (MEPLT) and the peripheral motor conduction time (PMCT). Both groups were required to walk on a flat surface until they had a reproduction of their symptoms, after which electrophysiological tests were recorded again. The walking did not create claudication in the control group participants. Twenty-seven of the LSS patients had symptoms of claudication. MEPLT in the control group pre and post-exercise were within normal limits. In the LSS group, 19 patients had higher pre-exercise values for MEPLT to at least one of the recorded muscles. In patients that had signs of neurological deficit, there was a significant difference between the MEPLT and PMCT values pre and post exercise. This difference was not significant in patients without a neurological deficit.
Neurogenic claudication in lumbar spinal stenosis is thought to be the result of an acute ischemic process acting on the spinal root. This causes changes in the conduction of MEPs which changes motor function. There are physical signs of compression in 30% of patients with LSS. MEPs are prolonged in 66% of patients which increases to 76% following exercise1. The authors of the study conclude that under in patients with LSS, exercise increases the sensitivity of MEPs in detecting the roots that are under functional compression.
The results of this study help to explain how patient’s reports symptoms of decreased walking ability with lumbar spinal stenosis and adds to our understanding of the condition.
References
1. Baramki H, Steffen T, Schondorf R, Aebi M. Motor conduction alterations in patients with lumbar spinal stenosis following the onset of neurogenic claudication. European Spine Journal: Official Publication Of The European Spine Society, The European Spinal Deformity Society, And The European Section Of The Cervical Spine Research Society [serial on the Internet]. (1999), [cited August 2, 2016]; 8(5): 411-416. Available from: MEDLINE with Full Text.
