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World J Orthop. Apr 18, 2014; 5(2): 134-145
Published online Apr 18, 2014. doi: 10.5312/wjo.v5.i2.134
Pathophysiology, diagnosis and treatment of intermittent claudication in patients with lumbar canal stenosis
Shigeru Kobayashi
Shigeru Kobayashi, Department of Orthopaedics and Rehabilitation Medicine, Faculty of Medical Sciences, and the Research and Education Program for Life Science, the University of Fukui, Fukui 910-1193, Japan
Author contributions: Kobayashi S solely contributed to this paper.
Supported by Grant-in Aid from the Ministry of Education, Science and Culture of Japan, No, 25460719
Correspondence to: Shigeru Kobayashi, MD, PhD, Department of Orthopaedics and Rehabilitation Medicine, Faculty of Medical Sciences, and the Research and Education Program for Life Science, the University of Fukui, Shimoaizuki 23, Fukui 910-1193, Japan. kshigeru@u-fukui.ac.jp
Telephone: +81-776-618383 Fax: +81-776-618125
Received: October 30, 2013
Revised: December 17, 2013
Accepted: March 3, 2014
Published online: April 18, 2014
Processing time: 200 Days and 20.1 Hours
Abstract

Spinal nerve roots have a peculiar structure, different from the arrangements in the peripheral nerve. The nerve roots are devoid of lymphatic vessels but are immersed in the cerebrospinal fluid (CSF) within the subarachnoid space. The blood supply of nerve roots depends on the blood flow from both peripheral direction (ascending) and the spinal cord direction (descending). There is no hypovascular region in the nerve root, although there exists a so-called water-shed of the bloodstream in the radicular artery itself. Increased mechanical compression promotes the disturbance of CSF flow, circulatory disturbance starting from the venous congestion and intraradicular edema formation resulting from the breakdown of the blood-nerve barrier. Although this edema may diffuse into CSF when the subarachnoid space is preserved, the endoneurial fluid pressure may increase when the area is closed by increased compression. On the other hand, the nerve root tissue has already degenerated under the compression and the numerous macrophages releasing various chemical mediators, aggravating radicular symptoms that appear in the area of Wallerian degeneration. Prostaglandin E1 (PGE1) is a potent vasodilator as well as an inhibitor of platelet aggregation and has therefore attracted interest as a therapeutic drug for lumbar canal stenosis. However, investigations in the clinical setting have shown that PGE1 is effective in some patients but not in others, although the reason for this is unclear.

Keywords: Lumbar canal stenosis; Cauda equine; Nerve root; Prostaglandin E1; Blood flow

Core tip: The radicular symptoms associated with degenerative disease of the lumbar spine are reported to be attributable to a combination of mechanical nerve root compression and resultant circulatory disturbance. Disturbance of blood flow in the cauda equina and nerve roots is reported to play an important role in the mechanism of intermittent claudication in patients with lumbar canal stenosis. Prostaglandin E1 (PGE1) is a potent vasodilator as well as an inhibitor of platelet aggregation and has therefore attracted interest as a therapeutic drug for lumbar canal stenosis with intermittent claudication. However, investigations in the clinical setting have shown that lipo-PGE1 is effective in some patients but not in others, although the reason for this is unclear.