Morishita Yuichiro, Hida Shinichi, Naito Masatoshi, Arimizu Jun, Takamori Yoshihiro
Department of Orthopaedic Surgery, Fukuoka University, Jyonan-ku, Fukuoka, Japan.
J Spinal Disord Tech. 2009 Apr;22(2):130-4. doi: 10.1097/BSD.0b013e318167b054.
The clinical relationship between the local pressure of the intervertebral foramen and the clinical findings in lumbar spinal canal stenosis were evaluated.
To investigate the pathogenesis of neurogenic intermittent claudication in lumbar spinal canal stenosis.
The genesis of neurogenic intermittent claudication is generally considered to result from nerve root ischemia; however, the exact pathogenesis of neurogenic intermittent claudication remains uncertain.
From a total of 20 lumbar spinal canal stenosis patients, 29 L5/S1 vertebral foramens were studied. All patients showed neurogenic intermittent claudication, and also showed neurologic abnormalities in L5 area. Intraoperatively, the local pressure of the intervertebral foramen was continuously measured using a micro-tip catheter transducer whereas the lumbar spine postures were changed under passive movement, and the relationships between the local pressure and the preoperative clinical findings in lumbar spinal canal stenosis were analyzed.
The local pressure of the intervertebral foramen significantly increased during lumbar spine extension (P<0.001). The patients who demonstrated large changes in the local pressure between flexion and extension showed a significantly poor walking ability (P=0.003). Moreover, the patients who had 2-level lumbar spinal canal stenosis showed significantly smaller changes in the local pressure between flexion and extension than 1-level lumbar spinal canal stenosis patients (P=0.01).
The present study suggests that the genesis of neurogenic intermittent claudication in lumbar spinal canal stenosis may be greatly affected by the variation of the dynamic mechanical stress on the spinal nerve roots of the lumbar spine, rather than the static mechanical stress on the spinal nerve roots with each posture. Moreover, 2-level lumbar spinal canal stenosis patients demonstrated radicular symptoms with relatively less external stress on their spinal nerve roots in the vertebral foramen than that observed in 1-level lumbar spinal canal stenosis patients.
评估椎间孔局部压力与腰椎管狭窄临床症状之间的临床关系。
探讨腰椎管狭窄症神经源性间歇性跛行的发病机制。
神经源性间歇性跛行的发病通常被认为是由神经根缺血引起的；然而，神经源性间歇性跛行的确切发病机制仍不明确。
对20例腰椎管狭窄症患者的29个L5/S1椎间孔进行研究。所有患者均表现为神经源性间歇性跛行，且L5区域存在神经功能异常。术中，使用微尖端导管传感器连续测量椎间孔局部压力，同时在被动运动下改变腰椎姿势，并分析局部压力与腰椎管狭窄术前临床症状之间的关系。
腰椎后伸时椎间孔局部压力显著升高（P<0.001）。屈伸过程中局部压力变化较大的患者行走能力明显较差（P=0.003）。此外，与单节段腰椎管狭窄患者相比，双节段腰椎管狭窄患者屈伸过程中局部压力变化明显较小（P=0.01）。
本研究表明，腰椎管狭窄症神经源性间歇性跛行的发病可能受腰椎神经根动态机械应力变化的影响较大，而非各姿势下神经根的静态机械应力。此外，与单节段腰椎管狭窄患者相比，双节段腰椎管狭窄患者椎间孔内神经根受到的外部应力相对较小，但仍出现了神经根症状。
