Lumbar canal stenosis is most commonly due to degenerative changes in older individuals. Multiple factors can contribute to the development of spinal canal stenosis. The degeneration of vertebral disc often causes a protrusion, which leads to ventral narrowing of the spinal canal. Then the height of the intervertebral space is further reduced, which causes the recess and the intervertebral foramina to narrow, exerting strain on the facet joints. Such an increase in load can lead to hypertrophy of the facet joint, particularly the superior articular process, which in combination propagate spinal instability and hypermobility. The reduced height of the segment leads the ligamentum flavum to form creases. Initial relative instability and hypermobility of the facet joints create the characteristic trefoil-shaped narrowing of the central canal. The resultant venous congestion and hypertension around nerve roots are likely to be responsible for the symptom complex known as neurogenic intermittent claudication. Based on the pathology, spinal stenosis can be categorized into the congenital and the acquired forms. Anatomically, the stenosis can be classified as central, lateral or foraminal. Central stenosis results from the hypertrophy of the inferior facet articular process of cephalic vertebra. Lateral recess and foraminal stenosis are the result of the hypertrophy of the superior facet articular process of caudal vertebra. Neurogenic intermittent claudication resulted from the mechanical compression to the nerve root, the artery and vein surrounding the nerve root, provoking venous congestion or arterial ischemia of nerve root due to hypertension. This vascular compromise leads to an ischemic neuritis that contributes to the clinical symptoms of stenosis. Additionally, moderate constriction induced pressure involving the cauda equina has experimentally been shown to disturb their nutrition and lead to demyelination of the nerve roots.