spinal stenosis

[문형철]

About spinal stenosis
1. 역사.
 Verbiest in 1954 was the first to recognize that structural narrowing of the vertebral canal could compress the cauda equina and produce claudication symptoms.

2. 개괄.
 50-70대의 symptomatic lumbar spinal stenosis incidence : 1.7 - 10%이다.
 Symptoms usually affect men aged more than 50 years. They complain of discomfort in the thighs, calves, and feet when walking. Bilateral symptoms occur with a male:female ratio of 8:1, whereas the ratio in unilateral claudication is 3:1
 참고) Males and females seem to be affected equally with spinal stenosis, however, women are afflicted with associated with degenerative spondylolithesis 4 times more often than men.

3. spinal stenosis의 분류.
 1) Central stenosis.
 2) Lateral stenosis.
 3) Mixed type stenosis.
 참고) 증상에 의한 분류 1) Bilateral claudication. 2) Unilateral claudication.

4. 진단도구.
 1) walking tolerance - exercise treadmill.
 2) EMG - motor, somatosensory evoked potential.
 3) plain radiograph.
 4) CT - Measured spinal dimension
    가. pedicle length.
    나. interpedicular distance.
    다. AP diameter : 대개 13-20mm까지를 정상으로 보고 11.5mm이하를 비정상으로 해석.
    but, there is no general agreement concerning the most relevant structure to measure.
 5) MRI.
 6) Myelography is the best diagnostic modality to eval‎uate the spine dynamically.
 7) 참고) peripheral circulation진단을 위해 Doppler studies.

 참고) CT AND MRI 진단의 Interobserver and Intraobserver Reliability 문제.....
 참고) 질문지에 의한 SEVERITY등의 감별....

5. Pathology.
 1) disc herniation(barrel contents mechanism 또는 container content difference).
 2) ligamentum flavum hypertrophy(정상치는 2-4mm) - greater contributor.
 3) facet hypertrophy
   cf) facet joint는 다른 synovial joint와 마찬가지로 arthritic change, degenerative change,
     osteosclerotic change, hypertrophic change를 보인다.
     ---> pseudospondylolithesis가 가장 큰 영향을 준다.
 4) spondylolysis and spondylolithesis - anterior spondylolithesis는 대개 L4-5, L5-S1에서 발생
                                       posterior spondylolithesis는 대개 L3위에서 발생.
                                    - second contributor.
 5) cyst of the facet capsule and ligamentum flavum - L 4-5에서 가장 흔하게 발생.
 6) vertebral compression fracture - 하지만 most osteoporotic compression fracture affect the anterior
    body causing a wedge-shaped deformity.
 7) lumbar spine after surgery.

1. Spinal stenosis has unfortunately become synonymous with neurogenic claudication, but a shallow canal is only one factor in the pathology. Spinal stenosis is sometimes entirely symptomless, 2 and stenosis is also a factor in other back pain syndromes, including disc protrusion and root entrapment from degenerative change. In addition, symptoms of claudication are unusual before the sixth decade of life, even though the vertebral canal will have been narrow for many years. Even in ach[안내]태그제한으로등록되지않습니다-[안내]태그제한으로등록되지않습니다-ondroplasia, with marked development stenosis, symptoms are not present in early life. The small canal is, therefore, but one factor in the pathology.

2. Degenerative soft tissue and bony pathology is invariably present in patients with neurogenic claudication. The ligamentum flavum is usually thickened or ossified. Some patients have diffuse idiopathic spinal hyperostosis (DISH) or Paget's disease(변형성 골염).

3. Vertebral displacement with an intact neural arch will critically narrow an already small canal. Degenerative spondylolisthesis effectively reduces the canal size at the level of displacement. Although degenerative spondylolisthesis is more common in women, bilateral neurogenic claudication is more common in men, and approximately half the men with bilateral claudication have a degenerative spondylolisthesis.7 The rotatory effect of a degenerative lumbar scoliosis can be an important factor in unilateral claudication.

4. The neuropathology is probably the result of inadequate oxygenation or accumulation of metabolites in the cauda equina. Nerve function is probably just adequate at rest but inadequate during exercise. The ischemic effect of compression on nerve function has been studied in animal models.3,4 However, it is of interest that ablation of the lumbar arteries after aortic surgery is rarely followed by claudication symptoms.

5. Central stenosis at one level does not account for the symptoms. There are a number of clinical reasons why central stenosis alone does not explain the mechanism of claudication.
First, a steadily progressing spinal tumor can completely block the central vertebral canal without
      producing claudication.
Second, a large central disc protrusion can block the canal without claudication.
Third, a single level stenosis from degenerative change at L3-L4 or L4-L5 may almost occlude
       the dural sac and yet produce only back pain.
Furthermore, imaging of asymptomatic subjects confirm‎s that stenosis is common, and
     patients who present with claudication must have had symptomatic stenotic canals for many years.
Again, it is surprising that in canine(개과의) studies a single level experimental stenosis constricting
      the cauda equina by 25% did not cause neurologic deficit.3

6. Root canal stenosis does not account for the symptoms. A number of authors have thought that root canal stenosis or foraminal stenosis is responsible for claudication symptoms. However, isolated root canal stenosis may be asymptomatic or on other occasions responsible for the constant root pain of root entrapment but not claudication. If root canal pathology was important, why do patients with neurogenic claudication invariably have central canal stenosis?

7. One of the radiologic features of neurogenic claudication is the high frequency of multiple level stenosis in the central or root canals(Figure 1). The venous anatomy of the roots of the cauda equina make them vulnerable to congestion at multiple levels. The veins of the roots (which do not anastomose between roots) generally drain distally to the foramen or, if this is occluded, proximally to the conus. A single low pressure block will affect only a small section of the root and probably not disturb conduction. However, in the presence of two low pressure blocks, there will be venous congestion in the intervening segment. The arterioles will continue to feed the segment at the higher arterial pressure, but impaired drainage will reduce the blood flow, the oxygen supply, and the nutrition, with a build-up of metabolites in the uncompressed segment between the two blocks (Figure 2).This hypothesis is compatible with experimental studies. A single level compression of 10 mm Hg in a porcine cauda equina model had little effect on the function, but a two-level compression of 10 mm Hg caused marked reduction of blood flow by 64%, 9 and there was significant reduction in protein transport and nerve conduction.4 A two-level compression below arterial pressure is also supported by the myeloscopy studies, which show congested cauda equina in claudicating patients.5 A two-level stenosis hypothesis must include at least one level of central canal stenosis, but the second level of stenosis could either be in the central or in the root canal. Two levels of central stenosis will cause venous congestion in all the roots of the cauda equina between the two blocks. However, central stenosis at one level and bilateral root canal stenosis at the lower level will congest only two roots. Proximal central stenosis and distal unilateral root canal stenosis will produce single root congestion (Figure 3). This would explain why the symmetrical displacement in a degenerative spondylolisthesis is usually associated with bilateral and not unilateral claudication. The degenerative process is symmetrical, with central stenosis at one level and bilateral root canal stenosis at a more distal level. With degenerative lumbar scoliosis, however, the asymmetrical degenerative process is more likely to produce root claudication.

8. If venous pooling of the nerve roots of the cauda equina between two levels of low pressure stenosis is responsible for the symptoms of neurogenic claudication, one has to ask why are symptoms usually not present at rest but only when walking. One might argue that the block pressure at each level of stenosis will increase with the dynamic activity of walking. There will be local vasodilatation of the radicular arteries in response to exercise. Exercising the single limb of a mouse will produce vasodilatation in the ipsilateral region of the spinal cord. Blood flow in the nerve root is also increased with peripheral nerve stimulation. One might expect, therefore, that the arteries of the cauda equina will dilate with exercise, and if space is already at a premium, the stenosis block pressure will rise to a critical level. Other features associated with walking will tend to increase the block pressure. Movement in the sagittal plane alters the epidural pressure at the site of stenosis, being above normal pressure even in flexion (15-18 mm Hg) and greatly above venous pressure in extension (80-100 mm Hg). Segmental rotation associated with walking might also significantly affect the root canal where the degenerate capsule of the facet joint limits available space for the nerve root complex. In addition, the increased venous return from the exercising lower limbs will be accompanied by engorgement of the pelvic veins and Batson's venous plexus, reducing the available space for the cauda equina. Extra dural venous engorgement will then contribute to the block pressure. There may be some patients with stenosis pressures at rest below the venous pressure, which rise above the venous pressure with exercise. However, one would expect that there will be some patients with multiple level stenosis who will have block pressures at rest above the venous pressure but not have leg symptoms at rest.
9. We have reported how there is considerable arterial vasodilatation of the porcine cauda equina to electrical stimulation and that this vasodilatation response is impaired in the presence of a two-level low pressure compression. We have observed that in the response to stimulation and in the absence of any compression, there is an arterial vasodilatation producing 200% increase in the blood flow of the cauda equina, and this is maintained over 30 minutes (Figure 4, 5). However, in the presence of a double level low pressure compression, the increase in blood flow after stimulation is less pronounced and is maintained only for a few minutes (Figures 6, 7). The blood flow then rapidly falls to approximately 60% below the resting level. There is then a failure of nerve conduction.