Lumbar spinal canal stenosis-special features

1. Introduction

Functional spinal canal stenosis is a treatable cause of mechanical back pain with or without claudication or neurological deficit. Spinal canal is the osteo-ligamentous canal which contains the spinal cord. This canal with its contents can be compared to a passage and passenger. A functional canal compromise occurs either due to decrease in size of the passage, due to increase in size of the passenger or space occupying lesion. It was found that some adults also develop progressive neurological deficits and low back pain in their latter part of life. It is due to acquired spinal canal stenosis due to degenerative spinal changes.

1.1. Functional lumbar canal stenosis

Lumbar canal stenosis can be defined as an anatomical or functional narrowing of the osteoligamentus vertebral canal and/or the intervertebral foramina causing direct compression or indirect compromise of dural sac, the caudal nerve roots and their vasculature, enough to cause symptoms or signs.¹ Schonstrome and others from Gothenberg² quantitatively studied the changes in the dimension of the spinal canal in physiological flexion and extension. They found that from flexion to extension the average reduction in the dimension, ranged from 12 to 30 percent. The majority of our daily activities are carried out by dynamically loaded spine in sagittal plane and therefore changes occurring during flexion, extension and by loading³ must be kept in mind. During flexion the laminae of the two adjacent vertebrae move apart and inter laminar space widens, producing lengthening and thinning of the ligamentum flavum. Dynamic changes in the lateral recess⁴ are less marked than in the central portion of the central canal. They are caused by bulging of the posterolateral annulus with or without disc, into the subarticular portion of the lateral recess. Rotational forces affect the subarticular portion of the lateral recess. Most of the patients are comfortable while they are lying down and have stenotic symptoms precipitated by dynamically loading the spine during standing, walking etc. There are two common types of clinical presentation of stenotic symptoms on loading. The first group of patients have well-localized radicular symptoms and signs, often involving a single root, and their symptoms are produced almost immediately or within a few minutes on spinal loading. The other group of patients complains of ill localized symptoms, which are produced after prolonged walking or standing.⁵ The degenerative process involving the disc begins as early as the late teens or early twenties. Initially, an increase in the water content of the nucleus pulposes predisposes it to generalized bulges or focal herniation through the cartilaginous endplates of the adjacent vertebra (Schmorl's node).⁶ With time, the nucleus pulposus undergoes progressive dehydration which results in loss of height of the disc space. With further loss of water and proteoglycans, the disc becomes brittle and fibrotic and is unable to provide the necessary elasticity for proper support of the vertebral column, a process known as disc desiccation.⁵ A reliable indicator of disc degeneration is the presence of intradiscal gas, which is referred to as vacuum phenomenon and may be visualized by plain radiographs or CT.⁷ The gas is predominantly nitrogen and is unusual in an infected disc space. Early disc desiccation presents as loss of signal intensity on T2 weighted images. Sagittal images are helpful in determining the degree of disc space narrowing. Magnetic resonance imaging also detects marrow changes within endplates adjacent to degenerative discs. Spondylosis is usually seen in association with facet joint degeneration, and multilevel disease is the rule. Degenerative spondylosis is the most common cause of spinal canal stenosis in adults.⁸

1.2. Neurogenic claudication

Neurogenic claudication^9–12 was the term recommended by Verbiest.¹² This is very similar to vascular intermittent claudication produced by occlusive aorto-iliac disease. Verbiest¹² reported symptoms of cauda equina compression simulating vascular claudication in patients with stenotic canals. Claudication means lameness or limping. The term pseudoclaudication was suggested by Kavanaugh¹³ et al in 1968.The pattern is fairly constant for each patient. Sensory symptoms almost invariably precede motor manifestations and patients discontinue activities before weakness develops.¹⁴ The pain rarely follows a sciatic, radicular pattern. It has paraesthetic and dysesthetic qualities described as numbness, coldness, burning and cramping. Coughing and straining has no effect 40. Discomfort may begin primarily in the buttocks, and spread to the posterior thigh and into the leg. Although walking most often precipitates manifestations, standing may also induce them, especially with the back in extension. Other causes of neural compression in a neural canal can result in neurogenic claudication. This includes large central disc herniation and lateral foraminal narrowing. None of these patients had evidence of vascular insufficiency. Both compressive and ischemic factors¹⁵ Claudication distance¹⁶ is not constant in intermittent neurogenic claudication.

1.3. Radiology

The AP diameter of the spinal canal increases caudally and should be considered abnormal if less than 12 mm¹⁷ Narrowing is critical if mid sagittal diameter is under 14 mm in the plain radiograph.¹⁸ Spinal canal stenosis can already be strongly suspected on plain radiographs,¹⁹ which are performed on any patient with back pain. The interpedicular distance was the first feature to draw attention, later, the AP diameter of bony canal was considered to be more worthy. Verbiest⁵ has measured the sagittal diameters of spinal canal during operation at the level of the cephalad and cauded borders of the neural and calculated ratio which is normally less than one and is equal or greater than one in narrow canal. A sagittal diameter of 12 mm is considered as narrow (relative stenosis) and a diameter of 10 mm or less is considered a severely narrowed (absolute stenosis) according to Verbiest.^5,12 Sagittal plane translation greater than 4.5 mm or 15 percent of the anteroposterior diameter of the vertebral body on dynamic (flexion-extension) radiographs should be considered potentially unstable. These values were obtained from the aforementioned experimental study. In CT scan^20,21 one may define 3 main different vertebral images corresponding to three different levels – pedicular image, articular image and discal image. The lateral measurement is more accurate with CT images.¹⁷MRI-^22,23 T1W images – Cortical bone is inseparable from CSF and ligaments. Fatty marrow produces high signal intensity on T1W spin echo and T2W fast spin echo images. In T2W spin echo or gradient echo, the vertebral bodies are of low signal intensity. Normal intervertebral disks are of low signal intensity. The Annulus fibrosis may be seen as a subtle and peripheral region of lower signal intensity in all T2W sequences. Nucleus pulposus is of higher signal Intensity and is traversed horizontally by a dark line that represents the normal inter nuclear cleft. Based on antero-posterior diameter of spinal canal or on the cross sectional area of the dural sac, lumbar canal stenosis can be diagnosed. Cross sectional area of dural sac >100 mm² at the narrowest point is normal and 76–100 mm² is moderately stenotic and <76 mm² are severely stenotic. MRI and CT scan have advantage of direct visualization of both central and lateral canal. MRI has additional benefit of visualization of soft tissue. Diagnostic value of imaging studies for lumbar spinal canal stenosis The term lumbar spinal canal was the word coined by Verbiest.¹² Initially it was described in patients with congenital bony abnormalities like achordroplasia. Later Verbiest(12⁾ found that similar syndromes also occurred in normal population. Even though previous studies were described bony spinal canal stenosis and its manifestations in relation to stenosis our study found that rather than bony spinal canal stenosis, it is the ‘Functional canal stenosis’ produced by various soft tissue components like disc protrusion into the canal, ligamentum hypertrophy and osteophytes of degenerative changes that determine the seventy of symptoms and neurological manifestations. Amudsen's¹¹ study. Examination of deep tendon reflexes shows involvement of ankle jerk in 27.7% of the patients and knee jerk in 17.7% of the patients.

3. Conclusion

Acquired lumbar canal stenosis is by far more common than congenital lumbar canal stenosis. spinal canal stenosis was an under recognized but potentially treatable cause of low back pain. Claudication distance was not constant and does not correlate with severity of disease. Among the evaluated symptoms best improvement after the surgery was seen for radicular pain, claudication distance and for motor weakness. Functional canal stenosis” is more important than bony spinal canal stenosis in clinical presentation.