Lumbar spondylosis
By Dr. A. Vincent Thamburaj, neurosurgeon.
SPONDYLO is a Greek word meaning vertebra. Spondylosis generally means changes in the vertebral joint characterized by increasing degeneration of the intervertebral disc with subsequent changes in the bones and soft tissues. Disc degeneration, spinal canal stenosis, spondylolisthesis are the resultant pathological changes.
Disc degeneration is the commonest pathological manifestation of lumbar Spondylosis.
Lumbar spinal stenosis can be defined as ‘narrowing of the lumbar canal in its central part, the lateral recess or the intervertebral foramen sufficient to impair one or more roots of the cauda, the impairment resulting in pain, unilateral or bilateral neurological deficit or neurogenic intermittent claudication’. Lumbar spinal stenosis appears in different pathological conditions. The form that is discussed here is mainly due to degenerative disease. The epidemiology of lumbar spinal stenosis has changed a great deal in the last few decades, related to the ageing population of industrialized countries, with a growing impact on national health systems.
Anatomy:
The spinal canal is formed anteriorly by the intervertebral disc or the vertebral body, lateral by the pedicles, posterolateral by the facet joints and posteriorly by the laminae or the yellow ligament. The spinal canal has paired lateral openings in each segment, the intervertebral foramina.
The lateral recess if the lateral part of the spinal canal. It begins at the tip of the superior articular process of the inferior vertebra, which is part of the facet joint. It is at this point where the recess is narrowest. After bending laterally around the pedicle it ends caudal in the broader lateral opening of the spinal canal, the intervertebral foramen. The anterior wall of the lateral recess is bounded by the intervertebral disc superiorly, and the vertebral body inferiorly. The lateral walls are formed by the vertebral pedicles. The dorsal wall is bounded by the superior articular process of the lower vertebra, to a small part by the lamina and also by the yellow ligament. In a narrow lateral recess, its dorsal walls built only by the articular process, and it is the degenerative changes of this structure that account for most of the nerve root compressions in lumbar spinal stenosis.
The nerve roots corresponding to each segment are separated from the dural sac at the level of the intervertebral space then they come to lie in the lateral recesses and exit the spinal canal a level below through the intervertebral foramina. At each of these points compression is possible.
Pathogenesis and classification:
The term idiopathic developmental by Verbiest in 1954 as a disease of unknown origin, with a genetic disturbance in which pathological effects are revealed in their entirely only when growth is complete and the vertebrae have attained full size’. This review will concentrate on the type of lumbar spinal stenosis that was classified as idiopathic developmental stenosis by Verbiest or considered to be degenerative lumbar spinal stenosis by other authors. Most authors accept the theory that explains lumbar spinal stenosis through degenerative changes that lead to instability and nerve root compression, which causes problems if the individual anatomy of the spinal canal is unfavorable.
Developmental and congenital factors include some of the anatomical variations that leave less space for the nerve roots, so even minor degenerative osseous changes can lead to nerve root compression: a shallow spinal canal, a trefoil shaped canal, or anomalies of the nerve roots.
Anatomical variations in the orientation, shape, or asymmetry of the facet joints make degeneration more likely that lead to nerve root compression. Degeneration is more likely to cause symptomatic nerve root compression in a narrow spinal canal, than in wide canal in which even pronounced spondylosis or spondylarthrosis may stay clinically silent.
The trefoil shape of the spinal canal is anatomical variation of the spinal canal, caused by the orientation of the laminae and facet joints. Most often it is found at the levels L3 to L5. This condition is considered to be a predisposing factor for the development of lateral recess stenosis through degenerative changes of the facet joints.
Anomalies of the nerve roots, (conjoined roots, redundant roots, transverse roots) can also contribute to the development of signs. A disproportion between the size of the lateral recess and the diameter of an aberrant root is needed to develop symptoms.
Asymmetric facet joints hasten disc degeneration; frontally oriented facet joints allow a wider range of lateral bending and therefore also have a negative impact on disc integrity. At the same time they leave less space in the lateral recess. Sagittally oriented joints allow easier sagittal displacement of a vertebra-development of degenerative spondylolisthesis. Acquired factors include all degenerative changes that lead to osseous and non-osseous nerve root compression.
Morphologically the following forms of impingement of nervous structures occur either alone or in combination can be differentiated in lumbar spinal stenosis:
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Central spinal stenosis
Lateral recess stenosis
Narrowing of the intervertebral foramen
Non-osseous nerve root compression |
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Spinal canal stenosis MRI axial |
Facetal hypertrophy MRI sagittal |
Spinal canal stenosis MRI sagittal |
The causes of central spinal stenosis are spondylarthrosis, formation of spondylotic ridges, thickened lamina, or degenerative spondylolisthesis. Spondylarthrotic facet joints can almost touch, narrowing the posterior portion of the spinal canal. Spondylosis with posteriorly directed oesteophytes, combined with spondylarthrosis can cause marked narrowing of the spinal canal with little space left for the nerve roots and an atrophy of the epidural fat. Thickening of the lamina occurs in advanced cases of degenerative changes and plays a minor role in reducing the diameter of the canal.
Different parameters have been used to measure the extent of central stenosis of the spinal canal, among them measurement of the sagittal diameters of the spinal canal and measurement of the dural tube in square millimeters are commonly employed. The traditional measurement of the sagittal diameter, fewer than 10 mm being considered pathological.
Lateral recess stenosis is the most common form of degenerative spinal stenosis that occurs either alone or in combination with central stenosis. Usually a spondylarthrotic facet joint that narrows the subarticular portion of the spinal canal causes the compression of the nerve root. Measurement of the width of the lateral recess with values of 2 mm and less is considered to be pathological. Another possible point of compression of the nerve root is a narrowing of the most distal part of the lateral recess, the intervertebral foramen.
Degenerative spondylolisthesis (pseudospondylolisthesis or degenerative anterior vertebral translation) affects older patients, but is increasingly seen in middle-aged patients, even at the age of 40, the L4/5 segment being most frequently involved. Sagittal orientation of the facet joints, surgical removal of the inferior articular process and degenerative changes of the superior articular process are the predisposing factors. Due to the anteriorly oriented facet joints, the L5/S1 segment is rarely involved. Typically, the degree of slipping in degenerative spondylolisthesis does not exceed 25%.
Degenerative changes are primarily due to disc degeneration, which occurs with ageing, infection or trauma. A degenerated disc leads to narrowing of the intervertebral space and usually is accompanied by spondylosis, with formation of spondylotic ridges. Degeneration and loss of height of the disc occurs first in the posterior part. This deformation of the disc, combined with the plane of orientation of the facet joints leads to retrolisthesis of the cranial vertebra, which is the most common form of degenerative vertebral translation. A change in the relationship of the facet joints causes subluxation, distension of the joint capsule and spondylarthrosis. Subluxation of the facet joint occurs first and leads to symptoms only in a lordotic posture. Degenerative listhesis may present as lumbar instability, with or without stenosis. In the advanced stage it is fixed, with a thickened capsule and joints, giving rise to permanent symptoms.
Clinical features:
Although a number of patients have permanent symptoms, the majority of patients with lumbar spinal stenosis experience symptoms while standing or walking. Symptoms or signs that occur while walking lead to neurogenic claudication. Over some time of walking distance shortens, sometimes so dramatically as to prevent the patient making more than a few steps. Paucity of findings at physical examination even in a patient with advanced symptoms is typical.
Permanent symptoms and signs unrelated to posture are caused by a permanent compression of the nerve roots. Leg pain, motor deficit sensory deficit and rarely, urinary dysfunction or impotence can be found in this order of frequency.
Intermittent symptoms and signs occur while the patient is standing, including low back pain, referred pain or back weakness. These symptoms are related to a narrowing of the lateral recess while the spine is extended. Therefore, symptoms are triggered or worsened in postures that aggravate lumbar lordosis, including standing, walking, especially downhill or downstairs, as well as while wearing shoes with high heels.
Low back pain is a common complaint for a long time before radicular compression occurs. Back weakness is a specific complaint described by patients as if their back is going to give away, probably caused by a proprioceptive sensation from vertebral joints and muscles. Both complaints, as well as the referred pain (pseudoradicular pain) are due to segmental instability of the spine and are relieved by a posture that diminishes lumbar lordosis: leaning forward while walking, standing, sitting or by lying down. While walking, permanent symptoms can spread to previously unaffected dermatomes or to the other leg, indicating involvement of other nerve roots. Leg pain can even diminish, which is an unexplained phenomenon. Due to postural widening of the foramina, some patients are able to ride a bicycle without complaints, at the same time having intermittent symptoms after only a short walking distance.
Neurogenic intermittent claudication is experienced by up to 80% of patients, depending on the severity of narrowing of the spinal canal. Symptoms and signs leading to it are motor deficit, sensory deficit, leg pain, in that order of frequency and rarely urinary incontinence. Resting with the lumbar spine flexed lessens the symptoms, but not resting in erect posture, in contrast t vascular intermittent claudication. Neurogenic intermittent claudication is caused by the insufficiency of vascular supply in one or more nerve roots of the cauda equine occurring during motor activity and the increased oxygen demand related to it. A focal area of deprived circulation occurs at the point of mechanical compression, with neuronal hyperexcitability that leads to pain or paresthesia. Demyelination or loss of large neuronal fibres leads to weakness and numbness. Another effect of mechanical compression is the archnoidal adhesions that fix the nerve root and impair CSF circulation around it with a negative impact on its metabolism.
Imaging:
Plain X-rays in anteroposterior, lateral and oblique views are useful in showing lumbarisation or sacralisation, in determining the shape of the intervertebral formina and the facet joints, showing spondylosis, spondlarthrosis, retrolisthesis, spondylolysis and spondylolisthesis. Central spinal stenosis or lateral recess stenosis cannot be quantified by this method.
Myelography (out dated now) was helpful in determining the degree and longitudinal extent of stenosis because more than one point of compression may be insufficient.
CT is the best method to evaluate osseous compression and at the same time other structures are visualized. With 3 mm thick slices the size and shape of the spinal canal, lateral recess, facet joints, laminae, as well as the morphology of the intervertebral disc, epidural fat and ligamentum flavum are shown.
MRI is clearly superior to CT in the visualization of non-osseous structures and currently the best method for evaluating the contents of the spinal canal. Despite this, apart of showing disc degeneration in T2-weighted images, it usually does not add substantial information necessary in the diagnosis of lumbar spinal stenosis. However, considering the rapidly growing experience with MRI, which is a non-invasive method the role of MRI in the diagnosis of this disease, will increase. Especially a possibility of performing functional sequences of the lumbar spine would be very valuable.
It is very important that all radiological findings are correlated with the symptoms, since asymptomatic narrowing seen on MRI or CT is often found, either as stenosis of an asymptomatic segment, or in completely asymptomatic patients and should be ignored.
Treatment:
The treatment has to be adapted to the patient, his age and aims. In the majority of patients a significant improvement or a relief of symptoms can be achieved. Radicular symptoms and neurogenic intermittent claudication are more likely to resolve with treatment than back pain, which persists in up to one third of patients.
Conservative treatment consists of analgesia and wearing a lumbar corset, which by alleviating lumbar lordosis can lessen symptoms and increase the walking distance. For a group of patients the relief they experience is satisfactory and the walking distance suffices for their daily needs.
A trial of three months’ duration is recommended as the initial form of treatment, unless motor deficit or progressive neurological deficit is present. Conservative therapy of lumbar spinal stenosis with permanent symptoms is rarely successful on a long-term basis, in contrast to conservative therapy of a herniated disc.
Surgical treatment is indicated if conservative therapy fails, and in the presence of incapacitating permanent symptoms, especially a motor deficit. Depending on the clinical symptoms and signs, and partly due to a different approach to lumbar spinal stenosis three groups of operative procedures are performed:
The decompression procedures are: decompression of the spinal canal, decompression of the spinal canal with decompression of the lateral recess and the intervertebral foramen, selective decompression of the nerve roots.
Weight reduction, and exercises to improve posture and strengthen abdominal and spinal muscles must accompany any form of treatment, surgical or conservative.
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