Elsevier; Wilke H-J, Volkheimer D. Basic Biomechanics of the Lumbar Spine. In: Biomechanics of the Spine. Disc Herniation. In: StatPearls [Internet]. Next Page: L3-L4 Treatment. So sciatic pain will potentially refer to any of those areas innervated from L3 to S3 levels these levels innervate the back of the leg and femoral nerve impingement will cause pain L2-L4 levels these dermatomes innervate the front of the thigh which provide both feeling and power to the front of the thigh.
Things to be aware of that are clinically significant and indicate that you need to take further action when you have sciatica are:. For the femoral nerve, this generally provides both feeling and power to the front of the thigh it innervates what we call the hip flexors and knee extensors. Movements such as climbing stairs the knee may unstable and prone to buckling will be difficult as your thigh muscles will feel weak.
Pain may also be felt on the side of the buttock, groin, inside of the knee and lower leg. It is also worth mentioning that all the muscles in the legs are also innervated by nerves from different levels in the spine as well. These are called myotomes. The information you give us in clinic and our clinical testing will help establish at which level in your spine you have a trapped nerve. There are a few terms commonly used when describing discs which we can quickly clarify.
A disc bulge is where the outer wall of the disc bulges out from its normal position. The disc wall is not broken, and the nucleus material is contained inside the disc. As the disc bulges, it may press against nerves directly. Often a bulge can be associated with a loss of disc height and this may lead to impingement of a nerve as it exits the spinal canal via a gap called a foramen between two vertebrae.
A herniated disc is the same as a prolapsed disc. This is where the nucleus of the disc breaks through the outer disc wall. There will be a loss of disc height as the disc loses pressure and the nucleus material can press directly on to the spinal nerves causing pain.
Or, the material of the disc nucleus may act as a biochemical irritation to the nerve in which case the result is the same… pain! It can imply a disc bulge or a herniation, usually a herniation.
Moreover, the intervertebral disc, which is composed of a gelatinous, centrally located nucleus pulposus and a peripherally located annulus fibrosus, is prone to rupture or herniate posteriorly or posterolaterally as a result of degenerative changes or trauma, producing neural element compromise. Normal anatomic structures of the lumbar spine at the third through the fifth lumbar levels.
Note the close association between the nerve roots and the dural tube, and the ligamentum flavum, the facet joints, the pedicles and the lamina. The ligamentum flavum inter-laminar ligament attaches laterally to the facet capsules.
Axial computed tomographic CT scan at a single lumbar vertebral level following injection of intrathecal contrast medium. Note the lumbar canal narrowing produced by hypertrophic lamina and pedicles.
In the lumbar regions, the cone-shaped terminus of the spinal cord conus medullaris normally ends at about the L1 or L2 level in adults. Caudal to these levels, the roots of the cauda equina are contained within the subarachnoid space of the dura-enclosed thecal sac Figure 3.
Thus, canal stenosis at lumbar levels results in nerve root dysfunction rather than spinal cord dysfunction. Posterior view of the lumbar region of the spinal canal, demonstrating the conus medullaris at the L1 to L2 level and the cauda equina nerve roots inferiorly.
Narrowing of the lumbar canal has many potential causes, and various classification schemes have been devised in order to better describe the pathophysiology of this condition. A classification system proposed by Verbiest 5 categorizes the multiple causes of lumbar stenosis into two types: conditions that lead to progressive bony encroachment of the lumbar canal including developmental, congenital, acquired and idiopathic causes or stenosis produced by nonosseous structures such as ligaments, intervertebral discs and other soft tissue masses.
For practical purposes, however, the etiologies of lumbar stenosis can be divided into congenital or acquired forms. Few causes of lumbar stenosis are truly congenital. These anatomic changes may lead to clinically significant stenosis if additional elements such as herniated intervertebral discs or other space-occupying lesions further narrow the canal and contribute to the compression. In most cases, stenosis of the lumbar canal may be attributed to acquired degenerative or arthritic changes of the intervertebral discs, ligaments and facet joints surrounding the lumbar canal.
These changes include cartilaginous hypertrophy of the articulations surrounding the canal, intervertebral disc herniations or bulges, hypertrophy of the ligamentum flavum and osteophyte formation. Some investigators have postulated that the pathologic changes that result in lumbar canal stenosis are the result of so-called micro-instability at the articular surfaces surrounding the canal. These movements are clinically silent yet may result in progressive loss of strength in the joint capsules and lead to reactive bony and cartilaginous hypertrophy, thickening or calcification of the ligamentum flavum, or subluxation of one vertebra on another spondylolisthesis , all of which may contribute to narrowing of the lumbar canal.
Compression of the microvasculature of the lumbar nerve roots, resulting in ischemia, is believed to be a major contributing factor in the development of neurogenic claudication. Wilson 8 classified neurogenic claudication into two major types based on the putative pathophysiologic mechanism: postural or ischemic.
Postural neurogenic claudication is induced when the lumbar spine is extended and lordosis is accentuated, whether at rest or during exercise in the erect posture.
With extension of the spine, degenerated intervertebral discs and thickened ligamenta flava protrude posteriorly into the lumbar canal, producing transient compression of the cauda equina. In the ischemic form, it is theorized that transient ischemia occurs in compressed lumbosacral roots when increased oxygen demand occurs during walking. Other acquired conditions that can be associated with lumbar canal stenosis as a result of osseous or fibrocartilaginous hypertrophy include fluorosis, hyperparathyroidism, Paget's disease, ankylosing spondylitis, Cushing's disease and acromegaly.
Men are affected with slightly higher frequency than women. Although symptomatic lumbar stenosis is usually a disease of the middle-aged and the elderly, younger patients may also be affected. Typically, the earliest complaint is back pain, which is relatively nonspecific and may result in delayed diagnosis. Patients then often experience leg fatigue, pain, numbness and weakness, sometimes several months to years after the back pain was first noticed.
Patients may undergo minor trauma that can exacerbate symptoms, which may lead to a more rapid diagnosis. Once the leg pain begins, it is most commonly bilateral, involving the buttocks and thighs and spreading distally toward the feet, typically with the onset and progression of leg exercise. The lower extremity symptoms are almost always described as burning, cramping, numbness, tingling or dull fatigue in the thighs and legs. Disease onset is usually insidious; early symptoms may be mild and progress to become extremely disabling.
Symptom severity does not always correlate with the degree of lumbar canal narrowing. Classically, the symptoms of lumbar canal stenosis begin or worsen with the onset of ambulation or by standing, and are promptly relieved by sitting or lying down. Thigh or leg pain typically precedes the onset of numbness and motor weakness.
Along with numbness and weakness, these symptoms and signs constitute the syndrome of neurogenic intermittent claudication. Patients commonly complain of difficulty walking even short distances and do so with a characteristic stooped or anthropoid posture in more advanced cases.
Although standing and walking exacerbate the extreme discomfort, bicycle riding can often be performed without much difficulty because of the theoretic widening of the lumbar canal that occurs with flexion of the back. Some patients actually obtain transient relief of pain by assuming a squatting position, which flexes the trunk. Conversely, lying prone or in any position that extends the lumbar spine exacerbates the symptoms, presumably because of ventral in-folding of the ligamentum flavum in a canal already significantly narrowed by degenerative osseus changes.
Other common symptoms include stiffness of the thighs and legs, back pain which may be a constant symptom and, in severe cases, visceral disturbances such as urinary incontinence that may be a result of impingement of sacral roots. Back pain, a symptom in nearly all patients with lumbar stenosis, 5 may be present with or without claudication, particularly in the earlier stages of the disorder.
Physical examination of patients with suspected lumbar stenosis should begin with examination of the back. The curvature of the spine should be noted, and the mobility and flexibility of the spine with any changes in neurologic symptoms during active flexion or extension should be recorded particularly the presence of leg pain, paresthesias or numbness with extension of the spine.
The skin should be inspected for the presence of any cutaneous signs of occult spinal dysraphisms. Occult spinal dysraphisms, or occult spina bifida, are failures in the complete closure of the neural vertebral arches, which often have external signs indicating their presence. These signs may include patches of hair, nevi, hemangiomas or dimples on the lower back in the midline.
These conditions are rare in the adult population, however. Most patients with a true positive straight leg raising sign complain of excruciating sciatica-like pain in the elevated leg at 30 to 40 degrees of elevation. This sign is usually absent in patients with lumbar stenosis. It should be noted that herniation of disc material and subsequent reparative processes may contribute to the overall picture of stenosis, but acute disc herniations generally produce a clinical picture that differs from the more chronic symptoms of canal stenosis.
Patrick's sign, which reproduces leg pain with lateral rotation of the flexed knee, implies ipsilateral degenerative hip joint disease. This is an important piece of the differential diagnosis in patients with stenosis, some of whom may have both conditions. The neurologic examination in patients with idiopathic degenerative lumbar stenosis may not reveal significant sensorimotor deficits at rest or in a neutral position.
Deep tendon reflexes may be decreased, absent or normal, depending on the chronicity of the caudal root compression.
Upper motor neuron signs, such as hyperactive deep tendon reflexes or the presence of pathologic reflexes, such as the Babinski's sign or Hoffmann's sign, are typically absent unless there is injury to descending long tracts.
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