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Klinische richtlijn rond lage rugpijn en radiculaire pijnPublished by: KCELast published: 2018Guide de pratique clinique pour les douleurs lombaires et radiculairesPublished by: KCELast published: 2018Key diagnostic factors
common
persistent low back pain
The pain in discogenic pathology is usually low back pain, which worsens with axial loading (standing or sitting) and improves with recumbence. The pain is frequently referred to the paraspinal muscles, buttocks, and the back of the thighs. Occasionally, there may be associated pain in a dermatomal distribution or in the groin or flank.
Reproduction of symptoms with spine flexion and ease of pain with extension has also been correlated with degenerative disc disease in the absence of other spine pathology.
There may be a previous episode of acute pain or trauma.
radicular leg pain
Results from nerve root compression. May range in severity from mild constant pain to excruciating pain in the dermatomal distribution of the affected nerve root.
activity-related symptoms
Pain is exacerbated by motion and relieved by rest (activity-related).
Degenerative pathology commonly presents with a limitation of functions and of activity. Daily chores can be affected and symptoms exacerbated by twisting or bending motion.
Other diagnostic factors
common
restriction in lumbar motion
Painful degenerative pathology can be associated with paraspinal muscle spasm. The range of spinal motion can be deranged.
uncommon
positive straight leg raise
If the pain is reproduced by passively raising the extended leg (positive Lasegue sign), it is suggestive of compressive or inflammatory nerve root pathology.
The presence of an acute disc prolapse can lead on to degeneration of the motion segment.
neurological deficit (leg weakness, sensory loss, bladder and bowel symptoms)
The presence of neurological deficit is associated with a dysfunction of the nerve root and/or the cauda equina. Can be caused by advanced degenerative changes, although it is uncommon.
Risk factors
strong
increasing age
Radiographic evidence of disc degeneration commences as early as the third decade of life. The changes increase in prevalence and severity with the passage of time by 3% to 4% per annum.[13][14] However, there is no clear correlation between symptoms and radiological findings.
Narrowing of disc space, loss of disc hydration, spondylophytes, and reactive endplate marrow (Modic) changes are the most common findings.[36] Facet joint degeneration lags behind the disc degeneration by a few decades.[37] Annular degeneration leads to a loss of the ability of the disc to resist torsion and places abnormal stresses on the facet joints.[38] With the passage of time the motion segment goes through the phase of instability to the phase of restabilisation.
genetic influence
The literature points to the fact that genetic influences are more important than the mechanical effects of sporting endeavours, sitting habits, or occupational factors.[20] A UK-based study of twins found the odds of the other twin also having clinically significant disc degeneration was higher in monozygotic twins (OR 6) than dizygotic (OR 2.2).[39]
Genes that are implicated with disc degeneration include the genes that code for collagen I, IX, XI, interleukin 1, aggrecan, vitamin D receptor, MMP-3, and cartilage intermediate layer protein.[40][41][42]
occupation (excessive axial loads, vibrations from transportation)
An association has been noted between occupation-related postures and stresses due to the abnormal loading and lifting mechanics.[19] The use of vibrating equipment is considered particularly hazardous.[36] A study comparing MRI-based disc degeneration between machine drivers, carpenters, and office workers in the 40- to 45-year-old age group noted that back injuries and driving are linked.[43] A longitudinal study involving concrete reinforcement workers and house painters demonstrated that disc space narrowing and spondylophyte formation was seen at least a decade earlier than controls. This indicates that physical work enhances degenerative process and that materials handling and postural loading are occupational factors.[44]
tobacco smoking
Smoking affects the intervertebral discs through several mechanisms. Nicotine-mediated vasoconstriction can lead to ischaemia that affects nutrient exchange in the disc.[45] Malnutrition of the discs can occur through carboxyhaemoglobin-induced anoxia.[46] A direct effect of the smoke condensate has been noted on the annular cell metabolism.
Experiments have demonstrated an inflammatory response, apoptosis, and attenuation of the gene expression of metalloproteinases, leading to a reduced matrix synthesis, and expression of structural genes.[45][47] The result of the faulty synthesis of disc macromolecules and the imbalance between disc matrix metalloproteinases and their inhibitors leads to an avascular disc becoming abnormally vascularised.[47] Passive smoking has been shown to manifest as changes in gene expression that precede histological changes.[48] Clinical results from the Swedish Spine Register demonstrate inferior surgical results in smokers, with inferior quality of health, a more regular analgesic use, and inhibition of fusion.[49]
facet joint tropism and arthritis
Facet joints are diarthrodial joints. Just like other diarthrodial joints, these show changes of osteoarthritis such as reduced joint space, loss of cartilage, sub-chondral sclerosis, and osteophytes. These changes may be associated with pain. The incidence of arthritis of these joints increases with increasing age and is more common at the lower levels.[50][51]
The risk of disc degeneration increases in the presence of facet arthritis. Arthritis changes the orientation of the joints to a more sagittal angulation.[52] This predisposes the motion segment to abnormal mobility.
Asymmetry between the right and left sides of the facet joints is termed facet tropism. This leads to abnormal mechanics that has a bearing on the further disc degeneration. The pattern of loading also has an implication on the type of disc prolapsed.[53]
abnormal pelvic morphology
The shape and morphology of the pelvis determines its ability to compensate for changes in the entire spinal column. Certain parameters can be measured, some of which are seen to deviate from normal values in pathological situations.[54] These include pelvic incidence, sacral slope, pelvic tilt, and lumbar lordosis. Pelvic incidence is the only parameter that is constant throughout adult life and does not change with position of the pelvis due to activities or with concomitant hip or lumbar pathology. This normally measures 60 degrees. The lumbar lordosis in health is within 9 degrees of the pelvic incidence. A pelvic incidence that is lower than the normal values implies a reduced ability of the pelvis to compensate in pathology. Compensation can be measured by parameters such as sacral slope and pelvic tilt.
changes in sagittal alignment
The sagittal alignment can be measured radiologically by way of a plumb line from the centre of the C7 vertebral body and the measurement from the posterosuperior corner of the sacrum. The value is positive if the line is anterior and negative if it is behind the sacrum. Changes in the sagittal alignment that cause the line to fall ≥8 centimetres in front of the sacrum lead to symptoms.[55] A situation of low pelvic incidence and low sacral slope can lead to an overload on the intervertebral discs and lead to a further loss of lumbar lordosis with loss in disc height. Conversely, a high pelvic incidence, high sacral slope, and a high lumbar lordosis load the facets much more and are 'protective' towards disc degeneration.
weak
obesity
diabetes mellitus
Diabetes mellitus is a systemic multi-organ disease that affects bone, cartilage, and connective tissue. Animal experiments have lead to a postulated mechanism for associated disc degeneration: premature and excessive apoptosis of nucleus pulposus cells occurs, which lead to an accelerated transition of these into fibrocartilage, leading to early degeneration.[57] People with diabetes are at higher risk than the normal population for disc degeneration and for spinal stenosis.[58] However, a study of monozygotic twins who are discordant for insulin-dependent diabetes has refuted this association.[59]
atherosclerosis
Aortic atherosclerosis leads to a reduction in blood flow, especially in older people. The association between atherosclerosis and disc degeneration is weak.[60] A significant association has been established between aortic calcification on CT scans and back pain. However, there is no correlation between the extent of calcification and the extent of degeneration demonstrated on CT discography.[61] High serum lipid levels are reported to be predictive of symptomatic disc degeneration.[14][60]
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