Abstract
Low back pain (LBP) is an acute or chronic pain in the lumbar or sacral regions [1], is highly prevalent and has substantial socioeconomic implications [2]. Jensen et al noted that low back pain is the second most common reason that patients seek medical care in the United States and that the estimated annual cost of related medical care is more than $8 billion [3]. Robertson noted also that the rate of low back–related disability has grown at a rate 14 times that of the population during the last 30 years [3]. MRI is established as the investigation of choice for assessing patients presenting with low back pain (LBP) and sciatica; recognised causes of nerve root compression include disc herniation and spinal stenosis, however many patients presenting with LBP and pain referred to the lower limb(s) show no evidence on imaging studies of nerve root compression, suggesting that there are other factors involved in the production of pain [4]. One of the prominent somatic sources of low back pain is the internal disc disruption of the lumbar spine, the socalled discogenic lumbar pain, which is the condition causing back pain without radiculopathy [5]. The annulus fibrosus is innervated by the recurrent meningeal nerve and by the small branches from the ventral ramus of the somatic spinal nerve; a proposed mechanism for such pain is inflammation of nerve roots (chemical radiculopathy) from leak of degenerative nuclear material through full-thickness annular tears [4, 5]. Compared with asymptomatic disks, painful disrupted lumbar intervertebral disks have higher concentrations of sensory fibers in their endplates and nucleus; this high concentration of sensory fibers, combined with increased levels of proinflammatory mediators such as IL-8 and PGE2, provides a substrate for hyperalgesia and presumably pain [6]. In this hyperalgesic state, even normal mechanical loading will be painful [6]. The concept of diskogenic pain caused by nocioceptive ingrowth into annular fissures has been supported only indirectly by observing a strong correlation between pain provocation and the presence of annular fissure during provocation diskography and subsequent CT imaging; annular fissures reaching the outer annular fibers are in fact the source of symptoms in patients suffering from chronic diskogenic LBP [6]. Discogenic lumbar pain is characterized by nonradicular pain, has a somatotropic rather than dermatomal pattern of pain projection; therefore, the use of symptoms and clinical findings to localize the level of abnormality is difficult; the source of discogenic pain is still unknown [7]. Ideally, a history and physical examination would consistently diagnose the source of a patient’s low back pain, and, if one diagnosed pain secondary to the intervertebral disc, one would be able to identify the exact level or levels involved; in reality, however, the exact source of low back pain is often illusive, because discogenic pain projects in a somatotropic rather than a dermatomal pattern, confirming and localizing a discogenic source, much less the exact level, using clinical findings alone remains unproven [8]. MR imaging provides an unique means to evaluate the morphologic status of intervertebral disks and their relationship to neural structures in patients with low back pain; moreover, the technique allows assessment of the biochemical status of the disk on T2-weighted spin-echo and fast spin-echo MR images [7]. One of the first structural abnormalities that predicted concordant pain provocation during disc stimulation was high-signal-intensity zones (HIZ) at first described by Aprill and Bogduk in 1992 [8]. HIZ are defined as small foci of high signal intensity at:
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