The Medical Bulletin

Magnetic resonance imaging (MRI) provides an accurate method of investigating diseases of the spine and spinal cord not previously accessible with other imaging techniques and has become the Agold standard@ in imaging pathologic lesions of all intervertebral disc disorders. [Yochum, TR and Rowe, LJ. Essentials of Skeletal Radiology, Lippincott Williams & Wilkins (3rd, 2005): 536.]

The clinical manifestation of lumbar disc degeneration varies by patient. Some patients may have an injury with an acute onset of pain, or patients may report an insidious onset of pain. Some patients may be completely asymptomatic. The use of MRI quantifies such aspects as loss of disk height, disk dehydration, posterior bulging, impingement due to herniation or facet degeneration, and the like. Despite the accuracy of these tests, it is critical to use imaging studies for confirmation of clinical diagnosis only. [Johnson, TR and Steinbach, LS, eds., Essentials of Musculoskeletal Imaging. American Academy of Orthopedic Surgeons. (2004)] MRI findings are only valuable when they correlate closely with clinical symptoms, as MRI results reveal only anatomic changes and not physiologic significance. [Wilkinson, HA. The Failed Back Syndrome: Etiology and Therapy. Springer-Verlag (2d 1992): 67, 81.]

The clinical meaningfulness of magnetic resonance imaging is uncertain. For example, large variations in lumbar disc and radicular canal morphology have been identified in both symptomatic and asymptomatic individuals. Given this fact, it is believed that the degree of nerve deformation in the spinal canal or intervertebral foramen is more critical to symptom generation than the magnitude of disc herniation. The relation between anatomic impairments and symptoms of lumbar pain, with few exceptions, remains controversial. For example, the presence of disc extrusion and/or ipsalateral, severe nerve compression at one or multiple sites is strongly associated with distal leg pain. Unfortunately, mild to moderate nerve compression, disc degeneration or bulging, and central spinal stenosis are not significantly associated with specific pain patterns. Although the segmental distributions of pain can be determined reliably from pain drawings, this finding alone is of little use in predicting lumbar impairment. The self-report of lower extremity dyesthesias is not significantly related to any specific lumbar impairments. Of the subjects studied, 63 percent had no evidence of nerve root compression on MRI, but 35 percent of these subjects had pain patterns referring distally to the knee. This may be accounted for by the taking of MRIs while patients are in the supine (lying) position rather than in an upright position with spinal loading. Of these subjects, 87 percent demonstrated positive results on straight leg raising testing. For this reason, the diagnosis of disc herniation must be based on history, physical examination findings, and imaging test results. Conventional physical testing does not relate directly to functional deficits. Further, tests for muscle weakness (motor deficit) are subjective in nature and depend on both the effort of the patient and the skills of the physician. This compression may also cause nerve root irritation via chemical mediators. [Beattie, PF, et al. “Associations between patient report of symptoms and anatomic impairment visible on lumbar magnetic resonance imaging.” Spine. 2000; 25(7): 819--828.]

The degree of disc displacement in magnetic resonance imaging did not correlate with any subjective symptoms, nor did nerve root enhancement or nerve compression. Magnetic resonance imaging classification was associated with straight leg raising restriction only to the extent that it could discern nonherniations from herniations. These findings demonstrate that a discogenic pain mechanism other than the nerve root entrapment generates the subjective symptoms among sciatic patients. Specifically, MRI imaging could not distinguish sciatic patients in terms of the severity of their symptoms. [Karppinen, K, et al. “Severity of symptoms and signs in relation to magnetic resonance imaging findings among sciatic patients.” Spine. April, 2001; 26(7): E149--E154.]

Magnetic resonance imaging has been found to underestimate root compression in 28 to 29 percent of cases in which root impingement is not surgically confirmed. [Bartynski, W and Lin, L. “Lumbar root compression in the lateral recess: MR imaging, conventional myelography, and CT myelography comparison with surgical confirmation.” Am J Neurorad. March, 2003; 24: 348--360.]

Similarly, it has been found that magnetic resonance scans were not predictive of the development or duration of low back pain. Individuals with the longest duration of low back pain did not have the greatest degree of anatomical abnormality on the original scans. For this reason, clinical correlation is essential to determine the importance of abnormalities found on magnetic resonance scans. [Borenstein, DG, et al. “The value of magnetic resonance imaging of the lumbar spine to predict low back pain in asymptomatic subjects. J Bone Joint Surg. September 2001; 83-A(9): 1306--1311.]

Results of another study found that disc disruption passing into the outer layers of the annulus, but not resulting in deformation of the outer annular wall, was as frequently associated with lower extremity pain as were discs with a greater degree of aching pain. These findings support the premise that lower extremity pain may be referred from the disc. [Ohnmeiss, DD, et al. “Degree of disc disruption and lower extremity pain.” Spine. 1997; 22(14): 1600--1605.]

Where an MRI reveals the presence of disc extrusion and/or ipsilateral severe nerve compression at one or multiple sites, there is a strong association with distal leg pain. With cases involving mild to moderate nerve compression, disc degeneration or bulging and central spinal stenosis are not significantly associated with specific pain patterns. [Beattie, PF, et al. “Associations between patient report of symptoms and anatomic impairment visible on lumbar magnetic resonance imaging.” Spine. 2000; 25(7): 819--828.]

Disc stimulation studies have found that pain can be referred from the low back to distal locations (lower extremity) extending below the knee. The distal extent of pain was found to depend on the intensity of stimulation. These findings confirm that fact that radiating pain is not necessarily the result of nerve root compression. [O=Neill, CW, et al. “Disc stimulation and patterns of referred pain.” Spine. 2002; 27(24): 2776--2781.]

Although pain drawings showed a significant relationship between pain location and lumbar disc levels identified by CT/discography, pain limited to the low back and buttocks was frequently associated with the absence of disc pathology. Even when limited, good associations of pain drawings and disc pathology were found, other assessments were still recommended. [Ohnmeiss, DD, et al. “Relationship between pain location and disc pathology: A study of pain drawings and CT/Discography.” Clin J Pain. 15: 210-217.] Unfortunately, thermal quantitative sensory testing had a poor predictive value for identifying the anatomic location of a herniated disc. [Samulesson, L, and Lundin, A. Eur Spine J (2002); 11: 71--75.]

Another complicating factor is the lack of understanding concerning the pathophysiologic mechanism causing sciatic pain. Two important mechanisms are believed to be mechanical nerve root compression and chemical irritation of the nerve root by nucleus pulposus tissue. It has been shown that nucleus pulposus tissue alone without compression can cause inflammation affecting nerve roots despite that fact that contact of this material with the nerve root is infrequently associated with such symptoms. In fact, 22 to 23 percent of subjects studied had contact of nucleus pulposus material with the nerve root. [Pfirrmann, CWA, et al. “MR image-based grading of lumbar nerve root compromise due to disk herniation: Reliability study with surgical correlation.” Radiology. 2004; 230: 583--588.]

Human experiments have shown that compression and traction can elicit radicular pain only when the nerve root is inflamed, but the underlying mechanism is poorly understood. Because myelograms, discograms, CT, and MRI frequently reveal abnormal findings in asymptomatic patients, it would appear that the true cause of pain production is more complex than traction or compression of the nerve root. Some secondary changes have been assumed to be critical factors in radicular pain. These include the possibility of chemical radiculitis from inflammatory mediators released by degenerated facets and discs or by an autoimmune reaction that occurs in response to disc herniation. This may be compounded by disturbed cerebrospinal fluid flow caused by compression or fibrosis which may aggravate local circulatory and inflammatory changes, resulting in malnutrition of the nerve root. [Yochum, TR and Rowe, LJ. Essentials of Skeletal Radiology, Lippincott Williams & Wilkins (3rd, 2005): 534--535.]

Further, compression itself can result in increased microvascular permeability of endoneurial capillaries causing intraradicular inflammation. [Kobayashi, S, et al. “Pathology of lumbar nerve root compression: Part 1: Intraradicular inflammatory changes induced by mechanical compression.” J Ortho Res. 2003; 22(1): 170--179.] It was further found that nerve root dysfunction occurred beyond the site of degeneration caused by compression, extending to the primary sensory neurons within the dorsal root ganglion as a result of axon reaction. [Kobayashi, S, et al. “Pathology of lumbar nerve root compression: Part 1: Intraradicular inflammatory changes induced by mechanical compression.” J Ortho Res. 2003; 22(1): 170--179. Kobayashi, S, et al. “Pathology of lumbar nerve root compression: Part 2: Morphological and immunohistochemical changes of dorsal root ganglion.” J Ortho Res. 2003; 22(1): 180.]