By Mark L. Dumonski, MD
Lumbar disc herniations represent one of the most common conditions encountered in a typical spine clinic. Symptoms can range from a patient being completely asymptomatic, to leg pain (commonly referred to as “radiculopathy” or “sciatica”), to a profound and debilitating loss of bowel and bladder control. The latter condition is called “cauda equina syndrome”, and while much less common than radiculopathy, does have the potential to lead to permanent bowel, bladder, and sexual dysfunction. Over the course of a lifetime, approximately 1% of people can expect to have symptomatic lumbar disc herniations. The known risk factors associated with disc degeneration include a history of smoking, heavy lifting, and increased age. However, the most significant influence in the advancement of disc degeneration is genetics.
How does a degenerated intervertebral disc differ from a “healthy” disc?
As intervertebral discs age, various biomechanical changes take place which, in turn, compromise their structural integrity. This inevitable process, commonly referred to as “degenerative disc disease”, has various implications. As the degenerative process ensues, the outer portion of the disc, termed the “annulus fibrosis”, weakens. In addition, the inner portion of the disc, known as the “nucleus pulposus”, also degenerates. This combination of the weakening annulus and the degenerating nucleus pulposus sets the stage for a disc herniation.
Patients with radiculopathy often complain of pain in a specific distribution that correlates to the nerve (or nerves) that are being compressed. For example, a patient with a disc herniation causing compression of the S1 nerve root (usually from an L5/S1 disc herniation) will typically complain of pain along the back of the thigh, the back of the calf, and the outside of the foot. Similarly, L4 and L5 nerve compression causes pain in their own characteristic patterns. Weakness may or may not be present. Impulses carried through the L4 and L5 nerves are responsible for keeping the toes pointed upward when walking. Therefore, weakness associated with compression of these nerves may lead to what is commonly referred to as a “foot drop”. This is tested in an examination by asking a patient to “heel-walk”. Alternatively, S1 nerve compression may cause weakness during the step-off phase of gait (when attempting to raise the heel off the ground), and is typically tested by asking a patient to “toe-walk”. Quite often, the weakness outlined above may not be noticed during day-to-day activities, but is readily detected on physical examination.
Magnetic resonance imaging (MRI) is the imaging study of choice in diagnosing lumbar disc herniations. Disc herniations are described as protrusions, extrusions, or sequestrations. A protrusion, simply put, is a disc “bulge”. This would appear similar to what one might see if a balloon was squeezed between the hands. A disc extrusion is present when a more significant portion of the inner disc material extrudes through the outer lining of the disc (figure 1). This situation is the most common cause of symptomatic disc herniations, and is frequently likened to the appearance of jelly being squeezed out of a jelly donut. A sequestered fragment is one in which there is no continuity between the fragment and the disc it came from (i.e. “a free fragment”). Some patients are unable to get an MRI due to the presence of a pacemaker, significant obesity, or claustrophobia. In these patients, CT-myelography is the test of choice. In this test, dye is injected into the spinal canal and a computerized tomogram (“CT scan”, or “CAT scan”) is obtained.
MRI image demonstrating a typical posterolateral disc herniation (white arrow)
In the acute setting, bed rest may be advised but should be limited to no more than 2-3 days. After this timeframe, patients are encouraged to pursue light activity as tolerated. It is important for patients to understand that, although significant discomfort with activities may be present, this is unlikely to cause any additional damage. In addition, prolonged immobilization is not without consequence and can have a number of deleterious effects (blood clots, depression, weight gain, altered pain thresholds, etc.). Additional nonoperative treatment options include anti-inflammatory medications, oral or injected steroids, and physical therapy. Nonoperative treatment should always be the initial treatment plan unless a significant neurologic deficit is present.
Patients with ongoing symptoms following at least 6 weeks of nonoperaive treatment are candidates for operative intervention. Various surgical techniques have been described to achieve fragment removal and decompression of the neural elements. In general, a midline 1-2 inch incision is made over the indicated segment, a “laminotomy” is performed, and the fragment is removed. “Laminotomy” refers to a procedure in which a small amount of bone is removed in order to gain access to the spinal canal, and ultimately to the herniated disc fragment. Typically, patients are discharged home the same day and are allowed to return to full activities shortly thereafter.
Lumbar disc herniations are common. When symptomatic, significant pain and disability may result. A patient’s history, physical examination and imaging studies are typically diagnostic. Radiculopathy, or “sciatica”, should be treated nonoperatively for at least 6 weeks, while cauda equina syndrome requires urgent attention as it may ultimately lead to permanent weakness and significant disability. In the absence of a profound neurological deficit (requiring urgent surgical intervention), patients with persistent symptoms following nonoperative treatment are candidates for surgical removal of the herniated fragment and decompression of spinal canal.
1. Battié MC, Videman T, Parent E. Lumbar disc degeneration: epidemiology and genetic influences. Spine: 2004 29:2679-90
2. Videman T, Battié MC, Parent E, et al. Progression and determinants of quantitative magnetic resonance imaging measures of lumbar disc degeneration: a five-year follow-up of adult male monozygotic twins. Spine. 2008: 33:1484-90
3. Battie MC, Videman T, Gibbons LE, et al. 1995 Volvo Award in clinical sciences. Determinants of lumbar disc degeneration. A study relating lifetime exposures and magnetic resonance imaging findings in identical twins. Spine 1995: 20:2601–12.
4. Sato K, Kikuchi S, Yonezawa T. In vivo intradiscal pressure measurement in healthy individuals and in patients with ongoing back problems. Spine 1999 24:2468-74
5. Fujiwara A, An HS, Lim TH, Haughton VM. Morphologic changes in the lumbar intervertebral foramen due to flexion-extension, lateral bending, and axial rotation: an in vitro anatomic and biomechanical study. Spine 2001 26:876-82.
6. Rabin A, Gerszten PC, Karausky P, et al. The sensitivity of the seated straight-leg raise test compared with the supine straight-leg raise test in patients presenting with magnetic resonance imaging evidence of lumbar nerve root compression. Arch Phys Med Rehabil 2007 88:840-3
7. Ohshima H, Hirano N, Osada R, et al. Morphologic variation of lumbar posterior longitudinal ligament and the modality of disc herniation. Spine 1993 18:2408-11
8. Forristall RM, Marsh HO, Pay NT. Magnetic resonance imaging and contrast CT of the lumbar spine. Comparison of diagnostic methods and correlation with surgical findings. Spine 1988 13:1049-54
9. Fardon DF, Milette PC; Combined Task Forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology. Nomenclature and classification of lumbar disc pathology. Recommendations of the Combined task Forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology. Spine 2001 26:E93-E113
10. Schaufele MK, Hatch L, Jones W. Interlaminar versus transforaminal epidural injections for the treatment of symptomatic lumbar intervertebral disc herniations. Pain Physician 2006 9:361-6
11. Vad VB, Bhat AL, Lutz GE, et al. Transforaminal epidural steroid injections in lumbosacral radiculopathy: a prospective randomized study. Spine 2002 27:11-6
12. Colonna PC, Fredienburg Z. The disc syndrome. J Bone Joint Surg [Am]
13. Bush K, Cowan N, Katz DE, et al. The natural history of sciatica with
associated disc pathology: A prospective study with clinical and independent
radiologic follow-up. Spine 1992 17:1205–12
14. Ahn UM, Ahn NU, Buchowski JM et al. Cauda equina syndrome secondary to lumbar disc herniation: a meta-analysis of surgical outcomes. Spine 2000 25:1515-22
15. Kohles SS, Kohles DA, Karp AP, et al. Time-dependent surgical outcomes following cauda equina syndrome diagnosis: comments on a meta-analysis. Spine 2004 29:1281-7
16. Atlas SJ, Deyo RA, Keller RB, et al. The Maine Lumbar Spine Study, Part II. 1-year outcomes of surgical and nonsurgical management of sciatica. Spine 1996 21:1777-86
17. Atlas SJ, Keller RB, Chang Y, et al. Surgical and nonsurgical management of sciatica secondary to a lum bar disc herniation: five-year outcomes from the Maine Lumbar Spine Study. Spine 2001 26:1179-87
18. Atlas SJ, Keller RB, Wu YA, et al. Long-term outcomes of surgical and nonsurgical management of sciatica secondary to a lumbar disc herniation: 10 year results from the maine lumbar spine study. Spine 2005 30:927-35
19. Weinstein JN, Lurie JD, Tosteson TD, et al. Surgical versus nonoperative treatment for lumbar disc herniation: four-year results for the Spine Patient Outcomes Research Trial (SPORT). Spine 2008 Dec 33:2789-800.