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Lumbosacral Disc Injuries Clinical Presentation

  • Author: Robert E Windsor, MD, FAAPMR, FAAEM, FAAPM; Chief Editor: Craig C Young, MD  more...
 
Updated: Oct 12, 2015
 

History

The natural history of LBP is frequently reported as being benign, with 40-50% of people becoming symptom free in 1 week and 90% having resolution without medical attention in 6-12 weeks. Recurrence rates are reported to be 60-85% in the first 2 years after an acute episode of LBP. Other studies have not shown such good outcomes. Deyo and Tsui-Wu found that 33.2% of patients with LBP had symptoms shorter than 1 month, 33% had pain for 1-5 months, and 32.7% reported pain lasting longer than 6 months.[6] Furthermore, 15-20% of patients showed moderate to severe activity limitations at a 1-year follow-up visit.

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Physical

Perhaps the best-known clinical entity involving the lumbosacral intervertebral disc is a protrusion or extrusion resulting in radiculopathy. Physical examination of the lumbar spine evaluating for radiculopathy should focus on a mechanical and neurologic examination.

A mechanical examination should evaluate for posture, segmental motion, lumbopelvic rhythm, and sacroiliac function.

Typical postural deficits include a rotation and listing to one side or the other. The direction of listing and rotation is determined by the direction of disc herniation and may cause the body to bend toward or away from the side of involvement. Other postural deficits include a loss of normal lordosis and/or being unable to stand erect.

Segmental examination focuses on the motion of one vertebra on another as the spine side bends to each side, flexes, extends, and rotates. Not only does the examiner focus on the normal, synergistic glide or lack thereof, but also on where or if the spine pivots at a particular segment and if the patient reports or demonstrates pain with a particular motion. Segmental examination should also be performed with the patient prone on an examination table by gently palpating the spinous process of each vertebra and evaluating it for its segmental motion in the axial plane and assessing whether it induces pain.

Neurologic examination evaluates for signs of nerve root inflammation and neural deficit.

Various methods exist for evaluating nerve root inflammation including the seated or supine straight-leg raise, the Braggart test, and prone hip extension test. The straight-leg and Bruggart tests evaluate the lower lumbar and upper sacral nerve roots, whereas the prone hip extension test test evaluates the upper lumbar nerve roots. A detailed sensory examination should also be performed to evaluate at least the L1-S1 dermatomes.

The motor examination should evaluate the strength of representative muscles of the L4 through S1 myotomes. The typical muscles that are examined include the tensor fascia lata, quadriceps, tibialis anterior, extensor hallucis longus, peroneal group, and posterior tibialis. Deep tendon reflexes (DTR) should also be performed, including the knee jerk (L4), medial hamstring (L5), and ankle jerk (S1).

The sacroiliac joints are evaluated in the standing, seated, and supine positions. A Gillet maneuver is performed in the standing position by evaluating the motion of the posterior superior iliac spine (PSIS) compared with the spinal midline and to the opposite side. This same maneuver should be also performed with the patient seated on a stool to differentiate between a sacroiliac (former) and an iliosacral (latter) dysfunction.

Indications of malingering include repetitive or inconsistent "give way" weakness that does not appear to be pain induced, pain out of proportion to examination maneuver, or pain in an area unrelated to the maneuver being performed.

Some typical features in the history of radiculopathy with a herniated nucleus pulposus are leg pain in a dermatomal distribution, exacerbation of pain with a sitting position, and amelioration of pain during standing or ambulation. This type of injury is typically a flexion, rotation, or combined flexion-rotation injury. On physical examination, root tension signs are positive and dermatomal or myotomal deficits are present. Based upon a typical history and physical examination, a presumptive diagnosis of radiculopathy secondary to herniated nucleus pulposus can be made. Appropriate care at this time may be 4-6 weeks of conservative, nonsurgical treatment.

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Causes

Disc degeneration

The widely accepted pathophysiologic process of the degenerative cascade has been well described by Kirkaldy-Willis and other investigators.[9] The following discussion highlights sequential changes that affect the entire motion segment during degeneration intermixed with how these anatomic changes relate to specific clinical presentations. The process has been described as occurring in 3 phases, which often overlap one another.

Phase I or the dysfunctional phase, is characterized anatomically by circumferential tears in the outer annulus, which may be accompanied by endplate separation or failure leading to an interruption of diffusion, resulting in impairment of the disc's nutritional supply and waste removal. These changes appear to be secondary to repetitive microtrauma.

Tears within the outer one third of the annulus may be painful because this portion of the disc is innervated. Strong evidence suggests that most episodes of acute LPB are due to disc injury rather than a musculotendinous strain and/or ligamentous sprain.

As the degenerative process advances, 2 structural changes may occur, heralding phase II of the degenerative cascade. Circumferential tears may coalesce to form radial tears, and/or the nucleus may lose its normal water-imbibing abilities. The latter phenomenon is a direct result of biochemical changes in aggregating proteoglycans.

Several studies suggest proteoglycan destruction results from an imbalance between matrix metalloproteinase-3 (MMP-3) and tissue inhibitor of metalloproteinase-1 (TIMP-1).[10] These alterations result in diminished water imbibing capacity. Morphologically, this manifests as a bulging disc and radiologically as a desiccated disc with diminished disc height. The bulging disc may result in a focal protrusion, and if a full-thickness radial tear develops, then an extrusion or sequestration may occur.

Structural changes of the facet joint are commonly accepted to follow discogenic degeneration; however, this pathologic alteration is not mandatory. Changes related to the zygapophyseal joints during the dysfunction phase are thought to include synovitis and hypomobility. Pain caused by the facet joint may occur during this and all subsequent phases.

Phase II, or the instability phase, is believed to result from the progressive loss of mechanical integrity of the 3-joint complex. Disc-related changes include annular tears, internal disruption and disc resorption, and possibly loss of disc height. Concomitant changes developing in the zygapophyseal joints include cartilage degeneration, capsular laxity, and subluxation. The biomechanical result of these alterations may lead to segmental instability.

Phase III, or the stabilization phase, is characterized by further disc resorption, intervertebral disc space narrowing, endplate destruction, disc fibrosis, and osteophyte formation and transdiscal bridging. Discogenic pain occurs less often in this phase than in either phase I or phase II. During this phase, degenerative scoliotic symptoms present.

Neurophysiology of LBP

The following 3 criteria must be met for a structure to be considered a pain generator: (1) it must have a nerve supply, (2) it must be susceptible to diseases or injuries known to be painful, and (3) it should be capable of causing pain similar to that which is seen clinically.

The first criterion necessary in identifying discs as a nociceptive source has been established. Weinstein et al identified substance P, calcitonin gene-related peptide (CGRP), and vasoactive intestinal polypeptides (VIP), important chemicals related to pain perception, in nerves among the outer annular fibers of the rat disc.[11] Further studies have demonstrated substances P, encephalon, dopamine, B-hydroxylase, and choline acetyltransferase immunoreactive nerve fibers among the surgically removed human longitudinal ligaments.

Several studies have revealed the presence of nerve fibers in the superficial layers of the annulus fibrosis. Malinsky demonstrated a variety of free and complex nerve endings in the outer one third of the annulus.[12] Several intrinsic painful disorders can affect lumbar discs, including discitis and internal disc disruption. Discitis often presents with complaints of LBP, whereas internal disc disruption has been shown to be a common cause of chronic LBP. These conditions satisfy the second criterion.

The third criterion has been evaluated through the performance of invasive imaging. Various investigators have demonstrated provocation of concordant pain with lumbar discography. Although pain can be evoked with provocative discography, it has not been demonstrated conclusively that this diagnostic technique actually elicits pain from the disc or that such pain is due to circumferential or radial tears in the annulus. Moneta et al provide the most suggestive evidence linking peripheral annular tears as the nociceptive source during discography.[13] Weinstein et al demonstrated that the disc has the capability of producing pain, thus satisfying the third criterion.[11]

Role of inflammation

Back pain without radicular symptoms may be a consequence of a biochemical and/or mechanical process, with the development of the latter entirely dependent on the former. Significant evidence indicates that it is inflammation that underlies the radicular pain associated with symptomatic lumbar disc herniation. The notion that lumbar radiculopathy secondary to a disc protrusion is not purely the result of mechanical compression of a spinal nerve or nerve root is widely accepted. The inflammatory process is believed to sensitize the dorsal root ganglion (DRG) to all incoming stimuli. In such a state, even minor mechanical stimulation of the DRG could evoke severe pain.

Acceptance of this paradigm by spine physicians has lead to interesting position papers concerning treatment of acute radicular pain. The North American Spine Society (NASS) recommended employing epidural steroid installation in the management of lumbar radicular syndromes.[14] In addition, Kraemer, in his presidential address to members of the International Society for the Study of the Lumbar Spine, implored them to use epidural perineural injection.[15] Of note is a meta-analytical study that demonstrated the statistically significant benefit of this therapeutic approach. Basic science evidence supporting this inflammatory model can be found in both animal and human research.

An autoimmune response has been suggested. Following embryologic formation, under normal conditions, the nuclear proteins are not in contact with the systemic circulation; therefore, it is postulated that a focal protrusion leads to exposure of nuclear material to the immune system. Because it will be detected as a foreign body, an autoimmune response may be mounted.

Bobechko and Hirsch demonstrated the inflammation-inducing potential of nuclear material using a rabbit model.[16] Olmarker et al showed that the epidural application of autologous nuclear material without mechanical compression in pigs may induce pronounced changes in nerve root structure and function.[17] An epidural inflammatory reaction occurred following the application of both nucleus pulposus and fat.

Olmarker et al implanted titanium chambers containing autologous nucleus pulposus and retroperitoneal fat or empty sham chambers subcutaneously into pigs.[18] They observed increased numbers of inflammatory cells in comparison to controls, thereby demonstrating the nucleus pulposus had marked inflammation-inducing properties. This study also contained a second experimental model in which local installation of suspensions of homologous nucleus pulposus and homologous subcutaneous fat were injected into the hamster cheek pouch. The results demonstrated that the nucleus pulposus suspension induced a rapid macromolecular leakage from blood vessels and also induced thrombus formation within vessels.

In a follow-up study, electron microscopic analyses of normal appearing neural tissue under light microscopy revealed axonal injury and Schwann cell damage.[17] These results demonstrate nuclear material can cause morphologic damage to neural tissue without a concurrent mechanical process such as compression.

McCarron et al also demonstrated the potential for the nucleus pulposus to produce an inflammatory reaction by injecting autologous nucleus pulposus suspension epidurally in dogs.[19] Histologic examinations revealed the nucleus pulposus suspension induced an epidural inflammatory reaction. A similar response was absent in a control group, which had been injected with normal saline.

Observations in human studies essentially mirror those obtained in animal studies.

Saal et al reported the presence of phospholipase A2 (PLA2) in human disc samples surgically removed for the treatment of radiculopathy secondary to lumbar disc disease.[7] PLA2 is an enzyme responsible for the liberation of arachidonic acid from cell membranes at the site of inflammation. It plays a central role in the inflammatory process via regulation of the arachidonic acid cascade and ultimately leads to the production of prostaglandin and leukotrienes. The activity of intervertebral disc–derived PLA2 was shown to be from 20-100,000 times greater than PLA2 activity derived from any other human source.

Franson et al demonstrated PLA2 extracted from human lumbar discs has a powerful ability to induce inflammatory activity in vitro.[20] Ozaktay et al demonstrated evidence of both neurotoxic and inflammatory effects by injecting PLA2 into the nerve receptive fields of surgically isolated facet joint capsules in rabbits.[21] The neurotoxic effects included loss of spontaneous nerve discharge after PLA2 injection and lack of response to mechanical stimulation in previously responsive units.

Histologically, typical leukocyte infiltration with polymorphonuclear leukocytes, vascular congestion, focal extravasation, and edema provided evidence for the inflammatory effects of PLA2. Following these reports, efforts have focused on understanding the relationship between painful herniations and inflammation.

Gronblad et al demonstrated the presence of an abundant number of macrophages in human disc herniation specimens removed at the time of surgery.[22] Control discs contained only a few macrophages. The authors also identified an important inflammatory cytokine, interleukin-β (IL-β) immunoreactive cells, in herniated disc tissue. IL-1β seems to be a significant element in the pathophysiology of rheumatoid arthritis and perhaps in osteoarthritis as well.

Haro et al obtained similar data on the presence of macrophage in painful disc herniations.[23] In addition, they were able to demonstrate statistically significant quantities of factor VII, monocyte chemotactic protein-1, and macrophage inflammatory protein-1 positive cells in symptomatic herniations.

Doita et al showed an infiltration of mononuclear cells along the margins of extruded discs that expressed inflammatory mediators.[24] Takahashi et al demonstrated the presence of inflammatory cytokines in human tissue adjacent to nerve roots at the level of a symptomatic herniated disc removed at the time of surgery.[25] The exact role IL-1a, IL-1b, IL-6, and tumor necrosis factor serve in the production of pain remains undetermined. One possibility involves the ability of these cytokines to stimulate production of prostaglandin E2, which Takahashi demonstrated in vitro. An interesting component of this study involved the demonstration that cytokine and prostaglandin E2 production was dramatically decreased following the addition of betamethasone.[25]

Internal disc disruption (IDD)

H.V. Crock proposed a hypothesis for IDD in his presidential address to the International Society for the Study of the Lumbar Spine.[26] He suggested the following[26] :

"...trauma to an intervertebral disc may damage disc components, resulting in the production of irritant substances, which may drain either into the spinal canal, irritating nerves or into the vertebral body, setting up an autoimmune reaction. The following clinical syndrome may develop: a) intractable back pain with aggravation of pain and loss of spinal motion with any physical exercise; b) leg pain; c) loss of energy; d) marked weight loss; e) profound depression."

"Patients with this syndrome will be found to have: a) normal plain spine x-rays; b) normal myelograms; c) normal CT [computed tomography] scans of the spine; d) usually normal blood examination; e) normal neurologic findings on clinical exam. Patients with this syndrome will have: a) abnormal discograms; b) pain will be reproduced by as small as a volume as 0.3 mL of contrast dye, due to the hypersensitivity of the pain fibers within the disc substance; c) the final volume of dye accepted will be in excess of normal; d) the discographic patterns on x-ray films will be abnormal."

This hypothesis suggests that a syndrome develops, resulting from the production of chemical substances by the damaged disc.

Treatment options for IDD include a chronic pain management program, intradiscal steroid injection, annular denervation, intradiscal electrothermy, or a surgical fusion procedure. Because these treatments vary greatly in their morbidity, mortality, and outcome, each option should be considered carefully on an individual basis.

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Contributor Information and Disclosures
Author

Robert E Windsor, MD, FAAPMR, FAAEM, FAAPM President and Director, Georgia Pain Physicians, PC; Clinical Associate Professor, Department of Physical Medicine and Rehabilitation, Emory University School of Medicine

Robert E Windsor, MD, FAAPMR, FAAEM, FAAPM is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine, American Medical Association, International Association for the Study of Pain, Texas Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Kevin P Sullivan, MD Consulting Staff, The Boston Spine Group

Kevin P Sullivan, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, North American Spine Society, International Spine Intervention Society

Disclosure: Nothing to disclose.

Erik D Hiester, DO Fellow in Interventional Pain Management, Georgia Pain Physicians, Emory University School of Medicine

Erik D Hiester, DO is a member of the following medical societies: American Academy of Family Physicians, American Medical Association, American Osteopathic Association, American Pain Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Henry T Goitz, MD Academic Chair and Associate Director, Detroit Medical Center Sports Medicine Institute; Director, Education, Research, and Injury Prevention Center; Co-Director, Orthopaedic Sports Medicine Fellowship

Henry T Goitz, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine

Disclosure: Nothing to disclose.

Chief Editor

Craig C Young, MD Professor, Departments of Orthopedic Surgery and Community and Family Medicine, Medical Director of Sports Medicine, Medical College of Wisconsin

Craig C Young, MD is a member of the following medical societies: American Academy of Family Physicians, American College of Sports Medicine, American Medical Society for Sports Medicine, Phi Beta Kappa

Disclosure: Nothing to disclose.

Additional Contributors

Andrew D Perron, MD Residency Director, Department of Emergency Medicine, Maine Medical Center

Andrew D Perron, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Sports Medicine, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous coauthor Dr Dennis P White to the development and writing of this article.

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