Lumbar Microdiscectomy: Indications and Techniques

History

Pain in the sciatic nerve distribution has been documented for centuries, beginning with ancient Greek and Roman physicians. Hippocrates was reportedly the first physician to use the term “sciatica,” deriving from the Greek word ischios , meaning hip. Sciatica pain was therefore attributed to disease of the hip joint until experiments by Cotugno in 1764 suggested that the pain might instead be of nervous origin. ^, The degenerative processes of the spine and intervertebral disc were described by Luschka in 1858; however, the nature of the disc itself remained unclear. It was not until the nineteenth century that sciatica became attributed to disc disease, after Lasegue described pain related to stretching of the nerve. ^, Mixter and Barr clarified the relationship between disc herniation and sciatica in 1934 in their landmark paper describing findings in 34 patients with herniated discs that were amenable to surgical intervention.

The first operative procedures for discogenic pain were in the early 1900s by Krause and Oppenheim, in which a laminectomy was performed for what was believed to be an enchondroma. In 1929, Walter Dandy performed surgery for low back and leg pain, discovering cartilaginous material in the spinal canal causing nerve root impingement. Many variations and advancements in this technique have since been described. The introduction of the operating microscope in 1977 by Yasargil and Caspar became one of the most significant modifications to this procedure in its history. The resultant microdiscectomy has since become the most commonly performed procedure for lumbar disc herniation. The past decade has brought innovations in imaging, retraction, and high-resolution endoscopic techniques that have provided further advancements in achieving successful treatment of sciatica.

Pathophysiology

Intervertebral disc degeneration is among the most common causes of chronic physical disability in adults, resulting in diminished mobility and a loss of functional independence. Both biomechanical and biochemical factors contribute to degenerative disc disease; however, knowing and understanding the anatomy of the disc provides insight into the physiology of its degeneration.

The intervertebral disc consists of three components: an inner nucleus pulposus, outer annulus fibrosus, and cartilaginous end plates superiorly and inferiorly. As the spinal column is formed in the embryo, the central notochord gives rise to the nucleus pulposus and mesenchymal tissue gives rise to the annulus fibrosus. The annulus fibrosus is composed mainly of type I collagen and provides resistance to tensile forces generated during bending or twisting. The nucleus pulposus is composed of the proteoglycan “aggrecan” and water, held together by elastin and type II collagen. The high concentration of proteoglycan serves to increase the osmotic gradient between the nucleus and adjacent plasma, allowing for an influx of water into the disc during recumbency. This process keeps the disc hydrated and increases its ability to withstand the mechanical forces of an upright posture. To counteract the influx of water due to osmotic forces, there is an efflux of water from the disc when upright resulting from the mechanical compressive force of the spine.

The intervertebral disc derives nutrition from vessels in the subchondral bone adjacent to the end plates. As such, it is believed that poor transport of nutrients into the disc contributes to disc degeneration. Intervertebral discs have been found to age earlier than other tissues of the body; accumulating tissue fissures, granular debris, and neovascularization. ^, Interestingly, however, unlike disc aging, disc degeneration is not exclusive to the elderly. Disc degeneration may be present in younger individuals due to injury or genetic predisposition. ^, Despite the fact that disc degeneration is progressive, the peak incidence of disc herniation is in the fourth decade of life (most commonly in the third through fifth decades). This is thought to be because a hydrated, expansive disc is necessary for herniation. As a person gets older, with continued disc desiccation, the nucleus becomes inflexible and unable to extrude past the annulus. During the third to fifth decades, the station of a hydrated, expansive disc exerting strain against a weakening annulus results in herniation. While many studies have attempted to define a causal relationship between aging and degenerative disc disease, none have been successful. The contribution of age to disc disease appears to be multifactorial, and results from decreasing concentration of cells in the annulus, cell senescence, and chronic mechanical loading. ^, Within the nucleus itself, the concentration of proteoglycans decreases with age, resulting in a decrease in water influx and a constant efflux due to compressive forces, yielding a net loss of water and elasticity of the disc. Meanwhile, over the years, the annulus wears down because of the strain of mechanical forces. These two changes do not necessarily happen at the same rate. It has been proposed that herniated discs may result if there is a preferential loss of annulus, resulting in a disproportionate strain on the nucleus. Over time, the weakened annulus gives way, with extrusion of disc material.

With increasing age, the nucleus pulposus becomes more fibrous as its aggrecan and hydration diminish, resulting in increased fissures and subsequent loss of height. ^, Loss of aggrecan occurs due to a decreased number and activity of disc cells. As a result, the load-bearing capability of the disc is diminished, resulting in a loss of height and bulging of disc material. The consequential alteration in facet joint mechanics results in formation of osteophytes at the disc margin. Additionally, osteoporosis and osteopenia, which are commonly observed in the aging spine, predispose it to microfractures of the adjacent subchondral bone, bone sclerosis, end-plate ossification, and a reduction in the number of vascular channels, limiting nutrient transport and creating abnormal stress on the adjacent disc. ^, As aging progresses, disease related to nutritional deficiency is accelerated by modifiable lifestyle factors, including tobacco use and dietary status.

Although disc herniation can present with back pain alone, it classically presents as radiculopathy, which may or may not be accompanied by a focal neurologic deficit. The radicular pain perceived is due to the location of the disc herniation. Herniations between the midline and neural foramen (posterolateral herniations) are by far the most common. By contrast, far lateral disc herniations comprise only about 10% to 15% of herniated discs. The classic posterolateral herniation is most common because of the anatomy of the posterior longitudinal ligament (PLL), which is thickest near the midline and weakens out near the lateral margin. When a disc herniates, it extrudes through the weaker, lateral margin of the PLL ( Fig. 145.1 ).

Before 1947, the lumbar disc itself was considered a nerve-free, painless structure. In 1947, Inman and Saunders discovered pain fibers in the annulus fibrosus. This was later confirmed by histologic studies revealing the presence of branches of the sinuvertebral nerves entering the outer third of the annulus and PLL. Discogenic back pain has since been linked to disc degeneration, as loss of disc structure under mechanical load results in abnormal motion, which stimulates nociceptors in the annulus fibrosus. The pathophysiology of radicular pain is not exactly known but does require a compressive component. Interestingly, however, as many as 20% of asymptomatic individuals will have a compressive disc herniation. The mechanism by which a compressed nerve root generates pain is incompletely understood. Prior study has revealed that compression of a noninflamed nerve root has been shown to produce sensory and motor symptoms without pain, while pain has been associated with manipulation of inflamed nerve roots. This concept helps to explain why some patients with small disc bulges may suffer from severe pain, whereas some large disc herniations produce only focal neurologic deficits without associated pain. Proposed theories, which have all been demonstrated in animal models, include nerve edema, alterations of nutritional transport, and axonal conduction inhibition. A complex interaction between proinflammatory cytokines and neurotrophins produced by disc cells and infiltrating immune cells is believed to mediate this process. This is supported by the success of antiinflammatory medications for symptomatic relief.

Patient Evaluation

In evaluating a patient with a herniated lumbar disc, great care must be taken to accurately correlate imaging findings with clinical picture. The incidence of a herniated disc is quite high in the general population, and radiographic presence alone is not a sufficient indication for surgical intervention. Proper patient selection (and not necessarily surgical technique) is believed to be the best predictor of a good outcome.

While trauma is not the sole cause of lumbar disc herniation, most patients will describe a specific incident preceding the onset of back pain, often involving a fall, twist, or lifting of a heavy object. Pain is the most common complaint and may be axial or radicular. As time progresses, back pain may yield to radicular symptoms, and, in fact, there is usually an inverse temporal relationship between the two. Often pain extends into the leg or foot in a dermatomal distribution. Severity of pain, on the other hand, can be quite difficult to interpret. For instance, the location of the disc has been shown to affect the severity of symptoms. Extraforaminal disc herniations have been found to be more painful, perhaps because of their direct compression of the dorsal root ganglion. Generally, in the scenario in which a patient has a true disc herniation but symptoms are inconsistent with what is expected, good outcomes cannot be expected from surgical decompression.

Using the patient’s history and presenting symptoms to localize the level of nerve compression is of utmost importance in choosing an appropriate surgical candidate. When assessing a patient, it is also important to look for red flag symptoms, i.e., acute bowel or bladder symptoms, which may be indicative of cauda equina syndrome. Once correctly identified as radiculopathy, the clinical observer can often (up to 70% to 80% of cases) predict the location of the pathologic disc based on clinical symptomatology alone. Below the level of the conus medullaris exists the cauda equina, with nerve roots departing one level above their exiting foramen. The nerve roots then course caudally in the spinal canal passing posterior to the intervertebral disc below and turn to exit the neural foramen. When exiting the neural foramen, sensory bodies form the dorsal root ganglion. The post-ganglionic nerve then passes across the lateral aspect of the intervertebral disc. For example, the L5 nerve root leaves the cauda equina at the level of the L4 vertebral body. The nerve courses posterior to the L4-5 disc and exits the spinal canal at the L5-S1 neural foramen where it is intimately associated with the inferomedial aspect of the L5 pedicle. In the event of a posterolateral L4-5 disc herniation, the L5 nerve root is most likely to be affected, resulting in pain radiating along the posterior thigh and posterolateral leg ( Fig. 145.2 ). In the case of a far lateral disc herniation, the herniation compresses the exiting root from the same level, i.e., the L4 nerve root. Specific tests including the straight-leg raise, Lasègue maneuver, slump test, bowstring test and femoral stretch test may be useful adjuncts to identifying or confirming a radiculopathy. While a useful examination finding when present, true weakness to confrontational testing may be masked from the examiner because of significant overlap in innervation. Of all the historical and examination findings, monoradiculopathic leg pain is the best clinical correlate, superior to straight leg raise and the presence of sensorimotor deficits.

Imaging

Advances in spinal imaging have markedly impacted our understanding of intervertebral disc herniation and the decision-making process when considering a patient for surgical intervention. That being said, the decision about when to pursue imaging has been a topic of much debate. In most centers, magnetic resonance imaging (MRI) is the standard imaging modality for evaluating back pain; however, modern imaging has failed to accurately correlate findings with the true cause of back pain. It is generally accepted that there is no role for advanced imaging in patients presenting with acute back or leg pain in the absence of symptoms suggesting underlying systemic disease or signs of neurologic impairment that may require intervention. Not only is early imaging costly, but a recent meta-analysis of randomized controlled trials comparing immediate versus clinically directed imaging in patients with acute back pain revealed no improvement in outcomes with lumbar spine imaging. ^, The common scenario involves the identification of imaging abnormalities without the known significance of these findings. For instance, the presence of a “dark nucleus” has been shown to predict the likelihood of back pain, and thus, patients with known pathologic imaging findings are more likely to experience poor outcome, ^, although a dark nucleus has not been definitively related to any pathologic condition.

The American College of Radiology practice guidelines were recently updated to state that imaging the patient who presents with acute low back pain is not indicated except in the presence of “red flag” features, which include recent significant trauma, minor trauma in a patient older than 50 years, weight loss, fever, immunosuppression, history of neoplasm, steroid use or osteoporosis, known intravenous drug abuse, or a progressive neurologic deficit with intractable symptoms. After proper evaluation, the clinician may proceed with imaging, which will typically begin with plain radiographs.