Microdiscectomy for the Treatment of the Herniated Lumbar Disc

CHAPTER PREVIEW

CHAPTER SYNOPSIS:

Intervertebral disc degeneration and herniation is a common and significant source of impairment for the general population. Discectomy has become the mainstay of treatment for symptomatic disc disease that has failed to respond to conservative treatment. Microdiscectomy has the advantage of lower morbidity when compared with traditional open procedures and has evolved to be associated with high success rates in the literature. This chapter reviews the pathophysiology, diagnosis, classification, and operative microsurgical techniques for the management of posterolateral herniated lumbar disc.

IMPORTANT POINTS:

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Pain in the nerve root distribution is the most common presenting complaint of patients with disc herniation.
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The physical examination is the key to localizing the affected spinal level because magnetic resonance imaging (MRI) may show asymptomatic disc herniations.
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MRI is the imaging modality of choice for confirming the affected level as initially suspected from the history and physical examination.
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Most cases of disc herniation are successfully treated by conservative means.
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Surgical discectomy is reserved for cases with significant neurologic compromise or failure of appropriate conservative treatment.
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The introduction of the operating microscope has allowed microsurgical techniques to replace traditional open discectomy.

CLINICAL/SURGICAL PEARLS:

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Conservative treatment should be initiated first in all cases except those representing severe neurologic compromise.
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Open microdiscectomy is the mainstay of current surgical treatment for symptomatic disc herniation and allows for smaller incisions, less dissection, less blood loss, shorter hospitalization, and improved outcomes.
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Minimally invasive discectomy has gained popularity but must be done with meticulous technique to achieve successful results.
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Preoperative and intraoperative localization of the herniated disc is imperative to ensure removal of the offending fragment.
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Alternative procedures, including percutaneous automated discectomy, chemonucleolysis, and annular repair, have variable results in the literature.

CLINICAL/SURGICAL PITFALLS:

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Cauda equina syndrome is an urgent surgical issue that must be promptly recognized and treated.
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Complications of surgical treatment must be carefully avoided and managed appropriately when they do occur. These include:
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  Surgery at the wrong spinal level
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  Dural tears and cerebrospinal fluid leak
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  Neurovascular injury
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  Persistent radicular symptoms
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  Disc reherniation
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  Iatrogenic spinal instability

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Lumbar disc degeneration and herniation is a common cause of low back pain and radiculopathy. Although the true impact of these disorders is difficult to quantitate, it remains a widespread but poorly understood phenomenon, affecting quality of life, health, and economic status of millions of Americans. In fact, because of the prevalence and predilection of the disease for affecting young, productive members of society, disc disease remains the leading cause of impairment in the United States. Improvements in radiographic imaging and microsurgery have since made the diagnosis and treatment of herniated lumbar discs a mainstay of orthopaedic and neurosurgical practice. The contemporary microdiscectomy in its various iterations has become a safe operation with low attendant morbidity and high success rates. This chapter reviews the pathophysiology, diagnosis, classification, and operative microsurgical techniques for the management of posterolateral herniated lumbar disc. Surgical management of the far lateral disc is discussed in chapter 15 .

PATHOPHYSIOLOGY

The normal lumbar spine sustains significant loading forces, resulting in high intradiscal pressures. The disc is an osmotic system, and as the load increases, water is expressed, concentrating proteoglycans and, therefore, osmotic pressure. As the osmotic pressure increases, fluid expression ceases, and a resultant water influx balances the applied load. The intervertebral disc is one of the first tissues to show degenerative changes.

The disc, particularly the nucleus pulposus, dehydrates with age because of a loss of proteoglycans. Chondrocytes, although occupying less than 1% of tissue volume, produce and maintain all extracellular matrix components throughout life. Cell loss, caused by apoptosis and necrosis beginning in the second to third decades of life, leads to loss of proteoglycans and dehydration, which causes decreased disc height and cracks and fissures in the annulus. The annulus and nucleus pulposus gradually become indistinguishable and change into a stiff, desiccated fibrocartilaginous ring. Normal tissue repair mechanisms do not seem to occur in the disc.

One of the primary causes of disc degeneration may be failure of the nutrient supply. Because the disc is largely avascular, nutrients are supplied by vertebral capillaries penetrating the subchondral plate, and then diffusing through the cartilaginous end plate and extracellular matrix to the cells, which may be as far as 8 mm from the capillary bed. Smoking has thus been identified as a risk factor for accelerated disc degeneration, with evidence of lower oxygen and increased lactic acid concentrations after a short exposure to cigarette smoke.

Controversy exists over the origin of pain caused by disc herniation. Certainly, an element of radicular pain is due to the mechanical compression of the nerve root by the disc, as evidenced by the edema and inhibition of axonal transport seen in experimental models of nerve compression. Back pain may be caused by mechanical stretch of the annulus, the only innervated portion of the intervertebral disc. Mechanical forces cannot, however, be the sole cause of pain. In addition, radiographic evidence of nerve root compression may not result in clinical symptoms, as evidenced by the 20% incidence rate of asymptomatic disc herniation in a review of routine magnetic resonance imaging (MRI) studies. Even after spontaneous resolution of pain, the radiographic compression from a disc herniation may remain unchanged. Thus, the role of inflammatory responses have also been implicated in both back and radicular pain.

DIAGNOSIS

Symptoms

Pain in a nerve root distribution is usually the initial symptom of herniated discs. Because the L4-5 and L5-S1 discs are the most frequently involved, patients typically describe radiating pain in the distribution of the sciatic nerve down to the ankle or foot. This may be accompanied by buttock pain, numbness, and weakness in a radicular distribution. Back pain may present insidiously or acutely and often precedes radicular pain, sometimes being relieved at the onset of severe sciatic symptoms. This pain is often worsened by movement, sitting, and standing.

Examination

Together with the history, the clinical examination is critical for helping to localize the symptomatic disc herniation, because it is not uncommon to have asymptomatic herniations on MRI. Therefore, knowledge of the dermatomal sensory and motor distributions, and associated reflexes for each of the lumbar nerve roots is essential for localizing the level of the disc herniation. Areflexia is more sensitive than gross muscle weakness and should be compared against the contralateral side. Provocative maneuvers such as the straight-leg raises, or Lasègue sign, can be used to show irritation of the nerve root from a herniated disc. With the patient supine, the leg is slowly raised from the ankle. If the patient experiences radicular pain with the leg between 30 degrees, at which the nerve root moves in the foramen, and 70 degrees, this test is considered positive and suspicious for acute disc herniation. When a large fragment is present, or if the fragment is in the axilla of the nerve root, contralateral leg raise may cause ipsilateral radicular pain. For the higher nerve roots, L1-3, nerve root irritation can be produced by extending the hip with the knee in flexion (femoral tension sign). The hip should always be examined to assess for arthritis, which can mimic radicular pain, and attention should also be paid to the possibility that sclerotomal pain from an arthritic facet can mimic sciatica.

Cauda Equina Syndrome

Cauda equina syndrome is an urgent surgical issue. Prompt treatment of this entity can result in a greater likelihood of neurologic recovery, but it should be noted that the speed of onset of the deficits can be highly predictive of the eventual outcome. The rapid onset of bowel and bladder or motor symptoms carries an ominous prognosis, even with urgent, or even emergent, surgical decompression. In the cauda equina syndrome, a large central disc herniation can affect multiple nerve roots of the cauda equina. The classic symptoms of saddle anesthesia, perianal numbness, and bowel and bladder symptoms may be subtle but must be carefully evaluated, because these nerve roots run centrally and are usually among the first affected. Checking sacral dermatomal sensation to pinprick testing is important, as is assessing volitional rectal tone. Symptoms of urinary retention are more common than urinary incontinence, which is usually a late sign because of overflow. A postvoid residual should always be checked, and it is concerning if greater than 50 to 100 mL. Varying degrees of sensory loss may occur in the legs and unilateral or bilateral motor involvement, which if absent, should never preclude this diagnosis.

IMAGING

MRI is the preferred imaging technique for the diagnosis of disc herniation. Localization of the disc herniation in relation to the spinal canal and neural foramen, as well as the cranial-caudal extent of the fragment, can be determined. In addition, the soft tissue detail of MRI allows the exclusion of neoplasms, cysts, infection, degenerative spondylosis, and other lesions that may mimic the symptoms of a herniated disc.

On MRI, disc desiccation results in darkening on a T2-weighted MRI scan, which heralds the beginning of disc degeneration. A disc herniation usually appears dark on both T1- and T2-weighted images, but hyperintensity on the T2 sequence is indicative of an acute rupture.

When evaluating a recurrent disc herniation, gadolinium should be administered to distinguish the marked enhancement of postoperative scarring from a disc fragment, which may show only rim enhancement. For best visualization, MRI should be deferred until 6 months after surgery, because postoperative edema, blood, and scar may make interpretation difficult.

Plain radiographs may demonstrate decreased disc height as an indirect measure of disc degeneration. Flexion-extension views may be used to evaluate for instability that might have contributed to cause of herniation and in the rare case may suggest the need for a fusion together with the decompression. Computed tomographic (CT) scan may be a useful adjunct in demonstrating associated osteophytes, which can help in the surgical planning. CT myelogram can be helpful if MRI is contraindicated.

CLASSIFICATION

The location of the disc herniation is paramount to which nerve root is affected and the proposed surgical treatment. Herniations may be classified as central, paracentral, foraminal, or far lateral ( Fig. 14-1 ). Central disc herniations occur between the lateral borders of the thecal sac. If large enough, it is these herniations that may cause the classic cauda equina syndrome, described later in this chapter. Paracentral disc herniations occur in the lateral recess, between the lateral thecal sac and the medial wall of the pedicle. These are the most common locations of herniated discs and cause compression of the descending nerve root as it travels from the cauda equina to the neural foramen (i.e., a L4-5 paracentral disc herniation causes L5 root radiculopathy). A foraminal herniation occurs where the nerve root traverses the foramen, between the medial and lateral walls of the pedicle. Far lateral disc herniations comprise only about 10% of all herniations but are clinically important, because they commonly impinge on the exiting nerve root (i.e., a L4-5 far lateral disc herniation causes L4 root compression) and require a modified surgical approach ( Fig. 14-2 ).