CLINICAL PROBLEMS AND CORRELATIONS OF THE THORACOLUMBAR SPINE
Low back pain, with or without leg pain, is very common in the population, particularly in middle-aged and older adults. Degeneration of the intervertebral disc and some degree of low back pain and stiffness are nearly universal features of aging. Degenerated discs have decreased height, increased posterior and lateral bulging, and reduced ability to dissipate compression forces. As a result, associated changes occur, including abnormal loading of the facet joints with development of facet arthritis, osteophyte formation, greater stress on adjacent ligaments and muscles, and thickening of the ligamentum flavum. In some patients, these changes may result in back pain, although it is difficult to isolate the primary source of low back pain in most instances. In some cases, back pain may become chronic. Chronic low back pain, defined as persistent symptoms for longer than 6 to 8 weeks, is common among people older than 40 to 50 years of age and those working in occupations requiring frequent bending, lifting, or exposure to repetitive vibration (e.g., truck drivers). Obesity, smoking, and poor physical fitness are all risk factors for disc degeneration.
A typical feature of back pain is its frequent radiation to one or both buttocks. The pain can additionally radiate to the posterior thigh. It is frequently exacerbated by lifting and bending activities and relieved with rest. As with all chronic pain conditions, depression may aggravate symptoms and make treatment more challenging.
|DEGENERATIVE DISC DISEASE|
Examination typically shows mild tenderness in the lower back or sacroiliac region. Flexion and extension of the spine may be limited and painful. The straight-leg raising sign is typically absent, and findings of the neurologic examination are normal. Patients with associated psychological issues may display nonorganic findings, such as exaggerated pain behaviors and non-anatomic localization of symptoms.
Radiographs and MR images of the spine reveal changes that are difficult to differentiate from normal age-related changes. These include decreased disc height, anterior vertebral body osteophytes, and decreased disc hydration (see Plate 1-21). Screening radiographs to rule out tumor, infection, or an inflammatory arthritic process are appropriate for patients with pain lasting longer than 6 weeks. MRI should be reserved for patients with unusual symptoms in whom an occult and sinister process is suggested, such as infection, tumor, or fracture. It is also utilized as a diagnostic tool for patients with unremitting symptoms in whom symptomatic nerve compression is suggested and who are surgical candidates.
Recurrent episodes of back pain are typical, and most can be managed nonoperatively with nonsteroidal anti- inflammatory drugs (NSAIDs), general conditioning exercises, active physical therapy, weight reduction, and smoking cessation. Unremitting pain necessitates further evaluation. Operative treatment is rarely indicated for back pain, and the role of fusion or arthroplasty for patients with discogenic low back pain is controversial.
LUMBAR DISC HERNIATION
The nucleus pulposus may herniate posteriorly or posterolaterally and compress a nerve root, resulting in lumbar radiculopathy (leg pain in a dermatomal distribution). The herniation may be protruded (with the anulus intact), extruded (through the anulus but contained by the posterior longitudinal ligament), or sequestered (free within the spinal canal). Pain results from nerve root compression and from an inflammatory response initiated by various cytokines released from the nucleus pulposus (see Plate 1-22).
Patients with lumbar disc herniation typically are young and middle-aged adults with a history of previous low back pain. The pain may be exacerbated by a bending, twisting, or lifting event but may also develop insidiously and abruptly. The central portion of the posterior longitudinal ligament is the strongest portion of the ligament and resists direct posterior extrusions. More than 90% of lumbar disc herniations occur posterolaterally at L4-5 and L5-S1. Posterolateral disc herniations may cause neural compression and radicular pain involving the traversing spinal nerve. For example, an L4-5 posterolateral disc herniation will typically affect the L5 nerve root. Occasionally, a disc herniation will be located far lateral and can affect the more proximal exiting nerve root within the foramen and can cause radicular pain corresponding to the vertebral level cephalad to the disc (e.g., an L4-5 far lateral disc herniation will affect the proximally exiting L4 nerve root).
Increasing pressure or stretch on the compressed nerve root exacerbates pain. Pain can also increase with any activity that increases intra-abdominal pressure, such as sitting, sneezing, and lifting. It is typically decreased by lying down with a pillow under the legs or by lying on the side with the hips and knees flexed (fetal position). Symptoms can be variable, but pain and sensory disturbances typically follow the dermatome of the nerve root(s) affected.
On examination, the patient may lean toward the affected side to relieve compression on the affected root. The straight-leg raise test (lifting the leg with the knee straight) is a classic sciatic nerve tension sign that indicates L5 or S1 root inflammation and should be performed on both legs. A positive test typically reproduces the patient’s radicular symptoms below the knee. The specificity of the test is heightened when raising the contralateral leg provokes symptoms on the affected side (the cross-leg sign). The comparable test for a more proximal lesion affecting the L4 root or higher is the femoral nerve stretch test, which is performed by having the patient lie on the nonaffected side and by having the examiner extend the affected hip with the knee flexed. A positive test reproduces the patient’s proximal leg pain.
Radiographs of the lumbar spine may be normal but are useful in ruling out other conditions such as fracture. MRI is the study of choice to delineate the location and type of disc herniation. Most patients respond to symptomatic treatment such as NSAIDs, muscle relaxants, oral narcotics, a short course of oral corticosteroids, or epidural corticosteroid injection and will note improvement of symptoms by 6 weeks.
Indications for surgery include cauda equina syndrome, urinary retention or incontinence, progressive neurologic deficit, severe single nerve root paralysis, and radicular pain lasting longer than 6 to 12 weeks. The goal of surgery is to relieve pressure on the affected nerve root or cauda equina. The procedure usually involves a small laminotomy and excision of the herniated disc fragment (see Plate 1-22). Lumbar discectomy typically provides dramatic relief of symptoms in 85% to 90% of patients. Recurrent disc herniations may occur in 5% to 10% of patients. Possible complications of surgery include injury to the neural elements, postoperative infection, durotomy, and persistent pain.
CAUDA EQUINA SYNDROME
Multiple nerve roots of the cauda equina may be severely compressed by a large central disc herniation or other pathologic process such as epidural abscess, epidural hematoma, or fracture, resulting in a rapid onset of neurologic deficit. Midline sacral nerve roots that control bowel and bladder function are particularly vulnerable to such compression. Typical symptoms include bilateral lower extremity radicular pain and motor/sensory dysfunction, saddle anesthesia in the perineum, difficulty voiding, or frank bowel or bladder incontinence. Patients with cauda equina syndrome require emergent surgical decompression. Even with prompt treatment, however, the return of neurologic function may be incomplete.
Lumbar spinal stenosis may result from any condition that causes narrowing of the spinal canal or neural foramina with subsequent compression of the nerve roots at one or more levels. The most common cause is degenerative changes in the disc and facet joints. These degenerative changes are often associated with a spondylolisthesis, which is an anterior slipping (anterolisthesis) of one vertebra on the subjacent level. Patients with achondroplasia or other conditions that alter growth of the posterior vertebral arch may also develop stenosis with progressive symptoms in the second or third decade of life. Lumbar stenosis may also be congenital or may be caused by traumatic or post-operative changes.
Narrowing of the spinal canal is common in persons older than 60 years of age, but most persons have minimal symptoms. The spine is a three-joint complex comprising the intervertebral disc anteriorly and the two facet joints posteriorly. It is thought that the pathology of spinal stenosis begins anteriorly in the disc and involves the facet joints secondarily. Skeletal changes associated with stenosis in the older population include disc bulging and narrowing, degeneration and osteophyte formation of the facet joints, and, occasionally, spondylolisthesis. Soft tissue changes associated with stenosis include buckling or thickening of the ligamentum flavum and posterior longitudinal ligament, as well as bulging or frank herniation of the disc.
Symptomatic lumbar spinal stenosis afflicts both sexes and typically does not develop until after 40 years of age, unless there is a congenital component. Typical symptoms include a diffuse pain in the buttocks and posterior thighs or pain in a dermatomal and radicular pattern. Back pain may or may not be present. Symptoms are frequently bilateral, but one extremity may be more severely affected than the other. Patients note pain and often numbness or weakness when walking, usually beginning in the buttocks or thighs, and often progressing to the calves and feet. This condition is also termed neurogenic claudication. Symptoms are typically relieved by sitting, bending forward, or leaning on an object. Forward-flexion of the lumbar spine reduces discomfort and improves exercise tolerance by expanding the spinal canal, thereby relieving neural compression. As a result, patients with symptomatic spinal stenosis sometimes walk with their hips and knees flexed to allow for lumbar flexion (see Plate 1-23). Patients typically report improved symptoms when leaning on a shopping cart, walking up hills, or exercising on a recumbent bike, all of which permit a slight degree of lumbar flexion, thereby relieving neural compression.
Vascular claudication may mimic neurogenic claudication and should be ruled out because they may coexist. As with neurogenic claudication, patients with vascular claudication may have increased leg pain with exercise that is relieved by rest. However, patients with vascular claudication do not have pain relief with lumbar flexion or walking uphill, have a fixed as opposed to variable claudication distance, rarely have back pain, often have loss of calf hair, and typically have diminished or absent peripheral pulses (see Plate 1-23).
Findings on examination are often limited in patients with spinal stenosis. Lumbar range of motion may be either normal or diminished. Muscle weakness, if present, is often subtle and may only be observed after having the patient walk. Weight-bearing radiographs should be obtained and usually demonstrate typical age-related changes of facet joint arthrosis, diminished disc height, or a degenerative spondylolisthesis, most common at L4-5 and L3-4. The differential diagnosis includes vascular claudication, peripheral neuropathy associated with diabetes mellitus or vitamin B12 or folic acid deficiency, abdominal aortic aneurysm, infection, and tumor.
|DEGENERATIVE LUMBAR SPONDYLOLISTHESIS|
Nonoperative management is initially symptomatic and includes physical therapy, NSAIDs, activity restriction, epidural corticosteroid injections, weight reduction, and smoking cessation. Membrane-stabilizing agents such as gabapentin have also been useful in reducing symptoms. When symptoms persist and surgery is an option, diagnostic imaging with either MRI or CT myelography should be performed. Weight-bearing lumbar radiographs are mandatory, and flexion and extension lumbar spine views may also be useful to rule out an associated degenerative spondylolisthesis. If spondylolisthesis is present, decompression is usually accompanied by spinal fusion of the affected levels. If no degenerative spondylolisthesis is present, surgical therapy usually involves neural decompression alone.
Surgery is most effective to relieve leg symptoms of neurogenic claudication. It is less successful in patients in whom back pain is the predominant symptom and in patients with significant comorbidities such as smoking, obesity, or diabetes. Surgical decompression of the stenotic level(s) is usually palliative (see Plate 1-25). This is most commonly achieved by a laminectomy, with foraminotomy as needed. Iatrogenic instability can occur after complete removal of a unilateral facet joint, by more than 50% facet resection bilaterally, or by removal of more than one third of the pars interarticularis bilaterally. In such cases, a concomitant spinal fusion should be considered. Recurrence of stenosis after decompression may occur, particularly at adjacent levels to a concomitant spinal fusion.
DEGENERATIVE LUMBAR SPONDYLOLISTHESIS
Spondylolisthesis is translation (slippage) of one vertebra in relation to an adjacent segment. The superior vertebra typically slips in an anterior (forward) direction in relation to the inferior vertebra (anterolisthesis) (see Plate 1-26). Retrolisthesis, in which the superior vertebra slips posteriorly, can also occur. This is occasionally observed in degenerative spondylolisthesis involving the upper lumbar levels. The causes of spondylolisthesis vary, but the vast majority of patients have either an isthmic or degenerative spondylolisthesis (see Plate 1-25). Isthmic spondylolisthesis typically occurs at L5-S1, begins during adolescence, and is discussed elsewhere.
In degenerative spondylolisthesis (spondylolisthesis with an intact neural arch), erosion and narrowing of the disc and facet joints lead to segmental instability. Because the posterior arch is intact, the slippage causes stenosis, which can be aggravated with flexion. This condition typically occurs in adults past age 40, is more common in women and blacks, and is most common at the L4-5 level. It can also occur at other levels, however, and can result in the appearance of a “cascading spine” (see Plate 1-26).
Symptoms include back pain, radicular pain, and neurogenic claudication. Indications for surgical management include persistent claudicatory leg pain, neurologic weakness, and, rarely, cauda equina syndrome. Because the affected segments are unstable, decompression is usually combined with fusion (arthrodesis). The addition of instrumentation improves fusion rate. Decom- pression alone is associated with poorer outcomes than decompression with concomitant fusion and may be associated with progression of spondylolisthesis. It is therefore typically reserved for elderly, low-demand patients with significant collapse of the disc and no motion detected on flexion-extension lumbar radiographs.