Anatomy and Physiology of the Lower Part of the Back
The bony spine is a complex structure, roughly divisible into an anterior and a posterior part. The anterior component consists of the cylindrical vertebral bodies, articulated by the intervertebral discs and held together by the anterior and posterior longitudinal ligaments. The posterior elements are more delicate and extend from the vertebral bodies as pedicles and laminae, which encircle the spinal canal. Large transverse and spinous processes project laterally and posteriorly, respectively, and serve as the origins and insertions of the muscles that support and protect the spinal column. The bony processes are also held together by sturdy ligaments, the most important being the ligamentum flavum, which runs along the ventral surfaces of the laminae. The posterior longitudinal ligament lies opposite it—on the dorsal surfaces of the vertebral bodies. These two ligaments define the posterior and anterior margins of the spinal canal, respectively.
The posterior parts of the vertebrae articulate with one another at the diarthrodial facet joints (also called apophysial or zygapophysial joints), each of which is composed of the inferior facet of the vertebra above and the superior facet of the one below. Figure 11-1 illustrates these anatomic features. The configuration and orientation of the facet joints differs in the cervical, thoracic and lumbosacral parts of the spine. The facet and sacroiliac joints, which are covered by synovia, the compressible intervertebral discs, and the collagenous and elastic ligaments, permit a limited degree of flexion, extension, rotation, and lateral motion of the spine.
A. The lumbar vertebrae viewed from above from B. the side and C. mid-sagittally. A and B show the bony structures and their relationships to the disc space, facet joints and intervertebral foramina. C demonstrates in a cutaway mid-sagittal view, the main ligamentous structures of the spine in relation to the bones and discs. The ligaments and articulations are critical to the mechanical integrity of the spinal column.
The stability of the spine depends on the integrity of the vertebral bodies, pedicles and intervertebral discs and on two types of supporting structures, ligamentous (passive) and muscular (active). Although the ligamentous structures are quite strong, neither they nor the vertebral body–disc complexes have sufficient integral strength alone to resist the enormous forces that may act on the spinal column. Consequently, the stability of the lower back is also largely dependent on the voluntary and reflex activity of the paraspinal, sacrospinalis, abdominal, gluteus maximus, and hamstring muscles.
The vertebral and paravertebral structures derive their innervation from the meningeal branches of the spinal nerves (also known as recurrent meningeal or sinuvertebral nerves). These meningeal branches spring from the posterior divisions of the spinal nerves just distal to the dorsal root ganglia, reenter the spinal canal through the intervertebral foramina, and supply pain fibers to the intraspinal ligaments, periosteum of bone, outer layers of the annulus fibrosus (which enclose the disc), and the capsule of the articular facets. Coppes and associates have found A-δ and C pain fibers extending into the inner layers of the annulus, and even into the nucleus pulposus.
Although the spinal cord itself is insensitive, many of the conditions that affect it produce pain by involving these adjacent structures. For example, the sensory fibers from the lumbosacral and sacroiliac joints enter the spinal cord via the fifth lumbar and first sacral roots. Motor fibers exit through the corresponding anterior roots and form the efferent limb of segmental reflexes.
The spinal roots in the lumbar region, after exiting from the spinal cord, course downward in the subarachnoid space of the spinal canal and are gradually displaced laterally until they angulate and exit at the intervertebral foramina. Prior to entering the proximal foraminal canal, the spinal root lies in a shallow furrow along the inner surface of the pedicle, the lateral recess. The lumbar nerve roots traverse this lateral recess one level superior to their exit through the foramen. The lateral recess is a common site of entrapment of the traversing root by posterolaterally herniated disc material and bony overgrowth.
The parts of the back that possess the greatest freedom of movement, and hence are most frequently subject to injury, are the lumbar, lumbosacral, and cervical. In addition to bending, twisting, and other voluntary movements, many actions of the spine are reflexive in nature and are the basis of erect posture.
General Clinical Features of Low Back Pain
Of the several symptoms of spinal disease (pain, stiffness, limitation of movement, and deformity), pain is foremost. Four types of pain may be distinguished: local, referred, radicular, and that arising from secondary muscular spasm. These several types of pain can often be discerned from the patient's description; reliance is placed mainly on the character of the pain, its location, and conditions that modify it.
Local pain is caused by any pathologic process that impinges on structures containing sensory endings, including the periosteum of the vertebral body, capsule of apophysial joints, annulus fibrosus, and ligaments. Destruction of the nucleus pulposus alone produces little or no pain but the annulus is innervated with small nerve fibers and, when subject to disruption, may produce considerable pain. This pain is steady and aching, but it may be intermittent and sharp, and, although not well circumscribed, is felt in or near the affected part of the spine. Pathologic change arising in spinal structures may also evoke discomfort in regions that share common innervation and thereby vaguely simulate the pain of radicular disease. These areas of projection may be considered similarly to the referred pain of the "sclerotomes" discussed in Chap. 8 and just below.
Referred pain in reference to the spine is of two types: one that is projected from the spine to viscera and other structures lying within the territory of the lumbar and upper sacral dermatomes, and another that is projected from pelvic and abdominal viscera to the spine. Pain caused by disease of the upper part of the lumbar spine may be referred to the medial flank, lateral hip, groin, and anterior thigh (sclerotomes; see Chap. 8). This has been attributed to irritation of the superior cluneal nerves, which are derived from the posterior divisions of the first three lumbar spinal nerves and innervate the superior portions of the buttocks. Pain from the lower part of the lumbar spine is usually referred to the lower buttocks and posterior thighs and is a result of irritation of lower spinal nerves, which activate the same pool of intraspinal neurons as the nerves that innervate the posterior thighs. Pain of this type is usually diffuse and has a deep, aching quality, but it tends at times to be more superficially projected. In general, the intensity of the referred pain parallels that of the local pain. Maneuvers that alter local pain have a similar effect on referred pain. McCall and colleagues and Kellgren have verified these areas of reference by the injection of hypertonic saline into the facet joints and the "sclerotomes" they determined are discussed in Chap. 8. But, as Sinclair and coworkers have pointed out, the sites of reference are inexact and cannot be relied on for precise anatomic localization.
In contrast to the movement-altered referred pain that originates in the spine, pain from visceral diseases felt within the abdomen, flanks, or lumbar region, is modified by the state of activity of the viscera and sometimes by assuming an upright or supine posture. In other words, its character and temporal relationships have little relationship to movement of the back.
Radicular or "root" pain has some of the characteristics of referred pain but differs in its greater intensity, distal radiation, circumscription to the territory of a root, and factors that excite it. The mechanism is stretching, irritation, or compression of a spinal root within or central to the intervertebral foramen. The pain is sharp, often intense, and usually superimposed on the dull ache of referred pain; it nearly always radiates from a paracentral position near the spine to some part of the lower limb. Coughing, sneezing, and straining characteristically evoke this sharp radiating pain, although each of these actions may also jar or move the spine and enhance local pain. Any maneuver that stretches the nerve root—e.g., "straight-leg raising" in cases of sciatica—evokes radicular pain. The specific patterns of radicular pain are described in the sections on prolapsed discs further on in the chapter, and the distribution of cutaneous innervation of the spinal roots is shown in Figs. 9-2 and 9-3. The most common pattern is sciatica, pain that originates in the buttock and is projected along the posterior or posterolateral thigh. It results from irritation of the L5 or S1 nerve root. Paresthesia or superficial sensory loss, soreness of the skin, and tenderness in certain regions along the nerve usually accompany radicular pain. If the anterior roots are involved as well, there is weakness, atrophy, or muscular twitching.
In patients with severe circumferential constriction of the cauda equina because of spondylosis (lumbar stenosis), sensorimotor impairment and referred pain are elicited by standing and walking. The symptoms are projected to the calves and the backs of the thighs thereby simulating the exercise-induced symptoms of iliofemoral arterial insufficiency—hence the term spinal claudication has been applied to the activity-induced symptoms of lumbar stenosis (see "Lumbar Stenosis and Spondylotic Caudal Radiculopathy" later in this chapter).
Referred pain from structures of the lower back (sometimes called pseudoradicular) does not, as a rule, project below the knees and is not accompanied by neurologic changes other than sometimes a vague numbness without demonstrable sensory impairment. This is quite in contrast to the pain of root compression. Pain resulting from muscular spasm usually occurs in relation to local spinal irritation and may be thought of as a nocifensive reflex for the protection of the diseased parts against injurious motion. Chronic muscular contraction may give rise to a dull, sometimes cramping local ache. One can sometimes feel the tautness of the sacrospinalis and gluteal muscles and demonstrate by palpation that the pain is localized to them. However, except for the most severe degrees of acute injuries of the back, the spasms are difficult to detect and their contribution to back pain has appeared to us to be relatively small.
In addition to assessing the character and location of the pain, one should determine the factors that aggravate and relieve it, its constancy, and its relationship to activity and to rest, posture, forward bending, coughing, sneezing, and straining. Frequently, the most important lead comes from knowledge of the mode of onset and the circumstances that initiated the pain. Inasmuch as many painful conditions of the back are the result of injuries incurred during work or in automobile accidents, the possibility of exaggeration or prolongation of pain for purposes of compensation must always be kept in mind.
Examination of the Lower Back
The main goals of the examination of the back are to differentiate pain that is caused by nerve root compression from those of musculoskeletal strains, metastatic spinal tumor, and infectious and inflammatory diseases of the spine and hips.
Some information may be gained by inspection of the back, buttocks, and lower limbs in various positions. The normal spine shows a thoracic kyphosis and lumbar lordosis in the sagittal plane, which in some individuals may be exaggerated. In the coronal plane, the spine is normally straight or shows a slight curvature, particularly in women. One should observe the spine for excessive curvature, a list, flattening of the normal lumbar lordosis, presence of a gibbus (a sharp, kyphotic angulation usually indicative of a fracture), pelvic tilt or obliquity (Trendelenburg sign), and asymmetry of the paravertebral or gluteal musculature. A sagging gluteal fold suggests involvement of the S1 root. In sciatica one may observe a flexed posture of the affected leg, presumably to reduce tension on the irritated nerve root. Or, patients in whom a free fragment of lumbar disc material has migrated posterolaterally may be unable to lie down and extend the spine.
The next step in the examination is observation of the spine, hips, and legs during certain motions. No advantage accrues from determining how much pain the patient can tolerate. More important is to determine when and under what conditions the pain begins or worsens. Observation of the patient's gait may disclose a subtle limp, a pelvic tilt, a shortening of step, or a stiffness of bearing—indicative of a disinclination to bear weight on a painful leg—the "antalgic gait". Analysis of this type of gait is covered in greater detail in Chap. 7. One looks for limitation of motion while the patient is standing, sitting, and reclining. When standing, the motion of forward bending normally produces flattening and reversal of the lumbar lordotic curve and exaggeration of the thoracic curve. With lesions of the lumbosacral region that involve the posterior ligaments, articular facets, or sacrospinalis muscles and with ruptured lumbar discs, protective reflexes prevent flexion, which stretches these structures ("splinting"). As a consequence, the sacrospinalis muscles remain taut and prevent motion in the lumbar part of the spine. Forward bending then occurs at the hips and at the thoracolumbar junction; also, the patient bends in such a way as to avoid tensing the hamstring muscles and putting undue leverage on the pelvis. In the presence of degenerative disc disease, straightening up from a flexed position is performed only with difficulty.
Lateral bending is usually less revealing than forward bending but, in unilateral ligamentous or muscular strain, bending to the opposite side aggravates the pain by stretching the damaged tissues. With unilateral sciatica, the patient lists to one side and strongly resists bending to the opposite side, and the preferred posture in standing is with the leg slightly flexed at the hip and knee. When the herniated disc lies lateral to the nerve root and displaces it medially, tension on the root is reduced and pain is relieved by bending the trunk to the side opposite the lesion; with herniation medial to the root, tension is reduced by inclining the trunk to the side of the lesion.
In the sitting position, flexion of the hips can be performed more easily, even to the point of bringing the knees in contact with the chest. The reason for this is that knee flexion relaxes tightened hamstring muscles and relieves the stretch on the sciatic nerve. This feature may also be evident in instances of lumbar disc disease, making the maneuver less sensitive than others.
Examination with the patient in the reclining position yields much the same information as in the standing and sitting positions. With lumbosacral disc lesions and sciatica, passive lumbar flexion causes little pain and is not limited as long as the hamstrings are relaxed, and there is no stretching of the sciatic nerve. Thus, with the knees flexed to 90 degrees, sitting up from the reclining position is unimpeded and not painful; with knees extended, there is pain and limited motion (Kraus-Weber test). With vertebral disease, passive flexion of the hips is free, whereas flexion of the lumbar spine may be impeded and painful.
Among the most helpful signs in detecting nerve root compression is passive straight-leg raising (possible up to almost 90 degrees in normal individuals) with the patient supine. This places the sciatic nerve and its roots under tension, thereby producing radicular, radiating pain from the buttock through the posterior thigh. This maneuver is the usual way in which compression of the L5 or S1 nerve root is detected (Lasègue sign), however, it may also cause an anterior rotation of the pelvis around a transverse axis, increasing stress on the lumbosacral joint and causing milder radiating pain if this joint is arthritic or otherwise diseased. Straight raising of the opposite leg ("crossed straight-leg raising," Fajersztajn sign) may cause sciatica on the opposite side and is a more specific sign of prolapsed disc than is the Lasègue sign. Several of the many derivatives of the straight-leg raising sign are discussed in the section on lumbar disc disease. Asking the seated patient to extend the leg so that the sole of the foot can be inspected is a way of checking for a feigned Lasègue sign.
A patient with lumbosacral strain or disc disease (except in the acute phase or if the disc fragment has migrated laterally) can usually extend the spine with little or no aggravation of pain. If there is an active inflammatory process or fracture of the vertebral body or posterior elements, hyperextension may be markedly limited. In disease of the upper lumbar roots, hyperextension of the leg with the patient prone is the motion that is most limited and reproduces pain; however, in some cases of lower lumbar disc disease with thickening of the ligamentum flavum, this movement is also painful.
Maneuvers in the lateral decubitus position yield less information but are useful in eliciting joint disease. In cases of sacroiliac joint disease, abduction of the upside leg against resistance reproduces pain in the sacroiliac region, sometimes with radiation of the pain to the buttock, posterior thigh, and symphysis pubis. Hyperextension of the upside leg with the downside leg flexed is another test for sacroiliac disease. Rotation and abduction of the leg evoke pain in a diseased hip joint and with trochanteric bursitis. A helpful indicator of hip disease is the Patrick test: with the patient supine, the heel of the offending leg is placed on the opposite knee, and pain is evoked by depressing the flexed leg and externally rotating the hip.
Gentle palpation and percussion of the spine are the last steps in the examination. It is preferable to first palpate the regions that are the least likely to evoke pain. The examiner should know what structures are being palpated (Fig. 11-2). Localized tenderness is seldom pronounced in disease of the spine because the involved structures are so deep. Nevertheless, tenderness over a spinous process or jarring by gentle percussion may indicate the presence of deeper, local spinal inflammation (as in disc space infection), pathologic fracture, metastasis, epidural abscess, or a disc lesion.
(1) Costovertebral angle. (2) Spinous process and interspinous ligament. (3) Region of articular facet (fifth lumbar to first sacral). (4) Dorsum of sacrum. (5) Region of iliac crest. (6) Iliolumbar angle. (7) Spinous processes of fifth lumbar and first sacral vertebrae (tenderness = faulty posture or occasionally spina bifida occulta). (8) Region between posterior superior and posteroinferior spines. Sacroiliac ligaments (tenderness = sacroiliac sprain, often tender, with fifth lumbar or first sacral disc). (9) Sacrococcygeal junction (tenderness = sacrococcygeal injury; i.e., sprain or fracture). (10) Region of sacrosciatic notch (tenderness = fourth or fifth lumbar disc rupture and sacroiliac sprain). (11) Sciatic nerve trunk (tenderness = ruptured lumbar disc or sciatic nerve lesion).
Tenderness over the interspinous ligaments or over the region of the articular facets between the fifth lumbar and first sacral vertebrae is consistent with lumbosacral disc disease (Fig. 11-2, sites 2 and 3). Tenderness in this region and in the sacroiliac joints is also a frequent manifestation of ankylosing spondylitis. Arthritic changes at a facet may cause the same tenderness. Tenderness over the costovertebral angle often indicates genitourinary disease, adrenal disease, or an injury to the transverse process of the first or second lumbar vertebra (Fig. 11-2, site 1). Tenderness on palpation of the paraspinal muscles may signify a strain of muscle attachments or injury to the underlying transverse processes of the lumbar vertebrae. Focal pain in the same parasagittal line along the thoracic spine points to inflammation of the costotransverse articulation between spine and rib (costotransversitis). Other sites of tenderness and the structures implicated by disease are shown in the figure.
In palpating the spinous processes, it is important to note any deviation in the lateral plane (this may be indicative of fracture or arthritis) or in the anteroposterior plane. A "step-off" forward displacement of the spinous process and exaggerated lordosis are important clues to the presence of spondylolisthesis (see further on).
Many of the processes discussed above can coexist, especially in the older individual, who may have hip and lumbar spine osteoarthropathy. This makes the interpretation of various signs difficult unless the symptoms are first analyzed properly.
On completion of the examination of the back and legs, one turns to a search for motor, reflex, and sensory changes in the lower extremities (see "Herniation of Lumbar Intervertebral Discs," further on in this chapter).
Conditions Giving Rise to Pain in the Lower Back
Congenital Anomalies of the Lumbar Spine
Anatomic variations of the spine are frequent and, though rarely themselves the source of pain and functional derangement, they may predispose an individual to discogenic and spondylotic complications by virtue of altering the mechanics and alignment of the vertebrae or size of the spinal canal.
A common anomaly is fusion of the fifth lumbar vertebral body to the sacrum ("sacralization") or, conversely, separation of the first sacral segment, giving rise to 6, rather than the usual 5 lumbar vertebrae ("lumbarization"). However, neither of these is consistently associated with any type of back derangement. Another less-common finding is a lack of fusion of the laminae of one or several of the lumbar vertebrae or of the sacrum (spina bifida). Occasionally, a subcutaneous mass, hypertrichosis, or hyperpigmentation in the lumbar or sacral area overlying the bony separation betrays the condition, but in most patients it remains occult until it is disclosed radiologically. The anomaly may be accompanied by malformation of vertebral joints and usually induces pain only when aggravated by injury. The neurologic aspects of defective fusion of the spine (dysraphism) are discussed in Chap. 38, with developmental abnormalities of the nervous system.
Many other congenital variants affect the lower lumbar vertebrae: asymmetrical facet joints, abnormalities of the transverse processes, are seen occasionally in patients with low back symptoms, but apparently with no greater frequency than in asymptomatic individuals. Spondylolysis consists of a congenital and probably genetic bony defect in the pars interarticularis (the segment at the junction of pedicle and lamina) of the lower lumbar vertebrae. It is remarkably common, affecting approximately 5 percent of the North American population and mainly a disease of children (peak incidence between 5 and 7 years of age). The defect assumes importance in that it predisposes to subtle fracture of the pars articularis, sometimes precipitated by slight trauma but often in the absence of an appreciated injury. In some young individuals, it is unilateral and may cause unilateral lumbar aching back pain that is accentuated by hyperextension and twisting. In the usual bilateral form, small fractures at the pars interarticularis allow the vertebral body, pedicles, and superior articular facets to move anteriorly, leaving the posterior elements behind. This leads to an anterior displacement of one vertebral body in relation to the adjacent one, spondylolisthesis. Considerable dull, aching back pain can result.
The main cause of spondylolisthesis in older adults is degenerative arthritic disease of the spine as discussed further on. Patients with progressive vertebral displacement and neurologic deficits require surgery. Reduction of displaced vertebral bodies before fusion and direct repair of pars defects are possible in special cases. Back pain is relieved in the majority of cases.
Traumatic Disorders of the Low Back
These constitute by far the most frequent causes of low back pain. In severe acute injuries from direct impact the examiner must be careful to avoid further damage and movements should be kept to a minimum until an approximate diagnosis has been made. If the patient complains of pain in the back and cannot move the legs, the spine may have been fractured and the cord or cauda equina compressed or crushed. (See Chap. 44 for further discussion of spinal cord injury.) Lesser degrees of injury, such as sprains and strains, are ubiquitous and can be handled with less caution because they do not involve compression of neural structures or displacement of spinal elements.
Acute Sprains and Strains
The terms lumbosacral strain, sprain, and derangement are used loosely, and it is probably not possible to differentiate them. Furthermore, what was formerly referred to as "sacroiliac strain" or "sprain" is now known to be caused by, in some instances, disc disease. The term acute low back strain may be preferable for minor, self-limiting injuries that are usually associated with lifting heavy loads when the back is in a mechanically disadvantaged position, or there may have been a fall, prolonged uncomfortable postures such as in air travel or car rides, or sudden unexpected motion, as may occur in an auto accident.
Nonetheless, the discomfort of acute low back strain can be severe, and the patient may assume unusual postures related to spasm of the lower lumbar and sacrospinalis muscles. The pain is usually confined to the lower part of the back, in the midline, across the posterior waist, or just to one side of the spine. The diagnosis of lumbosacral strain is dependent on the biomechanics of the injury or activity that precipitated the pain. The injured structures are identified by the localization of the pain, the finding of localized tenderness, augmentation of pain by postural changes—e.g., bending forward, twisting, or standing up from a sitting position, and by the absence of signs of radicular involvement. In more than 80 percent of cases of acute low back strain of this type, the pain resolves in a matter of several days or a week, even with no specific treatment.
Sacroiliac joint and ligamentous strain is the most likely diagnosis when there is tenderness over the sacroiliac joint and pain radiating to the buttock and posterior thigh, but this always needs to be distinguished from the sciatica of a herniated intervertebral disc (see further on). Strain is characteristically worsened by abduction of the thigh against resistance and may produce pain that is also felt in the symphysis pubis or groin.
Treatment of Acute Low Back Strain
The pain of muscular and ligamentous strains is usually self-limiting, responding to simple measures in a relatively short period of time. The basic principle of therapy in both disorders is to avoid reinjury and reduce the discomfort of painful parts. As a result of several studies that have failed to demonstrate a benefit of bed rest, the recent practice has been to mobilize patients as soon as they are able and to prescribe exercises designed to stretch and strengthen trunk (especially abdominal) muscles, overcome faulty posture, and increase the mobility of the spinal joints. Despite this approach, the authors can affirm from personal experience that some injuries produce such discomfort that arising from a bed or chair is simply not possible in the early days after injury (see Vroomen et al). Lying on the side with knees and hips flexed, or supine with a pillow under the knees favor relief of pain. With strains of the sacrospinalis muscles and sacroiliac ligaments, the optimal position is hyperextension, which is effected by having the patient lie with a small pillow under the lumbar portion of the spine or by lying prone. Local physical measures—such as application of ice in the acute phase and, later, heat diathermy and massage—often relieve pain temporarily. Nonsteroidal antiinflammatory drugs (NSAIDs) may be given liberally during the first few days. Muscle relaxants (e.g., cyclobenzaprine, carisoprodol, metaxalone, and the diazepams) serve mainly to make bed rest more tolerable but have little primary effect. Traction, formerly a popular treatment, is infrequently used. When weight bearing is resumed, discomfort may be diminished by a light lumbosacral support, but many orthopedists refrain from prescribing this aid.
Spinal manipulation—practiced by chiropractors, osteopaths, and others—has always been a contentious matter partly because of unrealistic therapeutic claims made in treating diseases other than low back derangements. A type of slow muscle stretching and joint distraction (axial traction on a joint) administered by physiatrists and physical therapists is quite similar. It must be recognized that many patients seek chiropractic manipulation for back complaints, often before seeing a physician, and may not disclose this information. When the supporting elements of the spine (pedicles, facets, and ligaments) are not disrupted, chiropractic manipulation of the lumbar spine has provided acute relief to a number of our patients with low back strain or facet pain. At issue is the durability of the effect, particularly the need for repeated spinal adjustments. One randomized British trial has shown manipulation to be faster than analgesics and bed rest in returning patients to work after minor back injury (Meade et al). Some trials have corroborated this finding (Hadler et al), whereas others have not, or, often, the results have been ambiguous. In the study by Cherkin and colleagues comparing chiropractic, physical therapy (McKenzie method), and simple instruction to the patient from a booklet, manipulation yielded a slightly better outcome at the end of a month. Despite several hypotheses offered by practitioners of spinal manipulation, the mechanism of pain relief is not known. The cracking sound created by rapid distraction of the facet joints (and attributed to gas coming out of solution in the joint fluid) seems not to be necessary for pain relief. It is unlikely that mundane low back pain represents minor subluxation, as claimed by chiropractors. In the authors' clinical experience, chronic low back pain, discussed below, has been less successfully treated by manipulative procedures than has acute pain, but there are some patients who testify to improvement in their clinical state and admittedly, the medical profession has little to offer in most cases of chronic low back pain. The results for acute and chronic back pain with another popular approach, acupuncture, have been even more uncertain, most studies showing it to be no more effective than a sham treatment (Tudler et al). It should be emphasized, however, that the chronic use of NSAIDs or narcotic analgesics is hazardous and is not an appealing alternative.
Chronic and Recurrent Low Back Syndrome
Often the symptoms of low back strain are recurrent and more chronic in nature, being regularly exacerbated by bending or lifting, suggesting that postural, muscular, and arthritic factors play a role. This is the most common syndrome seen in spine clinics, more often in men than in women.
Insidiously, or after some unusual activity, raising the question of trauma, especially if it happens in the work-place, the patient develops aching pain in the low back, increased by certain movements and attended by stiffness. The pain may additionally have a restricted radiation into the buttocks and posterior thigh, thereby simulating root compression. There are no motor, sensory, or reflex abnormalities. Radiographs and imaging procedures usually reveal some combination of osteoarthropathy, changes in vertebral discs, osteoarthritic changes in apophysial joints, and sometimes osteoporosis or slight spondylosis, or they may be entirely normal. Treatment with short-duration bed rest, analgesics, and physiotherapy, as outlined for acute strains, helps to relieve the symptoms, and the majority of patients recover within a few weeks, only to have a recurrence of similar pains in the future. Recurrent attacks are typical of degenerative spine disease that affects the vertebrae and facet joints. Usually, the origin of the pain cannot be assigned with certainty to spinal, joint, or muscular injury, but direct percussion tenderness of one vertebral segment always raises concern of metastatic disease as noted above. Quite often, changing the firmness of the mattress (in either direction) is helpful. Compensation relating to injuries at work or to an accident and related legal matters often add to the disability, but there are, of course, many legitimate injuries that occur in these circumstances.
Fractures of lumbar vertebral bodies are usually the result of flexion injuries. Such trauma may occur in a fall or jump from a height (if the patient lands on his feet, the calcanei may also be fractured) or as a result of an auto accident or other violent injury.
If the injury is severe, it may cause a fracture dislocation, a "burst" fracture of one or more vertebral bodies, or an asymmetrical fracture of a pedicle, lamina, or spinous process; most often, however, there is asymmetrical loss of height of a vertebral body (wedge compression fracture), which may be extremely painful at the onset. When compression or other fractures occur with minimal trauma (or spontaneously), the bone has presumably been weakened by some pathologic process. Most of the time, particularly in older individuals, osteoporosis is the cause of such an event, but there are many other causes, including osteomalacia, hyperparathyroidism, prolonged use of corticosteroids, myeloma, metastatic carcinoma, and a number of other conditions that are destructive of bone. Spasm of the lower lumbar muscles, limitation of all movements of the lumbar section of the spine, and the radiographic appearance of the damaged lumbar portion (with or without neurologic abnormalities) are the basis of clinical diagnosis. The pain is usually immediate, although occasionally it may be delayed for days.
A fractured transverse process, which is almost always associated with high-impact rotary injury of the spine and causes tearing of the paravertebral muscles and a local hematoma, produces deep tenderness at the site of the injury and limitation of all movements that stretch the lumbar muscles. The imaging findings, particularly MRI, confirm the diagnosis. In some circumstances, tears of the paravertebral musculature may be associated with extensive bleeding into the retroperitoneal space; this produces paraspinal or groin pain and proximal leg weakness with loss of the patellar reflex on the affected side. There may be a delayed subcutaneous hematoma in the flanks (Grey-Turner sign).
A problem not easily classified but having a distinctive clinical profile that should be known to neurologists is that of an osteoid osteoma. These benign tumors characteristically cause severe nocturnal pain located in one region of the parasagittal spine that awakens the patient from a peaceful sleep; also typical is complete relief after aspirin or small doses of other NSAIDs. MRI or CT is required to detect the lesion, as it may not be evident on plain radiographs of the spine. The typical appearance is a well-demarcated lytic lesion surrounded by a rim of bony sclerosis.
Treatment of Vertebral Compression Fracture
For the mundane thoracic and lumbar fracture associated with osteoporosis, bed rest, and analgesics are usually adequate. In the past two decades several mechanical approaches to reducing pain have been investigated. The injection of various materials directly into the fracture site within the vertebral body (vertebroplasty) attained popularity because of reports of marked pain relief. Several large trials have addressed the use of vertebroplasty and given conflicting results. The best conducted of these, with a placebo control groups (see Buchbinder et al and Kallmes et al) concluded that there was no durable benefit, however, these two studies included patients with fractures up to a year old. Having witnessed a few patients with almost immediate and remarkable relief of severe pain, we are uncertain of the best course but acknowledge that this is probably not an effective treatment for the majority of patients. Further discussion can be found in the review by Ensrud and Schousboe.
Herniation of Lumbar Intervertebral Discs (Table 11-1)
This condition is a major cause of severe and chronic or recurrent low back and leg pain. It occurs mainly during the third and fourth decades of life when the nucleus pulposus is still gelatinous. The disc between the fifth lumbar or first sacral vertebrae (L5-S1) is most often involved, and, with decreasing frequency, that between the fourth and fifth (L4-L5), third and fourth (L3-L4), second and third (L2-L3), and—quite infrequently—the first and second (L1-L2) lumbar vertebrae. Relatively rare but well described in the thoracic portion of the spine, disc disease is again frequent in the cervical spine at the fifth and sixth and the sixth and seventh cervical vertebrae (see further on).
Table 11-1 Features of the Main Root-Compressive Syndromes Due to Cervical and Lumbar Disc Herniation* ||Download (.pdf)
Table 11-1 Features of the Main Root-Compressive Syndromes Due to Cervical and Lumbar Disc Herniation*
INTERVERTEBRAL DISC SPACE
Supra- and infraspinatus deltoid, slight biceps weakness
Slightly diminished biceps jerk
Trapezius ridge and tip of shoulder, radiation to anterior upper arm, thumb, and index finger
Biceps, brachioradialis, extensor carpi radialis
Diminished biceps and supinator jerk
Tenderness over spine or scapula and suprascapular region; paresthesias in thumb and index finger
Shoulder, axilla, posterolateral arm, elbow, and middle finger
Triceps, wrist extensors
Diminished or absent triceps jerk
Tenderness over medial scapula and supraclavicular region or triceps. May complain of paresthesias in most of the fingers
Intrinsic hand muscles
Slight or no decrease in triceps jerk
Mimics ulnar palsy
Anterior thigh, over knee
Thigh adductor, quadriceps
Absent or diminished knee jerk
Anterolateral thigh, medial foreleg
Anterior tibial, sometimes with partial foot drop
Diminished or normal knee jerk
Posterolateral gluteal sciatica; lateral thigh, anterolateral foreleg, dorsal foot, lateral malleolus and great or second and third toe
Extensor hallucis longus and extensor digitorum brevis; some weakness of anterior tibialis, sometimes with foot drop
Unaffected (except posterior tibial)
Pain with straight-leg raising and variant tests; tenderness over fourth lumbar lateral process and lateral gluteal region
Midgluteal sciatica; posterior thigh, posterolateral leg, lateral foot, heel, or lateral toes
Plantar-flexor and hamstring weakness
Absent or diminished ankle jerk
Pain with straight-leg raising and variant tests; tenderness over lumbosacral (L5-S1) joint and sciatic notch; discomfort walking on heels
The cause of a herniated lumbar disc in any individual case is often not identifiable and flexion injury is often imputed, but a considerable proportion of patients do not recall an inciting episode. Degeneration of the annulus and the posterior longitudinal ligaments, and changes nuclei pulposis itself may have taken place silently or have been manifest by mild, recurrent lumbar ache. A sneeze, lurch, or other trivial movement may then cause the nucleus pulposus to prolapse, pushing the frayed and weakened annulus posteriorly. Fragments of the nucleus pulposus protrude through rents in the annulus, usually to one side or the other (sometimes in the midline), where they impinge on one or more nerve roots and cause the characteristic sciatic or other radicular pains and neurologic signs. In more severe cases of disc disease, a small piece of the nucleus may be entirely extruded as a "free fragment", sometimes called a sequestered disc fragment, and be mobile enough to affect a root at an adjacent level or to give rise to unusual precipitating features of radicular pain. Large protrusions cause pain by compressing the adjacent root against the articular apophysis or lamina. The protruded material may become reduced in size over time, presumably from desiccation, but often there is continued chronic irritation of the root or a discarthrosis with posterior osteophyte formation.
The Clinical Syndrome of Lumbar Disc Herniation
The fully developed syndrome of the common prolapsed intervertebral lower lumbar disc consists of (1) pain in the sacroiliac region, radiating into the buttock, thigh, and the calf, a symptom broadly termed sciatica; (2) a stiff or unnatural spinal posture; and often (3) some combination of paresthesia, weakness, and reflex impairment.
The pain of herniated intervertebral disc varies in severity from a mild aching discomfort to severe knife-like stabs that radiate the length of the leg and are superimposed on a constant intense ache. Sciatic pain is usually perceived by the patient as originating deep in the buttock and radiating to the posterolateral thigh; it may progress to the calf and ankle—to the medial malleolus (L4), lateral malleolus (L5), or heel (S1); however, distal radiation to the foot is less frequent. There are variations in the sciatic syndrome. Abortive forms may produce aching discomfort only in the lower buttock or proximal thigh and occasionally only in the lower hamstring or upper calf. With the most severe pain, the patient is forced to stay in bed, avoiding the slightest movement; a cough, sneeze, or strain is intolerable. The most comfortable position may be lying on the back with legs flexed at the knees and hips and the shoulders raised on pillows to obliterate the lumbar lordosis. For some patients, a lateral decubitus position is more comfortable. Free fragments of disc that find their way to a lateral and posterior position in the spinal canal may produce the opposite situation, one whereby the patient is unable to extend the spine and lie supine. Sitting and standing up from a sitting position may be particularly painful. It is surprising to patients that a lumbar disc protrusion may cause little or no back pain. If there is back discomfort, it tends to be just paraspinal on the side of sciatica and mainly in the acute stages.
In cases of root compression, pain is also characteristically provoked by pressure along the course of the sciatic nerve at the classic points of Valleix (sciatic notch, retrotrochanteric gutter, posterior surface of thigh, and head of fibula). Pressure at one point may cause radiation of pain and tingling down the leg. Elongation of the nerve root by straight-leg raising or by flexing the leg at the hip and extending it at the knee (Lasègue maneuver as discussed earlier) is the most consistent of all pain-provoking signs. During straight-leg raising, the patient can distinguish between the discomfort of ordinary tautness of the hamstring and the sharper, less-familiar root pain, particularly when asked to compare the experience with that on the normal side. Many variations of the Lasègue maneuver have been described (with numerous eponyms), the most useful of which is accentuation of the pain by dorsiflexion of the foot (Bragard sign) or of the great toe (Sicard sign). The Lasègue maneuver with the healthy leg may evoke sciatic pain on the contralateral side), but usually of lesser degree (Fajersztajn sign). However, this "crossed straight-leg-raising sign" is highly indicative of a ruptured disc as the cause of sciatica (56 of 58 cases in the series of Hudgkins). With the patient standing, forward bending of the trunk may induce reflexive flexion of the knee on the affected side (Neri sign). Sciatica may be provoked by forced flexion of the head and neck, coughing, or pressure on both jugular veins, all of which increase intraspinal pressure (Naffziger sign). Marked inconsistencies in response to these tests raise the suspicion of psychologic factors or of referred muscular pain.
An antalgic posture, referred to as sciatic scoliosis, is maintained by reflex contraction of the paraspinal muscles, which can be both seen and palpated. In walking, the knee is slightly flexed, and weight bearing on the painful leg is brief and cautious on the ball of the foot, giving a limp. It is particularly painful for the patient to go up and down stairs.
The signs of more severe spinal root compression are impairment of sensation, loss or diminution of tendon reflexes, and muscle weakness, as summarized in Table 11-1.
Generally, disc herniation compresses the root on one side, at the level just below the herniation (see below). Hypotonia may be evident on inspection and palpation of the buttock and calf. In a few patients, foot drop (L5 root) or weakness of plantar flexion (S1 root) is a main feature of disc protrusion, and some of these patients have little associated pain. The reflex changes noted below have little relationship to the severity of the pain or sensory loss. Furthermore, compression of the fourth, or sometimes fifth, lumbar root may occur without any change in the tendon reflexes. Bilaterality of symptoms and signs is rare, as is sphincteric paralysis, but they occur with large central protrusions that compress the cauda equina. The cerebrospinal fluid (CSF) protein is often elevated with disc rupture, more predictably with central rupture and then, usually in the range of 55 to 85 mg/dL, sometimes higher.
As emphasized earlier, herniations of the intervertebral lumbar discs occur most often between the fifth lumbar and first sacral vertebrae (compressing the traversing S1 or exiting L5 root; Fig. 11-3) and between the fourth and fifth lumbar vertebrae (compressing the traversing L5 or exiting L4 root).
Mechanisms of compression of the fifth lumbar and first sacral roots by herniated lumbosacral discs. A lateral disc protrusion at the L4-L5 level usually involves the fifth lumbar root and spares the fourth; a protrusion at L5-S1 involves the first sacral root and spares the fifth lumbar root. Note that a more medially placed disc protrusion at the L4-L5 level (cross-hatched) may involve the fifth lumbar root as well as the first (or second and third) sacral root.
Lesions of the fifth lumbar root (L5) produce pain in the region of the hip and posterolateral thigh (i.e., sciatica) and, in more than half such cases, lateral calf (to the lateral malleolus), and less often, the dorsal surface of the foot and the first or second and third toes. Pain is elicited by the straight-leg raising test or one of its variants, and protective nocifensive reflexes come into play, limiting further elevation of the leg. Paresthesia may be felt in the entire territory or only in its distal parts. The tenderness is in the lateral gluteal region and near the head of the femur. Weakness, if present, involves the extensors of the big toe and foot and the foot invertors (a distinguishing feature of foot drop originating in peroneal nerve damage). The ankle jerk may be diminished (more often it is normal), but the knee jerk is hardly ever altered.
With lesions of the first sacral root (S1), the pain is felt in the midgluteal region, mid-posterior part of the thigh, posterior region of the calf to the heel, outer plantar surface of the foot, and fourth and fifth toes. Tenderness is most pronounced over the midgluteal region. Paresthesia and sensory loss are mainly in the lower part of the leg and outer toes, and weakness, if present, involves the plantar flexor muscles of the foot and toes, abductors of the toes, and hamstring muscles. The Achilles reflex is diminished or absent in the majority of cases. In fact, loss of the Achilles reflex may be the only objective sign. Walking on the toes is more difficult and uncomfortable than walking on the heels because of weakness of the plantar flexors.
The less-frequent lesions of the third (L3) and fourth (L4) lumbar roots give rise to pain in the anterior part of the thigh and knee and anteromedial part of the leg (fourth lumbar), with corresponding sensory impairment in these dermatomal distributions. The knee jerk is diminished or abolished with compression of either root. Third lumbar (L3) motor root lesions may weaken the quadriceps, thigh adductor, and iliopsoas; L4 root lesions weaken the anterior tibial innervated muscles, sometimes with a mild foot drop. First lumbar (L1) root pain is projected to the groin, and L2, to the lateral hip.
Some patients have a distinctive syndrome associated with extreme lateral disc protrusions, particularly those situated within the proximal portion of the intervertebral spinal foramina. Unremitting radicular pain without back pain and a tendency to worsen with extension of the back and torsion toward the side of the herniation are characteristic. Also, in rare instances of lumbar intradural disc rupture, there may not be sciatic pain because the free fragment in the subarachnoid space does not impinge on the roots of the cauda equina. Both of these configurations may confound clinical and radiologic diagnosis and make surgery more difficult.
Rarer still, and often clinically obscure, are protrusions of thoracic intervertebral discs (0.5 percent of all surgically verified disc protrusions, according to Love and Schorn). The four lowermost thoracic interspaces are the most frequently involved. Trauma, particularly hard falls on the heels or buttocks, is an important causative factor. Deep boring spine pain; root pain circling the body or projected to the abdomen or thorax (sometimes simulating visceral disease); paresthesias below the level of the lesion; loss of sensation; both deep and superficial; and paraparesis or paraplegia are the usual clinical manifestations.
A herniated lumbar disc at one interspace may compress more than one root (Fig. 11-3), and it follows that the symptoms will then reflect this. Furthermore, the above descriptions of single root compression refer mainly to signs and symptoms of typical posterolateral disc protrusion. Very large central disc protrusions may compress the entire cauda equina with a dramatic syndrome that includes intense low back and bilateral sciatic pain, incomplete paraparesis, loss of both ankle jerks, and, most characteristic, varying degrees of urinary retention and incontinence. This circumstance demands surgical attention.
Anomalies of the lumbosacral roots may lead to errors in localization (see descriptions by Postacchini et al). The combined rupture of two or more discs occurs occasionally and complicates the clinical picture. When both the L5 and S1 roots are compressed by a large herniated disc, the signs of the S1 lesion usually predominate.
Herniation may occur directly into the adjacent vertebral body, giving rise to a Schmorl nodule. In such cases there are no signs of nerve root involvement although back pain may be present, sometimes recurrent and referred to the thigh. Most often, these well-circumscribed rounded radiographic densities adjacent to the endplate of the vertebral body are found incidentally on CT or MRI.
When all components of the lumbar disc syndrome are present, the diagnosis can be made with reasonable confidence. With persistent symptoms, many neurologists prefer to corroborate their clinical impression with MRI of the lumbar spine (Fig. 11-4). In the absence of neurological deficits, imaging generally need not be undertaken until the pain has persisted for several weeks (see Chou and colleagues). This, of course, may not be necessary if the pain is manageable and surgery is not contemplated (see further on). MRI is favored over CT because of the advantages of the distinction that can be made between disc material, annulus, nerves and bones and the clarity of their anatomic relationships. MRI also excludes disc herniations at other sites or an unsuspected tumor. As indicated earlier, in cases in which MRI is not possible or it has been unrevealing, we often turn to CT or CT with myelography for a refined definition of the root sleeves and use the EMG to corroborate subtle findings.
Lumbar disc herniation as shown by T2-weighted MRI. A. Sagittal view of a large herniated nucleus pulposus at L5-S1. The posteriorly protruding disc material indents and elevates the anterior thecal sac and narrows the spinal canal. The extruded material has the same signal characteristics of the parent disc. The disc space at this level is narrowed and the disc is less hyperintense than normal because of desiccation and the extruded component. B. Axial view showing the focal right paracentral posterior disc herniation (large arrow) protruding into the canal and compressing the traversing nerve root (the right S1 nerve root) at this level. The exiting L5 roots above are not affected and can be seen laterally to the disc (small arrows).
The needle EMG study is abnormal, showing fibrillation potentials in denervated muscles after 1 or 2 weeks, but it may remain normal in 10 percent of cases according to Leyshon and colleagues. Loss or marked asymmetry of the H reflex is another useful indication of S1 radiculopathy, but this simply corroborates the loss of an Achilles reflex. The finding of denervation potentials in the paraspinal muscles (indicating root rather than peripheral nerve lesions) and in muscles that conform to a root distribution is also helpful, but again, some weeks must have elapsed from the onset of root pain for these findings to be present. We emphasize that, while useful information is to be gained from EMG, it is required in only a limited proportion of cases and often provides mainly corroborating data. It is more helpful when the diagnosis is uncertain. An entirely normal study should lead to reconsideration of the diagnosis, particularly if surgery was planned for relief of a compressive radiculopathy.
Many disc abnormalities observed on MRI and loosely referred to as "herniation" are incidental findings, unrelated to the patient's symptoms, or are simply bulges of the annulus. Jensen and colleagues, in an MRI study of the lumbar spine in 98 asymptomatic adults, found that in more than half, there was a symmetrical extension of a disc (or discs) beyond the margins of the interspace (bulging). In 27 percent, there was a focal or asymmetrical extension of the disc beyond the margin of the interspace (protrusion), and in only 1 percent was there more extreme extension of the disc (extrusion or sequestration). These findings emphasize the importance of using precise terms in describing the imaging abnormalities and evaluating them strictly in the context of the patient's symptoms.
Treatment of Ruptured Lumbar Disc
In the treatment of an acute or chronic rupture of a lumbar disc, many patients have found it nearly impossible to participate in physical activities and to assume certain positions that cause pain. However, the time-honored tenet of prolonged bed rest has been questioned by the results of several randomized studies (Vroomen et al). It would appear that the main benefit is simply that time has passed and the expected resolution of pain has taken its course in many patients. Traction is probably of little value. Analgesic medications, either NSAIDs or opioids, may be required for a few days. In a few patients with severe sciatica we have been impressed with the temporary relief afforded by administration of oral dexamethasone (4 mg every 8 h) for several days, although this approach has not been studied systematically and several of our colleagues decry it. The treatment of nerve root compression with repeated epidural injections of corticosteroids has enjoyed periods of popularity, but controlled studies have failed to confirm sustained efficacy (White et al; Cuckler et al), and it is not without complications including the rare but widely publicized outbreak of fungal meningitis from contaminated steroids. As with many similar studies, Carette and colleagues (1997) found only short-term improvement with epidural steroid injection and the ultimate need for surgery was not altered. Nevertheless, some pain specialists have not discarded this form of treatment in view of success in selected patients, even if short-lived.
Surgical Treatment of Lumbar Disc Disease
An indication for emergency surgery is an acute compression of the cauda equina by massive disc extrusion, causing bilateral sensorimotor loss and sphincteric paralysis. Although not the recommended course, it should be pointed out that there have been instances in which even a dramatic syndrome of cauda equina compression had resolved spontaneously after several weeks.
If the pain and neurologic findings have not subsided in response to conservative management or the patient has suffered frequent disabling acute episodes, surgical treatment must be considered. Useful information regarding surgery and its timing can be ascertained from a randomized trial conducted by Peul and colleagues and from the Spine Patients Outcomes Research Trial (SPORT) conducted by Weinstein and coworkers (2006). In the first study, a large proportion of patients assigned to treatment with physical therapy and pain medications had enough pain that they required surgery within several months. In addition, patients assigned initially to surgery by microdiscectomy had considerably faster relief of back and sciatic pain, but at the end of a year, both groups had minimal disability and similar degrees of minor pain. The implications of this study are that avoiding surgery initially does not have adverse consequences but if more rapid pain relief and mobilization are the aims, surgery is preferable. In the second cited study there was even greater crossover between conservative and surgically assigned groups and there was a slightly more favorable outcome in those who underwent early surgery.
The surgical procedure most often indicated for lumbar disc disease is one of the variants of a hemilaminectomy with excision of the disc fragment introduced almost a century ago by Mixter and Barr. Questions relating to the relative merits of limited ("microscopic"), or minimally invasive excision of the lamina are often raised by patients and no clear answer can be given except that individual surgeons excel at one or another technique and the outcomes are similar. Eighty-five to 90 percent of cases with sciatic pain because of L4-L5 or L5-S1 disc ruptures are relieved by operation, are home in days or less, and are resuming activities within weeks. Rerupture occurs in approximately 5 percent of operated cases according to Shannon and Paul. Spinal fusion of the involved segments is indicated in cases in which there is instability, usually related to extensive or prior surgery or to an anatomic abnormality.
The features that are predictive of better outcome from decompressive surgery are a clearly delineated radicular leg pain, in contrast to general back pain alone, younger age, an identifiable precipitating event for the back and sciatic pain, clinical features that are restricted to compression of a single nerve root, and the absence of chronic or frequently recurrent back pain. Curiously, Barzouhi and colleagues found that the presence or absence of disc herniation in the MRI a year after operation had little relationship to the persistence of sciatica.
Other Causes of Sciatica and Low Back Pain
An increasing experience with lumbar back pain and sciatica has impressed the authors with the large number of such cases that have no clear cause. At one time, all these cases were classified as sciatic neuritis or "sacroiliac strain." After Mixter and Barr popularized the concept of herniated disc, all sciatica and lumbar pains were ascribed to this condition. Operations became somewhat indiscriminately practiced, not only for frank disc protrusion but also for "hard discs" (unruptured) and related pathologies of the spine. In large referral centers, the surgical results became decreasingly satisfactory until recently, as many patients were being seen with unrelieved postlaminectomy pain as with unoperated ruptured discs. This is no longer the case as selection of patients has been refined.
Other cases of chronic sciatic pain are due to one of a number of pathologic entities. Entrapment of lumbar roots may be the consequence not only of disc rupture but also of spondylotic spurs with stenosis of the lateral recess, cysts of the synovium derived from degenerative disease of the facet joint, hypertrophy of facets, and, rarely, arachnoiditis. Lateral recess stenosis in particular may be a cause of sciatica not relieved by conventional disc surgery (see below, under "Lumbar Stenosis"). Synovial cysts arising from a facet joint are not uncommon, and even very small ones may be situated in the proximal portion of the foramen, thereby causing sciatica. If pain is intractable, surgical removal of the cyst is indicated. Another surprising finding in the course of imaging the spinal canal is a cyst-like dilatation of the perineurial sheath (Tarlov cysts). One or more sacral roots may be involved at points where they penetrate the dura and may be associated with radicular symptoms. There are reports of relief from opening the cysts and freeing the roots, but the results seem more uncertain to us. Sciatica that is temporally linked to the premenstrual period is usually a result of endometriosis involving the nerve at the sciatic notch ("catamenial sciatica"). We have also observed cases of sciatica that occurred with each pregnancy, presumably from uterine traction on the nerve.
The notion of a pyriformis (piriformis) syndrome, so named by Kopell and Thompson, has arisen as a cause of otherwise unexplained buttock pain or vague sciatica. The muscle overlies or, in a small proportion, embeds the peroneal trunk of the sciatic nerve. Hypertrophy, spasm, or simply the anatomic variation in which the nerve is entrapped in the tendinous origin of the muscle have all putatively caused local and some degree of sciatic pain. Sciatica in these cases is elicited by stretching the muscle through flexion, adduction, and internal rotation of the hip. The validity of this syndrome is uncertain and it has been the subject of polemical discussions in the literature. EMG data are ambiguous but reportedly show distal denervation, sparing more proximally innervated muscles. Our practice would be to avoid surgery in such cases, but to endorse physical therapy.
Compression of the cauda equina by epidural masses, as described further on, most often begins with
back pain or sciatica. The sciatic nerve or the plexus from which it originates may be directly implicated in tumor (lymphoma, neurofibrosarcoma).
Several inflammatory diseases of the cauda equina produce back pain and bilateral sciatica and may be mistaken for the more usual types of cauda equina compression; cytomegalovirus infection in AIDS patients, Lyme disease (Bannwarth syndrome), herpetic infection (Elsberg syndrome), and neoplastic meningitis at times behave in this fashion. In all of these, the CSF shows a pleocytosis. The Guillain-Barré syndrome may also produce misleading back and radicular pain before weakness is apparent. The caudal roots in these diseases usually enhance with gadolinium on MRI.
An unusual lumbosacral plexus neuritis (Wartenberg plexitis) is a unilateral (occasionally bilateral) disorder akin to brachial neuritis, which may cause sciatica, as does occasionally nerve infarction or damage from diabetes, herpes zoster, parvovirus, or a retroperitoneal mass (see Chap. 46).
Again, if one sees enough of these cases, the cause of a number of them, particularly those with bilateral burning along the sciatic nerve, cannot be determined.
Lumbar Spinal Canal Stenosis ("Lumbar Stenosis" and Neurogenic Claudication)
The term spondylosis is often applied to a general constellation of bone, joint and ligamentous changes that narrow the spinal canal and neural foramina. In the lumbar region, these osteoarthritic and related degenerative changes lead to compression of one or more lumbar and sacral roots because of narrowing of the spinal canal. The problem is more likely to occur if there is a congenitally narrow canal. The roots are typically compressed between the posterior surface of the vertebral body anteriorly, the facet joint laterally, and the ligamentum flavum posteriorly. Lateral recess stenosis and foraminal stenosis are common effects of spondylosis (as mentioned above in relation to disc disease) and either or both may be the main cause of individual root compression.
The usual features of lumbar stenosis are of fluctuating aching and sharp pain in the low back, buttock and sciatic distribution, occasionally including femoral areas, and generally elicited by prolonged sitting, standing, or walking and relieved by rest. Some patients have virtually constant pain in these areas but still have relief with rest in one or another body position.
In the distinctive syndrome of "neurogenic claudication", standing or walking causes a gradual onset of numbness and weakness of the legs, usually with asymmetrical sciatic, calf, or buttock discomfort that forces the patient to sit down. When the condition is more severe, the patient gains relief by squatting or lying with the legs flexed at the hips and knees, or in a forward leaning position with the hips and knees slightly flexed, as if in a bicyclists position. Often the numbness begins in one leg, spreads to the other, and ascends as standing or walking continues. The ankle tendon reflexes may disappear after walking a distance, only to return on flexing the spine. Pain in the low back and glutei is variable. Disturbances of micturition and impotence are infrequent unless there has been an additional more acute disc herniation. In some patients with lumbar stenosis, neurologic symptoms persist without relation to body position. The process is distinguished from vascular claudication of the legs by its appearance in the standing position, the prominence of numbness in some cases, and, of course, by the preservation of distal leg pulses and loss of ankle reflexes in the neurogenic variety.
This "claudication of the cauda equina" was described by van Gelderen in 1948, and it was shown by Verbiest to not be caused by ischemia but by encroachment on the cauda by hypertrophied joints, thickened ligaments, and protrusions of disc material on a developmentally shallow canal. A subluxation may contribute to the stenosis in the anteroposterior dimension. Later, the canal is also narrowed from side to side (reduced interpedicular distance).
A prominent feature of many cases of the degenerative spinal disorder is displacement and malalignment of one vertebral body in relation to the adjacent one, or spondylolisthesis. This may cause little difficulty at first but eventually the patient complains of limitation of motion and pain in the low back radiating into the thighs. In the extreme case, examination discloses tenderness near the segment that has "slipped" anteriorly (most often L5, occasionally L4 in middle-aged women) or a palpable "step" of the spinous process forward and shortening of the trunk with protrusion of the lower abdomen (anterior shift of L5 on S1, spondyloptosis). Compression of the corresponding spinal roots by the displaced vertebrae causes paresthesia and sensory loss, muscle weakness, and diminished reflexes. These neurologic features, however, tend not to be severe. When spondylolisthesis is unstable, new symptoms may appear abruptly in the form of a foot drop, urinary retention, or overflow incontinence. The spinal instability is evidenced on conventional radiographs by a change in the diameter of the spinal canal as the patient moves between the flexed and extended position of the back.
A striking syndrome that has been attached to lumbar stenosis consists of painful legs–moving toes, described by Spillane. There is burning leg pain and continuous and complex rhythmic movements of the toes, as the name implies. Symptoms may begin on one side but become bilateral. Lumbar nerve root compression, most often from lumbar stenosis, or other types of peripheral damage underlie most cases.
Treatment of Lumbar Stenosis
Decompression of the spinal canal relieves the symptoms of lumbar stenosis in a considerable proportion of cases, but the results have been inconsistent. Patients must be chosen carefully for surgery, and success is likely if the clinical features conform to the typical syndrome, mainly pain that altered in various positions and at least partially relieved by rest, with definite evidence of root compression by imaging. In perhaps the most careful, controlled trial comparing surgery to conservative treatment for lumbar spinal stenosis, pain and overall function at 2 years was several-fold better in those who had operations (Weinstein et al, 2008). However, interpretation was hampered by a large number of patients who crossed over between arms of the study. Issues pertaining to the methodology of operation, the need for fusion of the lumbar spine to limit mobility, and various forms of "instrumentation" are of great interest, but are best discussed in textbooks of neurosurgery and orthopedics.
Insofar as lumbar stenosis is a cauda equina syndrome, its differential diagnosis is also considered in Chap. 44.
Atherosclerosis of the Distal Aorta (Vascular Claudication)
Atherosclerosis of large and medium-sized arteries often leads to symptoms that are induced by exercise (intermittent claudication) but may also occur at rest (ischemic rest pain) as already mentioned. The diabetic patient is especially susceptible. The muscle pain that is brought on by exercise and promptly relieved by rest most frequently involves the calf and thigh muscles. If the atherosclerotic narrowing or occlusion implicates the aorta and iliac arteries, it may also cause hip and buttock claudication and impotence in the male (Leriche syndrome). Ischemic rest pain—and sometimes attendant ulceration and gangrene—is usually localized to the foot and toes; it is the consequence of multiple sites of vascular occlusion. Pain at rest is characteristically worse at night and totally or partially relieved by dependency.
The examination of such patients will reveal a loss of one or more peripheral pulses, trophic changes in the skin and nails (in advanced cases), and the presence of bruits over or distal to sites of narrowing. The ankle reflexes are often diminished. The similarities to a claudicatory syndrome of lumbar spine stenosis have already been discussed.
Degenerative Osteoarthritis, or Osteoarthropathy
Independent of stenosis of the lumbar canal is chronic and recurring back pain caused by degenerative arthritic disease. It occurs in later life and may involve all or any part of the spine but is most prevalent in the cervical and lumbar regions. The pain is described as a stiffness that is centered in the affected part of the spine. It is increased initially by movement and is associated with limitation of motion but is often worse on arising in the morning. In contrast to the spinal claudicatory syndrome, warming up and progressive mobilization make the pain better. There is a notable absence of systemic symptoms such as fatigue, malaise, or fever, and, more importantly, there are limited or no features of radicular compression. Some patients complain of vague and intermittent pains in the upper or posterior legs, but sciatica is not a component and the straight-leg raising tests do not elicit pain. The sitting position is usually comfortable, although stiffness and discomfort are accentuated when the erect posture is resumed.
The severity of the symptoms often bears little relation to the radiologic changes; pain may be present despite minimal radiographic findings; conversely, marked osteophytic overgrowth with spur formation, ridging, bridging of vertebrae, narrowing of disc spaces, subluxation of posterior joints on flexion, and air in the disc spaces can be seen in both symptomatic and asymptomatic persons.
This syndrome has been somewhat clarified in recent years, but its definition and nature remain imprecise. In the typical instance, osteoarthritic degeneration of the facet joint gives rise to a focal parasagittal lumbar back pain, with tenderness over the joint (Fig. 11-2, location 3) but without signs of root compression. The pain can be severe, worse at night, and prevent sleep if no comfortable position can be found. Nonsteroidal drugs are helpful. The diagnosis is confirmed when the pain is relieved for a variable period by injection of the joint with local anesthetic.
Often one is uncertain whether it was the analgesic effect on the joint or the infiltration of the region around the nerve root that relieved the pain. Two controlled studies have provided evidence of the inefficacy, both in the short and long term, of corticosteroid injections into the facet joints (Carette et al, 1991; Lilius et al). Notwithstanding these reports, we have found the injection of analgesics and steroids in and around the facet to be a useful temporizing measure in some patients. Some patients have discovered that they may obtain temporary relief from facet pain by forcefully twisting or stretching the back and creating an audible pop at the affected joint, comparable to chiropractic manipulation. Over time, they acquire a laxity of the supporting structures of the joint, which may actually perpetuate the problem.
If the diagnosis is established by local injection, pain centers offer radiofrequency ablation of the small recurrent sensory nerves that innervate the joint as a means of permanent relief. This has met with some success but has not been studied systematically.
Some writers have used the term facet syndrome to describe a painful state from facetal hypertrophy that gives rise to a lumbar monoradiculopathy indistinguishable from that caused by a ruptured disc or spondylosis. Reynolds and coworkers have documented such cases. At operation, the spinal root is compressed against the floor of the intervertebral canal by overgrowth of an inferior or superior facet. Foraminotomy and facetectomy, after exploration of the root from the dural sac to the pedicle, have relieved the pain in many operated cases.
Lumbar Adhesive Arachnoiditis
This is a somewhat vague entity in which the arachnoid membrane is thickened and opaque in the vicinity of the cauda equina. The term is also applied to thickening of the arachnoidal sheaths around roots (normal roots have essentially no epineurium). According to one review, lumbar arachnoiditis is rare, having been seen in only 80 of 7,600 myelograms, and it should virtually vanish as the use of MRI and water-soluble dyes for myelography take precedence. The usual clinical features are intractable low-back and leg pain and paresthesia, all positionally sensitive, in combination with neurologic abnormalities referable to lumbar spinal roots. In our few patients, multiple previous myelograms with lipid contrast agent (a problem of the past), disc rupture, operative procedures, infections, and subarachnoid bleeding have been causal. Some cases have followed spinal anesthesia and even epidural anesthesia by a period of months or years. The presumption is that the dura had been breached, and often, there were clinical signs of aseptic meningitis soon after the procedure. In the absence of such an acute reaction, the later diagnosis of arachnoiditis rests on less-certain grounds.
The MRI shows eccentrically thickened meninges in the spinal canal with arachnoid adhesions and collections of CSF that displace nerve roots (Fig. 11-5). Abnormalities are even more striking on CT myelographic studies in which the contrast is broken up and fails to outline the roots. Treatment is unsatisfactory. Lysis of adhesions under an operating microscope and administration of intrathecal steroids have been of limited value, although some experienced surgeons claim otherwise. Epidural injection of steroids is occasionally helpful according to some of our orthopedic surgeon colleagues.
Lumbosacral MRI of a patient with lymphoma, with radiation-induced arachnoiditis causing severe back pain and leg weakness. A. Sagittal T2-weighted MRI showing clumping of the nerve roots of the cauda equina. B. Axial T2-weighted image at the L3 vertebral level showing clumping of the nerve roots. C. Axial T2-weighted image at the L5 vertebral level showing lateral displacement of nerve roots by acquired arachnoid cysts. There are bilateral metallic pedicle screws.
This disorder, referred to in the past as rheumatoid spondylitis and as von Bechterew or Marie-Strümpell arthritis, affects young adult males predominantly. Approximately 95 percent of patients with ankylosing spondylitis are marked by the histocompatibility antigen HLA-B27 (which is present in only 7 percent of nonaffected persons of European extraction). Pain, usually centered in the low back, is the main early complaint. Often it radiates to the back of the thighs and groin. At first, the symptoms are vague (tired back, "catches" up and down the back, sore back), and the diagnosis may be overlooked for many years. Although the pain is recurrent, limitation of movement is constant and progressive and comes to dominate the clinical picture. Early in the course of disease there is only "morning stiffness" or an increase in stiffness after periods of inactivity similar to lumbar osteoarthritis but unusual for the affected age group. In advanced stages, a cauda equina compression syndrome may complicate ankylosing spondylitis, the result apparently of an inflammatory reaction and proliferation of connective tissue (Matthews). Limitation of chest expansion, tenderness over the sternum, decreased motion and tendency to progressive flexion of the hips, and the characteristic immobility and flexion deformity of the spine ("poker spine") may be present early in the course of the disease.
The radiologic hallmarks are destruction and subsequent obliteration of the sacroiliac joints, followed by bony bridging of the vertebral bodies to produce the characteristic "bamboo spine." When this change becomes apparent, the pain usually subsides, but the patient by then has little motion of the back and neck. An unusual additional feature, almost unique to this condition but not present in all cases, is an extreme dilatation of the lumbar thecal sac. Ankylosing spondylitis may also be accompanied by the Reiter syndrome, psoriasis, and inflammatory diseases of the intestine (see also Chap. 44). The great risk in this disease is fracture dislocation of the spine from relatively minor trauma, particularly flexion-extension injuries.
Occasionally, ankylosing spondylitis is complicated by destructive vertebral lesions. This complication should be suspected whenever the pain returns after a period of quiescence or becomes localized. The cause of these lesions is not known, but they may represent a response to nonunion of fractures, taking the form of an excessive production of fibrous inflammatory tissue. When it is severe, ankylosing spondylitis may involve both hips, greatly accentuating the back deformity and disability.
Rheumatoid arthritis of the spine may be confined to the cervical region and creates risk of fracture–dislocation; it is considered further on in this chapter.
Neoplastic and Infectious Diseases of the Spine (See Also Chap. 44)
Metastatic carcinoma (breast, bronchus, prostate, thyroid, kidney, stomach, uterus), multiple myeloma, and lymphoma are the common malignant tumors that involve the spine. The primary lesion may be small and asymptomatic, and the first manifestation of the tumor may be pain in the back caused by metastatic deposits. The pain is constant and dull; it is often unrelieved by rest and is generally worse at night, interrupting sleep. Radicular pain may be added if the metastasis extends laterally. A fracture of a vertebral body in an otherwise healthy young or middle-aged person should alert the physician to the possibility of an underlying metastasis. At the time of onset of the back pain, there may be no radiographic changes on plain radiographs; when such changes do appear, they usually take the form of destructive lesions in one or several vertebral bodies with little or no involvement of the disc space, even in the face of a compression fracture. However, the changes are evident on CT and MRI or radioactive isotope scan, including PET, and demonstrate areas of osteoblastic activity caused by neoplastic or inflammatory disease.
Infection of the vertebral column, osteomyelitis, is usually caused by staphylococci and less often by coliforms and mycobacteria. The patient complains of subacute or chronic pain in the back, which is exacerbated by movement but not materially relieved by rest. Motion becomes limited, and there is percussion-induced tenderness over the spine in the involved segments and pain with jarring of the spine, as occurs when the heels strike the floor. Often these patients are afebrile and do not have a leukocytosis. The erythrocyte sedimentation rate and C-reactive protein are elevated as a rule. Highly characteristic is the demonstration by CT scanning and MRI of involvement of both the vertebral body and the adjacent intervertebral disc, and the finding of a breached disc space with involvement of two adjacent vertebral bodies is one of the features that differentiates infectious from neoplastic diseases of the spine. A paravertebral mass is often found, indicating an abscess, which may, in the case of tuberculosis, drain spontaneously at sites quite remote from the vertebral column. In the postoperative setting or following trauma, a disc infection can occur by direct microbial seeding. It should be remembered that the intervertebral disc is an avascular structure, and therefore blood-borne pathogens first infect the bone and then secondarily spread to the adjacent disc. This is not the case in the neonatal period when the discs are directly perfused, for which reason neonates are subject to hematogenously seeded discitis.
We have also encountered a number of patients with bacterial endocarditis who complained of severe midline thoracic and lumbar back pain but had no evident infection of the spine.
Tuberculous spinal infection and the resultant kyphotic deformity (Pott disease) represent a special condition that is common in developing countries (see Chaps. 32 and 44).
Special emphasis is placed on this condition, which usually necessitates urgent surgical treatment. Failure to properly identify this lesion has led to paraplegia or death from sepsis. Most often this is caused by staphylococcal infection, which is carried in the bloodstream from a septic focus (e.g., furuncle) or is introduced into the epidural space from an osteomyelitic lesion. Another important avenue of infection is the intravenous self-administration of drugs and use of contaminated needles. Rarely, the infection is introduced in the course of a lumbar puncture, epidural injection, or laminectomy for disc excision. In some instances, the source of an epidural abscess cannot be ascertained. The main symptoms are low-grade fever, leukocytosis, and persistent and severe localized pain that are intensified by percussion and pressure over the vertebral spines. Additionally, the pain may acquire radicular radiation. These symptoms usually require investigation by MRI or CT myelography and surgical intervention, preferably before the signs of paraplegia, sphincter dysfunction, and sensory loss become manifest. Small abscesses and granulomas that are the residua of previous and partially treated abscesses can be sometimes treated successfully with antibiotics alone as discussed further on.
Intraspinal Hemorrhage (see Chap. 44)
Sudden, excruciating midline back pain (le coup de poignard or "the strike of the dagger")—often with rapidly evolving paraparesis, urinary retention, and numbness of the legs—may announce the occurrence of subarachnoid, subdural, or epidural bleeding. The most common causes of such an event are a coagulopathy (mainly from warfarin), and a spinal arteriovenous malformation (AVM), as discussed in Chap. 44. Spinal arterial aneurysms are much less common underlying lesions. It should be mentioned that focal back pain of comparable intensity may mark the onset of acute myelitis, spinal cord infarction, compression fracture, and occasionally, Guillain-Barré syndrome.
Back Pain from Visceral Disease
Peptic ulcer disease and carcinoma of the stomach and pancreas most typically induce pain in the epigastrium. However, if the posterior stomach wall is involved, particularly if there is retroperitoneal extension, the pain may be felt in the thoracic spine, centrally or to one side, or in both locations. If intense, it may seem to encircle the body. The back pain tends to reflect the temporal characteristics of the pain from the affected organ; e.g., if caused by gastric ulceration, it appears about two hours after a meal and is relieved by food and antacids.
Diseases of the pancreas are apt to cause pain in the back, being more to the right of the spine if the head of the pancreas is involved and to the left if the body and tail are implicated. Retroperitoneal neoplasms—e.g., lymphomas, renal cell tumors, sarcomas, and other malignancies—may evoke pain in the lower thoracic or lumbar spine with a tendency to radiate to the lower part of the abdomen, groins, anterior thighs, or flank. A tumor in the iliopsoas region often produces a unilateral lumbar ache with radiation toward the groin and labia or testicle; there may also be signs of involvement of the upper lumbar spinal roots. An aneurysm of the abdominal aorta may induce pain localized to an analogous region of the spine. The sudden appearance of lumbar pain in a patient receiving anticoagulants should arouse suspicion of retroperitoneal bleeding; this pain may also be referred to the groin.
Inflammatory diseases and neoplasms of the colon cause pain that may be felt in the lower abdomen, the midlumbar region, or both. As with intense pain higher in the spine, it may have a belt-like distribution. Pain from a lesion in the transverse colon or first part of the descending colon may be central or left-sided; its level of reference is to the second and third lumbar vertebrae. If the sigmoid colon is implicated, the pain is lower in the upper sacral spine and anteriorly in the suprapubic region or left lower quadrant of the abdomen. Retroperitoneal appendicitis may have an odd referral of pain to the low flank and back.
Gynecologic disorders often manifest themselves by back pain, and their diagnosis may prove difficult. Thorough abdominal palpation, as well as vaginal and rectal examination by an experienced physician, supplemented by ultrasonography and CT scanning or MRI, usually discloses the source of pain. The uterosacral ligaments are a pelvic source of chronic back pain. Endometriosis or carcinoma of the uterus (body or cervix) may invade these structures, causing pain localized to the sacrum either centrally or more to one side. In endometriosis, the pain begins premenstrually and often merges with menstrual pain, which also may be felt in the sacral region. Rarely, cyclic engorgement of ectopic endometrial tissue may give rise to sciatica and other radicular pain. Changes in posture may also evoke pain here when a fibroma of the uterus pulls on the uterosacral ligaments. Low back pain with radiation into one or both thighs is a common phenomenon during the last weeks of pregnancy.
The pain of neoplastic infiltration of pelvic nerve plexuses may be projected to the low back and is continuous, becoming progressively more severe; it tends to be more intense at night and may have a burning quality. The primary lesion can be inconspicuous and may be overlooked on pelvic examination.
This is the name applied to pain localized to the coccyx, the three or four small vestigial bones at the lower-most part of the sacrum. The trauma of childbirth, a fall on the buttocks, avascular necrosis, a neurofibroma or glomus tumor, or one of a variety of other rare tumors and anal disorders, and, of course, pilonidal cyst, can sometimes be established as the cause of pain in this region. Far more often, the source remains obscure. In the past, patients in this latter group were indiscriminately subjected to coccygectomy, but more recent studies have demonstrated that most cases respond favorably to injections of local anesthetic and methylprednisolone or to manipulation of the coccyx under anesthesia (Wray et al).
Obscure Types of Low Back Pain and the Question of Psychiatric Disease
Even after careful examination, there remains a sizable group of patients in whom no basis for the back pain can be found. Two categories can be recognized: one with postural back pain and pain after injury, and another with psychiatric illness, but there are always cases where the diagnosis remains obscure.
Low back pain may be a major symptom in patients with hysteria, malingering, anxiety, depression, and hypochondriasis as well as in many persons whose symptoms do not conform to any of these psychiatric illnesses. It is good practice to assume that pain in the back in such patients may signify disease of the spine or adjacent structures, and this should always be carefully sought. However, even when some organic factors are found, the pain may be exaggerated, prolonged, or woven into a pattern of invalidism because of coexistent primary or secondary factors. This is especially true when there is the possibility of secondary gain (notably workers' compensation or settlement of personal injury claims). Patients seeking compensation for protracted low back pain without obvious structural disease tend, after a time, to become suspicious, uncooperative, and hostile toward their physicians or anyone who might question the authenticity of their illness. One notes in them a tendency to describe their pain vaguely and a preference to discuss the degree of their disability and their mistreatment at the hands of the medical profession. The description of the pain may vary considerably from one examination to another. Often also, the region(s) in which pain is experienced and its radiation are nonphysiologic, and the condition fails to respond to rest and inactivity. These features and a negative examination of the back should lead one to suspect a psychologic factor. A few patients, usually frank malingerers, adopt bizarre gaits and attitudes, such as walking with the trunk flexed at almost a right angle (camptocormia), and are unable to straighten up. Or the patient may be unable to bend forward even a few degrees, despite the absence of muscle spasm, and may wince at the slightest pressure, even over the sacrum, which is seldom a site of tenderness unless there is pelvic disease.
The depressed and anxious patient with back pain represents a troublesome problem. The disability seems excessive for the degree of spinal malfunction. Anxiety and depression may become important components of the back syndrome, and the patient may ruminate about an undiagnosed cancer or other serious illness. In these circumstances, common and minor back ailments—e.g., those caused by osteoarthritis and postural ache—are enhanced and rendered intolerable. Such patients are still subjected to unnecessary surgical procedures. It is not clear if one can depend on the diagnostic features of a response to drugs that alleviate depression.