9
Back Pain in Adults
Max Aebi
■ Introduction
The aging of the population in industrialized countries appears to be a nonreversible phenomenon. Increasing life expectancy, due in a great part to advances in health care, combined with a drastic decrease in the birth rate, has led to this situation.1 World demographics have shifted from a pattern of high birth rates and high mortality rates to one of low birth rates and delayed mortality.1,2 In Europe, the proportion of the population over the age of 65 was 10.8% in 1950, 14% in 1970, and 19.1% in 1995, and is projected to be 30.1% in 2025 and 42.2% in 2050.3 The proportion of the population over the age of 75 has grown from 2.7% in 1950 to 5.2% in 1995, and is projected to be 9.1% in 2025 and 14.6% in 2050.3 And this trend is not limited to industrialized countries; the developing countries’ share of the world’s population over the age of 65 is projected to increase from 59% to 71%. The global consequences of this distortion of the age pyramid on health care development, access, and costs are huge.4 For example, 59% of United States residents over the age of 65 have osteoarthritis, which is the main cause of disability and the most frequent cause of back and neck pain. Osteoarthritis is the most frequently encountered complaint of people of all ages, and the nature of the spine renders this problem difficult to investigate and to treat.
The aging of the spine is characterized by two major parallel and independent processes, which lead to different clinical situations:
- The reduction of bone mineral density, hence bone mass
- The development of degenerative changes of the diskoligamentous complex (disks, ligaments, facet joint capsules, and facet joints), resulting in instability, deformity, and narrowing of the spinal canal and the exit of the nerve roots (spinal and foraminal stenosis), with secondary neurologic problems such as myelopathy, cauda equina, radicular syndromes, and disability
Hence, degeneration alone, or in combination with bone mass reduction by osteoporosis or metastatic tumor involvement, contributes to a different degree to the development of a variety of lesions and often to several painful and invalidating disorders.
■ Osteoporotic Compression Fractures
Osteoporotic compression fractures of vertebral bodies as an expression of age-related diminution of the bone mass is an increasing problem due to aging of the Western population as well as the Japanese and Chinese population, resulting in increasing numbers of severely osteoporotic patients, mostly women. Recent studies have shown that osteoporotic vertebral fractures are associated with an increased risk of mortality and a decreased quality of life.5,6 The prevalence of these fractures is 39% in patients over the age of 65 years.4,7
■ Degeneration of the Spinal Structures
Degeneration of the spinal structures induces interactive alterations at many levels: bones, disks, facet joints, and ligaments. Some of these degenerative lesions can be responsible for compressive damage to the neural elements, as in the case of disk herniation or spinal stenosis.
Disk degeneration begins when the balance between synthesis and degradation of the matrix is disrupted; at the microscopic level, disk degeneration includes a net loss of water as a consequence of a breakdown of proteoglycans in so-called short chains, which are unable to bind water.8,9 Furthermore, there is disruption of collagen fiber organization, specifically in the annulus, and increased levels of proteolytic enzymes. Disk degeneration can be seen in 16% of 20-year-olds and 98% of 70+-year-olds10,11 (Fig. 9.1).
Women reach the same level of degeneration about 10 years later than men (Fig. 9.1). In the aging of the spine there is a predetermined cell viability (endogenous = genetic) and decreasing cellular activity in the disk over the years due to exposure of the disk to repetitive mechanical loads.9,12,13 This leads to a loss of extracellular matrix, with proteoglycans degrading, and decreased capability to bind water. The collagen organization is dissociated, which leads to a loss of height of the disk. This is always combined with a secondary deterioration of the facet joints, ligaments, and muscles. Through this process, the boundaries between the annulus and nucleus are less distinct, and the collagen is increasing in the nucleus and replacing the proteoglycans. With that we see concentric fissuring at radial tears, which weakens the disk, starting in the third and fourth decade of life. There is substantial variation in this cascade of events. But these changes clearly have biomechanical consequences for the motion segment.12
The role of vascularization in the aging disk is most crucial. The nutritional supply of the cells in the disk diminishes because the adjacent vertebral end-plate permeability is decreasing, leading to a blood supply decrease with a secondary tissue breakdown, which starts in the nucleus, and mechanical impact on the cells (sensitive to mechanical sickness), which leads to a qualitative and quantitative modulation of the matrix proteins.13–15 The variation of the proteoglycan content as well as the water content is age-dependent and operating in parallel: more degradation of the proteoglycans, less water content, and higher probability of disintegration of the disk (Fig. 9.2).
Thus, we can see that orthopedic surgeons, musculoskeletal specialists, and dedicated spine specialists are going to be treating huge numbers of patients affected by diseases that result from the aging of the musculoskeletal system.
■ Typical Disorders of the Aging Spine
Typical disorders of the aging spine that express themselves as back or neck pain with or without neurologic symptoms or signs include the following:
- Degenerative disease of the disks, osteochondrosis, and disk prolapse/herniation
- Degenerative disease of the facet joints resulting from joint incongruences due to disk height loss and arthritis, secondary instability, and deformity
- Degenerative spondylolisthesis with or without spinal stenosis and instability
- Spinal stenosis: central, recess, and foraminal stenosis due to narrowing of the elements of the spinal canal, following hypertrophy of the ligamentum flavum and the joint capsules and the facet joint by itself—pathomorphology that may lead to compression of the neural structures of the spinal canal
- Spinal deformities: scoliosis, kyphosis, and concomitant secondary instability and neurologic deficit
- Osteoporosis with vertebral compression fractures (VCFs) alone or in combination with degenerative defects, which may be followed by a secondary deformity
- Pathological fractures of the vertebrae due to metastatic disease
- Infection of the spine, spondylodiskitis, and spondylitis
Disk Degeneration, Osteochondrosis, and Disk Herniation
Symptomatic, isolated, or multilevel disk degeneration can be seen in the lumbar and cervical spine.16 The clinically most relevant disk degeneration with subchondral edema, possible secondary spondylolisthesis or translational and rotatory dislocation, and consecutive spinal deformity is most frequently seen in the lumbar spine at the following levels, in decreasing order: L3-L4, L2-L3, L4-L5, and L1-L2. The asymmetrical degeneration may lead to a disk herniation with major or mass dislocation of whole disk fragments (annulus and nucleus parts), leading usually to at least a major neurologic complication, such as root compression or cauda compression with significant radicular pain or sensorimotor deficit.
This pathology can occur in the context of previous surgery in the lower lumbar spine that led to a fusion or at least a poorly mobile spinal segment, with overload and stress rising to the adjacent superior or inferior segment, with rapid degeneration of the disk and with potential instability, spinal stenosis, and possible extrusion of major disk fragments as an acute event. In almost all these situations, decompression of the segment and a stabilization may become necessary17–19 (Fig. 9.3).
Fig. 9.3 Multilevel disk degeneration with instability in LH, a 72-year-old female. Arrow: maximum reklination demonstrates air inclusion L2-L3 and then L12 as an expression of a pathological movement.
Asymmetric degeneration of the disk may lead to further deterioration of the adjacent motion segments and may end with a progressive degenerative scoliosis5 that may need surgical treatment (see below). This may also occur as a long-term process in patients who suffer from an asymmetric transitional anomaly of the lumbosacral junction or early disk pathology at the lower lumbar spine (Fig. 9.3).
It is sometimes difficult to differentiate the active subchondral bony damage from osteoporotic compression fractures. Obtaining a thorough history, performing a physical examination, and requesting imaging scans such as magnetic resonance imaging (MRI) with short tau inversion recovery (STIR) sequences, computed tomography (CT), and bone scintigraphy will facilitate arriving at a diagnosis.
Symptomatic isolated or multilevel disk degeneration can be seen in the lumbar spine as well as in the cervical spine. This disk degeneration with osteochondrosis and sometimes significant subchondral edema, as an expression of inflammation, and occasionally combined with significant disk protrusion, can occur in elderly patients primarily without relevant deformity or instability. This degeneration can start at a younger age and can be asymptomatic or can be combined with off-and-on back pain over the course of years and even decades.16
For mostly mechanical reasons, disk degeneration can aggravate and become highly symptomatic, specifically when it is combined with segmental instability and osteochondritis (Fig. 9.4). Because these disks are severely degenerated and dehydrated over many years, a herniation consists almost always of a large, combined annulus and fibrotic nucleus sequester. The consequence of this disk degeneration may be a secondary deformity, with typical translatory dislocation of vertebrae in a segment or several segments, rotation and scoliosis, and kyphoscoliosis.5,16 It is also possible that disk degeneration and facet joint arthritis can lead to a degenerative spondylolisthesis.20–22 As long as the disk degeneration is isolated on one to three levels without a major deformity, a typical axial “instability” pain may occur, mostly during rotational movement, lifting when upright, or turning in bed during sleep. If conservative treatment with isometric reinforcement exercises of the abdominal and paravertebral muscles is not successful, surgery may be necessary.21,23–26
Fig. 9.4 Adjacent segment disease. (a) A 57-year-old woman with severe back pain but no leg pain. Segment L2-L3 osteochondrosis with beginning degenerative lumbar scoliosis. Nonsurgical treatment. (b) A 59-year-old woman with severe back pain and new leg pain and claudication symptomatology. Clear progression of the degenerative scoliosis. (c) Decompression, correction, and stabilization of the degenerative deformity of the same patient, with pedicular screw system and transforaminal lumbar interbody fusion (TLIF) in L2-L3 and L3-L4. (d) The now 65-year-old woman, who was almost pain-free for 5 years, experiences back pain in the upper lumbar spine. (e) Now 66 years old and more than 6 years postoperative, the woman experiences severe back pain and irradiation into the groin on the right more than on the left. (f) Severe adjacent segment degeneration noted at L1-L2 and beginning at L4-L5.
If surgery is necessary, many minimally invasive surgical techniques have been suggested, using a retroperitoneal anterior approach, a posterior approach, a far lateral approach (extreme lateral interbody fusion [XLIF]) (Fig. 9.5), or a combination of these approaches. Anterior surgery with stand-alone cages (anterior lateral interbody fusion [ALIF]) that are fixed with screws is straightforward in nonobese patients, and is quite feasible from L3-L4, L4-L5, and L5-S1, that is, in the lower lumbar spine. In obese or osteoporotic patients, or in those with previous abdominal surgery, it is advisable not to do an anterior surgery (ALIF or XLIF) alone, but rather combined with a posterior surgery with pedicle fixation and posterior lateral interbody fusion (PLIF) or transforaminal lumbar interbody fusion (TLIF) procedure, or just as an isolated posterior surgery. This is particularly true when decompression of the neurostructures in the spinal canal is the main purpose of the surgery.
Fig. 9.5 A 68-year-old woman with severe movement- and activity-dependent left leg pain. (a) Degenerative left convex lumbar scoliosis with significant osteophyte formation in several segments, except at L3-L4 (circle). Here a translational rotatory instability can be demonstrated (circle), which is most probably the cause of motion-dependent pain. Therefore, only this “strategic” segment has been immobilized and fixed by a stand-alone extreme lateral interbody fusion (XLIF) cage with plate fixation, leaving the deformity otherwise alone. (b) Instant pain relief and improved sagittal alignment are noted postoperatively.
Specifically in the frail elderly, where surgery is the only remaining option after all other treatments have failed, minimally invasive surgery, such as a far lateral approach (XLIF),27–30 is most appropriate, as it entails little blood loss, little surgical trauma, and brief anesthesia duration. However, to avoid posterior surgery, stand-alone cages should be used that can be fixed either by an additional plate or with the plate incorporated with the cage (Fig. 9.5). This technique facilitates achieving indirect decompression of a foraminal and sometimes a recess stenosis. However, it is limited in osteoporotic bone (the cage may migrate in the vertebral body) and in central stenosis, which is fixed, but nevertheless it may be appropriate in dynamic (mechanical unstable segment) central stenosis.29,31 In these cases it is sometimes necessary to do a posterior pedicle screw fixation with cement reinforcement and even to fill the intervertebral space after removing the disk with cement, that is, a so-called diskoplasty. In some cases where the disk height is significantly reduced and there is significant concomitant facet joint arthritis, which contributes to the pain generation, a microsurgical interlaminar decompression with resection of the flavum, capsule, and partial arthrectomy, combined with a translaminar facet screw fixation, may be sufficient (Fig. 9.6). This is an atraumatic surgery suitable for very elderly patients who have considerable morbidity, a reduced life expectancy, and little demand for physical activity; this surgery entails little blood loss, and one of its major purposes is to control pain, which is fulfilled by immobilizing each facet joints with a screw and with sufficient decompression.
Fig. 9.6 Translaminar screw fixation as a minimal intervention for decompression and immobilization of arthritic facet joints in a 79-year-old polymorbid patient. The markings outline the poorly identifiable contours of the vertebral bodies.
Spinal Stenosis in the Elderly
Spinal stenosis is a very common condition in the elderly, and it is important to differentiate among central stenosis, lateral stenosis, and root canal stenosis. In some cases there can be combination of two of these types, or one type can be combined with degenerative spondylolisthesis. Other conditions include Paget’s disease, a degenerative disease that may cause spinal stenosis with or without neurologic complications, and secondary spinal stenosis due to fracture, mostly osteoporotic fracture, or due to tumor compression of the spinal canal, mostly from metastatic disease. Finally, there is iatrogenic stenosis, which can occur as a late result after any spine surgery at any age. In these cases, spinal stenosis may occur as a so-called adjacent segment problem after fusion surgery, or it may be a part of a degenerative deformity (scoliosis and kyphosis).32
In most cases, spinal stenosis is due to degenerative changes or a preexisting narrow canal. These changes can lead to symptoms, but so-called stenotic images sometimes are present on imaging studies in several symptom-free individuals. The relationship among degenerative lesions, abnormal imaging, and patient complaints is still unclear. Lumbar stenosis with a claudication symptomatology, however, is a common reason for decompressive surgery or fusion. The investigation of stenotic symptoms should be extremely careful and thorough, and should include the appropriate auxiliary examinations, such as infiltration techniques (extraforaminal root blocks, epidural blocks, facet joint infiltrations, diskography, sacral blocks) as well as functional X-rays (flexion/extension lateral view with the patient in the supine position, and traction films), including vascular investigation. This is of the utmost importance, especially if surgery is deemed necessary for good results.33
Surgical management of spinal stenosis can consist of purely decompressive surgery. Different techniques are available, such as classic laminectomy, laminotomy, partial laminectomy, resection of ligamentum flavum and scar tissue, simple foraminal decompression, and others. In recent years it has been suggested in some cases to use a so-called interspinous process distraction, in which the foramina are opened and the canal is widened and indirectly decompressed.23,33 The interspinous process distraction also unloads the disks as well as the facet joints. The most appropriate patients for this procedure are those with increasing symptoms when doing lumbar extension movements. There is still a quite significant debate about whether a decompression needs to be accompanied by instrumentation.23,33 Depending on the osteophyte formations in the anterior column as well as the osteoarthritis of the facet joints, and in the absence of any instability, such as degenerative spondylolisthesis, a simple decompression without instrumentation may be sufficient. If there is a need for significant resection of hypertrophic facet joint parts to decompress the dural sac as well as the exiting roots, it may be necessary to stabilize the segment either by simple translaminar/ transarticular screw fixation or by pedicle fixation. The first method provides a less rigid fixation than the alternative with pedicle fixation. The risk of pedicle fixation in spinal stenosis patients without a deformity or obvious instability is that is generates a rigid spine section, which affects the adjacent segment, including the disks as well as the vertebral bodies.17,18,34–36 This increases the risk of fatigue fractures in these vertebral bodies and a disruption of the posterior ligament complex as an expression of the aging of ligaments and muscles (Fig. 9.7).
In a patient with a severely degenerated cervical spine with spinal stenosis, compression of the cord may be treated with consecutive myelopathy or root compression. The spinal stenosis of the cervical spine often goes together with a deformity usually in kyphosis and sometimes in a minor scoliotic deformity in the frontal plane. If there is a relevant deformity of the cervical spine combined with a narrow spinal canal, diagnostic traction may be applied to explore how far the deformity can be reduced and the cervical spine can be realigned. In case this is possible, surgery may be done under traction in the reduced position. In this case there is no manipulation for reduction necessary during the surgery, but only the decompressive, and if necessary, the stabilization part.
In the cervical spine, there are different ways in which the spinal stenosis can be addressed. It can be done with an anterior surgery, either by a uni- or multilevel diskectomy, and resection of the posterior, inferior, and superior corner of the adjacent vertebra. In cases in which the compression of the spinal cord is mainly due to disks on several levels, this technique can be applied on each individual level by maintaining the main part of the vertebral body. This method facilitates placing intervertebral spacers and restoring the cervical lordosis. In cases in which there is more compression due to relevant osteophytes, extension of the compression beyond the disk space, or concomitant ossification of the posterior longitudinal ligament (OPLL), one or even two level vertebrectomies may be necessary, with an anterior reconstruction with (expandable or rigid) cages or bony struts (fibula or iliac crest) and plate fixation. If this stabilization seems to be insufficient and does not restore the lordosis, a combined posterior fixation with tension banding and realigning of the cervical spine in lordosis may be necessary. There is also the option of posterior surgery through laminectomy, laminotomy on several levels, or laminoplasty. In cases in which there is insufficient physiological lordosis (in fact kyphosis), a simultaneous fixation of the decompressed cervical spine along with the decompression may be necessary. Most often, the technique of choice is lateral mass screws combined with rod systems. This surgery is combined with a posterolateral fusion, either by bone substitutes or with cancellous bone from the iliac crest. Because cervical spine surgery is not as invasive as lumbar spine surgery, elderly people with significant comorbidities can be treated specifically by anterior surgery under neuromonitoring, as it entails relatively little blood loss, and the surgical trauma is mostly “local,” not involving the homeostasis of the body, as in a surgery of the lumbar spine performed with the patient in the prone position which takes longer.
