Abstract
Low back pain (LBP) is a common condition that affects millions of Americans on a yearly basis. As we age, all anatomic components of the spine are affected: bone, muscles, discs, ligaments, and joints. The three-joint complex is the functional unit of the lumbar spine and comprises two consecutive vertebrae, the intervertebral disc, and the zygapophyseal (facet) joint. As the mechanical load on the spine is altered, forces are distributed through the surrounding facet joints, leading to facet hypertrophy, joint laxity, subluxation, and narrowing of the lateral recess. Disc height loss can then lead to central canal stenosis. Levels L4-L5 and L5-S1 are most commonly involved, as they undergo the most torsion and compressive forces during activity. Symptoms range from acute to chronic LBP. Positioning such as lumbar flexion/extension, rotation or lateral bending, or lumbar palpation can exacerbate symptoms. Pain quality can be sharp, dull, achy, or shock-like. Pain can be localized at a specific region; it can radiate locally or to a distant site. Approximately 90% of people who develop acute LBP experience a resolution of the symptoms within 6 weeks; hence, conservative management during this period is paramount. This includes anti-inflammatory medications, muscle relaxants, heat, ice, and rehabilitation comprising three phases (acute, recovery, and functional). Fluoroscopic-guided injections could be used to manage pain at any stage. If these options fail, then surgery can be considered.
Keywords
Degenerative disc disease, low back pain, Lumbago, lumbar degenerative disc disease, lumbar disc disease, three-joint complex
| Synonyms | |
| |
| ICD-10 Codes | |
| M47.817 | Spondylosis without myelopathy or radiculopathy, lumbosacral region |
| M47.899 | Other spondylosis, site unspecified |
| M51.36 | Other intervertebral disc degeneration, lumbar region |
| M51.37 | Other intervertebral disc degeneration, lumbosacral region |
| M54.5 | Low back pain |
Definition
Low back pain (LBP), also known as lumbago, is a common condition that according to observational studies occurs in about 80% of people. In the United States, respondents of a survey of adults 18 and over by the National Center for Health Statistics revealed that LBP was the most common type of pain (28.1%) when compared to severe headache or migraine (16.6%) and neck pain (14.6%).
Normal aging is a key component of the degenerative spine process and at times both are hard to differentiate. As such, literature has shown an increased prevalence in spine degeneration with age in asymptomatic individuals. When comparing prevalence estimates of degenerative spine imaging findings in asymptomatic patients aged 30 and aged 80, disc degeneration (52% vs. 96%, respectively), disc bulge (40% vs. 84%), facet degeneration (9% vs. 83%), and spondylolisthesis (5% vs. 50%) increased with age. With age, all anatomic components of the spine are affected: bone, muscles, discs, ligaments, and joints. As a result of the alteration of the “spinal structural equilibrium,” this can lead to spinal instability, clinical syndromes, restricted range of motion (ROM), pain, and in worst cases, disability. The three-joint complex is the functional unit of the lumbar spine and comprises two consecutive vertebrae, the intervertebral disc, and the zygapophyseal (facet) joint ( Fig. 45.1 ).
The lumbar disc can be separated into three components: the nucleus pulposus, annulus fibrosus, and cartilaginous endplates. When axial forces are placed upon the nucleus, it distributes the tensile forces via the annulus and the endplates. The degeneration of the intervertebral discs has been thought to be the catalyst leading to secondary degeneration of the surrounding spinal elements. Degeneration of the discs has been shown to be nutrition-related. The main source of nutrition to the intervertebral discs is derived from the cartilaginous endplates and as one ages, permeability of the nutritional gradient from endplates decreases as well as blood supply. An imbalance between extracellular matrix synthesis and degradation occurs, which leads to loss of disc structure and function. There is histological evidence showing cracks and microfractures in the cartilaginous endplates, concentric tears (cleft formation) in the nucleus pulposus, and radial tears in the annulus fibrosus. The intervertebral discs receive innervation anteriorly and laterally from the gray ramus communicans and posteriorly from the sinuvertebral nerve, with a majority of free nerve endings found in the outer third of the annulus. With age, collagen content within the nucleus increases and the junction between the nucleus and the annulus becomes less demarcated. Thus tears in the annulus lead to degeneration, prolapse, extrusion, and then sequestration, which can all be sources of pain.
As the mechanical load on the spine is altered, forces are distributed through the surrounding facet joints which, depending on one’s position, are responsible for 10% to 30% of lumbar weight bearing. These joints are diarthrodial synovial joints and, like all synovial joints, are subjected to degradation of cartilage, subchondral bone sclerosis, osteoporosis, osteophyte formation, and inflammation. This results in facet hypertrophy and, with increased repeated mechanical loading, can lead to joint laxity, subluxation, and narrowing of the lateral recess. In concert with disc height loss, it can then lead to central canal stenosis. Other bony elements of the spine (i.e., vertebral bodies, endplates, spinous and transverse processes) also undergo this degeneration process.
The ligamentum flavum is a ligament that runs from C2 to S1, connecting lamina of adjacent vertebrae together. It is 80% elastin and 20% collagen and occupies the posterior lateral borders of the spinal canal. Aging causes ligament hypertrophy and in association with disc degeneration leads to bucking, seen as thickness on imaging. This results in spinal canal narrowing and can lead to compression of neural elements. The cause of ligamentum flavum hypertrophy is unknown, but has been postulated to be due to age-related fibrosis secondary to a decrease in elastin-to-collagen ratio.
The spine is surrounded by a “core” group of muscles that aid in maintaining stability and equilibrium. These muscles are the abdominals (mostly transversus abdominis), diaphragm and pelvic floor muscles, erector spinae, and spinal multifidi. As time passes, a degenerative myopathy occurs which contributes to the alteration of vector forces upon the spine, thereby shifting it out of equilibrium. An example of this is seen in primary camptocormia, also referred to as bent spine syndrome, relating to primary idiopathic axial myopathy.
The most commonly involved lumbar levels are L4-L5 and L5-S1, as they undergo the most torsion and compressive forces during activity. Factors contributing to lumbar degeneration include environmental (diabetes mellitus, smoking, obesity), occupational (jobs with repetitive bending, stooping, prolonged sitting or vibratory stress), and psychosocial (stress, anxiety, depression), which can contribute to the perception of LBP).
Symptoms
As previously described, lumbar degenerative disease is associated with the normal aging process. Findings on imaging such as intervertebral disc degeneration, facet joint osteoarthritis, spondylolysis, spondylolisthesis, spinal stenosis, and degenerative changes in paraspinal muscles are also seen in asymptomatic individuals. Approximately one third of individuals with substantial abnormalities on magnetic resonance imaging do not manifest any clinical symptoms.
For those with symptoms, common complaints range from acute to chronic LBP. Onset can range from days to months. Positioning such as lumbar flexion, extension, rotation or lateral bending, or lumbar palpation can exacerbate symptoms. Pain with flexion, coughing, sneezing, or Valsalva can be associated with disc disease. Pain quality can be sharp, dull, achy, or shock-like. Severity can range from mild to severe. Pain can be localized at a specific region, as the patient will be able to point to exact location; or it can radiate locally or to a distant site. The presence of stiffness in the morning could be due to osteoarthritis. However, atypical symptoms of pain at night, fever, and recent weight loss could be due to malignancy or infection. Alleviating factors such as forward bending could signify compression of neural elements.
Leakage of pain-related neuropeptides (e.g., substance P) from the disc secondary to annulus tears to surrounding free nerve endings or onto the nearby dorsal root ganglion can cause pain. Clinicians should also inquire about psychological symptoms such as anxiety, depression, or sleep disturbance as contributing factor symptoms.
Physical Examination
Many structures comprise the spinal element; therefore a physical examination should be geared toward discerning one of the five most common sources of LBP: discogenic, facet arthropathy or instability, radiculopathy or neural compression, myofascial or soft tissue, and psychogenic. Although usually found alone, they can also be found in combination. Hence, the goal of the physical examination is to narrow one’s differential diagnosis to lead to more cost effective testing and therapeutic strategies ( Table 45.1 ).
| Condition | Diagnostic Keys | |
|---|---|---|
| Vascular | Abdominal aortic aneurysm | Older than 50 years Abdominal and back pain Pulsatile abdominal mass |
| Gynecologic | Endometriosis | Women of reproductive age Cyclic pelvic and back pain |
| Pelvic inflammatory disease | Young, sexually active women Systemically ill (fever, chills) Discharge, dysuria | |
| Ectopic pregnancy | Missed period Abdominal or pelvic pain Positive pregnancy test result | |
| Genitourinary | Prostatitis | Men older than 30 years Dysuria Low back and perineal pain |
| Nephrolithiasis | Flank and groin pain Hematuria | |
| Gastrointestinal | Pancreatitis | Abdominal pain radiating to back Systemic signs (fever, nausea, vomiting) Elevated serum amylase |
| Penetrating or perforated duodenal ulcer | Abdominal pain radiating to back | |
| Rheumatologic | Fibromyalgia | Young to middle-aged women Widespread pain Multiple tender points Disrupted sleep, fatigue Normal radiographs and laboratory values |
| Polymyalgia rheumatica | Older than 50–60 years Hip or shoulder girdle pain and stiffness Elevated erythrocyte sedimentation rate Dramatic response to low-dose prednisone | |
| Seronegative spondyloarthropathies (ankylosing spondylitis, Reiter syndrome, psoriatic, enteropathic) | Younger men (ankylosing spondylitis, Reiter syndrome) Lower lumbosacral pain Morning stiffness (“gel”) Improvement with activity Radiographic sacroiliitis | |
| Diffuse idiopathic skeletal hyperostosis (Forestier disease) | Older than 50–60 years Thoracolumbar stiffness or pain Flowing anterior vertebral calcification | |
| Piriformis syndrome | Buttock and leg pain Pain on resisted hip external rotation and abduction Transgluteal or transrectal tenderness | |
| Scheuermann kyphosis | Age 12–15 years Thoracic or thoracolumbar pain Increased fixed thoracic kyphosis 3 or more wedged vertebrae with endplate irregularities | |
| Trochanteric bursitis, gluteal fasciitis | Pain or tenderness over greater trochanter | |
| Adult scoliosis | Back pain Uneven shoulders, scapular prominence Paravertebral hump with forward flexion | |
| Metabolic | Osteoporosis | Women older than 60 years Severe acute thoracic pain (fracture) Severe weight-bearing pelvic pain (fracture) Aching, dull thoracic pain; relieved in supine position (mechanical) Loss of height, increased thoracic kyphosis |
| Osteomalacia | Diffuse skeletal pain or tenderness Increased alkaline phosphatase | |
| Paget disease | Bone pain: low back, pelvic, tibia Increased alkaline phosphatase Characteristic radiographic appearance | |
| Diabetic polyradiculopathy | Older than 50 years Diffuse leg pain, worse at night Proximal muscle weakness | |
| Malignant neoplasia | Older than 50 years Back pain unrelieved by positional change—night pain Previous history of malignant disease Elevated erythrocyte sedimentation rate |
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