Disorders of the lumbosacral spine cause pain, disability, suffering, public health issues, and socioeconomic issues with far greater impact than disorders of any other part of the body.
Most adults will experience several episodes of low back pain during their lifetime. It is estimated that 80% of workers will lose work time because of this complaint. On the basis of primary diagnosis only, a National Ambulatory Medical Care Survey in 1989 to 1990 ranked low back pain as the fifth most frequent reason for adults to visit an office-based medical practice. In surveys employing a wider definition of low back pain, it was found to be the second most frequent symptom prompting physician office visits in the United States. In 2010, low back pain was ranked third next only to ischemic heart disease and chronic obstructive pulmonary disease in poor health and mortality burden in United States.

A global review of the prevalence of low back pain in the adult general population has shown its point prevalence to be approximately 12%, with a 1-month prevalence of 23%, a 1-year prevalence of 38%, and a lifetime prevalence of approximately 40%. Furthermore, as the population ages over the coming decades, the number of individuals with low back pain is likely to increase substantially. Low back pain usually begins in early life, with the highest frequency of symptoms occurring between ages 35 and 55 years. Of all adults in industrialized societies, 60% to 80% are affected at some point in their lives. Work absence and symptom duration increase with aging. An acute episode of low back pain usually resolves within 6 weeks. More persistent pain lasting beyond 3 to 6 months occurred in only 5% to 10% of patients with back pain. The U.S. Agency for Health Care Policy and Research reported that 90% of patients with acute low back pain recover their usual activity tolerance within 4 weeks of injury. The remaining 10% of patients who do not recover with time or routine therapy go on to develop chronic symptoms and secondary problems. At 1 year, the incidence of acute back pain conversion to chronic back pain is 20%. Recurrences of low back pain are also common, with the percentage of subsequent low back pain episodes ranging from 20% to 44% within 1 year for working populations to lifetime recurrences of up to 85%.

The costs of low back pain include functional impairment, activity limitations, reduced quality of life, disability, underemployment, reduced work productivity, and direct medical cost. It appears that the societal perception of disability has changed dramatically over period of time. This has resulted in an increased rate and cost of disability and overutilization of medical care, including surgical treatments. Back pain in workers 40 to 65 years of age costs employers an estimated $7.4 billion per year. Duke University Medical Center researchers found that patients suffering from back pain consume more than $90 billion annually in health care expenses, with approximately $26 billion of that amount directly attributable to treating the back pain. Their results demonstrate the enormous economic impact of back pain. The total $90 billion spent in 1998 represented 1% of the U.S. gross domestic product (GDP), and the $26 billion in direct back pain costs accounted for 2.5% of all health care expenditures for that year. These data came from the Medical Expenditure Panel Survey (MEPS) in 1998. The MEPS is a national survey conducted by the Agency of Healthcare
Research and Quality (AHRQ) and the National Center for Health Statistics. The team found that 25.9 million adults reported back pain in 1998, with 172.7 million reporting no back pain. The figures do not include information about back pain in nursing home patients, who in the 1977 research accounted for about 20% of medical costs. As a result, the costs of care for back pain almost certainly top $100 billion. In addition, the Duke study did not include nonmedical cost of back pain, such as lost productivity. A study in the Journal of the American Medical Association found chronic pain conditions, including arthritis, back problems, and other ailments, drain $61.2 billion a year from the U.S. economy. Back pain accounted for about a quarter of the lost or unproductive work, second only to headaches as the most frequent pain complaint of workers.

Majority of low back pain is mechanical in nature caused by injury, compression, tears, and bone and disc degeneration. Common causes include the following:

Traditional beliefs suggested that heavy physical jobs required high energy demand and significant stress and strain on the spine, whereas light jobs required low energy demand. Many lowenergy jobs, nevertheless, are static, which is an inherent risk factor for low back pain. Low back pain, degenerative disc disease, and disc herniation are associated with the following:

The “oxidative stress hypothesis of aging” theory proposed that enhancement of oxygen consumption resulting from increased physical activity may accelerate disc degeneration. On the other hand, strenuous exercises may contribute to positive nutritional effect by facilitating the transport of small solutes into and out of the disc. Generally, it is believed that persons who are physically fit or who maintain a balanced exercise program appear to have a lower risk for chronic low back pain and a more rapid recovery after an episode of acute back pain.

In order to more easily identify the various sources of pain, the spine may be divided into three compartments: anterior, middle, and posterior.

The anterior compartment consists of the vertebral body and intervertebral disc. The anterior unit is bound together by cephalocaudal ligaments: anterior longitudinal ligament and posterior longitudinal ligament (PLL). The anterior longitudinal ligament is anatomically much broader and stronger than the PLL. The PLL is intact throughout the length of the vertebral column until it reaches the lumbar vertebrae. From L1, it becomes progressively narrower until at L5-S1 it is only half of its original width. This anatomic feature contributes to an inherent structural weakness in the lumbar spine. Hence, the lower lumbar spine is the region subjected to the greatest static stress and most spinal movement resulting in the greatest kinetic strain.

The middle (neuraxial) compartment contains all of the structures within the bony and ligamentous boundaries of the spinal canal. This includes the PLL, epidural space, meninges, spinal cord, dorsal and ventral nerve roots, root sleeves, dorsal root ganglia, and ligamentum flavum.

The posterior compartment contains the facet joints, laminae, vertebral arches, and structures posterior to the plane of the transverse processes and innervated by the dorsal rami of the spinal nerves. The ligaments are extremely important in stabilizing the vertebral column. The ligamentum flavum (yellow ligament), which connects the laminae of adjacent vertebrae, is the thickest and strongest ligament in the lumbar region. It can contribute to spinal stenosis by folding inward during upright posture, extension of the back, and hypertrophy.

The sinovertebral nerve originates lateral to the neural foramina and enters the spinal canal anterior to the dorsal root ganglion. It is a branch of the somatic ventral nerve root and the sympathetic grey ramus communicans. This specific nerve, also known as the nerve of Luschka, innervates the outer annulus of the disc, PLL, epidural membranes, and dura at the segmental level of origin and adjacent levels. It is important to note that central low back pain, with or without referred pain to the buttocks, may derive from irritation of the outer part of the annulus fibrosis or the PLL.

In summary, the potential sources of low back and radicular pain include the bony structure of vertebrae, muscles attached to the spine and hips, fasciae, ligaments, discs, facet joints, meninges, vessels, nerve roots, dorsal root ganglia, and nerves in the surrounding areas.

The natural wear and tear on the discs and facet joints results in microtrauma and degeneration. This can induce the release of neurohumoral mediators such as phospholipase A₂, serotonin, H⁺, substance P, prostaglandin E₂, and so on, to produce inflammation of the nerve roots or meninges and sensitize local nociceptors. Furthermore, it has been theorized that material from the nucleus pulposus, sheltered from the immune system by the presence of the annulus fibrosis, might act as a foreign protein and trigger an autoimmune reaction. The recent demonstration of an activated immunocompetent cellular response at the epidural interface of the herniation of the nucleus pulposus supports the concept of the immunogenic capacity of the nucleus pulposus. Tissue injury or inflammation can cause a barrage of nociceptive input into the spinal cord. This may lead to a phenomenon called central sensitization or windup of neurons in the dorsal horn of the spinal cord. The release of excitatory amino acids and neuropeptides in the dorsal horn is thought to be the mechanism underlying the phenomenon of central sensitization. At the cellular level, there is an increase in spontaneous discharge and an expansion of neural receptive fields of wide-dynamic-range neurons located in Rexed lamina V of the spinal cord. Clinically, this is characterized by sensation of pain when exposed to nonnoxious stimuli (allodynia), significantly increased response to painful input (hyperalgesia), and increased response to repetitive stimulation (hyperpathia).

The intervertebral disc is a ring-like structure composed of a centrally located well-hydrated pliable proteoglycan matrix, the nucleus pulposus, which comprises two-thirds of the surface area of the disc. Surrounding the nucleus is a fibrocartilaginous ring composed predominantly of type I collagen, the annulus fibrosus, which makes up the remaining one-third of the surface area of the disc. The annulus fibrosus is stronger anteriorly but often defective posteriorly. As a self-contained fluid system, the disc absorbs shock, permits transient compression, and allows movement. It provides a cushion between the vertebral bodies and allows for greater flexibility.

As the disc ages, the number of viable cells in the nucleus pulposus decreases, and the proportion of cells that exhibit necrosis changes from 2% in infancy to 50% in young adults and 80% in the elderly. The water content in the young disc is 80% to 90% in the nucleus pulposus. With aging, the discs tend to dehydrate, losing up to 70% of their water content. As the nucleus pulposus further dehydrates, it becomes more fibrous and less compliant. A disc will usually herniate under strain and pressure. When overstressed, it will protrude along in the path of least resistance, usually posterolaterally. This can cause direct mechanical pressure on the nerve roots resulting in radiculopathy.

In the healthy back, only the outer third of the annulus fibrosus is innervated. In the degenerative or disrupted disc, small unmyelinated nerve fibers grow into the inner third of the annulus fibrosus and even into the nucleus pulposus. Internal disc disruption is a condition characterized by a degenerated nucleus pulposus with radial fissures extending into the peripheral annulus fibrosus. Upon rupture of the disc, the release of irritative material near the meninges can induce radiculitis and symptoms of radiculopathy without actual herniated disc material compressing the nerve roots. Under such circumstances, significant disc herniation might not be visualized on MRI or computed tomography (CT) scan. In brief,
the proposed mechanisms of radiculopathy include direct pressure on nerve fibers as a result of compression injury and indirect impact through impairment of microcirculation, chemical irritation and inflammation, immune reaction, edema formation secondary to permeability changes of the intraneural capillaries, and impairment of the nutritional transport to the nerve root.

Compression of the nerve roots is dependent upon the effective space available within the neural foramina, the osseous structures surrounding the neural foramina, and the tethering effects of the intraspinal and extraspinal ligaments. Posterolateral disc herniations can impinge on the lumbar dorsal root, which then initiates electrical discharges for as long as 25 minutes after the mechanical stimulus has been removed. Radiculopathy can be produced by either biochemical or mechanic stimulation of a swollen, stretched, or compressed nerve root. Approximately 3% to 12% of all lumbar disc herniations occur laterally and extend into or beyond the foraminal zone; in this setting, the patients will complain of sudden and severe radicular pain, often with dysesthesia. On the other hand, discogenic pain resulting from a central disc bulge or herniation stimulates several lumbar tissues such as the outer layer of the annulus fibrosus or PLL. Clinically, this is manifested as central low back pain without any radicular symptoms.

The facet, or zygapophysial, joints consist of two arthrodial joints superiorly and inferiorly, each lined with synovium, lubricated by synovial fluid, and contained within a joint capsule. These synovial joints enhance spinal stability and flexibility. In the upper part of the lumbar spine (L1-L3), the facet planes lie in a generally vertical sagittal plane and permit flexion and extension but prevent lateral flexion or bending in the lordotic curve. The lumbosacral facet joints at the level of L5-S1 depart the farthest from the sagittal plane, allowing some rotation of the lower part of the lumbar spine. With slight forward flexion, the facets of the other lumbar vertebrae separate and permit a modest degree of lateral movement and rotation. Facet loading, if of a repetitive nature, may play a role in the degeneration of the facet joint. After repeated wear and tear, these joints are susceptible to osteoarthritis and associated synovial cyst formation. Hypertrophic facet joints or cysts can encroach on the spinal canal or the intervertebral foramina and contribute to the development of central spinal or foraminal stenosis.

A problem-focused pain history should include onset, location, intensity (e.g., pain scale 0 to 10), characteristics (achy, spasmodic, stabbing, burning, shooting, etc.), and duration plus aggravating and alleviating factors. The essential purpose in the initial evaluation is to differentiate patients with serious underlying pathology from those with mild problems.