Low Back Pain: Pathophysiology, Mechanisms, and Pain Generators

Low back pain (LBP) is the most common musculoskeletal condition affecting the adult population and a leading cause of disability worldwide, with a prevalence of 84%.1 Chronic LBP has a significant impact on functional capacity and occupational activities, is a major cause of absenteeism, and represents a major social and economic burden.1  One study estimates the cost of chronic LBP at $10 billion annually due to reduced productivity, while another study estimates a total of $100 billion annually due to healthcare costs, lost wages, and reduced productivity combined.2 Considering the many physiological, neurological, and psychological factors implicated in LBP, the diagnostic evaluation of patients is very challenging and requires complex clinical decision-making.3 Nevertheless, identifying the source of pain is of fundamental importance in determining a therapeutic approach for patients with LBP.3

LBP can derive from many different anatomical sources, such as muscle, bones, joints, nerve roots, fascial structures, intervertebral discs (IVDs), and organs within the abdominal cavity.3 In addition, symptoms may emerge from aberrant neurological pain processing causing neuropathic LBP.4-5 During the evaluation, the clinician must also consider the possible influence of psychological factors, such as stress, depression, and anxiety.6-7 In diagnosing LBP, clinical information is the key element as opposed to MRI. In fact, the American College of Radiology advises against MRI in the first 6 weeks (unless red flags appear) because imaging data is weakly related to symptoms. Overall, chronic LBP may arise from multiple pain generators simultaneously and therefore requires a multidisciplinary diagnosis with an accompanying multimodal treatment plan.8

The type of LBP depends on the pain generator. One example is radicular pain, which refers to pain due to ectopic discharges from an inflamed or lesioned dorsal root or its ganglion.3 Typically, pain radiates from the back and buttock into the leg in a dermatomal pattern. The most common pathophysiological cause of radicular pain is disc herniation, which results in inflammation at the nerve. Furthermore, radicular pain differs from radiculopathy in that the latter impairs conduction down a spinal nerve, leading to numbness and muscle weakness.3 Although the two often accompany each other, radicular pain can appear in the absence of radiculopathy and vice versa.3

Another example is facet joint syndrome, which accounts for up to 30% of chronic LBP cases.9 The lumbar zygapophyseal joints are formed from the inferior process of upper vertebra and the superior articular process of lower vertebra; furthermore, these joints have a large amount of free and encapsulated nerve ending, which activate nociceptive afferents.3 Patients with facet joint syndrome typically complain of LBP, sometimes with somatic referred pain in the legs and often radiating to the thigh or groin. Back pain tends to be off-center and of lower intensity than leg pain; pain also increases with hyperextension, rotation, lateral bending, and uphill walking.3 Lastly, patients may report back stiffness, especially during the morning.

Other pain generators associated with LBP include sacroiliac joint pain (SIJ), lumbar spinal stenosis (LSS), and discogenic pain. SIJ is well recognized as a source of pain in patients with chronic LBP. Pain associated with SIJ can arise from ligamentous or capsular tension, altered joint mechanics, extraneous compression or shear forces, hypermobility, and myofascial or kinetic chain dysfunction leading to inflammation.10 LSS is determined by progressive narrowing of the central spinal canal and lateral recesses, which consequently leads to compression of neurovascular structures.3 Most cases of LSS are degenerative and associated with structural changes in the spine due to aging. Lastly, disc degeneration is the pain generator in 39% of chronic LBP cases.3 In terms of the pathophysiology, disc degeneration is characterized by degradation of the nucleus pulposus matrix with accompanying radial and concentric fissures in the annulus fibrosus.3 Overall it is critical that clinicians perform a thorough evaluation to accurately diagnosis the cause of LBP and develop an effective multimodal treatment plan that rapidly alleviates symptoms.


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