3 Pathophysiology of Spinal Pain and Pain Pathways Spinal pain or pain originating from structures of the spine is the most common chronic pain condition and has a lifetime prevalence of 54 to 80%.1 It has significant health, economic, and societal impact. Spinal pain can arise from the myofascial layers, facet joints, intervertebral disks, vertebral bodies, or sacroiliac joint, or from compression of the nerve root or the spinal cord. In this chapter, we provide an overview of the pathophysiology of certain commonly encountered conditions in clinical practice. Degenerative changes can occur in cervical, thoracic, lumbar, and lumbosacral region of the spine but are most common in the midcervical and lower lumbar regions. • The three-joint complex between vertebral bodies consists of an intervertebral disk and two facet joints on each side. Because the three of them form “functional unit of spine,” changes in one will be followed by changes in the other.2 Disk changes usually precede changes in other structures ( • Loss of disk vascularity and hydration causes fibrosis of nucleus pulposus, and fissure formation in the annulus. Eventually, radial and circular tears occur in the annulus ( Fig. 3.1 Superior view at the level of the L4–L5 intervertebral disk. Normal relationship between the intervertebral disk and L4 exiting nerve root and L5 traversing nerve root. Fig. 3.2 Pain mechanism generation. Superior view at the level of the L4–L5 intervertebral disk. A posterolateral annular tear generates pain signal through the sinuvertebral nerve and gray ramus communicans. The pain signal is transmitted to the DRG. Fig. 3.3 Superior view at the level of the L4–L5 intervertebral disk. A non–contained-herniated nucleus pulposus is seen compressing the exiting L4 nerve root as well as the traversing L5 nerve. • Loss of disk height, facet joint hypertrophy, buckling of ligamentum flavum, and osteophytosis result in encroachment of central canal or neural foramen, causing neurogenic claudication, myelopathy, or radiculopathy ( • Neurogenic claudication can be attributed to either direct mechanical compression or indirect vascular insufficiency from venous congestion in the upright posture. Sitting posture or forward flexion may unbuckle the ligamentum flavum, open the canal and lateral recess, and allow adequate oxygen delivery ( • Asymmetric degeneration of disks or facet joints can lead to varying degrees of instability and cause either anterolisthesis or retrolisthesis, resulting in stenosis or scoliosis ( Fig. 3.4 T2-weighted sagittal magnetic resonance imaging of the lumbar spine demonstrating severe central canal stenosis at L3–L4 and L4–L5 due to ligamentum flavum hypertrophy and disk herniation. • Internal disruption of the disk (IDD) can cause axial spine pain. IDD consists of radial tears in the annulus, degradation of nucleus, and disk collapse with endplate failure in the absence of significant modifications of the external contour of disk and with no compression of neural structures. • Within healthy disks, nerve endings are restricted to the outer 2 to 3 mm of annulus fibrosus due to high intradiskal pressures. With degeneration, nociceptor nerve fibers may reach as far inward as the nucleus and this neoinnervation may lead to discogenic pain. Fig. 3.5 T2-weighted axial magnetic resonance imaging of the lumbar spine at L3–L4 demonstrating severe central canal and lateral recess stenosis due to ligamentum flavum hypertrophy. Fig. 3.6 Positional effects on the neural foramen. Extension causes narrowing of the foramen, while flexion increases the size of the foramen. • Facet joints or zygapophyseal joints are synovial joints that allow certain ranges of motion of the spine and also support its stability by preventing excessive rotation of the spine. • These are important pain generators in the back by virtue of abundant nociceptor innervation. Each joint is innervated by two medial branches: one from the dorsal ramus at its corresponding level and the other from the level above ( • Inflammation and arthritic changes in joints, facet joint effusions/cysts, compression of nerve roots by hypertrophied joints, and entrapment of the medial branches by calcified mamilloaccessory ligament are some of the proposed mechanisms for facetogenic pain.4 • Myofascial pain is associated with postural derangements such as unbalanced gait, fatigue, and dystonia, as these conditions cause asymmetric tone in extensor or flexor group of paraspinal muscles. Repetitive stress on specific muscle groups can be a triggering factor. • Other causes include spondylolisthesis with painful muscle spasms, medial branch irritation causing muscle spasm, emotional stress, and deconditioning. • Pathophysiologic changes may begin in the motor endplate zone. Increased acetylcholine release results in sustained muscle contractions and release of vasoactive and neuroactive substances. Central sensitization with malfunction of supraspinal inhibitory pathways may also play a role.
3.1 Introduction
3.2 Degenerative Disease of the Spine
Fig. 3.1).
Fig. 3.2). Mechanical stresses such as flexion can cause herniation of the nucleus along a radial tear. The herniated disk can impinge upon the exiting nerve root in the lateral recess or far lateral zone, causing pain and weakness in nerve root distribution (
Fig. 3.3). Inflammatory mediators released from the herniated nucleus also contribute to pain.
3.2.1 Lumbar Spinal Stenosis
Fig. 3.4, 
Fig. 3.5).
Fig. 3.6).
3.2.2 Degenerative Spondylolisthesis
Fig. 3.7). Once spondylolisthesis sets in, the imbalance in stress and deformity can cause self-propagating instability.
3.2.3 Discogenic Pain
3.2.4 Facet Arthropathy
Fig. 3.8).3
3.2.5 Myofascial Pain Syndrome
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