5 Pathophysiology of Back Pain Abstract This chapter reviews the definition of back pain and some of the pathophysiological factors leading to back pain. Back pain can be generated from a number of sources, including compression of nerve roots, the disc, ligaments, facets, sacroiliac joint, bone, and musculature. The goal of the minimally invasive spine surgeon is to identify the source of pain so that the least invasive procedure can be performed to achieve lasting pain resolution. Treating those levels or area of the spine not responsible for the patient’s symptoms can lead to iatrogenic tissue damage and less than optimal patient outcomes. Thus, understanding the pathophysiology of back pain disorders is critical to successful patient care. Keywords: back pain, pathophysiology, etiology, focused treatment, nociceptors, anatomy Low back pain continues to be a major global health problem and a leading cause of disability.1 To better understand the complex nature of low back pain and to identify potential targets for treatment, previous studies have investigated patient characteristics associated with the course and severity of low back pain and associated disability. Factors identified to date include high baseline levels of pain and disability, older age, obesity, smoking, unemployment, poor general health, depression, anxiety, and widespread pain.2 The International Association for the Study of Pain3 defines lumbar spinal pain as pain perceived anywhere within a region bounded by the last thoracic spinous process, the first sacral spinous process, and the lateral borders of the erectors spinae muscles ( In the light of these definitions, back pain can be defined as lumbar spinal pain or sacral spinal pain or any combination of the two. The significance of this definition is not so much to establish what low back pain is, but to establish what it is not. Pain over the posterior thorax is not low back pain, but thoracic spinal pain ( Pain over the gluteal region, not encompassing the lumbar spine or sacrum, does not constitute low back pain ( Pain has been categorized by duration (acute vs. chronic), location (superficial, deep, bone, muscle, or visceral), and cause or type (inflammatory, neuropathic, cancer). Generally, activation of activity in nociceptors underlies the experience of pain regardless of how it is categorized. The nociceptors are key players in understanding mechanisms of and managing pain. Nociceptors are sensory neurons with a cell body located in dorsal root, trigeminal, or nodose ganglia. All sensory neurons arising from these ganglia are pseudounipolar neurons with a central process terminating in the central nervous system (CNS; spinal dorsal horn) and a peripheral process terminating in a peripheral target such as the skin, muscle, or viscera5 ( Four distinct events are necessary for a nociceptor to convey information to the CNS about noxious stimuli impinging on peripheral tissues: 1. “Energy” from the stimulus (mechanical, thermal, or chemical) must be converted into an electrical signal. This process, referred to as signal transduction, results in a generator potential or depolarization of the peripheral terminal. 2. The generator potential must initiate an action potential, the rapid “all or nothing” change in membrane potential that constitutes the basic unit of electrical activity in the nervous system. 3. The action potential must be successfully propagated from the peripheral terminal to the central terminal. 4. The propagated action potential invading the central terminal must drive a sufficient increase in intracellular calcium ions to enable release of enough transmitters to initiate the whole process once again in the second-order neuron. Distinct sets of proteins underlie each of these processes, and are therefore the targets of a wide variety of therapeutic interventions. The primary afferent’s presynaptic nerve terminal in the dorsal horn of the spinal cord represents a site for a therapeutic intervention. Primary afferent fibers transmit the pain signal to the spinal cord and possess numerous receptor systems that can reduce this transmission by reducing transmitter release such as the alpha2-adrenergic, glycinergic, serotoninergic, opioidergic, and GABAergic receptors as well as ion channels sensitive to local anesthetics and anticonvulsants including voltage-gated calcium, sodium, and potassium channels. Fig. 5.1 (a,b) Topographic location of what is low back pain; (c,d) what is not low back pain. Aδ and C fiber neurons synapse primarily within laminae I, II, and V of the dorsal horn of the spinal cord. These primary afferents release neurotransmitters and neuropeptides that activate the second-order projection neurons of the spinal cord. Pain transmission through the spinal cord may be modulated by an endogenous descending pain inhibitory system and may be influenced by exogenously administered medications. The primary components of this descending pain inhibition system are the “triad” of the: 1. Periaqueductal gray (PAG). 2. Rostral ventromedial medulla (RVM). 3. Dorsal lateral pontine tegmentum (DLPT), which includes the locus coeruleus (LC) and the A7 nuclei. The PAG is an important site for the production of analgesia following systemic administration of opioids. The endogenous opioid [Met5]-enkephalin is present within this nucleus and opioid receptors of each subtype are present in this region. The PAG provides dense projections to the RVM and brainstem noradrenergic nuclei LC and A7. Although each of these regions has direct projections to the spinal cord, it has been proposed that their projections to the RVM are important components in the modulation of pain by these regions. The RVM can function as a relay nucleus in the production of antinociception by more rostral midbrain structures (PAG), but it also has a primary role in the suppression of nociceptive transmission at the level of the spinal cord. The suppression of nociceptive reflex behavior is thought to be mediated by the axons of RVM neurons that descend within the dorsolateral funiculus and terminate bilaterally in laminae I, II, V, VI, and VII of the spinal cord. Anatomical studies have shown these axons terminate coincident with spinothalamic tract cells and interneurons of the dorsal horn that are related to pain transmission. Consistent with the anatomical terminations of the RVM axons, physiological studies have shown that stimulation of the RVM results in the inhibition of a population of pain-specific neurons within the dorsal horn. Spinally projecting neurons of the RVM possess numerous neurotransmitters including serotonin, enkephalin, GABA, glutamate, and substance P. The DLPT contains all of the noradrenergic neurons that project to the RVM and the spinal cord. In animal models, electrical stimulation of the DLPT sites produces analgesia and the analgesia produced by the activation of these nuclei is mediated by the alpha-2 adrenergic receptor. The physician can pharmacologically manipulate each of these neurotransmitter systems to modulate pain transmission throughout the CNS.
5.1 Introduction
5.2 Definition of Low Back Pain
Fig. 5.1a, b). They define sacral spinal pain as pain perceived anywhere in a region bounded by the first sacral spinous process, the posterior sacrococcygeal joints, and the posterior superior iliac spines.
Fig. 5.1c). For thoracic spinal pain, the differential diagnosis is different from that for low back pain, and a different evidence base applies.4
Fig. 5.1c). This type of pain could originate from the hip joint and surrounding structures (e.g., the sacral iliac joint). Pain over the loin is not back pain, and could have an etiology originating from the urinary tract or other viscera (
Fig. 5.1d).
5.3 Peripheral Pain Mechanisms
5.3.1 Anatomy of Nociceptors
Table 5.1). Nociceptors are said to have “free” (unencapsulated) nerve endings because peripheral terminals of these afferents do not appear to be associated with any specific cell type.
5.4 Spinal Cord and Supraspinal Structures
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