Porth's Essentials of Pathophysiology, 4e

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Somatosensory Function, Pain, and Headache

C h a p t e r 3 5

occur at several levels of the CNS rostral to the input seg- ment. Perhaps the most puzzling aspect of locally applied stimuli, such as brushing, that can block the experience of pain is the relatively long-lasting effect (minutes to hours) of such treatments. This prolonged effect has been difficult to explain on the basis of specificity theories, including the gate control theory. Other important fac- tors include the effect of endogenous opioids and their receptors at the segmental and brain stem level, descend- ing feedback modulation, altered sensitivity, learning, and culture. More recently, Melzack has developed the neuroma- trix theory to further address the brain’s role in pain as well as the psychological and emotional dimensions of pain. 7 This theory proposes that the brain contains a widely distributed neural network, called the body–self neuromatrix, that has multiple somatosensory, limbic, and thalamocortical components. Genetic and sensory influences determine the architecture of each individ- ual’s neuromatrix, which integrates multiple sources of inputs. These include somatosensory inputs; other sensory inputs affecting interpretation of the situation; inputs from the brain addressing such things as atten- tion, expectation, culture, and personality; various com- ponents of stress regulation systems; and other sources. The neuromatrix theory of pain, which places genetic and neuroendocrine mechanisms on a level equal to that of neural transmission, has important implications for research and therapy. 7 Pain Mechanisms and Pathways Pain can be either nociceptive or neuropathic in origin. The term nociception, which means “pain sense,” comes from the Latin word nocere, “to injure.” Nociceptive pain is initiated by nociceptors that are activated by injury to peripheral tissues. Neuropathic pain, on the other hand, arises from direct injury or dysfunction of the sensory axons of peripheral or central nerves. Two aspects of pain affect an individual’s response to a painful stimulus—pain threshold and tolerance. Although the terms often are used interchangeably, they have distinct meanings. Pain threshold is closely asso- ciated with the point at which a nociceptive stimulus is perceived as painful. Pain tolerance relates more to the total pain experience; it is defined as the maximum intensity or duration of pain that a person is willing to endure before the person wants something done about the pain. Psychological, familial, cultural, and environ- mental factors significantly influence the amount of pain a person is willing to tolerate. The threshold for pain is fairly uniform from one person to another, whereas pain tolerance is extremely variable. The mechanisms of pain are many and complex. As with other forms of somatosensation, the pathways are composed of first-, second-, and third-order neurons 1,2 (Fig. 35-7). The first-order neurons and their recep- tive endings detect stimuli that threaten the integrity of innervated tissues. Second-order neurons are located in the spinal cord and process nociceptive information.

Pain

Somatosensory cortex

3

Thalamus

RAS

2

Spinothalamic pathway

1

Dorsal root ganglion

Nociceptor

Substance P Prostaglandins Serotonin Acetylcholine

Mediator release

Inflammation

Tissue injury

Third-order neurons project pain information to the brain. The thalamus and somatosensory cortex integrate and modulate pain as well as the person’s subjective reaction to the pain experience. Pain Receptors and Primary Afferent Pathways Nociceptors, or pain receptors, are activated by noxious insults to peripheral tissues. Structurally, they are free nerve endings of the peripheral pain fibers. These recep- tive endings translate noxious stimuli into signals that are transmitted by a dorsal root ganglion to the dorsal horn of the spinal cord. Nociceptive Simulation. Unlike other sensory recep- tors, nociceptors respond to several forms of stimula- tion, including mechanical, thermal, and chemical. Some receptors respond to a single type of stimuli (mechani- cal or thermal) and others, called polymodal receptors, FIGURE 35-7. Mechanism of acute pain.Tissue injury leads to release of inflammatory mediators with subsequent nociceptor stimulation. Pain impulses are then transmitted to the dorsal horn of the spinal cord, where they make contact with second- order neurons that cross to the opposite side of the cord and ascend by the spinothalamic tract to the reticular activating system (RAS) and thalamus.The localization and meaning of pain occur at the level of the somatosensory cortex. 1, first- order sensory neurons; 2, second-order sensory neurons; 3, third-order sensory neurons.