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Pain Sensations interpreted as pain, including burning, aching, stinging, and soreness, are the most distinctive forms of sensory input to the central nervous system. Pain serves an important protective function because it causes awareness of actual or potential tissue damage. Furthermore, it stimulates an individual to react to remove or withdraw from the source of the pain. Nociceptors Nociceptors are bare or free nerve endings; therefore, they do not adapt, or stop responding, to sustained or repeated stimulation. Nociceptors are widely distributed in the skin, dental pulp, periosteum, joints, meninges, and some internal organs. The three major classes of nociceptors are: • Thermal nociceptors • Mechanical nociceptors • Polymodal nociceptors Thermal nociceptors Thermal nociceptors are activated by extreme temperatures, especially heat. One group of these receptors is stimulated by noxious heat (>45 °C) and a second group is stimulated by noxious cold (<5 °C). Mechanical nociceptors Mechanical nociceptors are activated by mechanical damage, such as cutting, pinching, or tissue distortion, as well as by intensive pressure applied to the skin. Polymodal nociceptors Polymodal nociceptors are activated by all types of damaging stimuli (thermal, mechanical, chemical), including irritating exogenous substances that may penetrate the skin. Endogenous substances that may stimulate these receptors to elicit pain include potassium released from damaged cells; bradykinin; histamine; substance P; acids; and proteolytic enzymes. The two types of pain are: • Fast pain • Slow pain Fast pain may be described as sharp or prickling pain. This pain is perceived first (within 0.1 sec) as it is carried by the more rapidly fibers. Slow pain may be described as dull, aching, or throbbing pain. This pain is perceived second (only after 1 sec or more) because it is carried by fibers. Slow pain persists longer and is typically more unpleasant; in fact, it tends to become greater over time. Hyperalgesia An injured area is typically more sensitive to subsequent stimuli. As a result, painful stimuli, or even normally nonpainful stimuli, may cause an excessive pain response. An increase in the sensitivity of nociceptors is referred to as primary hyperalgesia. A classic example of hyperalgesia is a burn. Even light touch of a burned area may be painful. The sensitization of nociceptors following tissue damage or inflammation results from a variety of chemicals released or activated in the injured area. These substances decrease the threshold for activation of the nociceptors. One such substance that seems to be more painful than the others is bradykinin. Activated by enzymes released from damaged cells, bradykinin causes pain by several mechanisms. First, it activates A-delta and C fibers directly. Second, along with histamine, it contributes to the inflammatory response to tissue injury. Third, it promotes synthesis and release of prostaglandins from nearby cells. The prostaglandins sensitize all three types of pain receptors, thus enhancing the response to a noxious stimulus. In other words, it hurts more when prostaglandins are present. Aspirin and nonsteroidal antiinflammatory drugs (NSAIDs) inhibit the synthesis of prostaglandins, which accounts, in part, for their analgesic effects. Endogenous analgesic system The endogenous analgesic system is a built-in neuronal system that suppresses transmission of nervous impulses in the pain pathway. It functions by way of the following neurotransmitters produced in the CNS: • Endorphins • Enkephalins • Dynorphin Endorphins are found primarily in the limbic system, hypothalamus, and brainstem. Enkephalins and dynorphin (in smaller quantities) are found primarily in the gray matter of the midbrain, the limbic system, and the hypothalamus. These endogenous substances mimic the effects of morphine and other opiate drugs at many points in the analgesic system, including in the dorsal horns of the spinal cord. Opioid receptors are highly concentrated in the gray area of the midbrain. Stimulation of this region produces long-lasting analgesia with no effect on the level of consciousness. For these reasons, this gray area is often referred to as the endogenous analgesia center, The endogenous analgesic system is normally inactive. It remains unclear how this system becomes activated. Potential activating factors include exercise, stress, acupuncture, and hypnosis. Cutaneous pain Cutaneous pain is felt in superficial structures such as the skin and subcutaneous tissues. A pin prick and a paper cut are examples of cutaneous pain. It is a sharp pain with a burning quality that may be easily localized. This pain may be abrupt or slow in onset. Deep somatic pain As its name implies, deep somatic pain is generated in deep body structures, such as the periosteum, muscles, tendons, joints, and blood vessels. This type of pain is more diffuse than cutaneous pain. It may be elicited by strong pressure, ischemia, and tissue damage. Tissue ischemia When blood flow to a tissue is decreased or interrupted, the tissue becomes painful within a few minutes. In fact, the greater the rate of metabolism in the tissue, the more rapid is the onset of pain. The causes of pain due to tissue ischemia include: • Accumulation of lactic acid due to the anaerobic metabolism that occurs during ischemia • Release and activation of noxious chemicals in the area of tissue ischemia due to tissue damage. The lactic acid and other noxious chemicals stimulate polymodal nociceptors. Muscle spasm The pain induced by muscle spasm results partially from the direct effect of tissue distortion on mechanical nociceptors. Muscle spasm also causes tissue ischemia. The increased muscle tension compresses blood vessels and decreases blood flow. Furthermore, the increased rate of metabolism associated with the spasm exacerbates the ischemia. As discussed earlier, ischemia leads to stimulation of polymodal nociceptors. Visceral pain Visceral pain occurs in organs and tissues of the thoracic and abdominal cavities. It may be caused by several factors, including: • Inflammation • Chemical stimuli • Spasm of a hollow organ • Overdistension of a hollow organ Referred pain Referred pain is felt in a part of the body different from the actual tissue causing the pain. Typically, the pain is initiated in a visceral organ or tissue and referred to an area of the body surface. Classic examples of referred pain include headache and angina. Interestingly, the brain does not contain nociceptors; therefore, pain perceived as a headache originates in other tissues, such as the eyes; sinuses; muscles of the head and neck; and meninges. Angina, or chest pain, is caused by coronary ischemia. It may be accompanied by pain referred to the neck, left shoulder, and left arm. Referred pain most likely results from the convergence of visceral and somatic afferent fibers on the same second-order neurons in the dorsal horn of the spinal cord (see Figure 8.3). Therefore, the brain has no way of identifying the original source of the pain. Because superficial inputs normally predominate over visceral inputs, higher centers may incorrectly attribute the pain to the skin instead of the deeper tissue. Phantom pain Phantom pain is pain that appears to arise from an amputated limb or body part; as many as 70% of amputees experience phantom pain. This pain may begin with sensations of tingling, heat and cold, or heaviness, followed by burning, cramping, or shooting pain. Phantom pain may disappear spontaneously or persist for many years. The exact cause of phantom pain is not clearly understood. One proposed mechanism involves stimulation of the sensory pathway that had once originated in the amputated body part. An important point is that the sensory pathway originating in a given body part transmits impulses to the region of the somatosensory cortex devoted to that body part regardless of amputation. Stimulation at any point along this pathway results in the same sensation that would be produced by stimulation of the nociceptor in the body part itself. Following amputation of a body part, the ends of the afferent nerves arising from that body part become trapped in the scar tissue of thestump. These afferent nerve endings exhibit increased sensitivity and are easily stimulated. Therefore, action potentials are generated at these nerve endings and transmitted to the area of the somatosensory cortex devoted to the amputated body part. This results in the perception of pain arising from the amputated portion of the body. A second theory of phantom pain suggests that second-order neurons in the dorsal horn of the spinal cord become hyperactive. Spontaneous firing of these neurons causes transmission of nerve impulses to the brain and the perception of pain.