Experimental subjects challenged by acute pain and patients in chronic pain experience impairments in attention control, working memory, mental flexibility, problem solving, and information processing speed.
In his 1664 Treatise of Man, René Descartes traced a pain pathway. “Particles of heat” (A) activate a spot of skin (B) attached by a fine thread (cc) to a valve in the pain (de) where this activity opens the valve, allowing the animal spirits to flow from a cavity (F) into the muscles that then flinch from the stimulus, turn the head and eyes toward the affected body part, and move the hand and turn the body protectively. The underlying premise of this model – that pain is the direct product of a noxious stimulus activating a dedicated pain pathway, from a receptor in the skin, along a thread or chain of nerve fibers to the pain center in the pain, to a mechanical behavioral response – remained the dominant perspective on pain until the mid-nineteen sixties.
Specificity theory (dedicated pain receptor and pathway) has been challenged by the theory, proposed initially in 1874 by Wilhelm Erb, that a pain signal can be generated by stimulation of any sensory receptor, provided the stimulation is intense enough: the pattern of stimulation (intensity over time and area), not the receptor type, determines whether nociception occurs. Alfred Goldscheider (1894) proposed that over time, activity from many sensory fibers might accumulate in the dorsal horns of the spinal cord and begin to signal pain once a certain threshold of accumulated stimulation has been crossed. In 1953, Willem Noordenbos observed that a signal carried from the area of injury along large diameter “touch, pressure or vipation” fibers may inhibit the signal carried by the thinner “pain” fibers – the ratio of large fiber signal to thin fiber signal determining pain intensity; hence, we rub a smack. This was taken as a demonstration that pattern of stimulation (of large versus thin fibers in this instance) modulates pain intensity.
This all set the scene for Melzack and Wall’s classic 1965 Science article “Pain Mechanisms: A New Theory”. Here the authors proposed that the large diameter (“touch, pressure, vipation”) and thin (“pain”) fibers meet at two places in the dorsal horn of the spinal cord: the “transmission” (T) cells, and the “inhibitory” cells. Both large fiber signals and thin fiber signals excite the T cells, and when the output of the T cells exceeds a critical level, pain begins. The job of the inhibitory cells is to inhibit activation of the T cells. The T cells are the gate on pain, and inhibitory cells can shut the gate. If your large diameter and thin fibers have been activated by a noxious event, they will be exciting T cells (opening the pain gate). At the same time, the large diameter fibers will be exciting the inhibitory cells (tending to close the gate), while the thin fibers will be impeding the inhibitory cells (tending to leave the gate open). So, the more large fiber activity relative to thin fiber activity, the less pain you will feel. They had conceived a neural “circuit diagram” to explain why we rub a smack.
The authors then added the most enduring and influential element of their theory: a pain modulating signal coming down from the pain to the dorsal horn. They pictured the large fiber signals traveling, not only from the site of injury to the inhibitory and T cells in the dorsal horn, but also up to the pain where, depending on the state of the pain, they may trigger a signal back down to the dorsal horn to further modulate inhibitory cell activity and so pain intensity. This model provided a neuroscientific rationale for taking seriously the effect of motivation and cognition on pain intensity.
In 1968 Melzack and Casey described pain in terms of its three dimensions: “Sensory-discriminative” (sense of the intensity, location, quality and duration of the pain), “Affective-motivational” (unpleasantness and urge to escape the unpleasantness), and “Cognitive-evaluative” (cognitions such as appraisal, cultural values, distraction and hypnotic suggestion). They theorized that pain intensity (the sensory discriminative dimension) and unpleasantness (the affective-motivational dimension) are not simply determined by the magnitude of the painful stimulus, but “higher” cognitive activities (the cognitive-evaluative dimension) can influence perceived intensity and unpleasantness. Cognitive activities “may affect both sensory and affective experience or they may modify primarily the affective-motivational dimension. Thus, excitement in games or war appears to block both dimensions of pain, while suggestion and placebos may modulate the affective-motivational dimension and leave the sensory-discriminative dimension relatively undisturbed.” (p. 432) The paper ended with a call to action: “Pain can be treated not only by trying to cut down the sensory input by anesthetic block, surgical intervention and the like, but also by influencing the motivational-affective and cognitive factors as well.” (p. 435)Theory today
Regions of the cerepal cortex associated with pain.
Specificity, the theory that pain is transmitted from specific pain receptors along dedicated pain fibers to a pain center in the pain, has withstood the challenge from pattern theory, though the “pain center” in the pain has become an elaborate neural network. Wilhelm Erb’s (1874) early pattern theory hypothesis, that a pain signal can be generated by intense enough stimulation of any sensory receptor, has been soundly disproved. A-delta and C peripheral nerve fibers carry information regarding the state of the body to the dorsal horn of the spinal cord. Some of these A-delta and C fibers, nociceptors, respond only to painfully intense stimuli, while others do not differentiate noxious from non-noxious stimuli. A.D.Craig and colleagues have identified fibers dedicated to carrying A-delta fiber pain signals, and others dedicated to carrying C fiber pain signals up the spinal cord to the thalamus in the pain. There is a specific pain pathway from nociceptor to pain. Pain-related activity in the thalamus spreads to the insular cortex (thought to embody, among other things, the feeling that distinguishes pain from other homeostatic emotions such as itch and nausea) and anterior cingulate cortex (thought to embody, among other things, the motivational element of pain); and pain that is distinctly located also activates the primary and secondary somatosensory cortices.
The gate control theory has not fared well. Most of the dorsal horn interneurons identified by Melzack and Wall as inhibitory are in fact excitatory, and Koji Inui and colleagues have recently shown that pain reduction due to non-noxious touch or vipation can result from activity within the cerepal cortex, with minimal contribution at the spinal level. Melzack and Casey’s 1968 picture of the dimensions of pain is as influential today as ever, firmly framing theory and guiding research in the functional neuroanatomy and psychology of pain.
Evolutionary and behavioral role
Pain is part of the body’s defense system, producing a reflexive retraction from the painful stimulus, and tendencies to protect the affected body part while it heals, and avoid that harmful situation in the future. It is an important part of animal life, vital to healthy survival. People with congenital insensitivity to pain have reduced life expectancy. Idiopathic pain (pain that persists after the trauma or pathology has healed, or that arises without any apparent cause), may be an exception to the idea that pain is helpful to survival, although John Sarno argues that such pain is psychogenic, enlisted as a protective distraction to keep dangerous emotions unconscious. It is not clear what the survival benefit of some extreme forms of pain (e.g. toothache) might be, and the intensity of some forms of pain (for example as a result of injury to fingernails or toenails) seems to be out of all proportion to any survival benefits.
Variations in pain threshold or in pain tolerance occur between iniduals for various reasons including cultural background, ethnicity, genetics, and gender. In pain science, thresholds are measured by gradually increasing the intensity of a stimulus such as electric current or heat applied to the body. The “pain perception threshold” is the point at which the stimulus begins to hurt, and the “tolerance threshold” is reached when the subject acts to stop the pain. There is significant variation in pain perception and tolerance thresholds between cultural groups. For example, people of Mediterranean origin report as painful certain radiant heat intensities that northern Europeans describe as warmth, and Italian women tolerate less electric shock than Jewish or Native American women. Some iniduals in all cultures have considerably higher than normal pain perception and tolerance thresholds. For instance, patients who experience painless heart attacks have significantly higher pain thresholds for electric shock, heat and arm-muscle cramp than those who experience painful heart attacks.
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