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In this chapter we review the anatomy and physiology of pain pathways. We also discuss some of the physiological processes that modify the pain experience and that may contribute to the development of chronicity. For obvious reasons, most of this information comes from animal experiments. However, in recent years, experimental studies of human subjects using physiological, pharmacological, and psychophysical methods indicate that much of what has been learned in animals is applicable to humans (National Academy of Sciences, 1985). Research into basic mechanisms underlying pain is an increasingly exciting and promising area. However, most of what is known about the anatomy and physiology of pain is from studies of experimentally induced cutaneous (skin) pain, while most clinical pain arises from deep tissues. Thus, while experimental studies provide fairly good models for acute pain, they are poor models for clinical syndromes of chronic pain. Not only do they provide little information about the muscles, joints, and tendons that are most often affected by chronically painful conditions, but they do not address the vast array of psychosocial factors that influence the pain experience profoundly. To improve our understanding and treatment of pain we will need better animal models of human pain and better tools for studying clinical pain.
It is possible to place an electrode into a human peripheral nerve and record the activity of primary afferent nociceptors (Fitzgerald and Lynn, 1977; Torebjork and Hallin, 1973). The nociceptor is characterized by its response to noxious heat, pressure, or chemical stimuli. The ''pain'' message is coded in the pattern and frequency of impulses in the axons of the primary afferent nociceptors. There is a direct relation between the intensity of the stimulus and the frequency of nociceptor discharge (Figure 7-3). Furthermore, combined neurophysiological and psychophysical studies in humans have shown a direct relation between discharge frequency in a primary afferent nociceptor and the reported intensity of pain (Fitzgerald and Lynn, 1977; LaMotte et al., 1983). Blocking transmission in the small-diameter axons of the nociceptors blocks pain, whereas blocking activity of the larger-diameter axons in a peripheral nerve does not. These identified primary afferent nociceptors are thus necessary for detecting noxious stimuli.
The axons of some of these second-order cells cross over to the opposite side of the spinal cord and project for long distances to the brain stem and thalamus. The pathway for pain transmission lies in the anterolateral quadrant of the spinal cord. Most of our information about the anatomy and physiology of pain-transmission pathways in the central nervous system is derived from animal studies. However, it is known that in humans, lesions of this anterolateral pathway permanently impairs pain sensation and that electrical stimulation of it produces pain (Cassinari and Pagni, 1969; White et al., 1950; Willis, 1985).
There are two major targets for ascending nociceptive axons in the anterolateral quadrant of the spinal cord: the thalamus and the medial reticular formation of the brain stem. Our knowledge is most extensive for the spinal cells whose axons project directly to the thalamus, that is, the spinothalamic tract cells. The spinothalamic pathway is implicated in human pain perception because lesions of it, at any level, produce lasting impairments of pain sensation.
Studies of the properties of spinothalamic tract cells have been carried out in several species. In all these species, a major proportion of spinothalamic neurons respond maximally to noxious stimulation. Furthermore, there is a direct relationship in spinothalamic tract cells of firing frequency to stimulus intensities in the noxious range for human subjects (Kenshalo et al., 1980; Willis, 1985). These observations, coupled with decades of careful clinical studies, strongly implicate the spinothalamic tract as a major pathway for pain in humans.
The abovementioned processes were discussed in terms of a highly reliable pain-transmission system, the assumption being that pain intensity is a direct function of nociceptor activity. In fact, the excellent correlation among stimulus intensity, impulses in primary afferent nociceptors, and reported pain intensity demonstrated in human subjects under experimental conditions often does not apply to the clinical situation. The most remarkable observations are those in which patients subjected to injuries that ought to be very painful report no significant pain (Beecher, 1959).
Is there any physiological basis for differentiating between acute and chronic pain? Little is known about the effects of prolonged pain on the central nervous system. There is some evidence that the transition from acute pain to chronic pain alters patients' neurophysiology in a way that makes them somewhat different from people with acute pain. In arthritic rats, for example, there are changes in the peripheral nerves that alter their range of response to applied stimuli, and there may be changes in the central pathways for pain transmission as well (Guilbaud et al., 1985; Kayser and Guilbaud, 1984). Experiments with rats in which nerves have been injured and observed over time have shown changes in the central nervous system, but it is not known how these changes relate to pain (Markus et al., 1984).
In this chapter we have briefly surveyed the anatomy, physiology, and pharmacology of nociceptive transduction, transmission, and modulation. These are objective and potentially observable phenomena initiated by stimuli that damage or threaten tissue.
The monitoring of central pain transmission pathways is not practical with the technology available. Although it is theoretically possible, recording single units within the human nervous system requires a potentially dangerous surgical procedure. Multiunit, or evoked-potential, studies do not have the required specificity or spatial resolution to permit collecting meaningful data about clinical pain. It is technically possible to measure the chemicals released at spinal synapses by primary afferent nociceptors. If the concentration of such chemicals in the cerebrospinal fluid could be shown to correlate with either the activity of the primary afferent nociceptors or with the severity of clinical pain, this could provide evidence similar to that derived from recording the activity of the primary afferents. However, at the present time, the transmitter or transmitters for the primary afferent nociceptors are unknown.
The Biology 256 Fundamentals of Human Physiology Laboratory course was designed to provide students with hands-on access to modern techniques in human physiological analyses using the course-based research pedagogical approach. In this course, students will learn how to perform literature searches; generate research questions and hypotheses; design experiments; collect, analyze, visualize and interpret data; and present scientific findings to others. The Biol 256L curriculum offers a high-impact human physiology experience that fosters the critical thinking skills required to be a successful citizen in a modern world filled with misinformation.","image":"https:\/\/iastate.pressbooks.pub\/app\/uploads\/sites\/37\/2020\/11\/CBRAHumanPhysiology-cover.png","author":[{"@type":"Person","contributor_first_name":"Karri","contributor_last_name":"Haen Whitmer","name":"Karri Haen Whitmer","slug":"karri-haenwhitmer"}],"editor":[],"translator":[],"reviewedBy":[],"illustrator":[],"contributor":[],"about":[{"@type":"Thing","identifier":"MFG","name":"Physiology"},{"@type":"Thing","identifier":"PDM","name":"Scientific research"}],"publisher":{"@type":"Organization","name":"Iowa State University Digital Press","address":{"@type":"PostalAddress","addressLocality":"Ames, IA"}},"datePublished":"2021-02-01","copyrightYear":"2021","copyrightHolder":{"@type":"Organization","name":"Karri Haen Whitmer"},"license":{"@type":"CreativeWork","url":"https:\/\/creativecommons.org\/licenses\/by-sa\/4.0\/","name":"CC BY-SA (Attribution ShareAlike)","code":"CC BY-SA","description":"You are free to copy, share, adapt, remix, transform, and build upon the material for any purpose as long as you follow the terms of the license.Suggested citation: Haen, K.M. (2021). A Mixed Course-Based Research Approach to Human Physiology.\u00a0Ames, IA: Iowa State University Digital Press.\u00a0DOI: https:\/\/doi.org\/10.31274\/isudp.2021.67Suggested attribution: A Mixed Course-Based Research Approach to Human Physiology\u00a0by Karri Haen Whitmer is available under a Creative Commons Attribution ShareAlike 4.0 International License.Published by the Iowa State University Digital Press, a division of the University Library at Iowa State University.701 Morrill Rd, Ames, IA 50011, USAE-mail: digipress@iastate.edu"},"identifier":{"@type":"PropertyValue","propertyID":"DOI","value":"10.31274\/isudp.2021.67"},"sameAs":"https:\/\/doi.org\/10.31274\/isudp.2021.67","bookDirectoryExcluded":false,"language":{"@type":"Language","code":"en","name":"English"}}:root{--primary:#c8102e;--accent:#c8102e;--accent-fg:#ffffff;--primary-dark:#7c2529;--accent-dark:#7c2529;}:root{--reading-width:40em;}window.dataLayer = window.dataLayer || [];function gtag(){dataLayer.push(arguments);}gtag('js', new Date());gtag('config', 'G-61KW6RBW32');Skip to contentToggle MenuPrimary Navigation 0852c4b9a8
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