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An understanding of the mechanism of pain production was not required by the physicians who developed the use of general anesthesia in the second half of the 19th century (see Chapter 73 ). Although inhalation of vapors produced lack of awareness during surgery, anesthesiologists learned that control of perioperative nociception would require a more thorough understanding of pain. Fortunately, by the beginning of the 20th century, there was already a large body of knowledge on pain mechanisms, dating from the earliest days of medical inquiry.
In antiquity, pain was thought to be an emotion rather than a sensory modality. Pain control was a function of religious authorities and shamans in primitive cultures, and relief of pain was sought through incantations and prayers. Pain was then often considered to be a punishment for committed sins or a form of religious suffering. The word pain is derived from the Greek term poine ("penalty"). Aristotle thought pain was an emotion emanating from the heart, but Galen correctly observed that the brain was required for pain to be manifested in animals. Galen also proposed that sensation was a property of nervous tissue, but his physiologic system was altogether hampered by his idea that an invisible psychic pneuma traveled within hollow nerves. [6]
The 18th and 19th centuries witnessed considerable progress in understanding the mechanisms of pain. Albrecht von Haller[82] (1708–1777) (see Fig. 1-3B ) observed that some tissues in the body have a property that he called sensibility: "I call those parts sensible, if the irritation occasions evident signs of pain and disquiet in the animal." Other tissues were insensible, which "if touched occasioned no sign of pain nor convulsion." Some tissues were irritable. "I call that part of the human body irritable, if it becomes shorter upon being touched."
Haller's landmark contribution in 1752[83] concluded that only those parts of the body supplied with nerves possess sensibility, whereas irritability is a property of the muscular fibers. The idea of specific neural pathways for painful sensations began with Charles Bell[84] (1774–1842) and François Magendie[85] (1783–1855), who both demonstrated that the dorsal roots transmitted sensory information and that the ventral roots were for motor transmissions. Johannes Müller (1801–1858), in his 1826 paper entitled "Of the Peculiar Properties on Individual Nerves," proposed that each sense organ gave rise to its own characteristic sensation and to no other; electrical or mechanical stimulation of the optic nerve, for example, gives rise to only to a sensation of light.[86] [87] The evidence that pain was a separate and distinct sense with separate end organs was formulated in 1858 by Moritz S. Schiff (1823–1896). [88]
By the end of the 19th century, the idea was firmly established that acute pain was a distinct sensory modality that was susceptible to interruption through conduction block initiated with local anesthetics. Pain as a separate sensation that was transmitted through separate neural fiber tracts was supported by clinical observations after neural blockade. Several investigators found, for example, that acute pain could be abolished with cocaine injections that left some sensory modalities unaffected.[89]
Developments in pain theory led to considerable modifications in the theory that pain was a hard-wired sensory connection between the nociceptor and the brain and that the intensity of the pain was directly proportional the extent of tissue injury. Consider the frightening experience of the missionary, David Livingstone (1813–1873), who spent 16 years in Africa exploring the interior of the continent. He offers this account[90] of his thoughts while being attacked by a lion:
When in the act of ramming down the bullets I heard a shout, and, looking half round, I saw the lion in the act of springing upon me. He caught me by the shoulder, and we both came to the ground together. Growling horribly, he shook me as a terrier dog does to a rat. The shock produced a stupor similar to that which seems to be felt by a mouse after the first grip of the cat. It caused a sort of dreaminess, in which there was no sense of pain nor feeling of terror, though I was quite conscious of all that was happening.
Livingstone miraculously survived this attack and was left with crushed bones and 11 of the lion's teeth in his arm. It would seem from his account that Livingstone's central nervous system was providing its own powerful analgesic agents, not unlikely in the light of recent evidence that the brain can produce its own opioids that are capable of suppressing nociception. Livingstone compared his experience with what patients describe when partially under the influence of chloroform.
There is evidence that operations undertaken in the battlefield may be associated with less pain compared with similar elective operations performed without anesthesia. The amputation of Lord Horatio Nelson's right arm in the battle at Tenerife, Canary Islands, was performed aboard ship after he sustained a musket shot above the elbow, dividing the artery and shattering the humerus. Nelson complained only that the knife felt cold and thereafter ordered that all knives on board be heated before entering into conflict, because his personal experience had indicated a warm knife would produce almost no discomfort.[91] Henry Beecher[92] (1904–1976) confirmed during World War II that wounded soldiers had surprisingly little pain.
To further explain some of these central influences on nociception, Melzack and Wall proposed the gate control theory of pain in 1965.[93] They proposed that as the nociceptive afferent pain fibers entered the spinal cord, they synapsed in the dorsal horn, where the input was subjected to the modulating influence of a "gate" before it was transmitted rostrally. The theory further suggests that large-fiber inputs tend to close the gate (i.e., inhibit nociceptive transmission), small-fiber inputs open it, and descending influences from the cortex and midbrain [94] also profoundly influence the gate. Endogenous opioids, first discovered in 1974 by A. Goldstein[95] and later confirmed by J. Hughes[96] in 1975 and S. H. Snyder and coworkers[97] in 1977, are located at diverse sites in the pain pathway, including the dorsal horn, and they can influence the rostral transmission of pain sensations. Several modalities of pain therapy, such as acupuncture and biofeedback, attempt to activate these endogenous systems to suppress chronic pain syndromes.
The gate theory of pain has had considerable influence on the anesthesiologist's management of pain by focusing attention on the unique pharmacology of the dorsal horn of the spinal cord. By using intrathecal and epidural injections, [98] anesthesiologists have learned to suppress nociceptive transmission at the first synaptic relay in the spinal cord. The technique has implications in acute and chronic pain therapy because neuraxially administered drugs can provide analgesia without some of the systemic side effects of intravenously administered drugs. A typically modern view of perioperative pain is to view it as an impediment to recovery. Aggressive methods are often used to minimize pain to facilitate hospital discharge and a rapid return to normal functional activity.[99]
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