2008 The gain from pain- minimizing potential damage to the body

2008 The gain from pain- minimizing potential damage to the body

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Temporal Dimensions of Pain Acute pain in response to identified stimulus Long lasting pain in response to ongoing process, e.g., inflammation, that disappears after the process is resolved Persistent pain that outlasts the initiating process, e.g., post- herpetic neuralgia, phantom limb, nerve or CNS damage
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Nociceptors • Sensory neurons selectively activated by potentially damaging stimuli: mechanical, thermal, chemical. •W h y nociceptors and not pain neurons ? Because nociceptive stimuli do not always result in pain. • Nociceptors conduct to the spinal cord via small diameter axons- makes them susceptible to block by local anesthetics. • Properties of small diameter axons: slow conduction, high threshold to electrical stimulation, selectively blocked by local anesthetics.
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Nociception Involves Specialized Neurons
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Nociceptive sensory cells are small in diameter and express peptide neurotransmitters (in both cases unlike pressure sensitive neurons): Substance P and Calcitonin gene related peptide (CGRP)
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Small Fibers Are Responsible for Nociception
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First Pain and Second Pain • First pain is well localized “pricking” pain. • Second pain is diffuse “burning” pain. • First pain results from conduction in small myelinated fibers- A δ fibers. • Second pain results from conduction in C-fibers. • Small fibers are selectively blocked by “local anesthetics”
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Opiates inhibit release of transmitter from C- fiber nociceptors. Nociceptors responsible for pricking (1 st ) pain (A- δ fibers) have no opiate receptors 2 kinds of opiates: circulating: endorphins ; localized transmitters: enkephalins
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Discovery of opiates • “War on Drugs” in 1960s and 1970s • How do opiates (morphine,
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2008 The gain from pain- minimizing potential damage to the body

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