Chapter 012. Pain: Pathophysiology and Management (Part 4)

Chapter 012. Pain: Pathophysiology and Management (Part 4)

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Pain transmission and modulatory pathways. A. Transmission system for nociceptive messages. Noxious stimuli activate the sensitive peripheral ending of the primary afferent nociceptor by the process of transduction. The message is then transmitted over the peripheral nerve to the spinal cord, where it synapses with cells of origin of the major ascending pain pathway, the spinothalamic tract. The message is relayed in the thalamus to the anterior cingulate (C), frontal insular (F), and somatosensory cortex (SS). B. Painmodulation network. Inputs from frontal cortex and hypothalamus activate cells in the midbrain that control spinal pain-transmission cells via cells in the...

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Chapter 012. Pain: and (Part 4) Pain and pathways. A. system for messages. Noxious stimuli activate the sensitive ending of the primary afferent by the process of The message is then over the nerve to the spinal cord, where it synapses with cells of origin of the major ascending pain the tract. The message is relayed in the thalamus to the cingulate (C), frontal insular (F), and cortex (SS). B. network. Inputs from frontal cortex and activate cells in the midbrain that control spinal cells via cells in the medulla. Pain The pain produced by injuries of similar magnitude is variable in different and in different For example, athletes have been known to sustain serious fractures with only minor pain, and Beecher's classic World War II survey revealed that many soldiers in battle were by that would have produced agonizing pain in civilian patients. even the of relief can have a analgesic effect On the other hand, many patients find even minor injuries (such as and and the of pain has been to induce pain without a noxious powerful effect of and other variables on the perceived intensity of pain implies the of brain circuits that can modulate the activity of the One of these circuits has links in the midbrain, and and it controls spinal neurons through a pathway (Fig. 12-4). Human brain imaging studies have this circuit in the effect of and opioid analgesic each of the component of the pathway opioid receptors and is sensitive to the direct of opioid drugs. In animals, lesions of the system reduce the analgesic effect of opioids such as morphine. Along with the opioid receptor, the nuclei of this circuit contain opioid such as the and most reliable way to this system is by prolonged pain and/or fear. There is evidence that opioids are released surgical and in patients given a placebo for pain relief. circuits can enhance as well as suppress pain. Both and neurons in the medulla project to and control spinal neurons. Since neurons can be activated by neurons, it is possible to generate a pain signal with no noxious stimulus. In fact, human imaging studies have increased activity in this circuit during migraine headache. A central circuit that pain could account for the finding that pain can be induced by or enhanced by and it could provide a framework for how factors can to chronic pain. Pain Lesions of the or central nervous pathways for pain typically result in a loss or of pain damage to or of these pathways can produce pain. For example, damage to nerves, as occurs in diabetic or to primary as in herpes zoster, can result in pain that is referred to the body region by the damaged nerves. Though rare, pain may also be produced by damage to the central nervous system, the pathway or thalamus. Such pains are often severe and are to standard for pain. pains typically have an unusual burning, tingling, or electric quality and may be triggered by very light touch. These features are rare in other types of pain. On a sensory deficit is present in the area of the patient's pain. is also of pain; patients often complain that the very lightest moving stimuli evoke exquisite pain In this regard it is of clinical interest that a topical of 5% lidocaine in patch form is effective for patients with neuralgia who have prominent variety of to pain. As with primary afferent damaged primary including become highly sensitive to and begin to generate impulses in the absence of There is evidence that this increased and is due to an increased of sodium channels. Damaged primary afferents may also develop to spinal cord neurons cut off from their normal input may also become active. Thus, both central and nervous system to pain.