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18 Cards in this Set
- Front
- Back
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Define Allodynia |
pain from normally non-painful stimuli |
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Describe Peripheral Sensitization |
increased sensitivity of receptors to painful stimuli. 1. Increase in sensitivity of free nerve endings to original pain stimulus 2. Receptors respond to multiple pain stimuli - release substance-P & GCRP which recruit other nociceptor nerves. 3. Increase in # of free nerve endings responding to the pain stimuli
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Define primary hyperalgesia |
increase in sensitivity to painful stimuli in the area of original damage |
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List 2 methods to reduce peripheral sensitization |
Anti-inflammatory medications Nerve block |
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Substance P instigates what cells to release what two substances? |
MAST cells - Histamine & NGF |
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What 5 substances present in an "injury" will stimulate the nociceptive response? |
Bradykinin 5-HT Prostaglandin ATP H+ ions |
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The result of CGRP & Substance P release: |
Edema |
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Discuss the mechanism for Central Sensitization |
increase in the sensitivity of neurons within the CNS such that normal inputs begin to produce abnormal responses. Increased sensitivity of Dorsal Horn neurons Increase in receptive field of dorsal horn neurons to include areas not involved in the original injury. |
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Define secondary hyperalgesia |
occurs in the area surrounding the original damage - resultant of both peripheral & central sensitization |
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Describe the three results of central sensitization |
1. Increased neuron sensitivity or excitability. 2. Disinhibition 3. Microglia activation |
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Discuss increased neuron sensitivity or excitability:
[part of central sensitization] |
Following ‘intense’ nociceptive stimulation or persistent injury, activated C and A-delta nociceptors release a variety of neurotransmitters onto output neurons in the superficial dorsal horn (red). As a consequence, normally silent NMDA glutamate receptors located in the postsynaptic neuron can now signal, increase intracellular calcium, and activate a cascade of events that increase the excitability of the output neuron and facilitate the transmission of pain messages to the brain. |
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Discuss Disinhibition:
[part of central sensitization] |
Under normal circumstances, inhibitory interneurons (blue) continuously release GABA and/or glycine (Gly) to decrease the excitability of output neurons and modulate pain transmission. However, in central sensitization this inhibition is lost, resulting in hyperalgesia. Additionally, disinhibition can enable non-nociceptive myelinated A-beta primary afferents to interact with dorsal horn pain neurons such that normally innocuous stimuli are now perceived as painful. |
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Discuss Microglia activation:
[part of central sensitization] |
Pain activates microglial cells in the dorsal spinal cord. These cells release several factors which result in increased excitability of dorsal horn neurons and promote enhanced pain in response to both noxious and innocuous stimulation (that is, hyperalgesia and allodynia). Activated microglia release a host of cytokines, such as tumor necrosis factor α (TNFα), interleukin-1β and 6 (IL-1β, IL-6), and other factors that contribute to central sensitization. |
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Discuss the mechanism involved in primary and secondary hyperalgesia. |
Primary hyperalgesia - occurs in area of original damage, result of peripheral sensitization
Secondary Hyperalgesia - occurs in area surrounding original damage result of both peripheral & central sensitization |
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Discuss the peripheral pain system responsible for the transmission of fast, sharp pain, course touch, & Non-noxious temperature |
Transmitted via A-delta fibers (small, thinly myelinated, slow fibers (5-30 m/s) Modality specific- respond to non-noxious, high threshold pressure, non-noxious temperature, noxious pressure (tissue damage), or noxious temperature Detection of injured site / Good stimulus localization
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Discuss the peripheral pain system responsible for the transmission of slow, long-lasting, dull, aching or burning pain |
transmitted via C fibers (unmyelinated, very slow fibers (0.5-2 m/s)
Polymodal –respond to noxious (high threshold) mechanical, thermal and chemical stimuli
Protection of injured site / Poor stimulus localization |
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Discuss the Gate theory of segmental inhibition |
at each of the main relay points along the ascending pain pathways, there are “gates” that can be closed to make it harder for nociceptive impulses to get through thus, depending on how open the gates are at each of these relay points, the same level of activity in a nociceptor will not always lead to perception of the same intensity of pain stimulating Periaqueductal Gray (PAGs) will block the pain In absence of input from C fibers, tonically active inhibitory interneuron suppresses pain pathway With strong pain, C fiber stops inhibition of the pathway, allowing a strong signal to be sent to the brain Pain can be modulated by simultaneous somatosensory input TENS stimulates Ab fibers = closes the “gate” = helps block pain when you rub the painful part of your body |
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Where is the third neuron/termination of the spinothalamic tract & what is the tracts activity? |
Thalamus (VPL) - sensory cortex
Localization & discrimination of the pain |
