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7. Somatosensory System 3 - Pain, Itch, & Pain Modulation (Ruggieri)
Terms in this set (30)
types of somatosensation: what types are transmitted via DC-ML? ALS? trigeminal?
DC-ML: touch (tactile, 2-pt discrimination, vibration), proprioception, movement sense (kinesthesia)
ASL/CN V: temp (non-noxious cold & warmth), pain (fast/prick, slow/burning, noxious cold & heat), itch
pain vs. nociception?
P: unpleasant sensory + emotional experience due to tissue damage, subjective
Noc: neural processes of encoding + processing noxious stimuli, physiological
nociceptor pain vs. neuropathic pain?
nociceptor: caused by tissue injury, stimulus evoked, mediated by quiescent C polymodal nociceptors through DRG + spinal nerves, inc neural activity in wide range of neurons, managed by opioids
neuropathic: caused by injury or disease of NS (usually PNS), spontaneous origin or minor stimuli, develops days/months after injury, mediated by C polymodal nociceptors, often unmanageable to traditional therapies
mechanism of chronic pain (ie neuropathic pain)
inflammatory soup: tissue damage itself, macrophages + neurophils (release cytokines), mast cells (histamine + bradykinin <-- nociceptor activators), prostaglandins (NSAID targets)
all of these mediators activate the terminal nociceptor nerve ending
process of turning peripheral sensitivation into central sensitivation
how does this lead to chronic pain?
retrograde transport of inflammatory mediators from the terminal nerve end into the dorsal horn/DRG of the spinal cord --> activating the spinal cord (increases production of nociceptor-related NTs) --> increase recruitment/proliferation of non-neuronal elements (mast, macrophage, T cell, etc)
this response can maintain abnormalities in spinal cord after peripheral injury has healed (
define: peripheral sensitization, hyperalgesia (primary + secondary), allodynia
peripheral: nociceptors become more sensitive (lower threshold) + more responsive (inc firing rate)
hyperalgesia: exaggerated response to painful stimuli (primary = site of damaged tissue, secondary = skin bordering damaged tissue)
allodynia: exaggerated response to non-painful stimuli (hypersensitivity to touch, fibromyalgia)
nociceptor afferents enter spinal cord thru dorsal roots + take one of what 2 actions?
1. synapse + decassate at that level
2. ascend 2 spinal levels via posterolateral tract (or Lissauer's Tract)
<-- most common route
where is the lesion:
L side: numbness in dermatome T5, loss of fine touch, vibratory sense, + proprioception below dermatome T5
R side: loss of pain + temp sensation below dermatome T5
Brown-Sequard Syndrome (spinal cord hemisection)
tumor compressing the dorsal roots of spinal cord T5
multi-synaptic sites of ALS pathway: what are the 3 alternate site the axons of 2nd order neurons can ascend other than the VPL in the thalamus?
1. reticular nucleus = medulla
2. reticular nucleus = pons
3. PAG = midbrain
T/F: There is no humunclus in the ALS.
T -- only in the spinal cord levels (in the brain stem the ALS becomes too small to differentiate)
anterior white commissure is supplied by what artery
anterior spinal artery
diffuse collection of multi-synaptic, multi-functional neurons extending from the caudal medulla through the midbrain, send neurons to frontal + limbic lobe for affective response to pain, some project backwards to control pain
receives collateral branches from 2nd order ALS neurons, sends projections to thalamic nuclei that process nociception, major component of pain inhibitory system, modulates transmission btwn 1st + 2nd order pain neurons in brainstem + spinal cord
periaqueductal grey area
SUMMARY: Ascending Anterolateral System
sensations carried in the spinal trigeminal nucleus
crude touch, pain, itch from face, ear, + oral cavity
OVERVIEW: Trigeminal System
pain modulation by the CNS: examples of top down modulation (descending)? bottom up modulation (ascending)?
why does rubbing a painful area reduce the pain?
gating (post-synaptic inhibition)
large axons (A-alpha & A-beta) from the non-nociceptive mechanoreceptors release NTs (like glycine + enkephalin) to inhibit the 2nd order neuron and prevent it from responding to the nociceptive pain signal from the C fiber
(NOTE: presynaptic inhibition also exists)
why are opioids affected for alleviating pain?
what is deafferation pain?
they activate/participate in descending pain modulation pathways (decrease intensity of painful stimuli)
"phantom limb pain," suggests feedback loop in pain modulation, results from complete or partial interruption of afferent pain inputs
PAG in the descending pain modulatory system is sensitive to what NTs?
where/how are these NT produced?
opioids + serotonin
produced in the PAG + PAG also has receptors for them, produced from exercise or in response to pain or exogenously by drugs
LC produces what pain-modulating NTs?
NE, produced by the LC, strongly anti-nociceptive, suppress transmission of 1st + 2nd order pain neurons in the ALS
nucleus raphe dorsalis vs. nucleus raphe magnus?
dorsalis = part of Ret Nu
magnus = part of RVM
what NTs do the PAG and nucleus raphe dorsalis (reticular formation) produce? where do their axons project?
serotonin + neurotensin
project to the nucleus raphe magnus in the RVM
what is the blood supply to the RVM?
where are the noradrenergic sites of the descending pain modulatory pathway? how do they work?
locus coeruleus, send direct NE projections to the spinal cord, NE is strongly anti-nociceptive, supresses 1st + 2nd order pain neurons of the ALS
T/F: The pain modulatory system is an uncrossed system (no decussation).
what NTs are release at the level of the spinal cord in response to peripheral painful stimuli?
role of enkephalinergic interneurons in the release of these NTs?
substance P and glutamate
enkephalinergic intereneurons: activated by nuc raphe magnus (RVM) + LC, release
, which inhibits release of substance P + glutamate
OVERVIEW: descending pain modulatory pathway
Self Study: DC-ML vs. ALS (image)
Self Study: DC-ML vs. ALS (chart)
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