Final material Flashcards
How do we define “pain”
- -unpleasant sensory & emotional experience ~potential tissue damage
- -Pain = subjective
- -Each individual learns the meaning of the word “pain” through experiences related to injury in early life
Pain has survival value for all organisms
- -biologists see those stimuli or illnesses that cause pain are likely to damage tissue.
- -Pain = associate w/ actual/potential tissue damage
- -Pain = unpleasant = emotional experience
Pain vs. Nociception
Pain = conscious experience
–brain activity due to noxious (+) & uses sensory, emotional and cognitive processes
Nociception = information about a noxious stimulus is conveyed to the brain
–Total sum of neural activity that occurs prior to the cognitive processes that enable humans to ID pain
**Nociception is not sufficient alone for the experience of pain
Terminology Pain
- -unpleasant sensory & emotional experience resulting from actual or potential tissue injury
- -Subjective & associated w/ perception of nociceptive event
- -Influenced by past experiences
Terminology Nociception
–Electrochemical activity of nerve r/c & fibers caused by (+) that is potentially dangerous to the organism
Terminology Nociceptor
–nerve r/c preferentially sensitive to nociceptive stimulation or (+) that becomes nociceptive if it persists
Terminology Nociceptive
–A nociceptive (+) is by definition stimulation of sufficient intensity to activate nociceptors, and even produce a tissue lesion.
Terminology Algia
–Localized pain w/o presuming its cause (i.e.“lumbalgia”).
o Often used as an affix to indicate an increase or decrease in pain (hyperalgesia or hypoalgesia).
Terminology Antalgic/analgesic
reduction of pain.
Terminology Paresthesia
spontaneous or provoked unusual sensation (not painful).
Decreased Sensations (4)
1) Hypoesthesia
2) Hypoalgesia
3) Anesthesia
4) Analgesia
Hypoesthesia
decrease in sensitivity to non-noxious stimulation
Hypoalgesia
decrease in pain in response to a typically noxious stimulus
Anesthesia
loss of sensation
Analgesia
absence of pain following a typically noxious stimulus
Increased Sensations (3)
1) Hyperesthesia
2) Hyperalgesia
3) Allodynia
Hyperesthesia
increase in sensitivity to non-noxious stimulation
Hyperalgesia
exaggerated response to typically noxious stimulation, refers to an unusually low nociceptive threshold
Allodynia
pain produced by typically non-noxious stimuli
Pain: General Features
1) Pain is universal & context-dependent
2) Pain is context-dependent
o Ex: young man undergoing painful tribal rituals
o Ex: pain associated with a clinical pathology
3) Pain is clinically significant
o Part serious illness
o 2nd most common reason to seek medical attention
-#1 reason for chiropractic care
Nociception: General Features
- -highly conserved
- -homologous across all mammalian species
- -engages multiple physiological & neural systems
1) Neural networks
2) Neurohumoral systems
3) Neuroimmune systems
Paradoxical Qualities of Pain
pain = minimization of tissue damage
BUT…
chronic pain = decrease quality of life
The Paradox of Pain (3)
- Adaptiveness
- -experience of pain = warning sign, however; it appears to be negative in all respects - Lack of clear cortical representation
- -painful (+) = activate cortex - Presence of descending pain control mechanisms
- -cognitive & emotional can suppress pain
Goals of the Circular Pain Model
1) Explain multidimensional nature of pain experience
2) Emphasize complexity & interdependence of components
3) Provide model of pain that helps comprehend diff components of pain
o = appropriate treatment of all aspects of pain
2 basic principles governing the clinical measurement of pain
1) patient only can eval their pain
2) eval impact on person as a whole
quantifiable components of pain experience include:
1) pain intensity
2) physical capacity
3) spatial attributes
4) pain quality
5) psychological componet
pain intensity
how strong // intense
- -Wong-Baker FACES scale
- -visual analog scale (VAS)
- -oral pain scale (OPS)
- -LOCQSMAT (S)
physical capacity
does the pain prevent you from performing activities
–LOCQSMAT (S)
spatial attributes
where is the pain
- -pain drawing
- -LOCQSMAT (L)
pain quality
describe your pain in your own words
–LOCQSMAT (Q)
psychological component
affective response “how is the pain affecting your mood/ emotional well-being)
–beck depression inventory
4 distinct neurophysical events of nociception include:
1) transduction
2) transmission
3) modulation
4) perception
transduction
converting noxious stimuli into electrochemical inpulses
transmission
electrochemical impulses along afferent fibers to various nervous system regions
modulation
altering the perception of noxious stimuli by peripheral or central mechanisms
perception
conscious experience of pain
interpretation of nociceptive info by a higher center of CNS
nociceptor properties
- -free nerve endings of specialized afferent fibers
- -respond to intense noxious stimuli
- -primary cell bodies from the body = dorsal root ganglia (DRG)
- -primary cell bodies from the face = trigeminal ganglia
- -all nociceptive neurons utilize glutamate & substance P
- -peripheral nociceptors = myelinated Ad & unmyelinated C
myelinated Ad fibers (20%)
- -large
- -faster (~20m/s)
- -bimodal (mechanical & thermal)
- -small receptive field
- -projection to lamina 1
unmyelinated C fibers (80%)
- -small
- -slower (2m/s)
- -polymodal (mechanical & thermal & CHEMICAL)
- -large receptive field
- -project to lamina 2 & 3
first & second pain
1st pain = sharp & transient pain (Ad fibers)
2nd pain = delayed & diffuse & long lasting (C fibers)
inflammation can enhance the perception of pain via… (2)
1) modifying the degree of nociceptor activation
- -increase in transmission & enhanced perception
2) sensitization of nociceptors (peripheral sensitization)
- -increased responsiveness (lowered threshold)
peripheral sensitization
- -increased expression of Na+ ion channels
- -receptor upregulation
- -repeated application
- -inflammatory mediators
(origin & action) K+ ions & histamine
origin = escape from damaged cells actions = active polymodal nociceptors
(origin & action) prostaglandins
origin = synthesized by enzymes released from substrates created by tissue damage actions = sensitize nociceptors
(origin & action) bradykinin, 5HT & ATP
origin = arrive following plasma effusion or lymphocyte migration actions = activate & sensitize nociceptors
(origin & action) substance P, calcitonin gene-related peptide (CGRP)
origin = secreted by nociceptor activity actions = contribute to inflammatory response by initiating release of other substances
transmission of nociceptive information occurs from:
- -peripheral tissue to the horsal horn of the spinal cord via dorsal rootlets
- noxious info from body
- dorsal horn –> spinal cord –> thalamus
- -peripheral tissue to brainstem
- noxious info from face
- brainstem to thalamus
- -thalamus to cortex
entry of afferent fibers into the CNS
- -fibers split into 2 groups before spinal cord (Ab & Ad/C)
- -synapse on dorsal horn neurons
nociceptive neurons
projection neurons w.in spinal cord dorsal horn that participate in nociceptive in the CNS. 3 classes.... 1) nociceptive-specific 2) interneurons 3) wide-dynamic-range (WDR) neurons
nociceptive-specific neurons
receive info ONLY from primary nociceptive afferents and therefore ONLY respond to stimulation of specific intensity
- -2 groups = Ad and some activated by Ad & C fibers
- -contain small receptive fields
interneurons
mainly inhibitory, release GABA, and can be recruited by afferent fibers or by descending mechanisms
wide-dynamic-range (WDR) neurons
AKA- non-specific
receive afferents from Ab, Ad, C fibers therefore = respond to both innocuous & noxious stimuli
- -receive inhibitory contacts from interneurons
- -receive efferent contacts from descending p/way
- -utilize glutamate as main NT
- -large receptive fields
- -receive input from viscera, muscles, joints
- -can be sensitized via central sensitization mechanisms
WDR neurons : convergence
- -nociceptors via Ad & C fibers
- -non-nociceptive sensory r/c viz Ab fibers
- *can be summed together both temporally and spatially
temporal summation
high-frequency, repeated nociceptive (+) from Ad & C
- -perception of 2nd pain is increased
- -“wind-up”
- -spinal sensitization
spatial summation
(+) of large surface area will (+) an equally large # of nociceptors, thereby increasing nociceptive afferent impulses
necessary events for generation of an action potential (AP)
1) ligand binding to both AMPA & NMDA r/c (ligand=glutamate)
2) depolarization of postsynaptic WDR neuron’s membrane
3) removal of Mg+ ion blocking the ion channel of the NMDA r/c
4) intracellular Ca2+ ion influx into the WDR neuron
central sensitization
“sensitized” WDR neurons = lower threshold for activation = facilitating transmission of nociceptive info of higher center of nervous system = long term potentiation
mechanisms LTP leading to central sensitization in WDR neurons (4)
1) increased postsynaptic excitability
2) increased glutamate release per impulse from the presynaptic neuron
3) enhanced/sustained EPSP depolarization
4) changes in gene transcription
increased postsynaptic excitability =
lowered threshold for activation
–due to phosphorylation of ion channels on WDR neurons
increased glutamate release per impulse from the presynaptic neuron
following the release of the retrograde messenger nitric oxide (NO)
enhanced//sustained EPSP depolarization
resulting from an increase (up regulation) of AMPA receptors on the WDR neuron
changes in gene transcription
due to activation of intracellular STPs
central sensitization & WDR neurons
- -lowered threshold = previously sub-threshold (+) = APs (hyperalgesia)
- -non-nociceptive sources = perceived as nociceptive (allodynia)
- -reduce endogenous pain mod via disinhib interneurons
- -more ATP = more glial cell release cytokines
- -dynamic increase in dorsal horn neuron receptive field (~pain radiation)
primary hyperalgesia
develops at site of tissue injury
- *vasodilate –> edema –> swelling –> inflam
- *peripheral sensitization
secondary hyperalgesia
hypersensitivity that develops uninjured tissue surrounding site of injury
- -result of enhanced neural responsiveness of CNS
- -similar to chronic pain
- *more WDR neurons
- *central sensitization
(WDR neuron changes)
Increased impulse frequency from sensitized nociceptors =
hyperalgesia (primary)
(WDR neuron changes)
lowered activation threshold & increased impulse frequency to innocuous (non-noxious) stimuli
allodynia
(WDR neuron changes)
increase in WDR neuron receptive field
pain region expansion
secondary hyperalgesia/ pain radiation
(WDR neuron changes)
progressive EPSP size increase & impulse frequency with repeated noxious and non-noxious sensory stimulation
(temoral & spatial summation)
chronic pain
central pathways of pain perception
1) sensory-discriminative component
- -neural pathways & CNS targets
2) affective-emotional component
- -targets of a separate ascending somatosensory p.way
3) nociceptive component
- -involved in both other p.ways
sensory discriminative component
what.where.when.how strong
- lateral spinothalamic tract (body)
- trigeminal-thalamic tract (face)
—cortical targets = somatosensory areas
(post-central gyrus, regions of parietal lobe)
nociceptive neural pathways review
BODY
1’ neuron = DRG –>
spinal cord via rootlets –>
2’ @ dorsal horn –>
decussate & ascend up spinothalamic tract–>
ventral post lateral (VPL) nucleus of thalamus –>
1’ somatosensory cortex
nociceptive neural pathways review
FACE
1’ neuron = trigeminal ganglion –>
pons & descend to synaps on 2’ neuron –>
2’ neuron = spinal 5th nucleus (medulla) –>
decussate & ascend in 5th-thalamic tract –>
ventral post medial (VPM) of thalamus –>
1’ S-S cortex
affective-emotional component
- -utilizes spinoreticular tract
- -tragets = limbic system, amygdala, insula & periaqueductal grey
spinoreticular tract
- -1’ neuron = DRG –>
- -spinal cord via dorsal rootlets–>
- -2’ neuron = dorsal horn –>
- -SOME decussate ascend in bilateral spinoreticular tract ->
- -mediodorsal & intralaminar nuclei of thalamus AND reticular formation of the midbrain
- -limbic sustem = hypothalamus & amygdala & periaqueductal grey
receive nociceptive input from two groups…
1) VPL & VPM (ventrobasal complex)
2) mediodorsal & intralaminar complex
VPL & VPM (ventrobasal complex)
- -1’ & 2’ somatosensory cortex
- -sensory -discriminative component of pain
mediodorsal & intralaminar complex
- -send projections to structures of limbic system & frontal lobe
- -affective-emotional component of pain
referred pain
perception of pain remote from its actual origin
–viscerosomatic pain = common form
both discomfort & internal organ pain can be perceived as cutaneous pain because….
both have same ventral posterior lateral (VPL) nuclei of the thalamus receive afferent nociceptive projections from visceral & somatic body areas that are innervated by the same spinal cord segment
modulation
adjustments made by either “bottom up” or “top down”
endogenous mechanisms of pain modulation
bottom up pain gating
transitory pain suppression via non-noxious peripheral sensory stimulation
–effects last only as long as non-nociceptive stimulation
gate control theory
Melzack & Wall 1960
-spinal cord contained a neurological pain “gate” which could be “shut” in order to prevent nociception
bottom up pain & gate control theory
- -non-noxious (+) = activate peripheral mechanoreceptors
- -collaterals of these large non-noxious sensory fibers can facilitate inhibitory GABA-ergic interneurons which synapse on & inhabit WDR’s
–input from non-noxious (+) can override painful input which results in prevention of the nociceptive signal traveling to the CNS
“top down” pain gating
involves the exertion of conscious & unconscious cognitive control over the perception of pain and involves several mech….
- learned expectations w. implicit/explicit memory
- emotional priming effects
- conditioned emotional responses
- placebo eggects
- shifts in attention
- mirror therapy for phantom pain
the descending analgesic system involves…
- -somatosensory cortex
- -hypothalamus
- -thalamus
- -amydala
- -periaqueductal grey
- -several brainstem nuclei: locus coeruleus (NE/NA), raphe nuclei (5-HT), ventral tegmental area (VTA, DA)
perception
final output of nociceptive (+) being transmitted thru p/way of nervous system & interpretation of higher cortical regions
pain-related behaviours
- -protextive withdrawal relfexed (flexor reflex)
- -grimacing, shouting, crying, fainting
- -others may not be specific to occupation but can reflect perception of pain
- -response of ANS (diaphoresis, increased muscle tone, increased respiration rate, increased heart rate, pupil dilation)
