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Neurophysiology > Final material > Flashcards

Final material Flashcards

1
Q

How do we define “pain”

A
  • -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
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2
Q

Pain has survival value for all organisms

A
  • -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
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3
Q

Pain vs. Nociception

A

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

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4
Q

Terminology Pain

A
  • -unpleasant sensory & emotional experience resulting from actual or potential tissue injury
  • -Subjective & associated w/ perception of nociceptive event
  • -Influenced by past experiences
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5
Q

Terminology Nociception

A

–Electrochemical activity of nerve r/c & fibers caused by (+) that is potentially dangerous to the organism

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6
Q

Terminology Nociceptor

A

–nerve r/c preferentially sensitive to nociceptive stimulation or (+) that becomes nociceptive if it persists

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7
Q

Terminology Nociceptive

A

–A nociceptive (+) is by definition stimulation of sufficient intensity to activate nociceptors, and even produce a tissue lesion.

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8
Q

Terminology Algia

A

–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).

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9
Q

Terminology Antalgic/analgesic

A

reduction of pain.

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10
Q

Terminology Paresthesia

A

spontaneous or provoked unusual sensation (not painful).

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11
Q

Decreased Sensations (4)

A

1) Hypoesthesia
2) Hypoalgesia
3) Anesthesia
4) Analgesia

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12
Q

Hypoesthesia

A

decrease in sensitivity to non-noxious stimulation

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13
Q

Hypoalgesia

A

decrease in pain in response to a typically noxious stimulus

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14
Q

Anesthesia

A

loss of sensation

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15
Q

Analgesia

A

absence of pain following a typically noxious stimulus

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16
Q

Increased Sensations (3)

A

1) Hyperesthesia
2) Hyperalgesia
3) Allodynia

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17
Q

Hyperesthesia

A

increase in sensitivity to non-noxious stimulation

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18
Q

Hyperalgesia

A

exaggerated response to typically noxious stimulation, refers to an unusually low nociceptive threshold

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19
Q

Allodynia

A

pain produced by typically non-noxious stimuli

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20
Q

Pain: General Features

A

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

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21
Q

Nociception: General Features

A
  • -highly conserved
  • -homologous across all mammalian species
  • -engages multiple physiological & neural systems
    1) Neural networks
    2) Neurohumoral systems
    3) Neuroimmune systems
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22
Q

Paradoxical Qualities of Pain

A

pain = minimization of tissue damage
BUT…
chronic pain = decrease quality of life

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23
Q

The Paradox of Pain (3)

A
  1. Adaptiveness
    - -experience of pain = warning sign, however; it appears to be negative in all respects
  2. Lack of clear cortical representation
    - -painful (+) = activate cortex
  3. Presence of descending pain control mechanisms
    - -cognitive & emotional can suppress pain
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24
Q

Goals of the Circular Pain Model

A

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

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25
Q

2 basic principles governing the clinical measurement of pain

A

1) patient only can eval their pain

2) eval impact on person as a whole

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26
Q

quantifiable components of pain experience include:

A

1) pain intensity
2) physical capacity
3) spatial attributes
4) pain quality
5) psychological componet

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27
Q

pain intensity

A

how strong // intense

  • -Wong-Baker FACES scale
  • -visual analog scale (VAS)
  • -oral pain scale (OPS)
  • -LOCQSMAT (S)
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28
Q

physical capacity

A

does the pain prevent you from performing activities

–LOCQSMAT (S)

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29
Q

spatial attributes

A

where is the pain

  • -pain drawing
  • -LOCQSMAT (L)
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30
Q

pain quality

A

describe your pain in your own words

–LOCQSMAT (Q)

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31
Q

psychological component

A

affective response “how is the pain affecting your mood/ emotional well-being)
–beck depression inventory

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32
Q

4 distinct neurophysical events of nociception include:

A

1) transduction
2) transmission
3) modulation
4) perception

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33
Q

transduction

A

converting noxious stimuli into electrochemical inpulses

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34
Q

transmission

A

electrochemical impulses along afferent fibers to various nervous system regions

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35
Q

modulation

A

altering the perception of noxious stimuli by peripheral or central mechanisms

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36
Q

perception

A

conscious experience of pain

interpretation of nociceptive info by a higher center of CNS

37
Q

nociceptor properties

A
  • -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
38
Q

myelinated Ad fibers (20%)

A
  • -large
  • -faster (~20m/s)
  • -bimodal (mechanical & thermal)
  • -small receptive field
  • -projection to lamina 1
39
Q

unmyelinated C fibers (80%)

A
  • -small
  • -slower (2m/s)
  • -polymodal (mechanical & thermal & CHEMICAL)
  • -large receptive field
  • -project to lamina 2 & 3
40
Q

first & second pain

A

1st pain = sharp & transient pain (Ad fibers)

2nd pain = delayed & diffuse & long lasting (C fibers)

41
Q

inflammation can enhance the perception of pain via… (2)

A

1) modifying the degree of nociceptor activation
- -increase in transmission & enhanced perception
2) sensitization of nociceptors (peripheral sensitization)
- -increased responsiveness (lowered threshold)

42
Q

peripheral sensitization

A
  • -increased expression of Na+ ion channels
  • -receptor upregulation
  • -repeated application
  • -inflammatory mediators
43
Q

(origin & action) K+ ions & histamine

A 
origin = escape from damaged cells
actions = active polymodal nociceptors
44
Q

(origin & action) prostaglandins

A 
origin = synthesized by enzymes released from substrates created by tissue damage
actions = sensitize nociceptors
45
Q

(origin & action) bradykinin, 5HT & ATP

A 
origin = arrive following plasma effusion or lymphocyte migration
actions = activate & sensitize nociceptors
46
Q

(origin & action) substance P, calcitonin gene-related peptide (CGRP)

A 
origin = secreted by nociceptor activity
actions = contribute to inflammatory response by initiating release of other substances
47
Q

transmission of nociceptive information occurs from:

A
  • -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
48
Q

entry of afferent fibers into the CNS

A
  • -fibers split into 2 groups before spinal cord (Ab & Ad/C)
  • -synapse on dorsal horn neurons
49
Q

nociceptive neurons

A 
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
50
Q

nociceptive-specific neurons

A

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
51
Q

interneurons

A

mainly inhibitory, release GABA, and can be recruited by afferent fibers or by descending mechanisms

52
Q

wide-dynamic-range (WDR) neurons

AKA- non-specific

A

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
53
Q

WDR neurons : convergence

A
  • -nociceptors via Ad & C fibers
  • -non-nociceptive sensory r/c viz Ab fibers
  • *can be summed together both temporally and spatially
54
Q

temporal summation

A

high-frequency, repeated nociceptive (+) from Ad & C

  • -perception of 2nd pain is increased
  • -“wind-up”
  • -spinal sensitization
55
Q

spatial summation

A

(+) of large surface area will (+) an equally large # of nociceptors, thereby increasing nociceptive afferent impulses

56
Q

necessary events for generation of an action potential (AP)

A

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

57
Q

central sensitization

A

“sensitized” WDR neurons = lower threshold for activation = facilitating transmission of nociceptive info of higher center of nervous system = long term potentiation

58
Q

mechanisms LTP leading to central sensitization in WDR neurons (4)

A

1) increased postsynaptic excitability
2) increased glutamate release per impulse from the presynaptic neuron
3) enhanced/sustained EPSP depolarization
4) changes in gene transcription

59
Q

increased postsynaptic excitability =

A

lowered threshold for activation

–due to phosphorylation of ion channels on WDR neurons

60
Q

increased glutamate release per impulse from the presynaptic neuron

A

following the release of the retrograde messenger nitric oxide (NO)

61
Q

enhanced//sustained EPSP depolarization

A

resulting from an increase (up regulation) of AMPA receptors on the WDR neuron

62
Q

changes in gene transcription

A

due to activation of intracellular STPs

63
Q

central sensitization & WDR neurons

A
  • -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)
64
Q

primary hyperalgesia

A

develops at site of tissue injury

  • *vasodilate –> edema –> swelling –> inflam
  • *peripheral sensitization
65
Q

secondary hyperalgesia

A

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
66
Q

(WDR neuron changes)

Increased impulse frequency from sensitized nociceptors =

A

hyperalgesia (primary)

67
Q

(WDR neuron changes)

lowered activation threshold & increased impulse frequency to innocuous (non-noxious) stimuli

A

allodynia

68
Q

(WDR neuron changes)

increase in WDR neuron receptive field

A

pain region expansion

secondary hyperalgesia/ pain radiation

69
Q

(WDR neuron changes)
progressive EPSP size increase & impulse frequency with repeated noxious and non-noxious sensory stimulation
(temoral & spatial summation)

A

chronic pain

70
Q

central pathways of pain perception

A

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

71
Q

sensory discriminative component

what.where.when.how strong

A
  • lateral spinothalamic tract (body)
  • trigeminal-thalamic tract (face)

—cortical targets = somatosensory areas
(post-central gyrus, regions of parietal lobe)

72
Q

nociceptive neural pathways review

BODY

A

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

73
Q

nociceptive neural pathways review

FACE

A

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

74
Q

affective-emotional component

A
  • -utilizes spinoreticular tract

- -tragets = limbic system, amygdala, insula & periaqueductal grey

75
Q

spinoreticular tract

A
  • -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
76
Q

receive nociceptive input from two groups…

A

1) VPL & VPM (ventrobasal complex)

2) mediodorsal & intralaminar complex

77
Q

VPL & VPM (ventrobasal complex)

A
  • -1’ & 2’ somatosensory cortex

- -sensory -discriminative component of pain

78
Q

mediodorsal & intralaminar complex

A
  • -send projections to structures of limbic system & frontal lobe
  • -affective-emotional component of pain
79
Q

referred pain

A

perception of pain remote from its actual origin

–viscerosomatic pain = common form

80
Q

both discomfort & internal organ pain can be perceived as cutaneous pain because….

A

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

81
Q

modulation

A

adjustments made by either “bottom up” or “top down”

82
Q

endogenous mechanisms of pain modulation

A
83
Q

bottom up pain gating

A

transitory pain suppression via non-noxious peripheral sensory stimulation
–effects last only as long as non-nociceptive stimulation

84
Q

gate control theory

A

Melzack & Wall 1960

-spinal cord contained a neurological pain “gate” which could be “shut” in order to prevent nociception

85
Q

bottom up pain & gate control theory

A
  • -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

86
Q

“top down” pain gating

A

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
87
Q

the descending analgesic system involves…

A
  • -somatosensory cortex
  • -hypothalamus
  • -thalamus
  • -amydala
  • -periaqueductal grey
  • -several brainstem nuclei: locus coeruleus (NE/NA), raphe nuclei (5-HT), ventral tegmental area (VTA, DA)
88
Q

perception

A

final output of nociceptive (+) being transmitted thru p/way of nervous system & interpretation of higher cortical regions

89
Q

pain-related behaviours

A
  • -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)

Neurophysiology (3 decks)

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