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Neurophysiology Final > Neurophysiology of Nociception: Sensory Transmission > Flashcards

Neurophysiology of Nociception: Sensory Transmission Flashcards

1
Q

Reminder: What is transmission?

A

the process in which electrochemical energy (in the form of an action potential) is transmitted along afferent fibers to other locations in the nervous system

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2
Q

Where does transmission of nociceptive information occur from?

A
  • Peripheral tissue to the dorsal horn of the spinal cord via dorsal rootlets from body (dorsal horn –> brainstem & thalamus)
  • Peripheral tissue to the brainstem from face (brainstem –> thalamus)
  • Thalamus to the cortex
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3
Q

What two groups do afferent fibers split into before entering the spinal cord?

A
  • A-beta fibers

- A-delt and C fibers

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4
Q

Where do A-beta fibers assume their position before entering the spinal cord?

A

dorsomedial position

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5
Q

Where do A-delta & C fibers assume their position before entering the spinal cord?

A

Ventrolateral position

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6
Q

Where do the A-beta, A-delta & C fibers synapse after splitting?

A

on dorsal horn neurons

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7
Q

What are nociceptive neurons?

A

projection neurons within the spinal cord dorsal horn that participate in CNS nociception

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8
Q

What are the 3 classes that nociceptive neurons are split into?

A
  • Nociceptive-specific
  • Interneurons
  • Wide-dynamic-range (WDR) neurons
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9
Q

Nociceptive-specific neurons

A

receive information only from primary nociceptive afferents and therefore will only respond to stimulation of specific intensity

  • contain small receptive fields
  • 2 groups: those activated by A delta; A delta and C fibers
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10
Q

What are the two fields that Nociceptive-specific neurons are subdivided into?

A
  • those activated by A-delta fibers

- those activated by both A-delta and C fibers

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11
Q

Interneurons

A

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

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12
Q

Wide-dynamic-range (WDR) neurons

A

a.k.a. Non-nociceptive-specific

Receive afferent contacts from A-b, A-d & C fibers and therefore, respond to both innocuous and noxious stimuli

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13
Q

Characteristics of WDR neurons?

A
  • Receive inhibitory contacts from interneurons
  • Receive efferent contacts from descending pathways
  • Utilize glutamate as main NT
  • Have large convergent receptive fields
  • Receive input from viscera, muscles, and jts
  • Can be sensitized via central sensitization mechanisms
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14
Q

Which neurons utilizes glutamate as main NT?

A

WDR neurons

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15
Q

What is the phenomenon that refers to a single WDR neuron receiving multiple contacts (A-b,A-d, C fibers)?

A

convergence

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16
Q

Can the convergence of afferent impulses to the WDR neuron summed together both spatially and temporally?

A

YES

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17
Q

What will high-frequency, repeated nociceptive stimulation will result in?

A

Temporal summation of the nociceptive afferent impulses from C and A-d fibers

  • Perception of 2nd pain is increased
  • “wind-up”
  • Spinal sensitization
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18
Q

Spatial stimulation

A

Stimulation of a large surface area will stimulate an equally large number of nociceptors, thereby increasing the nociceptive afferent impulses
- Larger surface > nociception

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19
Q

Excitation of WDR neurons utilize which r/cs embedded in the plasma membrane in the neuron?

A

AMPA and NMDA

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20
Q

What are the AMPA and NMDA r/cs responsible for?

A

For LTP mechanisms induced by excitatory glutamatergic nociceptive input

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21
Q

What are the necessary events for generation of an AP (WDR neuron)

A
  • Ligand binding to both AMPA and NMDA r/c (ligand = glutamate)
  • Depolarization of postsynaptic WDR neuron’s membrane
  • Removal of Mg+ ion blocking the ion channel of the NMDA r/c
  • Intracellular Ca2+ ion influx into the WDR neuron
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22
Q

How can WDR neurons become sensitized?

A

in instances of high-frequency or prolonged activation

- as in the case of a chronic injury or disease

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23
Q

What can also be a contributory factor for WDR neuron sensitization?

A

Summation

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24
Q

What is the result of a “sensitized” WDR neuron?

A
  • Have a lowered threshold for activation –> increasing excitability –> facilitating transmission of nociceptive information to higher centers of the nervous system
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25
Q

What is it referred to when WDR neuron sensitization facilitates transmission of nociceptive information to higher centers of the nervous system?

A

Central sensitization

- considered to be a form of LTP

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26
Q

What can cause increased excitation of WDR neurons and activate “silent” NMDA receptors (NMDARs) on the WDR neurons?

A

NT’s that bind to the WDR neuron r/c

- glutamate, substance P, calcitonin-gene related peptide (CGRP), and ATP

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27
Q

What does activated NMDARs signal?

A

increase in intracellular Ca2+ and activate a host of calcium-dependent signaling pathways (STPs)
- leads to an increased excitability of the WDR neuron, enhance EPSPs, and facilitate the transmission of nociceptive messages to the brain

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28
Q

What are the 4 main mechanisms of plasticity in WDR neurons which lead to hypersensitivity in pain?

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
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29
Q

4 main mechanisms:

What is increased postsynaptic excitability of the WDR neuron due to?

A

due to phosphorylation of ion channels on the WDR neuron

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30
Q

4 main mechanisms:

What is increased glutamate release per impulse from the presynaptic neuron due to?

A

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

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31
Q

4 main mechanisms:

What is enhanced/sustained EPSP depolarization a result from?

A

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

32
Q

4 main mechanisms:

What are the changes in gene transcription due to?

A

activation of intracellular STPs

33
Q

Lowered excitation threshold of WDR neurons results in?

A

previously sub-threshold stimuli generating AP’s (hyperalgesia)

34
Q

Central sensitization & WDR neurons can result in afferent inputs form non-nociceptive sources being perceived as what?

A

nociceptive impulses (allodynia)

35
Q

What can reduce efficacy of endogenous pain modulatory mechanisms through disinhibition of typically inhibitory interneurons?

A

central sensitization & WDR neurons

36
Q

Enhanced release of ATP can activate local glial cells which release what?

A

cytokines and other irritative molecules

37
Q

What is the proposed mechanism of clinical pain radiation?

A

central sensitization & WDR neurons can result in a dynamic increase in dorsal horn neuron receptive field

38
Q

Primary hyperalgesia

A

develops at the site of tissue injury and is associated with an increased sensitivity of the peripheral nerve fivers involved in nociception

  • local vasodilation, followed by edema, swelling and release of inflammatory mediators
  • peripheral sensitization of nociceptors
39
Q

Secondary hyperalgesia

A

a hypersensitivity that develops in uninjured tissue surrounding the site of injury

  • increased receptive field of WDR neurons
  • Central sensitization of WDR neurons
40
Q

What does secondary hyperalgesia seem to be a result of?

A

an enhanced neural responsiveness of the CNS

41
Q

What does individuals with secondary hyperalgesia exhibit?

A

symptoms similar to those seen in chronic pain patients

42
Q

In many cases non-neurotypical input from nociceptive afferents plays a dynamic and ongoing role in what?

A

the maintenance of nociception, often long after injured tissue has healed

43
Q

Neuropathic pain is often described as

A

chronic intense perceived pain that arises in response to mild or no stimulation

44
Q

What mechanisms typically decline as tissue heals?

A

both peripheral and central sensitization

-threshold of nociception returns to pre-injury level

45
Q

In neuropathic pain both injured and non-injured peripheral nociceptors of the same afferent fiver can increase what?

A

firing rate (esp. in presence of inflammatory mediators)

46
Q

What happens with Increased nociceptor activity that can induce increased sympathetic activity?

A

prolonged nociceptor activity

- sympathetically maintained pain

47
Q

What often follows peripheral sensitization and can be enhanced by sympathetic activity?

A

central sensitization of the dorsal horn neurons

48
Q

WDR neuron:

increased impulse frequency from sensitized nociceptor results in?

A

hyperalgesia (primary)

49
Q

WDR neuron:

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

A

allodynia

50
Q

WDR neuron:

increased receptive field results in?

A

pain region expansion (secondary hyperalgesia / pain radiation)

51
Q

WDR neuron:
Progressive EPSP size increase & impulse frequency with repeated noxious and non-noxious sensory stimulation (temporal & spatial summation) results in?

A

Chronic pain

52
Q

What is the sensory-discriminative component of a pain experience is attributed to?

A

specific neural pathways and CNS targets

53
Q

What is the affective-emotional component of pain attributed to?

A

the targets of a separate ascending somatosensory pathway

54
Q

Physiological nociceptive component is involved in what two pathways?

A

Sensory-discriminative and the affective-emotional component

55
Q

Sensory discriminative component utilizes what tracts?

A 
spinothalamic tract (body)
trigeminal-thalamic (face)
56
Q

Cortical targets of sensory discriminative component of pain?

A

somatosensory areas of the cortex (post-central gyrus, regions of the parietal lobe)

57
Q

Nociceptive neural pathway review: Body

A

primary nociceptive neuron in DRG –> enter spinal cord via dorsal rootlets & synapse on secondary neurons in dorsal horn –> decussate to ascend in the contralateral spinothalamic tract–> synapse on VPL nucleus of thalamus–> primary S-S cortex

58
Q

Nociceptive neural pathway review: Face

A

primary nociceptive neurons in the trigeminal ganglion–> enter pons & descend to synapse on secondary neurons in the spinal trigeminal nucleus (medulla) –> decussate and ascend in the contralateral trigeminal-thalamic tract–> synapse on VPM nucleus of thalamus–> primary S-S cortex

59
Q

The affective-emotional component utilizes

A

spinoreticular tract

60
Q

Affective-emotional component targets include?

A

many regions of the limbic system

- amygdala, insula and periaqueducatal grey (PAG)

61
Q

Spinoreticular tract pathway review

A

primary nociceptive neurons in DRG –> enter spinal cord via dorsal rootlets & synapse on secondary neurons in dorsal horn –> some fibers decussate (some don’t) fibers then ascend in the bilateral spinoreticular tract –> synapse on mediodorsal and intralaminar nuclei of the thalamus and the reticular formation of the midbrain –> limbic system structure; hypothalamus and amygdala & PAG

62
Q

What is the center for the integration of nociceptive information and is responsible for the relay of this information to various regions?

A

Thalamus

63
Q

Nuclei of the thalamus that receive nociceptive input are divided into what two groups?

A

Nuclei of the ventrobasal complex

Nuclei of the mediodorsal and intralaminar complex

64
Q

Nuclei of the ventrobasal complex (VPL,VPM) send projections to?

A
  • the primary and secondary S-S cortex
65
Q

Nuclei of the mediodorsal and intralaminar complex send projections to?

A
  • to structures of the limbic system & frontal lobe
66
Q

What nuclei of the thalamus is associated with the sensory discriminative component of pain perception?

A

Nuclei of the ventrobasal complex (VPL,VPM)

67
Q

What nuclei of the thalamus is associated with affective-emotional component of pain perception?

A

Nuclei of the mediodorsal and intralaminar complex

68
Q

Referred pain can be defined as…

A

the perception of pain at a location remote from its actual origin

69
Q

What is a common form of referred pain?

A

Nociception of visceral origin that is perceived at a somatic location (viscerosomatic pain)

70
Q

How many neurons in the dorsal horn of the spinal cord are specialized solely for the transmission of visceral pain?

A

very few

71
Q

Somatic afferents and visceral afferents synapse on….

A

the same neurons in the spinal cord
- these visceral sensations are transmitted together in the spinal cord to central locations along with cutaneous (somatic) sensations

72
Q

What receives afferent nociceptive projections form visceral and somatic body areas that are innervated by the same spinal cord segment?

A

the same VPL nuclei of the thalamus

73
Q

Can discomfort of internal organs be perceived as cutaneous pain?

A

Yes

74
Q

What can being familiar with typical referral patterns aid in?

A

diagnosis

75
Q

Persistent pain may sensitize that spinal cord on several segments and how is this perceived?

A

as a gradually increase in pain

Neurophysiology Final (10 decks)

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