Neurophysiology of Pain Flashcards

1
Q

Lengthening of the axon

A

6-8% stretch –> blood flow slows
15% stretch –> blood flow stops
20% stretch –> cell death and demyelination

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2
Q

decreased blood flow –>

A

sensitization of PNS

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3
Q

increased blood flow –>

A

desensitization of PNS

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4
Q

Ia Nerve Fiber

A
  • Myelinated: 70-120 m/sec
  • location: muscle
  • ending: muscle spindle
  • sensation: proprioception
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5
Q

Ib Nerve Fiber

A
  • Myelinated: 70-120 m/sec
  • location: tendon
  • Ending: GTO
  • Sensation: Muscle contraction/stretch
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6
Q

A-Beta fibers (II)

A
  • Diameter: 10
  • Myelinated: 25-70 m/sec
  • location: skin, joint, muscle
  • ending: Meissener corpuscle, Merkel cell, pacinian corpuscle, Ruffini ending, hair follicle, Paciniform ending, muscle spindle
  • Sensation: touch, pressure, vibration, position sense, muscle stretch
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7
Q

A-Delta Nociceptor (III)

A
  • Diameter: 2.5 (thick)
  • Myelinated: 2-25 m/sec
  • Ending: Free nerve ending
  • High threshold
  • Small receptive field
  • Thermal: increased temp = more sensitive
  • mechanical: sensitized by thermal (50-55 degrees C)
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8
Q

C fibers - Nociceptors

A
  • Diameter: 1 (thick)
  • unmyelinated
  • endingL free nerve endings
  • high threshold
  • large receptive fields
  • thermal, mechanical, chemical, polymodal
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9
Q

location of nociceptors

A

skin, muscle, joint, tendon, IV disc, bone/periosteum, fascia

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10
Q

How inflammatory chemicals work on C fibers

A

bind to nociceptors –> lower membrane potential –> lower threshold

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11
Q

where is there an increased concentration of ion channels

A

non myelinated areas
- nodes of Ranvier
- DRG
- loss of myelin due to injury/disease

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12
Q

abnormal pulse generating sites

A
  • abnormal concentration of ion channels in axolemma
  • axon develops an ability to generate its own impulses, rather than just conducting one
  • may be explanation for “odd pains” or persistent pain
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13
Q

what’s one of the most sensitive areas in the body

A

DRG

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14
Q

what laminae do sensory fibers terminate on

A

I-IV

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15
Q

What laminae does noxious information from the skin go to?

A

I, II, V

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16
Q

what laminae does tactile information go to

17
Q

what laminae does noxious information form muscle/joints go to?

A

I and deeper dorsal horn

18
Q

Wide Dynamic Range 2nd Order Afferents

A
  • input from A delta, C fibers, and A-beta fibers
  • overlapping receptive fields
  • discriminate intensity and modality
  • most “day to day” information
19
Q

Nociceptive specific 2nd order afferents

A
  • receive input from A delta and C fibers
  • non-overlapping fields
  • localization and modality
  • higher threshold to activate
20
Q

light touch pathways

A

A-Beta stimulated –> releases GABA –> inhibits message from being passed on to 2nd order afferents

21
Q

A delta or C fibers stimulated –>

A

released glutamate –> chemically activates AMPA receptors on 2nd order neuron –> message gets related to brain

22
Q

what do glial cells in the dorsal horn do

A
  • express receptors for many NTs
  • involved in clearance of NTs from synaptic cleft
  • release neuroactive substances known to sensitize neurons (glutamate, NO, pro-inflammatory cytokines)
23
Q

Neospinothalamic tract

A
  • predominately nociceptive neurons
  • projects directly to VPL nucleus
  • VPL receives convergent info from STT and dorsal column
  • VP projects to S1 and S2 cortices
24
Q

What information does the STT give the VPL nucleus

25
what information does the dorsal column give the VPL nucleus
touch sensations
26
what do S1 and S2 somatosensory cortices do
- sensory-descriminative component of pain - location - duration - quality/modality - intensity
27
Paleospinothalamic tract
- predominantly WDR neurons (nociceptive and non-nociceptive, information on intensity, discriminated noxious from non-noxious) - diffuse projections to multiple areas of the thalamus - Reticular formation - pons/medulla - tectum - auditory/visual processing - periaqueductal gray
28
what is PAG involved in
- pain inhibition via medulla - input from hypothalamus, amygdala, and cortex, cingulate gyrus, limbic forebrain structures
29
Bulbospinal modulation
- rostral ventral medulla receives input from STT and PAG - on/off system - goal is to shift salience - gain low = more off cells - gain high = more on cells
30
PAG Effects
- release opioids to stimulate raphe nucleus --> release serotonin to inhibit 1st and 2nd order neurons - release opioids to stimulate reticular formation --> release NE into inhibitory interneurons - PAG-RVM pathway: can modulate activity of on/off cells
31
Hebbian Theory
- Nerves that fire together, wire together - Neurons out of sync fail to link - brain in persistent pain became more efficient at making pain - focused repetition of the pain neuromatrix leads to maladaptive changes
32
Change in ion concentration
- refractory channels become active - increase in channel density - change in type of ion channel (become more sensitive to stress chemicals)
33
Maladaptive plasticity at dorsal horn
- prolonged C fiber stimulus = increased ion channel concentration in DH - RMP of 2nd order decreased = less stimulus to activate - chemical changes lead to interneuron death - increased sensitivity of 2nd order afferents - increased discharge frequency - increased size of receptive fields - decreased endogenous inhibition - proprioceptive deficits
34
maladaptive plasticity in brainstem
- decreased threshold for perception of noxious/non-noxious stimuli - slow stimulus processing - incorrect localization - proprioceptive deficits
35
maladaptive plasticity in PAG-RVM
- Decreased PAG activation - shift from inhibition to maladaptive facilitation
36