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

A

III, IV

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

A

pain/temp

25
Q

what information does the dorsal column give the VPL nucleus

A

touch sensations

26
Q

what do S1 and S2 somatosensory cortices do

A
  • sensory-descriminative component of pain
  • location
  • duration
  • quality/modality
  • intensity
27
Q

Paleospinothalamic tract

A
  • 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
Q

what is PAG involved in

A
  • pain inhibition via medulla
  • input from hypothalamus, amygdala, and cortex, cingulate gyrus, limbic forebrain structures
29
Q

Bulbospinal modulation

A
  • 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
Q

PAG Effects

A
  • 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
Q

Hebbian Theory

A
  • 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
Q

Change in ion concentration

A
  • refractory channels become active
  • increase in channel density
  • change in type of ion channel (become more sensitive to stress chemicals)
33
Q

Maladaptive plasticity at dorsal horn

A
  • 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
Q

maladaptive plasticity in brainstem

A
  • decreased threshold for perception of noxious/non-noxious stimuli
  • slow stimulus processing
  • incorrect localization
  • proprioceptive deficits
35
Q

maladaptive plasticity in PAG-RVM

A
  • Decreased PAG activation
  • shift from inhibition to maladaptive facilitation
36
Q
A