Neurophysiology of Pain Flashcards
Lengthening of the axon
6-8% stretch –> blood flow slows
15% stretch –> blood flow stops
20% stretch –> cell death and demyelination
decreased blood flow –>
sensitization of PNS
increased blood flow –>
desensitization of PNS
Ia Nerve Fiber
- Myelinated: 70-120 m/sec
- location: muscle
- ending: muscle spindle
- sensation: proprioception
Ib Nerve Fiber
- Myelinated: 70-120 m/sec
- location: tendon
- Ending: GTO
- Sensation: Muscle contraction/stretch
A-Beta fibers (II)
- 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
A-Delta Nociceptor (III)
- 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)
C fibers - Nociceptors
- Diameter: 1 (thick)
- unmyelinated
- endingL free nerve endings
- high threshold
- large receptive fields
- thermal, mechanical, chemical, polymodal
location of nociceptors
skin, muscle, joint, tendon, IV disc, bone/periosteum, fascia
How inflammatory chemicals work on C fibers
bind to nociceptors –> lower membrane potential –> lower threshold
where is there an increased concentration of ion channels
non myelinated areas
- nodes of Ranvier
- DRG
- loss of myelin due to injury/disease
abnormal pulse generating sites
- 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
what’s one of the most sensitive areas in the body
DRG
what laminae do sensory fibers terminate on
I-IV
What laminae does noxious information from the skin go to?
I, II, V
what laminae does tactile information go to
III, IV
what laminae does noxious information form muscle/joints go to?
I and deeper dorsal horn
Wide Dynamic Range 2nd Order Afferents
- input from A delta, C fibers, and A-beta fibers
- overlapping receptive fields
- discriminate intensity and modality
- most “day to day” information
Nociceptive specific 2nd order afferents
- receive input from A delta and C fibers
- non-overlapping fields
- localization and modality
- higher threshold to activate
light touch pathways
A-Beta stimulated –> releases GABA –> inhibits message from being passed on to 2nd order afferents
A delta or C fibers stimulated –>
released glutamate –> chemically activates AMPA receptors on 2nd order neuron –> message gets related to brain
what do glial cells in the dorsal horn do
- 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)
Neospinothalamic tract
- predominately nociceptive neurons
- projects directly to VPL nucleus
- VPL receives convergent info from STT and dorsal column
- VP projects to S1 and S2 cortices
What information does the STT give the VPL nucleus
pain/temp
what information does the dorsal column give the VPL nucleus
touch sensations
what do S1 and S2 somatosensory cortices do
- sensory-descriminative component of pain
- location
- duration
- quality/modality
- intensity
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
what is PAG involved in
- pain inhibition via medulla
- input from hypothalamus, amygdala, and cortex, cingulate gyrus, limbic forebrain structures
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
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
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
Change in ion concentration
- refractory channels become active
- increase in channel density
- change in type of ion channel (become more sensitive to stress chemicals)
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
maladaptive plasticity in brainstem
- decreased threshold for perception of noxious/non-noxious stimuli
- slow stimulus processing
- incorrect localization
- proprioceptive deficits
maladaptive plasticity in PAG-RVM
- Decreased PAG activation
- shift from inhibition to maladaptive facilitation
