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65 Cards in this Set

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Gating Theory of Pain
the amt of stimulation of the receptor is NOT equivalent to the amount of pain perceived

anterolateral pathway

damage to SC
vib, prob, 2pt descrimination


loss of pain 1-2seg below the level of the lesion
Free nerve endings have cell bodies

depolarize and send AP
in the DRG, and projections into the CNS
3 Types of Nociceptors
1. Thermal- respond to extremes
-Alpha/Delta fibers- light myel
2. Mechanical Rec- intense press
-Alpha/Delta fibers
3. Polymodal- variety, long lasting pain.
-unmyelinated C fibers
tissue damage results in
1. vasodialation
2. abundance of chem rush in
-stimulate free nerve endings
3. cell ruptures
4. high K- depolarization
released chemicals cause a

tissue damage activates
Feed Forward Reaction

C-Fibers, AP travels to Dorsal Horn
what is released into dorsal Horn?

what is the result of histamine?
Substance P, CGRP->mast cells-->histamine

sensitizes free nerve endings
-pain rec become more sensitive
Secondary Pain response
1. Arachadonic acid-sens nociceptors
2. Bradykinin- acts directly on alpha/delta and C fibers
3. Histamine- sensitizes fibers
Pain fibers primarily enter through what layers of lissaur's tract?
layers 1 and 2 (substantia gelatinosa)
which fibers terminate in..

Layer 1
Layer 2
Layer 5
alpha/delta (marginal layer)
C Fibers
alpha/delta, alpha/beta, and C
Speed of Conductance..

Alpha/beta fibers
C fibers
Alpha/beta, alpha/delta, then C fibers

conduct fastest, sharp pain
relatively fast, sharp pain
slow(1-2m/s), dull pain
prolonged secondary pain is due to what?
1. latency in conduction of C fibers
2. release of chemicals that prolong the effect
C fibers release
1. Glutamate- for fast synaptic transmission
2. Substance P
-secondarily, need repetitive APs
Substance P actions in the Periphery...
1. histamine from mast cells
2. in dorsal horn, sensitizes post-syn AMPA rec to Glu
-amplify glu signaling
Thermoreceptors respond to temps

Thermal Nociceptors resond
not extreme, 20-40 deg C

extreme: x<5 or x>40 deg C
what does a pinprick activate?
2-pt discrimination
mechanonociceptors if extreme
-if press in a small area
when does a bigger response to a given stimuli happen?
after the initial reaction

because of sensitization
sensitization causes?
a decrease in pain thresholds
rel of chem alters the activity of the receptors

Surface area affected by pain inc in secondary reaction

sensitization of pain receptors that dec pain threshold

non-noxious stimulus now becomes noxious
-ie sunburn painful to breath
Persistent Injury causes
1. C fibers continuously rel Glu
2. activation of NMDA rec
3. synaptic plasticity into system
what does synaptic plasticity do?
keeps the signaling b/w the C-fibers and doral horn cells potentiated
Anterolateral (STT) contains 2 types of fibers that originate in the spine
1. Spinoreticular- goes to medulla/pons
2. Spinomesenscephalic- goes to med brain and terminates in Periaqueductal Grey matter
Spinomesencephalic terminates

what is this impt in
in periaqueductal grey matter

1. pain modulation
2. connections to limbic system
STT crosses
goes to VPL, then to somatosensory cortex

TTT goes to VPM
Primary Somatosensory Cortex

Insular Cortex

Ant Cingulate Cotrex
deals w/ location and intensity of pain
autonomic cmpt of pain

limbic assoc- emotional component of pain
pain is what type of phenomena

intensity signal by what
graded phenomena

frequency of AP
which receptors have the highest threshold?
C fiber contacts

A/B fiber contacts
projection neuron to AntLat sys

dorsal column, contacts some inhibitory interneurons
Summation results in
Less chance of projection neurons firing APs

1. inhib input from the A/B interneuron
2. excitatory input from C fiber
stimulating periaqueductal grey matter results in
reduced sensation of pain

1. causes stim of dorsal raphe nuc-->serotonin down dorsal horn
2. activates locus ceruleus->rel norepi to dorsal horn
how do descending projections regulate pain?
release opiods
mostly enkephalins

descending control prevents the signal from coming up the projection neuron
enkaphalins work by
presyn inhibition of voltage gated Ca channels to prevent NT rel
Referred pain
via non-somatic pain receptors in viscera
can become sensitized

refer to specific dermatome
what does visceral pain refer to dermatome?
visc and somatic pain fibers synapse on same projection neurons
acute pain

Chronic pain
not a treatment problem. usually resolves. tradit meds work well
greater clinical problem. "Pain that persists longer than it should"
-often w/o spec etiology
chronic pain
1. nociceptive- tissue damage
2. neuropathic- damage to nervous system proper
Nociceptive pain
1. tissue damage
2. responds to analgesics
3. activated C and A/delta fibers
4. definable pathology
symptoms of nociceptive pain
1. redness-rubor
2. swelling-tumor
3. temperature-calor
4. pain-dolor
effects of nociceptive pain
1. rel catecholamines (inc HR/BP)
2. altered respiration
3. sweating
4. inc cortisol
5. psychological distress
Neuropathic pain
Injury of nervous system proper
responds to ADJUVANT analgesics

can be from injury anywhere along the pain pathway
Neuropathic pain presentations
1. immed or delayed
2. bizzare- very emotional
3. way out of proportion to pathology
4. NONE of the traditional symptoms of redness/swelling
Effects of neuropathic pain
1. maybe inc catecholamines
2. mabye dec cortisol
3. psychological effects are reliable
Descriptions of Neuropathic pain
1. buring
2. paresthesia(pins/needles)
3. paroxysmal (sudden attacks)
4. lancinating
5. electrical, raw, shooting, deep, dull, ache
Cardinal Signs of Neuropathic pain
1. Allodynia- pain from a normally non-painful stimulus
2. Hyperalgesia- exaggerated pain response
clinical manifestations of neuropathic pain
1. autonomic dysfxn
2. vasoconstricion
3. trophic changes to bony structure
4. local motor impairment
5. other neural impairment
Types of Neuropathic pain(5)
1. Compressive- slipped disc, nerve compression
2. Inflammatory- neuritis
3. De-afferentation- complete TRANSECTION of nerve
4. Central injury- to cns
5. sympathetic NS
most neuropathic pain goes in what?
cycles- peaks and valleys

cycles thruout the day
common findings in neuropathic pain
1. lack of nociceptive findings
2. no evidence of disease
3. spontaneous pain
4. hyperalgesia
5. profound psych response
6. ANS abnormalities
possible reasons for neuropathic pain
1. altered phenotype
2. sprouting
3. misconnection
4. inc excitability
*Best answer is 'we dont know'
Treatent continuum
does not relatet to efficacy

most effective drugs NOT used first
-start w/ noninvasive, non-toxic first
treat nociceptive pain w/
traditional analgesics, opiods, nsaids, cox2 inhib, corticosteroids
synthetic opiates
tag the same receptor
-mu opiod receptor
optimal way to deliver morphine
into the CNS
more effective, less is needed
neuropathic pain meds
modulate CNS funciton. goal is to make peaks lower and farter apart. ADJUVANT ANESTHETICS

antidepressants, anticonvulsants, antiarrhythmics, antispastics (a-2 agonists)
side effects of neuropathic meds
orthostatic hypotension
renal/liver toxicity
arachadonic acid sensitizes what in the secondary pain response?
Bradykinin acts directly on what in the secondary pain response
1. Alpha/gamma
2. C-fibers
3. and other cells to release more compounds
major players in the secondary pain response
substance p
what releases substance P?

what does it do?
nociceptor terminals rel subP

stimulates mast cells to rel histamine, leads to vasodialation and extravasation
what releases Bradykinin?
damaged cells
some fibers in the spinomesencephalic tract travel in the?
dorsal horn
what happens to the surface area affected by pain?
continuous stimulation of C fibers leads to what change in receptors?
1. contin rel of Glu
2. inc NMDA receptors
3. introduces synaptic plasticity
what does the inc in NMDA receptors do?
1. induces synaptic plasticity
2. keeps the signal b/w C fibers and dorsal horn potentiated
medial thalmus projects to what?
1. insular cortex- ANS cmpt of pain
2. Ant Cigulate cortex- emotional cmpt of pain
3. somatosentory cortex- intensity and localization of pain