• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/77

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

77 Cards in this Set

  • Front
  • Back
pain relevant loci
1)periphery(skin,viscera,joints,muscles)
2)DRG
3)dorsal horn
4)brain
Ascending Pathway
Pain matrix
1)thalamus
2)S1,S2
3)limbic cortex
Descending Pathway
not motor
1)hypothalamus
2)midbrain
3)brainstem
4)spinal cord
nociceptor
unipolar neuron
has free nerve ending (not specialized structure)
looks for adequate stimuli
adequate stimuli
heat,pressure,chemical,noxious
multipolar neuron
multiple dendrites one axon. Major neuron in body
ex)motor,interneurons
bipolar neuron
one dendrite one axon
found only in ear and eye
unipolar neuron
ex)all sensory including nociceptor
cell body coming from single hole and have one left dendrite and on right axon
glove and stocking distribution
found in some pain syndromes
feel pain in toes then over time spreads to different parts
reason: large neurons are more fragile and affected first by injury.The largest neuron is the one going to toe.
endoneurium
membrane surrounding axon
perineurium
membrane surrounding nerve bundle
epineurial
running alongside nerve like a epineurial blood vessel
dermatome
part of body which the spinal nerve in question is coming from
afferent
periphery to brain
efferent
brain to periphery
ipsilateral
same side where you did something
contralateral
opposite side
dermatomal distribution
pain is on the nerve
ex)shingles
substantia gelatinosa
in dorsal horn
important for pain processing
dorsal horn
sensory afferent go into it
ventral horn
cell bodies of motor/interneurons (efferents) come out of it
dorsolateral fasciculus
has no cell bodies here just spot where axons coming into
rexed's laminae
particular parts of horns
second order neurons
in the spinal cord
cross the spine because all sensory info crosses side even pain
(interneuron is second order but doesnt cross)
cell bodies found in laminae 1 or 5
spinal reflex
caused at the level of spinal cord
interneuron gets info from sensory and transmits message to motor neuron of ventral horn. There is no ascending pathway activation
2 ways to get up spine
anterolateral column
dorsal column
where do second order neurons terminate
main three but many others
spinothalamic
spinoparabrachial (pons)
spinoreticular (middle of brainstem)
reticular system
sleep and arousal
somatotopy
from particular parts of body sensory info preserved and found together.in white matter medially get info from upper and laterally get info from lower body
found in thalamus and somatosensory cortex(S1)
ventrobasal nucleus
in thalamus
consists of VPL,VPM
all sensory info (including pain) goes thru here
visceral anatomy
has own ganlia
very different anatomy than for skin and muscles
trigeminal anatomy
above the neck also has different anatomy
trigeminal spinal tract (Vo,V1,Vc) equiv to spinal dermatomes
main nucleus equiv brainstem
trigeminal ganglion equiv DRG
from main nucleus info goes to thalamus and then cortex
third order neuron
from thalamus goes to S1 to tell where pain is
but also goes many other places to elicit emotional/behavioral response
spatial resolution(mm)
where something is happening
smaller=better
temporal resolution(s)
for changes in time
smaller=better
sensory discriminative
aspect of pain for
1)where pain is
2)intensity
3)quality(what it feels like)
suggestion changes activity in S1
motivational affective
aspect of pain for
1) unpleasantness
2) meaning of pain
changes activation in ACC
descending modulatory pathway
from cortex hypothalamus amygdala go down thru midbrain to spinal cord theres 2 paths
1)PAG(midbrain)->LC(pons)->VLF(dorsal horn)
2)PAG(midbrain)->RVM(medulla)
->DLF(dorsal horn)
collateral
when ascending pathway from dorsal horn goes up to thalamus it can split off and go to medulla,pons,midbrain
may modulate neurons
ed pearl
specificity theory
specificity theory
specific afferent will fire only to painful stimuli. will not respond to innocuous stimuli only to noxious
intensity theory
branch of specificity instead says that afferent will fire to innocuous but not as much
ron melzack/pat wall
pattern theory
pattern theory
decision that something is pain is made at the level of spinal cord or brain
and the pattern of afferent firing
gate control theory
branch of pattern
what are the 4 afferent fiber classes
1)Aalpha(muscle control)
2)Abeta(touch,vibration)
3)Adelta(pain,thermal)
4)C(pain,sweating)
draw gate control theory
...
rubbing inhibits pain because..
increased L input increases SG inhibition on S fibers therefore experience some analgesia
contradiction between afferent termination and gate theory
gate theory assume that L and S inputs on same neuron of SG that not the case. Gate theory anatomically incorrect. L and S interact via interneurons
somatic afferent termination is different from visceral because...
visceral has a lot more branching this explains why feel pain over stomach instead of localized spot
somatic-visceral convergence
afferent's from different body parts synapse onto same projection neuron
ex)skin afferent synapse on same projection neuron that an afferent from heart is
cause visceral pain to be referred to skin
is referred pain central or peripheral phenomenon?
Central
what is the efferent effect of nociceptor's?
neurogenic inflammation to help bring immune response. Seen mostly in C fibers(lack of myelin)
first pain vs second pain
caused by conduction velocities/how pain processed
first pain: short/sharp pain due to adelta's
second pain: longer/duller pain due to C's
three spinothalamic tract neurons in dorsal horn
wide dynamic range
nociceptive specific
low threshold mechanosensitive
anterior cingulate cells
part of limbic system
receptive field is whole body
unlike second order neurons which care about where pain is anterior cingulate don't they only care that there is pain
is it just the injured site of fiber that changes?
No, you can have some very important changes occur to surrounding uninjured fibers
counter irriation
is pain inhibiting pain in another spot
condition pain modulation
used to be called diffuse noxious inhibitory control
some people with certain pain disorder deficient in this therefore acupuncture,etc doesnt work
TENS
transcutaneuous electrical nerve stimulation
purpose it to activate abeta's(increase L input therefore act as analgesic)
acts superficial since abeta's more superficial
sensitization
central or peripheral
seen in pain causes increased sensitivity to pain
temporal summation "wind up"
central sensitization
more and more AP genereated if the stimuli freq is close enough to one another and therefore gets more and more painful.
spatial summation
stimuli given simultaneously in adjacent body parts. They cause more AP and therefore more pain more stimulation is given .
long term potentiation
in hypo-campus and spinal cord
for memory and learning
affect synaptic plasticity
primary hyperalgesia
site of injury is hyperalgesic to heat and touch
peripheral sensitization
secondary hyperalgesia
uninjured but hyperalgesic to mechanical stimuli
central sensitization (explained by capsaicin desensitization and mirror pain)
two types of secondary hyperalgesia
stroking (allodynia)-due to low threshold mechanoreceptors (recruited to deal with pain)
punctate (static hyperalgesia)-due to nociceptors
sensitization and symptoms describe them
-primary hyperalgesia/allodynia
-secondary hyperalgesia/allodynia
-ectopic activity (no peripheral stimuli)
paresthesia
spont pain
spont pain & dysethesia
plasticity after injury
functional changes (changes to things already there) like
1)molecular
2)synaptic
3)cellular
4)network
or structural changes involving new addition/losses like
1)addition/losses of synaptic spines
2)hypertrophy/hypotrophy of branching
silent nociceptors
become active only after injury
ex)silent C nociceptors
injury can cause
changes in phenotype different neurons can take on new functions like Abetas
neuroma
cutting nerve at free nerve ending
leads to ectopic firing and therefore spont pain
ectopic firing originates in the..
DRG after spinal injury
if you cut the nerve at the dorsal root you..
stop firing
cortical reorganization in phantom
amputees with no pain have same cortical activity as normal controls
phantom limb patients have different cortical activity with cortical representation of mouth extending to hands and arms
major glial cells of CNS
1)microglia(immune)
2)astrocytes(BBB,neural support)
3)oligodendrocytes (myelin)
astrocytes/microglia are like interneurons
glial cells for pain?
both astrocytes and microglia
microglia may be involved in central sensitization (during peripheral injury in CNS microglia thicken up and pump out more signals related to pain)