Topic Test 4 - Part 3B (pain) Flashcards
what are nociceptors?
receptors of painful stimuli
describe nociceptors
- activated by stimulus that may damage tissue
> (pick up on*) strong mechanical stimulation, temperature extremes, oxygen deprivation, chemicals; even substances released by damaged cells (lactic acid, histamine etc) - nociception is not pain!
*job is to manage pain information
why is nociception not equal to pain?
- nociception = sensory process that provides the signals that MAY trigger pain
- pain = sore, aching, throbbing sensations we “feel,” can be influenced by past experiences (our interpretation)
*can feel pain without experiencing tissue damage
> nociception can exist without pain
> pain can exist without nociception
nociceptors are _
free nerve endings which bring the sensation of pain to CNS
what are the 4 types of nociceptors?
- mechanical nociceptors
- thermal nociceptors
- chemical nociceptors
- polymodal nociceptors
what are mechanical nociceptors responsible for?
respond to damage such as cutting, crushing or pinching
what are thermal nociceptors responsible for?
respond to temperature extremes
what are chemical nociceptors responsible for?
respond to histamine and other chemicals
what are polymodal nociceptors responsible for?
respond equally to all kinds of damaging stimuli
different types of pain involve different types of fibers - for fast pain, list:
a) nociceptor
b) fiber
c) pain
d) localization
e) timing
a) mechanical and thermal
b) myelinated Ab(a delta) fibers
c) sharp, prickling sensation
d) easily localized
e) fast, occurs first
for slow pain, list:
a) nociceptor
b) fiber
c) pain
d) localization
e) timing
a) polymodal
b) unmyelinated C fibers
c) dull, aching, burning sensation
d) poorly localized
e) slow, occurs second and for longer time
why do we have slow pain?
exists so we can be sensitive about that area
what tract carries nociceptive information to the brain?
spinothalamic tract
- cell bodies in dorsal root ganglion
- axons enter dorsal horn of spinal cord
describe the pathway of the spinothalamic tract
1) enters zone of Lissauer (ascend or descend slightly)
2) synapse in the substantia gelatinosa (in the dorsal horn)
3) second order neurons in the spinal cord immediately decussate
4) ascend to the brain in the ventrolateral surface of the spinal cord
5) synapse with VP nucleus (and other areas) in the thalamus
6) Information then projected the somatosensory cortex
pain is complex and can be difficult to localize in the brain, it’s also highly integrated with _
medial structures related to emotion/memory
compare the 2 major ascending pathways, DCML and spinothalamic, in terms of neurons
both have 3
compare the 2 major ascending pathways in terms of ipsilateral vs contralateral
- touch and pain info is ipsilateral when it hits the spinal cord (ex. right hand goes to right side of spinal cord)
- pain info (spinothalamic) jumps over right away, contralateral sidfe
- touch info remains ipsilateral until crossover at medulla
compare the 2 major ascending pathways in terms of area of spinal cord
ventrolateral side vs dorsal
compare the 2 major ascending pathways in terms of types of neurons in pathways
DCML: primarily ABeta
Spinothalamic: primarily A delta and c
describe the general organization of the 2 major ascending pathways
DCML
- upper body tracts more lateral
- lower body tracts more medual
Spinothalamic
- upper body tracts more deep
- lower body tracts more superficial
describe afferent regulation (pain regulation)
- pain can be reduced by the activity of mechanoreceptors
- gate control theory of pain
describe the gait control theory of pain
neurons in the spinothalamictract may be inhibited by Aa or AB sensory nerves (touch) in the dorsal horn of the spinal cord
what’s a daily life example of how pain can be reduced with mechanoreceptors?
tactile info can reduce pain we are feeling (ex. hit head, rub it)
-overloading this area with tactile info and inhibiting some of the pain signals
ex. kt tape
ex. transcutaneous electrical nerve stimulation
describe the interneuron’s job in pain reduction through mechanoreceptors **
- connect things to potentially influence eachother
- can connect mechanical info onto nociceptive pathway
- if we have mechanical stimulus, can cause inhibiory response on nociceptive signal
on the topic of gate control theory of pain, what evidence was found on transcutaneous electrical nerve stimulation and foam rollers?
electrical stim, can potentially distract pain signals
- foam roller effect partially negligible but good for reducing muscle pain sensation
how has the PAG been used in rats to control pain?
activate the PAG, almost like local anaesthetic
describe pain regulation - descending regulation
- brain can do powerful things when it comes to controlling pain!
> strong emotion, stress, etc. can suppress pain (bunch of connections coming from cortex) - periaqueductal gret matter (PAG) (little area in midbrain, has direct path down to interact with the pain signals coming in)
- downregulating pain
describe the PAG
1) receives input from many areas in cortex (often emotional)
2) neurons descend to medulla (raphe nuclei)
3) neurons descend to spinal cord to depress activity
what effect does stress have on descending regulation?
- high stress state can activcate this area of the brain and the goal is to send these inhibitory signals down to the dorsal horn of the spinal cord
- this is where 2nd order neuron for spinothalamic tract exists
how come when you get injured you feel it later?
- high stress response, shut down the pain response because we need to get out of the danger first, then pain comes
- the descending regulation of pain has paradoxical gray matter that can come down and connect onto synapse and release things that will stop release of pain signals (internal opioids stopping the release of substance P/neurotransmitter sending pain signal)
describe hyperalgesia
- reduction in the pain threshold, increased sensitivity, or spontaneous pain
- primary changes occur peripherally
- hyperalgesia vs allodynia
*any small activation of free nerve ending can send signal out
*increased sensitivity to things that should cause pain
describe the 2 types of hyperalgesia
primary: super-sensitivity with the damaged area
secondary: super-sensitivity in the surrounding area
describe how primary changes occur peripherally in hyperalgesia
inflammation = bodies attempt to eliminate injury and stimulate healing
- a variety of neurotransmitters, peptides, lipids, etc. area released which can attach to receptors in/around injury to lower their threshold for activation
compare hyperalgesia vs allodunia
allodynia is a similar concept, but pain response from stimuli that would normally not cause pain (sensitivity to tactile response that shouldn’t be causing pain
describe central sensitization
amplifiation of neural signalling (eg. nociceptive information) within the CNS that elicits pain hypersensitivity or even normal stimuli (allodynia)
- changes in the synapses and potentially the organization of interconnecting neurons may increase excitability/reducing inhibition of pain pathways
- contributions are difficult to identify and treatments difficult to target
describe how normal sensitization vs central sensitization would look
normal sensitization
- normal response we would expect
- damaging tissue = sending Ps and creating pain response, and touch picking up touch info
central sensitization
- neuron is extra sensitive to info coming in
- not necessarily the peripheral, happening at central level
- secondary neuron is very sensitive, any small amount of pain response are amplified and become painful
*allodynia = supposed to be inhibitory, but activating pathway
initially debated, but now central sensitization is an accepted factor related to:
- osteoarthritis and various MSK disorders
- fibromyalgia (increased pain, unclear reason)
- other chronic pain conditions
describe referred pain
cross-talk between sensory neurons
- convergence of visceral and somatic afferent neurons
explain the referred pain example of the heart attac
- pain in chest and left arm
- dorsal root ganglion bringing in sensory info, have potential crossover
- have massive signals coming from heart and has sensory axon coming in and going through the doral root ganglion/similar areas
- if sensory axons coming in the same spinal nerve through same dorsal root ganglion, that’s were we feel crossover
*feel pain in areas of skin provided by dermatome
our pain goes to the cortex but this doesn’t mean we can’t have _ when we need to react to pain faster
local synapses
