Topic Test 4 - Part 3B (pain)

Question 1

what are nociceptors?

Answer 1

receptors of painful stimuli

Question 2

describe nociceptors

Answer 2

• 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

Question 3

why is nociception not equal to pain?

Answer 3

• 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

Question 4

nociceptors are _

Answer 4

free nerve endings which bring the sensation of pain to CNS

Question 5

what are the 4 types of nociceptors?

Answer 5

• mechanical nociceptors
• thermal nociceptors
• chemical nociceptors
• polymodal nociceptors

Question 6

what are mechanical nociceptors responsible for?

Answer 6

respond to damage such as cutting, crushing or pinching

Question 7

what are thermal nociceptors responsible for?

Answer 7

respond to temperature extremes

Question 8

what are chemical nociceptors responsible for?

Answer 8

respond to histamine and other chemicals

Question 9

what are polymodal nociceptors responsible for?

Answer 9

respond equally to all kinds of damaging stimuli

Question 10

different types of pain involve different types of fibers - for fast pain, list:
a) nociceptor
b) fiber
c) pain
d) localization
e) timing

Answer 10

a) mechanical and thermal
b) myelinated Ab(a delta) fibers
c) sharp, prickling sensation
d) easily localized
e) fast, occurs first

Question 11

for slow pain, list:
a) nociceptor
b) fiber
c) pain
d) localization
e) timing

Answer 11

a) polymodal
b) unmyelinated C fibers
c) dull, aching, burning sensation
d) poorly localized
e) slow, occurs second and for longer time

Question 12

why do we have slow pain?

Answer 12

exists so we can be sensitive about that area

Question 13

what tract carries nociceptive information to the brain?

Answer 13

spinothalamic tract
- cell bodies in dorsal root ganglion
- axons enter dorsal horn of spinal cord

Question 14

describe the pathway of the spinothalamic tract

Answer 14

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

Question 15

pain is complex and can be difficult to localize in the brain, it’s also highly integrated with _

Answer 15

medial structures related to emotion/memory

Question 16

compare the 2 major ascending pathways, DCML and spinothalamic, in terms of neurons

Answer 16

both have 3

Question 17

compare the 2 major ascending pathways in terms of ipsilateral vs contralateral

Answer 17

• 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

Question 18

compare the 2 major ascending pathways in terms of area of spinal cord

Answer 18

ventrolateral side vs dorsal

Question 19

compare the 2 major ascending pathways in terms of types of neurons in pathways

Answer 19

DCML: primarily ABeta
Spinothalamic: primarily A delta and c

Question 20

describe the general organization of the 2 major ascending pathways

Answer 20

DCML
- upper body tracts more lateral
- lower body tracts more medual

Spinothalamic
- upper body tracts more deep
- lower body tracts more superficial

Question 21

describe afferent regulation (pain regulation)

Answer 21

• pain can be reduced by the activity of mechanoreceptors
• gate control theory of pain

Question 22

describe the gait control theory of pain

Answer 22

neurons in the spinothalamictract may be inhibited by Aa or AB sensory nerves (touch) in the dorsal horn of the spinal cord

Question 23

what’s a daily life example of how pain can be reduced with mechanoreceptors?

Answer 23

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

Question 24

describe the interneuron’s job in pain reduction through mechanoreceptors **

Answer 24

• 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

Question 25

on the topic of gate control theory of pain, what evidence was found on transcutaneous electrical nerve stimulation and foam rollers?

Answer 25

electrical stim, can potentially distract pain signals - foam roller effect partially negligible but good for reducing muscle pain sensation

Question 26

how has the PAG been used in rats to control pain?

Answer 26

activate the PAG, almost like local anaesthetic

Question 27

describe pain regulation - descending regulation

Answer 27

- 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

Question 28

describe the PAG

Answer 28

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

Question 29

what effect does stress have on descending regulation?

Answer 29

- 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

Question 30

how come when you get injured you feel it later?

Answer 30

- 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)

Question 31

describe hyperalgesia

Answer 31

- 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

Question 32

describe the 2 types of hyperalgesia

Answer 32

primary: super-sensitivity with the damaged area secondary: super-sensitivity in the surrounding area

Question 33

describe how primary changes occur peripherally in hyperalgesia

Answer 33

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

Question 34

compare hyperalgesia vs allodunia

Answer 34

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

Question 35

describe central sensitization

Answer 35

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

Question 36

describe how normal sensitization vs central sensitization would look

Answer 36

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

Question 37

initially debated, but now central sensitization is an accepted factor related to:

Answer 37

- osteoarthritis and various MSK disorders - fibromyalgia (increased pain, unclear reason) - other chronic pain conditions

Question 38

describe referred pain

Answer 38

cross-talk between sensory neurons - convergence of visceral and somatic afferent neurons

Question 39

explain the referred pain example of the heart attac

Answer 39

- 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

Question 40

our pain goes to the cortex but this doesn't mean we can't have _ when we need to react to pain faster

Answer 40

local synapses