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Neuro > Pain > Flashcards

Pain Flashcards

1
Q

labeled line theory

A

Descartes (and others) believed pain was carried by specialized receptors (ie. We feel pain because pain receptors tell us that something is painful)

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2
Q

what fibers detect pain

A

free nerve endings

freen nerves are high threshold

everything else is low threshold so it is a mix of both theories

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3
Q

different types of nociceptors in free nerve endings

A
  • Nociceptoris umbrella term for “noxious” receptor
  • Thermal, mechanical, chemo
  • Silent/sleeping nociceptors
  • Polymodalnociceptors
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4
Q

polymodal nociceptros

A

one free nerve ending that can respond to abunch of things``

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5
Q

A alpha and Abeta

A 
myelinated
large diamet
proprioception and light touch
lowest intensity
fastes
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6
Q

Adelta

A 
lightly myelinated
medium diameter
nociception (mechanical themal chemical)
high intensity
free nerve endings
sharp pain
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7
Q

c fiber

A 
slowest 
dull pain
highest intensity
unmyelinated
small diameter
temp itch
nociception (mechanical thermal chemical)
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8
Q

glutamate nociception

A

released in lamina I-VI
ampa
nmda - learning in spinal cord
once active you get a bunch of ca in and it becomes responsive for a long time

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9
Q

substance P

A

neuropeptide
released with glutamate
nociception

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10
Q

calcitonin gener related peptide

A

released with glutamate nociception

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11
Q

what kind of pain is neospinothalamic

A

discriminatory pain

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12
Q

what kind of pain is paleospinothalamic and spinoreticular?

A

reflective pain

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13
Q

neospinothalamic tract is carried by what fibers

A

delta

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14
Q

delta and c fibers localized?

A

delata is localized

c is poorly localized and long lasting

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15
Q

phantom limbs

A

PAIN is psychological

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16
Q

pain on battlefield

A

gets blocked or modulated

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17
Q

depression and pain and sleep

A

more sensitive to pain with less sleep bc of the psychological aspect and with depression

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18
Q

chronic pain

A

like phatom pain had damage a long time ago but still there

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19
Q

nocebos

A

opposite of placebo

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20
Q

pain sensitization

A

somtimes when we feel it we get more sensitive other times we get less sensitive

it depends on the neuron and temporal order that the painful stimulus is presented

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21
Q

gate control theory of pains

A

inside spinal cord you have large and small neurons that converge in substantia gelatinosa, that are against each other whether we will receive pain or pressure or no, normal things are inhibited by substantia gelatinosa, and will inhibit other neurons from ascending also

22
Q

Specific properties of nociceptive and non-nociceptive signals togethercode for pain perception in the spinal cord
Some spinal cord layers contribute to pain-modulatory pathways by spino-bulbo-spinalmechanisms

A

spinal cord >brainstem> spinal cord

perabrachial nucleus is part of reticular formation

spinoreticular pathway

parabrachial nucleus talks to limbic so it adds to fer anxiety depression

limbic and cognitive systems both talk to pag (periaqueductal gray matter) which sends descding projection to rvm (rostral Ventral medulla) which is another part of the reticular system
rvm sends neurons down that will positively or negatively feedback so exacerbate or ameliorate the pain

on battlefield adrenalin is pumping and frontal lobe inhibits this system with limbic system and pag to say now is not the time, and norepi is released into psinal cord and you do not feel the pain

happnes when haveing a great time or really pumped really pumped

23
Q

2 pain modulatory pathways: Anterolateral system and Spino-bulbo-spinal pathways:

A

Spinoreticularand spinomesencephalictracts

24
Q

Spinoreticularand spinomesencephalictracts type of info

A

poorly localized pain

25
Q

Spinoreticularand spinomesencephalictracts point of origin receptors involved

A

free nerve endings (TRP Channels) in skin visceral and muscle

26
Q

Spinoreticularand spinomesencephalictracts cell bodies

A

drg

27
Q

Spinoreticularand spinomesencephalictracts first synapse

A

lamina 1-2

28
Q

Spinoreticularand spinomesencephalictracts enters and travels

A

dorsal horn (Lissauer’s Fassciculusto ascend at least 1 segment in lamina I), after 1stsynapse, travels bilaterally, ascends through anterolateral spinothalamictract

29
Q

Spinoreticularand spinomesencephalictracts decussates

A

spinal cord after 1st synapse

30
Q

Spinoreticularand spinomesencephalictracts second synapse

A

Medullary/Pontine reticular formation, parabrachialnucleus (spinoreticular); PeriaquedcucatalGrey Matter (spinomesencephalic)

31
Q

Spinoreticularand spinomesencephalictracts final destination

A

dorsal horn of spinal horn

32
Q

spinomesencephalic tracts

A

are at midbrain level

33
Q

spinoreticular tracts

A

are below midbrain

34
Q

pb is pathway into

A

limbic system

35
Q

main pathway of inhibition uses rvm

A

periaquaductal gray sends axons down to rvm of medulla and synapse there then those axons go to spinal cord and inhibit gray

2 axon system

5ht is released from rvm, snri is prescribed to put mroe serotonin in system for pain and depression

36
Q

rvm and locus cerulous sends fibers

A

straight back to spinal cord

37
Q

periaqueductal greay sends fibers

A

to rvm then to spinal cord

38
Q

raphe nuclei

A

in middle rostal ventral medulla

have serotonergic fibers that descend

39
Q

periaqueductal grey is good at

A

inhibiting pain signals

40
Q

endogenous opioids

A

are prescribed bc we have an endogenous opiod system that prevents transmission of pain signals acts at each system pag rvm and spinal cord

41
Q

pag signal

A

Major descending pathways form the PAGsignal through the Raphe nuclei of the RVMto either inhibit or excite the spinal cord nociceptive signals
(This is neurotransmitter specific

Endorphins
Enkephalins (these top two ar found in terminals of axons in all three areas of pain inhibition adding endorphins make pms stronger)
Norepinephrine
Serotonin

42
Q

tens

A

Transcutaneous Electrical Nerve Stimulation Effectiveness supports the Gate-Control Theory of Pain

43
Q

pain matrix

A

Emotional responses, previous pain experioence, placebo can also affect pain modulation

psychological aspect of pain exists all over and is affected by everything!

tell kids to toughen up!

44
Q

chronic pain

A

arises from central sensitization (spinal cord and brain-based sensitization) in the absence of nociceptive stimuli

hyperalgesia
allodynia

45
Q

hyperalgesia

A

after we fill pain after it is chronic

shouldnt hurt us but it is

axon terminal grew so you get hyper response

46
Q

allodynia

A

activate nociceptor and mechanoreceptor rececptor

everytime you activate mechanoreceptor you get painful response and things hurt that shouldnt

47
Q

windup

A

repeated stimulation from same source is interpreted as increasingly painful

neurons are closer to threshold when keep stimulating

not necessarily long term

windup happens in the moment
hyperalgesia is longterm

48
Q

axon reflex contributes to windup

A

psuedounipolar keep getting ap so you dont turn it up

create substance p and you get inflammatory response mast cells release histamine which aggravates neuron on prolongs response

49
Q

pain differences

A
  • Visceral pain info is ONLY carried by delta and delta-fibers
  • Visceral pain does not “feel like” the damage/disruption responsible for the pain
  • Female predominance
  • Psychological intervention improves “well-being,” not necessarily painful symptoms
50
Q

visceral pain paths

A

can travel in lateralspinotholamic or anterior and some will go through completely diff paths

most is reffered

not good at numbing just try to teach peole to deal with it

types of fibers that

51
Q

visceral pain is referred due to

A

convergence

Neuro (10 decks)

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