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Flashcards in Chronic pain Deck (32):
1

Superficial sharp pain

sensed with a little delay
usually short in duration
mediated by myelinated pain fibers (Adelta fibers)
Conduct AP btw 5-30 m/sec (medium speed)
Responds to either mechanical or temperature stimuli

2

Superficial dull, burning pain

Longer lasting - often "sore"
mediated through small, slowly conducting unmyelinated pain fibers (C fibers)
broad range of painful stimuli: mechanical, thermal, chemical

3

Deep/visceral pain

joints, muscles, bones, CT
aching sensation;difficult to localize
contraction of nearby skeletal muscle --> vicious cycle of increasing pain
unmyelinated C-fibers

4

Referred pain

pain perceived at a site adjacent to/at a distance from site of an injury's origin
Unmyelinated C-fibers
mechanism unclear

5

Adelta fiber

synapse on laminae I or V in dorsal horn
can be localized more exactly

6

C-fiber

terminate in laminae II/III of dorsal
more difficult to localize

7

Pain receptor stimulation +/- tactile stimulation

very poorly localized without tactile stimulation

8

Adaptive pain

coupled with a noxious stimulus / healing tissue
Nociceptive/inflammatory

9

Nociceptive pain

acute pain caused by a noxious stimulus
can be produced by direct mechanical deformation of nocicepter
OR activation of specific channels such as TRPV (cold/heat)

10

Inflammatory pain

increased sensitivity to prevent contact with/movement of injured part until repair is complete

11

Hyperalgesia

increased response to a normally painful stimuli

12

Allodynia

painful response to a normally benign stimulus

13

Maladaptive pain

uncoupled from a noxious stimulus/healing tissue
neuropathic/functional

14

Neuropathic pain

pain occurring in response to damage to nervous system

15

Shingles

VZV dormant following chicken pox
Reactivated virus migrates from DRG along nerves to spinal cord and skin
Painful blisters (crust over, heal in 4-6 weeks)

16

Post-herpetic neuralgia

continuation of pain long after the rash and blisters heal
Occur from nerve damage caused by virus
Burning, stabbing, gnawing
20% of patients with shingles

17

FUnctional pain

pain occurring in response to abnormal operation of nervous system

18

Fibromyalgia

medicall unexplained
no cure
chronic widespread pain, allodynia
muscle/CT pain with many systemic problems

19

Peripheral sensitization

reduction in threshold/increase in responsiveness of nociceptors
e.g. heat sensitivity after a sunburn
Inflammatory chemicals/mediators released around site of tissue damage --> alter nociceptive receptors/ion channels, increase excitability
1) post-translational processing
2) altered transcription

20

Kinins

e.g. bradykinin produced by proteolytic breakdown of kininogen in area of wound
most potent pain producing substance

21

Inflammatory chemicals involved in peripheral sensitization

Kinin
Substance P
Substance used elsewhere as synaptic transmitters: ACh, 5-HT

22

Substance P

can be released from peripheral terminals of sensory nerve fibers --> skin, muscle and joints
local inflammatory response

23

Post-translational processing of nociceptors

typically involve addition of phosphate groups
lower threshold/longer duration of opening
signals act locally
--> peripheral sensitization/early stages of primary hyperalgesia

takes minutes

24

Altered transcription of proteins made by nociceptors

Signals transported back to cell body of sensory neurons in DRG
--> change txn or tln
Increased protein shipped back to terminal --> increased responsiveness of terminal to stimuli
--> peripheral sensitization/ early stages of primary hyperalgesia

Happens in ~1 day

25

Central sensitization

increase in excitability of neurons within CNS
--> normal inputs produce abnormal responses

Hyperresponsive conditions of: post-op pain, migraine, neuropathic pain, fibromyalgia, GI tract pain

26

Acute phase of normal response to pain

Normal synaptic transmission via activation of AMPA receptors by glutamate
NMDA receptors are typically blocked by Mg

27

Acute phase of central sensitization

1) Summation of synaptic inputs from activation of nociceptors
2) removal of Mg block of NMDA receptors --> increased sensitivity to glutamate
3) postsynaptic receptors are phosphorylated
- increased recruitment to synaptic membrane
- increased receptor kinetics (longer opening)
- decreased opening threshold

get WINDUP

28

Windup

progressive increase in discharge of dorsal horn neurons in response to repeated low-frequency activation of nociceptors

can be decreased by using ketamine (competitive NMDA blocker) at a low dose

29

Persistent phase of central sensitization - gene regulation

Upregulation of genes encoding receptors locally
Upregulation of genes globally:
- COX-2
- initiated by a circulating factor released by inflammatory cells --> increase of PGE2 --> facilitate synaptic transmission and excitability

Widespread induction of COX-2: generalized aches/pains, loss of appetite, changes in mood and sleep cycle (features of inflammatory diseases)

30

Persistent phase of central sensitization - disinhibition

Inhibitory interneurons in spinal cord normally act to produce a limited, appropriate and brief response to any input
Disinhibition increases excitability and pain
Tx aimed at preventing loss of these interneurons

31

Persistent phase of central sensitization - structural reorganization

Following nerve injury vacant synapse sites
A/beta fibers sprout and form novel synapses in lamina II --> inappropriate functional connections --> persistent hypersensitivity and phenotype conversion

32

Gate theory

Transmission of pain from peripheral nerve through spinal cord can be modulated by:
- other afferent neurons
- controls emanating from brain

effect of transcutaneous electrical stimulation thought to be due to this effect (stimulate Abeta fibers, reduce flow of pain info to the brain)