Neuro- Pain

Front 1

Gating Theory of Pain

Back 1

the amt of stimulation of the receptor is NOT equivalent to the amount of pain perceived

Front 2

DCML

anterolateral pathway

damage to SC

Back 2

vib, prob, 2pt descrimination

pain

loss of pain 1-2seg below the level of the lesion

Front 3

Free nerve endings have cell bodies

depolarize and send AP

Back 3

in the DRG, and projections into the CNS

Front 4

3 Types of Nociceptors

Back 4

1. Thermal- respond to extremes
-Alpha/Delta fibers- light myel
2. Mechanical Rec- intense press
-Alpha/Delta fibers
3. Polymodal- variety, long lasting pain.
-unmyelinated C fibers

Front 5

tissue damage results in

Back 5

1. vasodialation
2. abundance of chem rush in
-stimulate free nerve endings
3. cell ruptures
4. high K- depolarization

Front 6

released chemicals cause a

tissue damage activates

Back 6

Feed Forward Reaction

C-Fibers, AP travels to Dorsal Horn

Front 7

what is released into dorsal Horn?


what is the result of histamine?

Back 7

Substance P, CGRP->mast cells-->histamine


sensitizes free nerve endings
-pain rec become more sensitive

Front 8

Secondary Pain response

Back 8

1. Arachadonic acid-sens nociceptors
2. Bradykinin- acts directly on alpha/delta and C fibers
3. Histamine- sensitizes fibers

Front 9

Pain fibers primarily enter through what layers of lissaur's tract?

Back 9

layers 1 and 2 (substantia gelatinosa)

Front 10

which fibers terminate in..

Layer 1
Layer 2
Layer 5

Back 10

alpha/delta (marginal layer)
C Fibers
alpha/delta, alpha/beta, and C

Front 11

Speed of Conductance..


Alpha/beta fibers
alpha/delta
C fibers

Back 11

Alpha/beta, alpha/delta, then C fibers

conduct fastest, sharp pain
relatively fast, sharp pain
slow(1-2m/s), dull pain

Front 12

prolonged secondary pain is due to what?

Back 12

1. latency in conduction of C fibers
2. release of chemicals that prolong the effect

Front 13

C fibers release

Back 13

1. Glutamate- for fast synaptic transmission
2. Substance P
-secondarily, need repetitive APs

Front 14

Substance P actions in the Periphery...

Back 14

1. histamine from mast cells
2. in dorsal horn, sensitizes post-syn AMPA rec to Glu
-amplify glu signaling

Front 15

Thermoreceptors respond to temps

Thermal Nociceptors resond

Back 15

not extreme, 20-40 deg C

extreme: x<5 or x>40 deg C

Front 16

what does a pinprick activate?

Back 16

2-pt discrimination
mechanonociceptors if extreme
-if press in a small area

Front 17

when does a bigger response to a given stimuli happen?

Back 17

after the initial reaction

because of sensitization

Front 18

sensitization causes?

Back 18

a decrease in pain thresholds
rel of chem alters the activity of the receptors

Surface area affected by pain inc in secondary reaction

Front 19

Hyperalgesia


Allodynia

Back 19

sensitization of pain receptors that dec pain threshold

non-noxious stimulus now becomes noxious
-ie sunburn painful to breath

Front 20

Persistent Injury causes

Back 20

1. C fibers continuously rel Glu
2. activation of NMDA rec
3. synaptic plasticity into system

Front 21

what does synaptic plasticity do?

Back 21

keeps the signaling b/w the C-fibers and doral horn cells potentiated

Front 22

Anterolateral (STT) contains 2 types of fibers that originate in the spine

Back 22

1. Spinoreticular- goes to medulla/pons
-arousal/attention
2. Spinomesenscephalic- goes to med brain and terminates in Periaqueductal Grey matter

Front 23

Spinomesencephalic terminates

what is this impt in

Back 23

in periaqueductal grey matter

1. pain modulation
2. connections to limbic system

Front 24

STT crosses

Back 24

immediately
goes to VPL, then to somatosensory cortex

TTT goes to VPM

Front 25

Primary Somatosensory Cortex

Insular Cortex

Ant Cingulate Cotrex

Back 25

deals w/ location and intensity of pain
autonomic cmpt of pain

limbic assoc- emotional component of pain

Front 26

pain is what type of phenomena

intensity signal by what

Back 26

graded phenomena

frequency of AP

Front 27

which receptors have the highest threshold?

Back 27

Nociceptors

Front 28

C fiber contacts

A/B fiber contacts

Back 28

projection neuron to AntLat sys

dorsal column, contacts some inhibitory interneurons

Front 29

Summation results in

Back 29

Less chance of projection neurons firing APs

1. inhib input from the A/B interneuron
2. excitatory input from C fiber

Front 30

stimulating periaqueductal grey matter results in

Back 30

reduced sensation of pain

1. causes stim of dorsal raphe nuc-->serotonin down dorsal horn
2. activates locus ceruleus->rel norepi to dorsal horn

Front 31

how do descending projections regulate pain?

Back 31

release opiods
mostly enkephalins

descending control prevents the signal from coming up the projection neuron

Front 32

enkaphalins work by

Back 32

presyn inhibition of voltage gated Ca channels to prevent NT rel

Front 33

Referred pain

Back 33

via non-somatic pain receptors in viscera
can become sensitized

refer to specific dermatome

Front 34

what does visceral pain refer to dermatome?

Back 34

visc and somatic pain fibers synapse on same projection neurons

Front 35

acute pain

Chronic pain

Back 35

not a treatment problem. usually resolves. tradit meds work well
greater clinical problem. "Pain that persists longer than it should"
-often w/o spec etiology

Front 36

chronic pain

Back 36

1. nociceptive- tissue damage
2. neuropathic- damage to nervous system proper

Front 37

Nociceptive pain

Back 37

1. tissue damage
2. responds to analgesics
3. activated C and A/delta fibers
4. definable pathology

Front 38

symptoms of nociceptive pain

Back 38

1. redness-rubor
2. swelling-tumor
3. temperature-calor
4. pain-dolor

Front 39

effects of nociceptive pain

Back 39

1. rel catecholamines (inc HR/BP)
2. altered respiration
3. sweating
4. inc cortisol
5. psychological distress

Front 40

Neuropathic pain

Back 40

Injury of nervous system proper
responds to ADJUVANT analgesics

can be from injury anywhere along the pain pathway

Front 41

Neuropathic pain presentations

Back 41

1. immed or delayed
2. bizzare- very emotional
3. way out of proportion to pathology
4. NONE of the traditional symptoms of redness/swelling

Front 42

Effects of neuropathic pain

Back 42

1. maybe inc catecholamines
2. mabye dec cortisol
3. psychological effects are reliable

Front 43

Descriptions of Neuropathic pain

Back 43

1. buring
2. paresthesia(pins/needles)
3. paroxysmal (sudden attacks)
4. lancinating
5. electrical, raw, shooting, deep, dull, ache

Front 44

Cardinal Signs of Neuropathic pain

Back 44

1. Allodynia- pain from a normally non-painful stimulus
2. Hyperalgesia- exaggerated pain response

Front 45

clinical manifestations of neuropathic pain

Back 45

1. autonomic dysfxn
2. vasoconstricion
3. trophic changes to bony structure
4. local motor impairment
5. other neural impairment

Front 46

Types of Neuropathic pain(5)

Back 46

1. Compressive- slipped disc, nerve compression
2. Inflammatory- neuritis
3. De-afferentation- complete TRANSECTION of nerve
4. Central injury- to cns
5. sympathetic NS

Front 47

most neuropathic pain goes in what?

Back 47

cycles- peaks and valleys

cycles thruout the day

Front 48

common findings in neuropathic pain

Back 48

1. lack of nociceptive findings
2. no evidence of disease
3. spontaneous pain
4. hyperalgesia
5. profound psych response
6. ANS abnormalities

Front 49

possible reasons for neuropathic pain
allodynia/hyperalgesia

Back 49

1. altered phenotype
2. sprouting
3. misconnection
4. inc excitability
*Best answer is 'we dont know'

Front 50

Treatent continuum

Back 50

does not relatet to efficacy

most effective drugs NOT used first
-start w/ noninvasive, non-toxic first

Front 51

treat nociceptive pain w/

Back 51

traditional analgesics, opiods, nsaids, cox2 inhib, corticosteroids

Front 52

opiods

Back 52

synthetic opiates
tag the same receptor
-mu opiod receptor

Front 53

optimal way to deliver morphine

Back 53

into the CNS
more effective, less is needed

Front 54

neuropathic pain meds

Back 54

modulate CNS funciton. goal is to make peaks lower and farter apart. ADJUVANT ANESTHETICS

antidepressants, anticonvulsants, antiarrhythmics, antispastics (a-2 agonists)

Front 55

side effects of neuropathic meds

Back 55

orthostatic hypotension
renal/liver toxicity

Front 56

arachadonic acid sensitizes what in the secondary pain response?

Back 56

nociceptors

Front 57

Bradykinin acts directly on what in the secondary pain response

Back 57

1. Alpha/gamma
2. C-fibers
3. and other cells to release more compounds

Front 58

major players in the secondary pain response

Back 58

bradykinin
substance p
histamine

Front 59

what releases substance P?

what does it do?

Back 59

nociceptor terminals rel subP

stimulates mast cells to rel histamine, leads to vasodialation and extravasation

Front 60

what releases Bradykinin?

Back 60

damaged cells

Front 61

some fibers in the spinomesencephalic tract travel in the?

Back 61

dorsal horn

Front 62

what happens to the surface area affected by pain?

Back 62

increases

Front 63

continuous stimulation of C fibers leads to what change in receptors?

Back 63

1. contin rel of Glu
2. inc NMDA receptors
3. introduces synaptic plasticity

Front 64

what does the inc in NMDA receptors do?

Back 64

1. induces synaptic plasticity
2. keeps the signal b/w C fibers and dorsal horn potentiated

Front 65

medial thalmus projects to what?

Back 65

1. insular cortex- ANS cmpt of pain
2. Ant Cigulate cortex- emotional cmpt of pain
3. somatosentory cortex- intensity and localization of pain