Pain

Front 1

What results from a combination of genetic, biologic,environmental, psychological, andsocial factors, often requiring comprehensive approaches to prevention andmanagement?

Back 1

pain

Front 2

What factors can lead to persistent pain conditions/amplification?

Back 2

genetic polymorphisms combined with environmental factors and psychological stress

Front 3

What is the difference in the sensation of pain and chronic clinical pain?

Back 3

-sensation of pain = nociception

-chronic clinical pain =

1) pain thatpersists for >3-6months,

2) is oftenprogressive,

3) andthe cause can be difficult to determine

Front 4

What do nociceptors sense?

Back 4

potential tissue damage

Front 5

What are free-nerve endings in skin or other tissues that actas sensors of noxious physical stimuli interpreted as painsensation?

Back 5

nociceptors

Front 6

What are specialized heat and cold sensors called?

Back 6

thermosensors

Front 7

What is nociception?

Back 7

-Transductionof Noxious Stimuli by Nociceptors

-conversionof physical energy imposed by noxious stimuli into neuronal action potentials

Front 8

mechanoreceptors

Back 8

transduce mechanicalpressure for transmission by primarily by A-delta fibers

Front 9

thermoreceptors

Back 9

transduce heat andcold for transmission, primarily byC- and A-delta fibers, respectively

Front 10

polymodal nociceptors

Back 10

combined mechanicaland thermal information is transmitted primarily by C-fibers

Front 11

chemoreceptors

Back 11

respond to H+ andother noxious chemicals for transmission by C- and A-delta fibers

Front 12

pain transduction occurs at...

Back 12

free nerve endings

Front 13

pain transmission occurs via...

Back 13

c and a-delta axons

Front 14

pain transduction and transmission process

Back 14

-peripheral activation

-receptor potential (merge to become...)

-generator potential (long enough duration and great enough strength becomes...)

-action potential

-central activation

-synaptic potential

Front 15

difference in conduction velocity (and myelination) of nociceptive afferent nerve fibers

Back 15

-A alpha and A beta pretty rapid

-much slower = C fibers and a-delta fibers

-C fibers = unmyelinated

-A delta fibers = lightly myelinated

Front 16

What is an area on the skinsurface where adequate stimulus activating the terminal endings of a particularneuron will fire an action potential?

Back 16

receptor field?

Front 17

What happens when you apply a stimulus outside the receptor field?

Back 17

will NOT generate an action potential

Front 18

example of two point discrimination

Back 18

< 5 mm on the finger tips = great sensitivity

vs.

40 mm on the thigh = lowsensitivity

Front 19

smaller receptive field =

Back 19

increased discrimination

Front 20

increased receptor density =

Back 20

increased sensitivity

Front 21

Receptive fields should not be confused with what?

Back 21

dermatomes

Front 22

Where do nociceptor afferents terminate?

Back 22

in the dorsal horn onto spinothalamic tract neurons

Front 23

lamina I spinothalamic tract

Back 23

-myelinated nociceptors (A-delta fiber)

-unmyelinated (C-fiber)nociceptors

Front 24

lamina V spinothalamic tract

Back 24

-polymodal (wide dynamic range) type

-nociceptive afferents(A-delta and C fibers)

-low-threshold input fromlarge-diameter myelinated fibers (A-beta) of mechanoreceptorswhen sensitized

Front 25

What is the result of sensory fiber release of substance P?

Back 25

-activates and internalizes NK1 receptors on spinothalamic and trigeminothalamic tract cells

-leads to release of glutamate

Front 26

main differences in somatosensation/fine touch pathway and pain/temp pathway (spinothalamic)

Back 26

-somatosensation/fine touch:

•1stsynapse and cross in medulla

•ascends in dorsalcolumn

-pain/temp:

•1stsynapse and cross in spinal cord

•ascends in ventrolateral white matter

Front 27

somatic and visceral pain pathway

Back 27

spinothalamic (anterolateral) tract

Front 28

fine, discriminative touch and post synaptic visceral pain pathways

Back 28

dorsal column, medial lemniscal system

Front 29

Where are collaterals dropped off on the way into the brain, and what is the significance of that?

Back 29

reticular formation - for sensitization

Front 30

Where does neural processing of sensory input occur?

Back 30

at specialized locations in the brain with point to point codingthroughout the pain signaling pathway

Front 31

What is the purpose/concept behind a somatotopic map?

Back 31

somatosensoryareas in the cortex of the brain are anatomically organized in relation to thesource of information, with larger areas dedicated to parts of the body withgreater discrimination and sensitivity

Front 32

What is the result of tissue damage in terms of peripheral sensitization?

Back 32

-releaseof ATP, H+,and oxidation product

-draws in mast cells releasing bradykinin (BK),serotonin, andprostaglandins (PG)

-which activate and sensitize nociceptors

Front 33

In peripheral sensitization, neuronal release of what producesdilationof peripheral blood vessels and protein/plasma extravasation, resulting in rednessand edema?

Back 33

CGRP & Substance P

Front 34

2 "steps" of spinal cord central sensitization

Back 34

-Activatedprimary afferent endings release glutamate, substance P, and other peptidescentrally

-Glialactivation near the central terminals releasescytokines and oxidants

Front 35

What is the net effect of spinal cord central sensitization?

Back 35

Overactivation of theCentral Nerve Endings, Postsynaptic Neurons and Glia

Front 36

What is the overall role of dorsal root reflexes in neurogenic inflammation?

Back 36

ActionPotentials Generated Both InwardAND Outward (orthodromic& antidromic)

-net effect: MORE PAIN

Front 37

What 3 specific things does neurogenic inflammation increase?

Back 37

1) peripheral& central release of transmitters

2) depolarizationof the central and peripheral nerveendings

3) peripheral& central sensitization

Front 38

What generally happens in pre-synaptic inhibition?

Back 38

1) Pre-synaptic inhibitory synaptic input

2) Hyperpolarizationof terminal

3) Decreasedsynaptic neurotransmitter release

4) Diminishedsynaptic transmission

Front 39

What 2 specific things happen in pre-synaptic inhibition?

Back 39

-Less Ascending Transmission of Pain Signaling

-Less Synaptic Transmission of C and AδFiber Signaling

(less info going to thalamus than normal)

Front 40

pre-synaptic excitation

Back 40

*More ascending transmission of pain signaling after K+/Cl- Co-Transporters (KCC2, NKCC1) Promote Switch toGABA Excitatory Activation!*

Persistent nociceptor firingincreases GABA, [Cl-]i & outward drive; Cl- reversal potential = Post-synapticDepolarization

Front 41

What may account for referred pain?

Back 41

convergence of visceral and somaticafferents on the same spinal neurons

Front 42

What is a scenario in which areas of deep and referred pain may occur?

Back 42

myocardial infarction and angina

Front 43

In the visceral pain system, pain is...

Back 43

-Typically silent orfelt as dull ache that is hard to localize.

-But, signals from visceral nociceptorscan be felt as painelsewhere in the body.

-The source of the pain can be readily predicted from thesite of referred pain.

Front 44

Visceral and Somatic Sensory Information Convergence Centrally in the Spinal Cord Results in

Back 44

specific regional patterns

Front 45

What does "the placebo effect" or "endogenous pain control" refer to?

Back 45

descending inhibition and action of endogenous opiates

Front 46

Generally speaking, how do descending axons from neurons in the brainstem modulate pain?

Back 46

byactivating opiate-containing interneurons within the brainstem and dorsal hornof the spinal cord

Front 47

What do these“naturalopioid”neuropeptides act to inhibit?

Back 47

activation of the spinothalamic tract and other sites

Front 48

Opiates reduce what to diminish pain?

Back 48

synaptic transmission

Front 49

In descending inhibition, brainstem neurons release serotonin, norepinephrine and opioids, activating local inhibitory interneurons & suppressing activity of spinothalamic tract neurons by at least 3mechanisms. What are they?

Back 49

Action of Endogenous Opioids & Opiates

1) Opioidsdecreasethe duration of the sensory neuron action potentials by decreasing Ca2+ influx and neurotransmitter release

2) Monoamines and opioids decreasethe postsynapticpotential amplitude

3) Opiates hyperpolarize the membrane of dorsal horn neurons by activating a K+ conductance

Front 50

individual differences in pain perception are due to...

Back 50

cognitivesupra spinalfocus, evident as increased cortical activation (ACC, PFC, and insula)

Front 51

"pain network"

Back 51

CORTICAL AND SUBCORTICAL AREAS ARE INVOLVED IN PAIN PERCEPTION AND PAIN AFFECT

Front 52

6 examples of pain as a disease

Back 52

1) inflammatory pain - ex) arthritis

2) neuropathic pain - ex) diabetic neurpathy

3) cancer pain - ex) pancreatic cancer

4) orofacial pain - ex) burning mouth

5) headache/migraine

6) central pain

Front 53

inflammatory pain

Back 53

1) back pain

2) arthritis

-rheumatoid

-osteoarthritis

3) vasculitis

4) hypoxia

-sickle cell anemia

Front 54

chronic pain conditions

Back 54

-neuropathic pain

1) diabetic neuropathy

2) post-herpetic neuralgia

3) phantom pain

4) trigeminal neuralgia

-complex regional pain syndrome