Pain

Front 1

What are the two ascending sensory pathways?

Back 1

-Dorsal columns
-Anterolateral system (including the spinothalamic tract)

Front 2

The dorsal columns carry ____ and _____ to the CNS.

Back 2

vibration and proprioception

Front 3

The anterolateral system (including ST tract) carries ____ and ____ to the CNS.

Back 3

pain and temperature

Front 4

What is nociception?

Back 4

the neural response to actual or perceived tissue damage

Front 5

What are nociceptors?

Back 5

peripheral free endings of primary sensory neurons origniating from the DRG and trigmenal ganglia neurons

Front 6

What activates nociceptors?

Back 6

harmful stimuli (damage releases chemicals that activate free nerve endings)

Front 7

What are the three classes of nociceptors?

Back 7

Thermal
Mechanical
Polymodal

Front 8

What temperatures activate thermal nociceptors?

Back 8

above 45 deg C and below 5 deg C

Front 9

Thermal nociceptors have _____ fibers to sense sharp pain

Back 9

A-delta

Front 10

What are the characteristics of A-delta fibers?

Back 10

-sharp pain
-least myelinated
-relatively small and slow compared to larger A-alpha and A-beta sensory fibers

Front 11

What activates mechanical nociceptors? What kind of fibers carry their sensory info?

Back 11

intense pressure; A-delta fibers (sharp pain)

Front 12

What activates polymodal nocieceptors?

Back 12

intense mechanical, chemical, or thermal stimuli

Front 13

What kind of fibers carry polymodal nociceptor sensory info?

Back 13

C fibers (dull, prolonged, burining pain) that are unmyelinated

Front 14

What are the two types of fibers that detect painful stimuli?

Back 14

C fibers and A-delta fibers

Front 15

What substances are released following tissue damage?

Back 15

histamine
bradykinin
potassium
substance P
serotonin
prostaglandins
leukotrienes

Front 16

What causes hyperalgesia?

Back 16

Substance P causing the release of histamine from mast cells and histamine acting on the free nerve terminals

Front 17

Explain the chemical cascade that causes pain.

Back 17

1. injury damages endothelial cells
2. ATP, Ach, 5-HT releaesd from damaged cells
3. Arachidonic acid is released and converted to PGE2 by cyclooxygenase
4. Bradykinin (potent) is released by damaged cells
5. Activated nociceptive terminals release peptides including substance P and CGRP
6. Substance P & CGRP activate mast cells and cause vasodilation/extravasation
7. Activated and damaged mast cells release histamine
8. Histamine activates polymodal nociceptors (C fiber endings)

Front 18

At what step in the chemical cascade of pain does aspirin act?

Back 18

the conversion of arachidonic acid to prostaglandin E2 by cyclooxygenase

Front 19

How do ATP, Ach, and 5-HT released from damaged endothelial cells work?

Back 19

they sensitize the endings of nerves (don't necessarily cause a full blown nociceptive response)

Front 20

Where does Bradykinin act? What does it do?

Back 20

directly on nociceptive endings of A-delta and C fibers;
it activates other cells to release more prostaglandins and inc. inflamm. response

Front 21

______ is a transmitter of C fibers

Back 21

Substance P

Front 22

T/F: A-alpha and A-beta fibers have outputs in both the dorsal and ventral horn

Back 22

True (they go all the way down to the ventral horn where they might be involved in sensorimotor reflexes)

Front 23

T/F: A-delta and C fibers generally terminated in the deeper layers of the dorsal horn.

Back 23

F (they generally terminate in the more superficial layers)

Front 24

Which specific lamina do A-delta fibers terminate in?

Back 24

usually layer I (marginal layer)
but can also synapse on layer V

Front 25

Which specific lamina do C fibers tend to synapse in?

Back 25

substantia gelatinosa (layer II) on interneurons (excit and inhib)

Front 26

What layer of the dorsal horn is most pain information coming from?

Back 26

superfical layers

Front 27

What is layer I lamina called? What terminates here?

Back 27

Marginal layer; nociceptive specific (A-delta) fibers and other somatosensory neurons

Front 28

What is layer II lamina called? What terminates here?

Back 28

Substantia gelatinosa; either nociceptive (C fibers) or responsive to non-noxious stimuli

Front 29

What terminates on level III/IV of lamina?

Back 29

A-beta fibers-responsive to non-noxious (not nociceptive)

Front 30

What fibers can synapse in layer V?

Back 30

A-beta, A-delta, C fibers, and nociceptive input from viscera

Front 31

What type of fibers can synapse in layer VI?

Back 31

A-beta fibers (muscle/joint input)

Front 32

What kind of input is there in layers VII/VIII?

Back 32

polysynaptic nociceptive inputs bilateral

Front 33

What is the pathway for pain and temperature sensation?

Back 33

1. come in Lissauer's tract
2. axons travel up or down a couple of segments before they enter SC
3. come into substantia gelatinosa
4. cross in ventral white commissure

Front 34

Do all pain/temp fibers cross to contralateral side?

Back 34

No, some stay ipsilateral but the majority do cross over to the contralateral side

Front 35

Which fibers conduct the fastest?

Back 35

A-alpha and A-beta

Front 36

Describe A-alpha and A-beta fibers.

Back 36

myelinated
conduct the fastest
have the largest axons

Front 37

Describe A-delta fibers.

Back 37

myelinated
smaller (than A-alpha & A-beta)
somewhat slower (than alpha and beta) but still pretty fast

Front 38

Describe C fibers.

Back 38

non-myelinated
conduct orders of magnitude slower (than A fibers)
repetitively activated
responsible for slow, dull, burning pain

Front 39

What type of transmitters are used by DRG?

Back 39

Glutamate and Substance P

Front 40

Where in nerve terminal is glutamate contained?

Back 40

Found in clear small vesicles

Front 41

Where in nerve terminal is Substance P found?

Back 41

dense core vesicles

Front 42

What causes release of glutamate at nerve terminal? Is release fast or slow?

Back 42

a single AP; release is fast

Front 43

What is glutamate responsible for in DRG? Through what type of receptor?

Back 43

fast synaptic signaling; largely through AMPA receptor

Front 44

What is required for the release of Substance P from DRG nerve terminals?

Back 44

repetitive stimulation of C fibers

Front 45

What is capsaicin?

Back 45

a member of the TRP (transient receptor potential) family that is specific for temperature

Front 46

What is hyperalgesia?

Back 46

with damage, pain pathways become more sensitive to pain (hypersensitivity to pain); occurs after tissue damage

Front 47

What is allodynia? What is the mechanism of action?

Back 47

when non-painful stimuli activate nociceptors; C fibers fire repetitively resulting in glutamate release onto spinal cord neurons also activating NMDA receptors

Front 48

What is thought to be responsible for phantom limb pain?

Back 48

Allodynia: after amputation C fibers are still "wound up" and could cause changes in the spinal cord

Front 49

What are the 3 tracts in the anterolateral system?

Back 49

Spinothalamic
Spinoreticular
Spinomesencephalic

Front 50

What is the pathway for the spinothalamic tract?

Back 50

from laminae I, V, VII to the thalamus VPM and VPL and then up to somatosensory cortex

Front 51

Do fibers in the spinothalamic tract cross? If so, where?

Back 51

yes, in the ventral white commissure

Front 52

Do fibers of the spinoreticular tract cross?

Back 52

some (has crossed and uncrossed fibers)

Front 53

Do fibers of the spinomesencephalic tract cross?

Back 53

yes

Front 54

What is the pathway for the Spinoreticular tract?

Back 54

From deeper lamina VII, VIII --> sends off collaterals to synapse in the reticular system of brainstem (pons & medulla) --> then they synapse in thalamus --> to somatosensory cortex

Front 55

What is the pathway for the spinomesencephalic tract?

Back 55

from cord laminae I, V to the mesencephalic reticulum, lateral periaqueductal grey matter --> to hypothalamus, limbic system, and midbrain

Front 56

Which tract in the anterolateral system synapses with other ascending pathways to communicate with other parts of the brain that have to deal with emotion (i.e. amygdala)?

Back 56

spinomesencephalic tract

Front 57

Whic tract of the anterolateral system goes directly to the hypothalamus?

Back 57

spinothalamic

Front 58

What are the 2 nuclei in the thalamus associated with pain?

Back 58

Lateral and Medial nuclear group

Front 59

What nuclei make up the lateral nuclear group?

Back 59

VPL/VPM and posterior nuclei

Front 60

What entes lateral nuclear group and where does it project?

Back 60

LNG receives nociceptive specific fibers and projections from the spinothalamic tract; it projects to the primary somatosensory cortex

Front 61

What makes up the medial nuclear group?

Back 61

intralaminar nuclei complex (paleospinothalamic)

Front 62

What inputs does the medial nuclear group receive? Where does the MNG project?

Back 62

nociceptive specific inputs and projections from the spinoreticulothalamic tract; diffuse projections to the cortex

Front 63

What are the 3 cortical areas responsible for pain processing?

Back 63

Anterior insular cortex
Anterior cingulated cortex
Primary somatosensory cortex

Front 64

What projects to the anterior insular cortex?
What kind of pain info does the AIC process?

Back 64

medial thalamus;
info about the internal state of the body (autonomic component of pain)

Front 65

What projects to the anterior cingulated cortex? What kind of pain info does the ACC process?

Back 65

intralaminar nuclei of medial thalamus;
emotional component of pain

Front 66

What projects to the primary somatosensory cortex? What kind of pain info does the PSC process?

Back 66

lateral thalamus (projects to primary then to secondary);
location and intensity of pain (via sensory homonculus)

Front 67

T/F: There is a conscious and unconscious ability to gate the amount of painful information sent to the cortex.

Back 67

True

Front 68

In the gating hypothesis of pain, which fibers activate the projection neuron and inhibit the inhibitory interneurons (disinhibition)?

Back 68

C fibers

Front 69

In the gating hypothesis of pain, which fibers interact with C fibers and may modify the pain signal?

Back 69

A-beta fibers (carry vibration)

Front 70

In the gating hypothesis of pain, which fibers decrease the strength of the pain signal?

Back 70

A-beta fibers

Front 71

What is the pain path descending from the cortex?

Back 71

somatosensory cortex --> periaqueductal grey (also receives from hypothal.) --> raphe nuclei --> dorsal horn neurons --> descending neurons terminate on opiod containing cells

Front 72

What are the transmitters for the locus ceruleus?
raphe nucleus?
spinal cord?

Back 72

norepinephrine
serotonin
opiod receptor system

Front 73

At the cellular level, what type of opiod receptors do neurons act on?

Back 73

pre- and post-synaptic mu type opiod receptors

Front 74

What is referred pain?

Back 74

deep nociceptors within viscera can send afferents into dorsal horn where they meet up with various nociceptors from other places such as the skin; the same nerve is stimulated and pain will be experienced froma specific dermatome