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Flashcards in Physiology of Pain Deck (37):
1

Pain is different from all other senses because

the sensation is elicited by multiple stimuli
it preempts all other signals
these differences result in multiple alterations in the physiological functioning of the pain pathways

2

pain can be characterized as

fast pain
slow pain

3

fast pain

generally associated with the immediate injury
aka sharp pain

4

slow pain

often characterized as dull or achy
often occurs after the injury

5

Pain can be characterized by location

deep pain
muscle pain
visceral pain
somatic/cutaneous pain

again the characteristics of these forms of pain vary due to physiological and anatomical considerations

6

Sensory receptors

many are bare nerve endings with specialized ion channels that open in response to specific stimuli (i.e. thermoreceptors)
some sensory receptors show quite extensive morphological specilization

7

Sensing Noxious Stimuli - the nociceptors
Two types of fibers

bare nerve endings can be
A delta fibers
C fibers

8

A delta fibers

small sparsely myelinated, fast, sharp pain

9

C fibers

unmyelinated fibers associated with dull pain (slow pain)

10

Nociceptors must be able to detect

a wide variety of damaging stimuli

11

Types of Nociceptors

sensitive to both thermal and mechanical stimuli (most)
sensitive to only thermal
sensitive to only mechanical
silent/sleepin

12

Many mixed modality nociceptors also express a

mechanosensitibe Na channel (SCN9A or Na1.7)

13

Mutations in the nocicieptive Na channels lead to

an absence of pain sensation
paroxysmal pain syndrome

14

Mutations in the nocicieptive Na channels lead to

an absence of pain sensation
paroxysmal pain syndrome

15

Unlike other receptors, nociceptors express _________ which alter the sensitivity of the nociceptors to input

number of ligand gated receptors (in addition to the stimulus gated channels)

16

Ligand gated receptors for ______(4) are found on the nocicieptors to alter sensitivity

Substance P
the kinins
ATP
H+
interestingly this collection of chemicals also exists in the spinal cord, where they also influence nociceptive inputs at those synapses

17

When ligands bind their ligand gated channels on the nociceptors,

they change the sensitivity of the nociceptors (usually increasing) and activate the silent receptors

18

The source of sensitivity-altering chemicals

activated nociceptors, the damaged tissue, and recruited WBC release these into the periphery as well as in the spinal cord.

19

There are multiple pathways to the brain
proprioceptive and discriminative touch
fast pain
slow pain

dorsal columns
spinothalamic tract
spinoreticulothalamic system

20

The NT released by nociceptive fibers

EAA (from A delta) acting primarily on non NMDA receptors

21

NT released by C fibers

Substance P
EAA

22

Nociceptors that travel with the spinoreticulothalamic pathway (slow pain) synapse on
what is this synapse important for

an interneruon in the spinal cord before crossing and ascending to the reticular formation

this synapse is the site of much modulation of spinal cord function
local (gate theory)
descending (opioid pathways)

23

Nociceptors that travel with the spinoreticulothalamic pathway (slow pain) synapse on
what is this synapse important for

an interneruon in the spinal cord before crossing and ascending to the reticular formation

this synapse is the site of much modulation of spinal cord function
local (gate theory)
descending (opioid pathways)

24

visceral afferent pain fibers travel with

autonomic nerves, rather than with either of the two spinal pathways already described

25

Unlike other senses, nociceptive input is distributed widely in the Cortex

insular cortex
post central gyrus
mediofrontal cortex

26

Pain and S1 and S2

S1 and S2 do receive input from the nociceptors and play a role in localizing the pain

27

Pain and the insular cortex

the insular cortex is particularly important in the interpretation of nociceptive inputs

processes information about the internal state of the body
contributes to the autonomic response to the pain
INTEGRATES ALL SIGNALS RELATED TO THE PAIN (ASYMBOLIA - occurs when insular cortex is lost)

28

Lesions in any one area

does not abolish the ability to experience pain, although the experience is changed

29

pan and the amygdala

many nociceptiv inputs go to the amygdala
this is particularly important for activating?producing the emotional components inherent in the sensation of pain

30

Visceral nociceptors, traveling with the autonomic nerves, have additional synapses within

the hypothalamus and the medulla - these form the basis of the physiological changes associated with visceral pain, including diaphoresis and altered BP

31

Visceral nociceptors, traveling with the autonomic nerves, have additional synapses within

the hypothalamus and the medulla - these form the basis of the physiological changes associated with visceral pain, including diaphoresis and altered BP

32

Gate theory based on

based in part on the observation that other somatic input can alleviate pain (rubbing the area)

33

Gate theory reminder

neurons traveling in the spinoreticulothalamic tract synapse on an interneuron within the spinal cord before ascending

34

Gate theory

Step 1 - activate an A beta fiber by the normal stimuli. The AB fiber has a branch that travels via the coral columns, but it ALSO BRANCHES WITHIN THE SPINAL CORD

Step 2 - the AB fiber releases EAA and activates an inhibitory interneuron in the spinal cord

Step 3 - the inhibitory interneuron releases glycine to inhibit the activity of the second order neuron in the pain pathway

End result - rubbing the area of skin activated by the AB fiber will reduce the sensation of pain

35

Basic idea of descending mechanisms of modification of painful inputs

use presynaptic inhibition to reduce activation of the second order nociceptive neuron in the spinal cord

36

Basic idea of descending mechanisms of modification of painful inputs

use presynaptic inhibition to reduce activation of the second order nociceptive neuron in the spinal cord

37

Descending modification of pain

Step 1 - neurons in the periaqueductal gray are activated by numerous inputs, including opiate, EAA and the cannibinoids

Step 2 - axons from the PAG neurons travel to the midline raphe nuclei and release ENKEPHALINS which activate the raphe neurons

Step 3 - axons from the raphe neurons travel to the spinal cord and release SEROTONIN, which activate inhibitory nterneurons, causing them to release opiates

Step 4 - the opiates released by the interneuron activate mu receptors on the presynaptic terminal of the C fiber

Step 5 - this produces pre-synaptic inhibition that reduces the release of substance P from the nociceptor and reduces pain transmission