Pain I and II

Question 1

What’s the pain cycle?

Answer 1

Painful dental therapy/
Post-op pain 
---> Apprehension
--->Avoidance
--->Pathology
--->Clinical pain
then back to painful dental therapy/post-op pain

Question 2

What is meant by levels of pain?

Answer 2

pain is detected (and is medicated) at many different levels of the nervous system

Question 3

What is the definition of pain?

Answer 3

…. “is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage” (Merskey, 1986)*

- individual variability
- treat it! (pain is not normal)

Question 4

What are factors affecting the perception of pain?

Answer 4

cultural background
 emotional state
 age
 previous experience
 fatigue
 distraction

Question 5

What are the two (three) different types of pain that can be experienced?

Answer 5

Two (3) different types of pain can be experienced

Acute (transient) Pain:
Pulled muscle, abrasion, cut skin, blunt needle inj.

Persistent (few days-wks); Chronic (3-6mos.) Pain Joint Pain – arthritis, degenerative disease
Lower back pain
Migraine headaches - neuralgia
Disease - terminal cancer

Question 6

Of all the senses what is the easiest to modify?

Answer 6

pain, use drugs, mind control.

Question 7

what does the reception of painful stimuli do for the receipient/

Answer 7

Reception of Painful stimuli motivates the recipient to attend to the stimulus (remove it) or else some form of tissue damage may result

Question 8

What happens if a painful stimuli occurs for a long time? What can higher centers do about incoming pain stimuli?

Answer 8

If the sensation continues for a long time, CNS characteristics may alter (change in mood)

Painful sensations can be modified by higher centres overriding the incoming stimuli to preserve current state

Question 9

What are the three categories of pain receptors (nociceptors)?

Answer 9

1. Mechanical
2. Thermal
3. Polymodal

Question 10

What are the mechanical nociceptors like?

Answer 10

both A delta and C fibres

supplied by both myelinated (A delta) & unmyelinated (C type) fibres

A delta fibres may be responsible to what is called the “first pain”

unimodal (will not respond to temperature stimuli)

only responsive to SEVERE forms of stimulation (pin prick, pinching)

Question 11

What are the thermal nociceptor like?

Answer 11

may be two types (hot vs. cold):
- mainly supplied by C-type fibres
- small latency indicating they are temp responsive
(and not just inflammation indicators)
- may also respond to extreme mechanical stimulation

Question 12

What are the polymodal nociceptors like?

Answer 12

• respond to a variety of painful stimuli
• thermal, mechanical (pressure) and chemical
  exclusively innervated by C-type fibres
  thought to transmit “second pain”

Question 13

What are the four characteristics of a nociceptor?

Answer 13

Four characteristics:

1) must have high threshold for appropriate stimulus
2) must possess small receptor field within tissue
3) must produce persistent discharge during suprathreshold stimulus
4) innervated by small diameter myelinated/ unmyelinated afferent fibres

Question 14

For the characteristic of a nociceptor of - must have high threshold for appropriate stimulus, what is the difference between A beta and A delta fibers?

Answer 14

• Lower stimulus intensity required at receptor level to elicit response from an Aβ non-nociceptive vs. Aδ and C nociceptive fibres

It’s like if you’re just walking then it doens’t hurt, you can tell there’s pressure, but when you stomp really hard then you start getting all of the other ones and it hurts.

If nociceptors were firing all the time you’d be in pain all the time

Question 15

For the characteristic of a nociceptor of - must possess small receptor field within tissue what does this mean for nociceptors?

Answer 15

Each single polymodal nociceptor as a very small receptive field (size of receptive field indicated by size of dot in diagram) and only fire when heat stimulus is over 46C

Question 16

For the characteristic of what does must produce persistent discharge during suprathreshold stimulus mean?

Answer 16

i.e., response dues not “fatigue out” during the stimulus
? Is this like a rapidly adapting or slowly adapting receptor? It is like a slowly adapting receptor because as you apply the stimulus it continues to fire, not when you put it on or take it off it fires.

Question 17

For the characteristic of a nociceptor of - innervated by small diameter myelinated/unmyelinated afferent fibers what type of fibers are they?

Answer 17

A delta or C-type fibers

slowest transmission of information in the body.

Question 18

What does the activation of peripheral nociceptors cause?

Answer 18

Activation of peripheral nociceptors causes the release of substances which report pain to the CNS

In the PNS, the depolarization of the free nerve endings results in perception of pain by the CNS

Initial discharge of primary afferents is mediated by chemicals

Released into the surrounding extracellular fluid in response to tissue damage

there are substances known to potentiate pain that are released right at the receptor level.
this is why you can ask a patient to take ibuprofen before they come in, because they will deaden the release of these or the response to them.

Question 19

What is peripheral sensitization?

Answer 19

Peripheral sensitization: peripheral receptors of nociceptors become easier to activate and fire more often – why?

Step 1 is tissue damage = release of K +, bradykinin (from the blood vessels), and prostaglandins to peripheral receptors.

Step 2: Increased neuronal excitability = release of Substance P, which causes release of 1) 5-HT from platelets, 2) histamine from mast cells, and 3) bradykinin from blood vessels

Step 3: Other neurons that formerly weren’t involved in the first pain response nevertheless receive the released serotonin and histamine, simply by being too close to the initial injury. Thus, pain spreads to these “non-affected” nerves.

Question 20

what is secondary hyperalgesia?

Answer 20

A single injection of a pain-causing substance into the epidermis/dermis may elicit a pain response that spreads to surrounding areas (therefore hyperalgesic area is secondary to the primary pain stimulus)

Question 21

Different fibre groups carry vastly different information, what info do group A alpha, A beta, A gamma, A delta, and C type fibers carry?

Answer 21

Pain Afferents: NB!!!!
Different fibre groups carry vastly different information

Group A-a and A-b DO NOT carry nocioceptive information
Carry low-threshold info regarding proprioception

Group A-g fibres are motor

Groups A-d and C type fibres are found to respond to high threshold mechanical and/or thermal stimuli.

Question 22

What is a nerve fiber like?

Answer 22

Although a typical nerve contains many types f nerve fibres, each of those individual fibres respond to different types of stimuli

Question 23

What are the two pain pathways?

Answer 23

Fast pain and slow pain.

Question 24

what’s fast pain?

Answer 24

Fast Pain

• the Group A-delta fibres carry nocioceptive information (Both thermal/mechanical)
• Conduction velocities 12 – 18 m/sec
• Responsible for conveying short latency pricking pain – the sharp first pain

THIS IS THE FIRST PAIN!!!!!!!!

Question 25

What is slow pain?

Answer 25

Slow Pain - Type C fibres have a much reduced conduction velocity (0.5 – 2 m/sec) - Endings are activated by high threshold mechanical, thermal (> 45°C and chemical stimuli - Responsible for mediating long lasting burning pain – the dull second pain If you stop the transmission of that fast pain, the A delta fibers, then the slow pain the C type fibers pain is increased with the same amount of stimuli.

Question 26

what do we know about the C-polymodal nociceptor?

Answer 26

not much, but evidence suggests that the terminals are sensitive to direct heat or mechanical distortion. Thus transduction can occur at the terminal.

Question 27

Are there more large myelinated or small unmyelinated?

Answer 27

The number of small diameter (likely C-type) fibres greatly outnumber larger (likely myelinated) fibres

Question 28

what is the duality of pain? What is the pathway for fast and slow or dull pain?

Answer 28

These two types of fibres are found throughout the skin and deeper tissues – Duality of pain is maintained at all levels. There are two fibre pathways that convey nocioceptive information to the CNS: One is believed to be responsible for fast pain – spinothalamic/trigeminothalamic The other conveys dull chronic pain - spino-reticulo-thalamic (trigeminal correlate too)

Question 29

There are pathway within the spinal cord (duplicated in the trigeminal nuceleus caudalis), what are they and what happens there?

Answer 29

Primary afferents enter spinal cord Eventually synapse in Lamina I, II/III, or V of the dorsal horn Lamina I (marginal zone) - synapses, receive from thermal and mechanical nocioceptors - A-d (fast pain) and C type fibres (slow pain) Laminae II/III (substantia gelatinosa) - synapses receive from polymodal nociceptors - only C type fibres Lamina V respond to info coming from both nocioceptive as well as non-nocicpetive origins - termed wide dynamic range neurons The neurotransmitter that conveys pain is not well defined Known that C-type fibres use Substance P Found anywhere you locate small unmyelinated fibres DON'T REALLY NEED TO KNOW THE TERMS SO MUCH AS JUST UNDERSTAND THE CONCEPT. (the laminae are diagrammed in the notes). the ones that cause fast pain are more superficial than the ones that cause dull pain. Non-pain fibers synapse a bit deeper and the major non-nociceptive information synapse in number V just like some pain does.

Question 30

Where in the brain do we have pain synapsing?

Answer 30

Thalamus - (VPM and VPL) has two areas it processes pain – reflects the duality areas for pain also process other modalities as well Cortex Generally held view that pain is not well represented at the cortical level - this view changing with PET scans – Known discriminative versus affective areas - found in deeper gray matter – in depths of sulcus

Question 31

What is the gate theory?

Answer 31

Many different theories – specificity theory, stimulus pattern theory, etc. In the early 60’s Melzack & Wall enunciated the Gate Control theory (stood the test of time for the most part)

Question 32

What are the four criteria of the gate control theory?

Answer 32

1) Transmission of impulses from afferents to the Spinal cord neurons is controlled by a gate 2) Gate is influenced by relative amounts of activity associated with large & small diameter fibres ``` Large fibre (non-nocioceptive) activity closes the gate (blocks transmission) Small fibre activity (nocioceptive) opens the gate (facilitates pain transmission) ``` Like when you hit your hand and then you rub it to make it feel better. 3) nerve impulses from higher centres can influence the gating mechanism 4) Once neurons of cord reach (exceed) a critical point, there is activation of the “Action system” Pain is perceived. Evasive action can be initiated

Question 33

What are the 4 main players involved in the gate control theory?

Answer 33

1) Myelinated non-nociceptive fibres (M) 2) Unmyelinated nociceptive fibres 3) Spinal interneurons 4) Wide dynamic range neurons

Question 34

When normal pain happens in the pain gate, explain what happens

Answer 34

Non-nociceptive fibres activate the interneuron, so the wide dynamic range neuron is inhibited (not activated) (look at the picture). In the picture the myelinated non-nociceptive fiber attach to both the wide dynamic range neuron and the interneuron. The unmyelinated neuron also synapses on both). Nociceptive fibres inhibit the interneuron, so the wide dynamic range neuron is not longer inhibited and fires… OUCH! When you get a mix of the two the myelinated non-nociceptive fibre will close the gate and the unmyelinated nociceptive fiber will open the gate.

Question 35

What happens at temperature extremes?

Answer 35

At temperature extremes, both nociceptors and thermal non-thermal nociceptors may fire

Question 36

What happens if you remove the FAST first pain fibres (the A deltas?)

Answer 36

If you don’t have the A deltas then the C pain gets worst and worst and worst every time you apply the stimuli.

Question 37

What has been occurring in the reducing/controlling painful stimuli?

Answer 37

In the last 15 years there has been a large increase in acceptance of acupuncture and TENS as methods of reducing/ controlling painful stimuli These practices have been v. beneficial in Dentistry

Question 38

What happens with the inhibition of pain with opiate-like substances?

Answer 38

Different opiate-like substances are located in various regions throughout the CNS including the - periaqueductal gray (around the cerebral aqueduct) - dorsal horn of spinal cord - laminae I, II and V - respiratory centers in brainstem - thalamus, anterior cingulate (when you take these, your anterior cingulate pretty much gets shut down) When these enkephalins, endorphins and dynorphins bind to neurons, they block activity and produce analgesia. Opiates have high addiction potential, but play an important role in pain management

Question 39

How many different opiate receptors are on the neuronal cell surface?

Answer 39

3

Question 40

What is the descending pathways for inhibition of pain?

Answer 40

Many of the areas that have opiate-like receptors receive from ascending pain pathways but they also have descending connections back to the same area The periaqueductal gray is a major reticular formation control site for descending modulation of pain Connects to other medullary nuclei (nucl. Raphe magnus – 5-HT) and dorsal horn (nucleus caudalis – pain nucl of mouth) When stimulated, all of these areas produce analgesia Neurotransmitter is thought to be Substance P. Effectively block/ suppress the activity of neurons in the nucleus caudalis – pain nucl of mouth. Inhibition is only to nociceptive specific neurons since wide-dynamic range neurons can still convey normal touch info -e.g.: can block jaw opening reflex elicited by stimulation of tooth pulp (touching tooth pulp really, really hurts) vs. tapping a tooth (which hopefully doesn’t hurt)