Pain I and II Flashcards
What’s the pain cycle?
Painful dental therapy/ Post-op pain ---> Apprehension --->Avoidance --->Pathology --->Clinical pain then back to painful dental therapy/post-op pain
What is meant by levels of pain?
pain is detected (and is medicated) at many different levels of the nervous system
What is the definition of pain?
…. “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)
What are factors affecting the perception of pain?
cultural background emotional state age previous experience fatigue distraction
What are the two (three) different types of pain that can be experienced?
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
Of all the senses what is the easiest to modify?
pain, use drugs, mind control.
what does the reception of painful stimuli do for the receipient/
Reception of Painful stimuli motivates the recipient to attend to the stimulus (remove it) or else some form of tissue damage may result
What happens if a painful stimuli occurs for a long time? What can higher centers do about incoming pain stimuli?
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
What are the three categories of pain receptors (nociceptors)?
- Mechanical
- Thermal
- Polymodal
What are the mechanical nociceptors like?
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)
What are the thermal nociceptor like?
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
What are the polymodal nociceptors like?
- respond to a variety of painful stimuli
- thermal, mechanical (pressure) and chemical
exclusively innervated by C-type fibres
thought to transmit “second pain”
What are the four characteristics of a nociceptor?
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
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?
- 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
For the characteristic of a nociceptor of - must possess small receptor field within tissue what does this mean for nociceptors?
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
For the characteristic of what does must produce persistent discharge during suprathreshold stimulus mean?
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.
For the characteristic of a nociceptor of - innervated by small diameter myelinated/unmyelinated afferent fibers what type of fibers are they?
A delta or C-type fibers
slowest transmission of information in the body.
What does the activation of peripheral nociceptors cause?
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.
What is peripheral sensitization?
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.
what is secondary hyperalgesia?
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)
Different fibre groups carry vastly different information, what info do group A alpha, A beta, A gamma, A delta, and C type fibers carry?
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.
What is a nerve fiber like?
Although a typical nerve contains many types f nerve fibres, each of those individual fibres respond to different types of stimuli
What are the two pain pathways?
Fast pain and slow pain.
what’s fast pain?
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!!!!!!!!
What is slow pain?
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.
what do we know about the C-polymodal nociceptor?
not much, but evidence suggests that the terminals are sensitive to direct heat or mechanical distortion. Thus transduction can occur at the terminal.
Are there more large myelinated or small unmyelinated?
The number of small diameter (likely C-type) fibres greatly outnumber larger (likely myelinated) fibres
what is the duality of pain? What is the pathway for fast and slow or dull pain?
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)
There are pathway within the spinal cord (duplicated in the trigeminal nuceleus caudalis), what are they and what happens there?
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.
Where in the brain do we have pain synapsing?
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
What is the gate theory?
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)
What are the four criteria of the gate control theory?
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
What are the 4 main players involved in the gate control theory?
1) Myelinated non-nociceptive fibres (M)
2) Unmyelinated nociceptive fibres
3) Spinal interneurons
4) Wide dynamic range neurons
When normal pain happens in the pain gate, explain what happens
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.
What happens at temperature extremes?
At temperature extremes, both nociceptors and thermal non-thermal nociceptors may fire
What happens if you remove the FAST first pain fibres (the A deltas?)
If you don’t have the A deltas then the C pain gets worst and worst and worst every time you apply the stimuli.
What has been occurring in the reducing/controlling painful stimuli?
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
What happens with the inhibition of pain with opiate-like substances?
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
How many different opiate receptors are on the neuronal cell surface?
3
What is the descending pathways for inhibition of pain?
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)
