Oral and Facial Pain Flashcards
(95 cards)
1
Q
Define pain
A
pain is an unpleasant sensory or emotional experience associated with actual or potential tissue damage, or described in terms of such damage
2
Q
What is nociception?
A
this refers to the activation of neural pathways by stimuli that damages or threathen to damage the tissues (noxious stimuli)
3
Q
Pain is one of the classical components of inflammation. List the others
A
calor
rubor
tumour
Functio lasae (loss of function)
4
Q
Pain is the result of ___________
A
nociception
5
Q
What is referred pain?
A
this is when the source and the site of the pain are different
6
Q
What types of structures usually experience referred pain?
A
usually occurs between structures of the same embryological origin
7
Q
When pain is described as being “segmental”, what does it mean?
A
it refers to the fact that both the source and the apparent location of the sensation fall within the same neural segment of the body
8
Q
What are the classifications of the origins of orofacial pain ?
A
- intracranial pain disorders
- primary headache disorders (neurovascular)
- Neurogenic pain disorders
- Intra-oral pain disorders
- Temporomandibular pain disorders
- Pain arising from disorders of associated structures (e.g. eyes, ear, nose, throat)
- pain associated with mental disorders (e.g. psychogenic pain)
9
Q
Give examples of neurogenic pain disorders
A
- paroxymal neuralgias
- continuous pain disorders
- sympathetically mediated pain
10
Q
Give examples of chemicals that can activate OR sensitise nociceptive nerve endings
A
- bradykinin
- histamine
- serotonin
11
Q
Give examples of chemicals that can active nociceptive nerve endings
A
Prostaglandins
Leukotrienes
12
Q
Give examples of chemicals that can only activate nociceptive nerve endings
A
- K+
- H+
13
Q
What is the function of neuropeptides released by nociceptive nerve endings?
A
contribute to a positive feedback mechanism
14
Q
Seemingly comparable injuries or disease states always produce the same level of pain in different people or even the same people. True or false
A
False
15
Q
Most of the knowledge on the mechanism of simple acute pain originates from studies on ___________.
A
Limbs
Not on orofacial region
16
Q
Why is the term “pain receptor” not acceptable? What is the more appropriate term of use?
A
This is because pain is a perception and not a stimulus
The more appropriate term to use is nociceptor
17
Q
Why is the term nociceptor more acceptable than “pain receptor”?
A
this is because some stimuli can activate nociceptors without causing pain e.g. temperatures around 41 degrees celsius
18
Q
Morphologically, all or most nociceptors are believed to be …
A
free nerve endings
19
Q
In what way do nociceptors differ?
A
they can be myelinated (A fibres) or unmyelinated (C fibres)
20
Q
In humans, most A-delta fibres respond to only what type of stimuli? What are these fibres referred to as?
A
most will respond to mechanical stimuli only
Adelta mechano-nociceptors
21
Q
What are A delta polymodal nociceptors?
A
these are the next largest group of A delta fibres which respond to all kinds of stimuli (mechanical thermal, chemical)
22
Q
Give examples of other types of Adelta fibres
A
- respond to only cold
- respond to hot and chemical but not mechanical
23
Q
What is the nature of most of the unmyelinated (C-fibres)?
A
they are polymodal - responding to strong mechanical stimuli, intense heat or cold and various pain producing chemicals
24
Q
Why are first (fast) and second (slow) pain components more difficult to distinguish in the orofacial region ?
A
this is because of the short conduction distances in the brain
25
What are the neural effects of chemicals released as a result of tissue damage?
activation or sensitisation to noxious stimuli
26
How can intradental nociceptors become activated?
hydrodynamic mechanisms
27
Chemicals that can activate nociceptors are knowns as ...
alogenic- pain producing
28
What occurs following activation of a nociceptor?
increased membrane permeability of the nerve ending, resulting in depolarisation which, if large enough, will generate action potentials in nerve fibres
28
Damaged/inflammed tissues display increased pain sensitivity. True or false
True
28
What is hyperalgesia?
a group of conditions where increased intensities of pain result from a stimulus that would usually produce a lesser level of pain
| heightened pain from things that are meant to hurt
28
What is Allodynia ?
It is a type of hyperaesthesia whereby pain is produced by stimuli which would not normally do so
| pain from things that are not supposed to hurt
29
What is the cause of allodynia ?
sensitisation of peripheral nociceptors by inflammatory alogenic substances when they are present in concentrations that are too low to produce a threshold potential
30
The inducible form of cycloxygenase enzyme is ...
COX2
31
The constitutive form of cycloxygenase enzyme is ...
COX1
32
What is the benefit of selective COX-2 inhibitors ?
analgesic and anti-inflammatory actions without the undesirable side effects that are accountable to COX-1 inhibition; GI disturbances, haematological (aspirin), some renal and respiratory (sensitive asthmatics)
33
Where are the cell bodies of most orofacial nociceptive neurons located?
trigeminal ganglion
34
Briefly outline the pathway of orofacial nociceptive receptors
Trigeminal ganglion ---> trigeminal sensory root ---> nucleus caudalis (caudate nucleus) ---> thalamus ---> somatosensory cortex
35
The nucleus caudalis is referred to anatomically as ...
the hindmost part of the trigeminal spinal nucleus
36
What are the types second order neurons in the nucleus caudalis?
* nociceptive specific cells which receive inputs from only nociceptors
* wide dynamic range (nonciceptive non specific)- receive input from nociceptors, mechanoreceptors and thermoreceptors
37
What is the main function of nociceptive specific neurons?
signal the presence and location of noxious stimulus
38
What is the main function of wide dynamic range cells/neurons?
they may grade the overall severity
39
Briefly describe neuronal divergence
primary afferent neuron terminals branch and synapse with several second order neurons
40
Briefly describe neuronal convergence?
this is where second order neurons receive inputs from many different primary afferents
41
Neuronal convergence may be implicated in what conditions?
Hyperalgesia
Referred pain
42
How do second order neurons (that receive input from superficial and deep structure) interpret input/signals?
they intepret them as originating from the more superficial structure since such inputs usually predominate
43
With regard to the trigemino-thalamic tract, describe the projection of second order neurons. What is the consequence of this ?
2nd order neurons cross the midline and project to the contralateral thalamus
sensation of pain is generation on the opposite side of the brain to the injury that causes the pain
44
In reference to the gate control theory of pain, what is the function of small inhibitory interneurons?
* they can reduce the amount of excitatory neurotransmitter released by primary afferent neurons
* they can also directly inhibit second order neuron
45
What is the potential role of large diameter mechanoreceptors in the gate control theory of pain?
segmental inhibition
they can activate inhibitory interneurons
46
What is the potential role of neurons in higher centres in the gate control theory of pain ?
descending inhibition
activation of inhibitory interneurons
47
Second order nociceptive cells that are concerned with the sensation of pain travel directly via the trigemino-thalamic tract and synapse at the ___________.
ventrobasal nuclei
(bypass the thalamus?)
48
Third order neurons from the ventrobasal thalamus project to ...
primary somatosensory cortex
49
Positron emission tomography has shown that the __________________ is uniquely activated by thermal noxious stimuli
anterior cingulate gyrus
50
Give an example of an instance where pain occurs without obvious tissue injury
trigeminal neuralgia
51
Surgical interruption of presumed nociceptive pathways always permanently removes pain. True or false
False
52
Why are nociceptive pathways described as dynamic?
this is because neural activity can be modified to suppress or enhance the amount of pain that is experienced in different circumstances
53
Give examples of chemicals that are involved in the mediation of transmission at the first synapse in nociceptive pathways. What is their function
* glutamate
* substance P
* calcitonin gene related peptide
they are excitatory substances that tend to depolarise (and thus produce activity in) the post synaptic neurons.
54
The inhibitory controls that modulate activity in nociceptive pathways are referred to as ...
Gate controls
55
The gate control theory of pain was proposed by ___________ in 1965
Melzack and Wall
56
Briefly explain the circumstances where resulting pain may be severe
when the gate is wide open allowing signals pass from the primary afferent nociceptive nerves to the second order cells
57
Briefly explain the circumstances where no pain would be felt
the gate between primary afferent nerves and second order cells are closed or partly open (the latter being the most often case)
58
What does the "gate" in the gate control theory of pain refer to?
interneurons
59
How are interneurons able to modify activity in the nociceptive pathway?
* Presynaptic inhibition- decrease the release of excitatory neurotransmitters
* Postsynaptic inhibition- inhibition of second order cells
60
What chemicals mediate the inhibitory effect of interneurons ?
by a variety of agents including:
* GABA
* Glycine
* endogenous opioid peptides such as enkephalins and dynorphins
61
How are inhibitory interneurons activated in nociceptive pathways?
* other afferents (mechanoceptors/Abeta mechanosensitive cells)
* descending signals from the brain
62
There is evidence that activity in large diameter Abeta afferent nerves from the same __________ of the body inhibit activity in second order nociceptive neurons.
the same neural segment
63
How are the vast majority of Abeta nerves activated following injury?
they can be activated by rubbing close to an injury or a diseased tooth as they are mechanosensitive
64
Why is there an assumption, from a clinical standpoint, that mechanoreceptive controls of pain will always be active to a limited extent?
this is because mechanoreceptors are constantly being excited by our movements
65
What is the likely consequence of reducing mechanoreceptive activity in a specific part of the body?
it can cause an increase in sensitivity to pain by "opening the gate"
66
What type of fibres are amongst the most easily damaged by physical insult ?
Abeta fibres
e.g. following pressure damage
67
Briefly explain why re-establishing normal mobility can contribute to successful treatment of some chronic pains?
reduced sensitivitity to pain in that area
due to activation of inhibitory interneurons by Abeta mechanoreceptive fibres
this effectively closes the "gate" and thus no pain experienced
68
Outline some of the ways in which a post synaptic neuron in the nociceptive pathway can be sensitised
* increase transmitter release from presynaptic neuron
* increased expression of receptors on post synaptic neuron
* enhanced post synaptic depolarisation
* metabolic changes in post synaptic neuron
69
What are some of the biological/molecular effects of the removal of inhibitory influences on the nociceptive pathway?
* increased transmitter release from pre-synaptic neuron
* enhanced post synaptic depolarisation
70
The knowledge of segmental control of pain gave rise to what principle? Give a brief summary of behind this principle
Transcutaneous electrical nerve stimulation (TENS)
selective activation of Abeta nerves with electric stimuli can be used to reduce pain
71
All forms of TENS work via Abeta fibres acting segmentally. True or false
False
they do not all work in this way
72
State the alternative ways in which different forms of TENS can work
electrical stimulation of sites in the brain and particularly in the brainstem
they inhibit the responses of second order nociceptive neurons
73
What sites in the brainstem can be targetted by TENS to produce analgesia?
* periaqueductal or periventricular grey matter
* raphe nuclei
74
What are the assumed mechanisms by which descending pathways inhibit nociceptive pathways?
* directly (without inhibitory interneurons)
* activation of interneurons- mediating gate controls
75
Where do NSAIDs and topical anaesthetics exert their effects?
nociceptors
76
Give examples of different classes of drugs that are used to control orofacial pain
* antidepressants
* membrane stabilising drugs e.g. carbamazepine
77
Following TENS, what do the descending fibres release ?
* serotonin (5HT)
* Noradrenaline
78
Although there is no evidence of how descending pathways are activated naturally, state some instances where their activation is possible (in line with current evidence)
* conditions of stress and anxiety
* when there is a noxious/painful stimulus in another part of the body
79
How can the role of descending pathways explain why there may be reduced levels of pain felt on a battlefield or sports field?
* this is because conditions of stress and anxiety can activate the descending pathways
* descending pathways can possibly activate inhibitory interneurons and thus reduce pain experienced
80
What is the counter irritation phenomena?
this is where one pain masks another
81
Give an example of a traditional therapy that may be a form of counter-irritation
acupuncture
82
How does the counter-irritation phenomena tie into the descending pathway?
a noxious/painful stimulus in another part of the body may activate the descending pathway on the contralateral side of the brain
Descending pathway can then work to inhibit the pain signals
83
What does facilitation refer to?
increase in transmission signals
84
What is the consequence of increasing transmission signals at the first synapse in nociceptive pathways?
increase in strength/duration of the resulting pain
85
Briefly describe the phenomena that is "wind-up"
this is where repetitive activation of nociceptive C-fibres brings about an enhanced response to subsequent activity in these fibres
86
What factors may bring about "wind-up"
* increased release of transmitters such as substance P (act on NK1 receptors) and glutamate (act on NMDA receptors) by presynaptic neurons
87
The mechanisms of wind up are similar to mechanisms which are responsible for ________________.
Long term potentiation
88
What is the role of long term potentiation in areas like the hippocampus?
underlies some forms of learning which result from repeated activation of the NMDA receptors
89
Central sensitisation occurs in response to ...
persistent nociceptive inputs and peripheral nerve injuries
90
Central sensitisation can contribute to ...
hyperalgesia and some forms of allodynia
91
Recent studies of some mammalian neurons which may be second order nociceptive cells have been described by engineers to be ...
bistable
92
What does the term bistable refer to in this context? What is its relevance clinically?
once these mammalian nerve cells are depolarised by transient excitatory influence, they remain partially depolarised until subjected to a transient inhibitory influence.
This may be fundamental in our understanding of how clinical pain outlast the injuries that initially produce them.
