OFS- special aspect of orofacial pain Flashcards
(28 cards)
What is allodynia and give an example of allodynia
pain due to stimulus that does not normally provoke pain eg trigeminal neuralgia
Factors affecting perception of pain
intensity, emotion, past experience, other concomitant sensory experience, race, placebo
Characteristic of fast pain
sharp pain, well localised, short duration, thermal and mechanical nociceptos, A-d fibers
Characteristic of slow pain
aching burning pain, poorly localised, long duration, polymodal nociceptors, C fibers
Where does double pain arise from
2 different fiber conducting at diff velocity
How does tissue damage cause stimulation of nociceptors
tissue damage will cause release of chemical to sensitise (prostaglandin- damaged cells, substance P-primary afferent) and activate (potassium-damaged cells. bradykinin-damaged vessel, serotonin damaged endothelial and platelet, histamin-mast cells) nociceptors
How is peripheral sensitisation occur
Antidromic activation cause neuron to release substance P
Describe the pain caused by hot pulps
antidromic activation cause release of SP and calcitonin gene related peptide.
SP cause plasma extravasation and mast cell degranulation and activate nociceptors . CGRP cause dilation of blood vessel and odema formation which cause release of bradykinin activating nociceptors
Process of central sensitization
tissue/peripheral nerve injury increases C fiber input–> increase in summation of slow synaptic potential–> alteration in second messengers–> activates protein kinase –> increase excitability and synaptic efficacy causing central sensitisation
How to prevent central sensitisation in dentistry ans why do we want to prevent central sensitisation
preventing CS will reduce post-op pain
Administer LA after GA for third molar exo to prevent CS
Differences between Allodynia vs Hyperalgesia
Allo: CS
Hyper:CS+PS
key effects of substance p in dental pulp
vasodilatory, histamine release, increase blood flow, increased vascular permeability, increase bp,
conditions or procedure that will increase substance p release
caries, pulpitis, granuloma, cavity prep, orthodontics, tooth beaching
2 types of 2nd order neuron and their effects
nociceptive and Wide dynamic range
3 nucleus of trigeminal sensory neuron
mesencephalic, chief and spinal
3 part of spinal nucleus of CNV
sub nucleus oralis, interpolaris and caudalis
describe the trigeminal pain pathway
1st order neuron enters at the level of pon, then descend to the medulla and synapses with 2nd order…….
5 theories of pain
specific, intensity, pattern, gate control, neuromatrix
What is the gate control theory and what are the 4 component
interaction between nociceptive and non-nociceptive input at the the spinal cord level in the form of a gating mechanism
4 component
large fibers (non-nociceptive, touch)
small fibers (nociceptive)
subsatantia gelotinosa (spinal gating system)
T- cells (transmission cells sending pain signals to the brain)
How does the gate control theory work
small fiber activation will inhibit inhibitory cells from inhibiting transmission of pain
Large fiber does opposite hence inhibiting pain transmission
What is the neuromatrix theory
The neuromatrix theory of pain states that the perception of painful stimuli does not result from the brain’s passive registration of tissue trauma, but from its active generation of subjective experiences through a network of neurons known as the neuromatrix.
What is referred pain
Pain from internal organ is felt as pain in a more superficial region, cz nociceptor fibers from viscera and cutaneous structure converge on the same pain pathway
What are 5 categories of special aspects of pain in the orofacial region
Referred pain, TMD, Headache, Neuralgia, Phantom pain
Common causes of TMD
Structural or mechanical displacement, functional or neuromuscular and psychological
