Pain and thermosensation Flashcards
Definition of pain?
-what are the 3 forms of pain?
“An unpleasant sensory and emotional experience, associated with actual tissue damage or described in terms of such damage”
-nocicpetive (acute pain) inflammatory (prolonged pain) Pathological (neurogenic pain i.e. no longer useful)
characteristics of pain vary according to point of origin:
describe the characteristics of pain originating from:
Skin
Muscle
Viscera
Skin
well localised
pricking, stabbing, burning
Muscle
poorly localised
aching, soreness/tenderness, cramping, stabbing, burning
Viscera
poorly localised
Dullness, vagueness, Fullness, Nausea
Nociceptive pain
- what is activated for this to occur?
- where are the cell bodies located?
-Nociceptors, specific peripheral primary sensory afferent neurones normally activated preferentially by intense stimuli
they are first order neurones
-in the dorsal root ganglia and trigeminal ganglia
Nociceptor subtypes
- where does transduction begin?
- what are the two types of fibres involved?
- How can they be sub classified? (2, 4)
-in free nerve endings
-A delta fibres
mechanical/thermal nociceptors, thinly myelinated, mediate first/fast pain
-C fibres unmyelinated and respond to all noxious stimuli, mediate second/slow pain
-A delta fibres can be sub classified:
Type I & Type II
Type I:
require strong mechanical stimuli for activation, activated by noxious heat
they show sensitisation to new stimuli
the threshold falls in tissue injury
mediates first pain to mechanical injury
Type II:
respond to noxious mechanical stimuli and also to noxious heat
Shows adaption
Mediates first pain to heat
C-fibres can be sub classified
C-MH, C-M, C-H, C-MiHi
(H= heat, M= mechano)
C-MH:
responds to noxious mechanical stimuli and activated by noxious heat
sensitive to capsaicin, contributes to heat pain and location of stimulus
C-M:
responds to noxious mechanical stimuli, insensitive to heat an capsaicin
C-H:
repsonds to noxious heat
normally insensitive to mechanical stimuli and sensitive to capsaicin
mediates heat hyperalgesia and does not contribute to localisation. sensitive to mechanical stimulate when there is inflammation
C-MiHi:
normally insensitive to both mechanical and heat stimuli but acquires sensitivity on inflammation. sensitive to capsaicin
Nociceptor structure
-name the 2 terminals present and how they affect function
Central terminal:
not responsive to environmental stimuli
Site of Ca dependent transmitter release
targeted by endogenous molecules that regulate activity
Peripheral terminal:
responsive to environmental stimuli
Site of release of molecules that influence local tissue environment (e.g. substance P)
targeted by endogenous molecules that regulate sensitivity
MEANS SIGNALLING CAN BE BIDIRECTIONAL
Inputs to the spinal cord:
- where are primary afferent cell bodies located?
- where do axons terminate?
- where do C-fibres and A delta fibres terminate?
- what cells synapse with C-fibres and A delta fibres?
- proprioceptive cells receive input from what fibres?
- what do Wide dynamic range fibres receive input from?
- in dorsal root ganglia
- centrally in the dorsal horn of the spinal cord in various laminae of Rexed
- superficially in laminae I and II
- nociceptive specific cells
- A beta fibres
- from all 3 types of fibre so respond to a wide range of stimuli
Neurotransmission between the primary afferent and second order neurone in the dorsal horn
- what is the NT?
- what is produced by ^?
- What receptors are involved?
- what role do peptides have?
- glutamate
- fast e.p.s.p.
- activates AMPA receptors with NMDA receptor participation
- substance P and CGRP also participate causing slow and prolonged e.p.s.p. that facilitates activation of NMDA receptors by relieving voltage dependent block by Mg
Sensitisation of the nociceptive pathway following tissue damage -what are the two distinct processes? -for each: mediated by? effect? (2) maintained by what? plays major role in what sensation?
-peripheral sensitisation & central sensitisation
peripheral sensitisation
mediated by nociceptors at the site of injury/tissue inflammation
causes primary hyperalgesia via reduced threshold and amplified response
requires ongoing peripheral pathology for maintenance
major role in heat, lesser extent mechanical sensitivity
Central sensitisation
Reflects an increase in CNS neurone activity and properties
causes secondary hyperalgesia & allodynia via recruitment of novel inputs to nociceptive pathways and abnormal processing of sensory input
underlies pain that persists after tissue healing
major role in mechanical sensitivity
Visceral, Viscerosomatic and referred pain
- where does visceral pain originate from? character?
- pathway of visceral afferents?
- how does referred pain occur?
- what symptoms are assoc with visceral pain?
- where does visceral pain refer to?
- what is viscerosomatic pain? how does it occur?
-nociceptors covering tissues or walls of hollow organs
originates from stretching, twisting, inflammation and ischaemia- but not cutting to burning
poorly localised, dull aching, throbbing character
- visceral afferents from nociceptors follow sympathetic pathways before entering dorsal horn
- some visceral and skin afferents converge upon the same spinothalamic neurones and the brain interprets the nociceptive information arising from the viscera as originating from an area of skin that may be distant to the internal organ
- autonomic features e.g. nausea, vomiting, sweating, paler
- to segmental dermatome
- it is sharp and well localised, occurs when inflammatory exudate from diseased organ contacts a somatic structure
The nociceptive tracts
- ascend the spinal cord in what system? comprised of? (2)
- where do neurones terminate for 1st & 2nd tract?
- 2nd tract function?
-anterolateral system
the spinothalamic tract (STT)
The spinoreticular tract (SRT)
-STT
in the posterior nucleus of the thalamus and ventroposterior nucleus of the thalamus
-SRT
reticular nuclei in the the brainstem
involved in autonomic response to pain, emotional response, fear of pain
Discriminatory and emotive components of pain
- name the 2 pathways involved?
- features of each? (signals fro where, function?)
-Fast pathway (STT) slow pathway (SRT)
-STT
signals from the thalamus are relayed by thalamocortical neurones to the primary sensorimotor cortices
warning system, signals location and severity of the injury and they duration of pain, analyses features
SRT
signals to the intralaminar nuclei of the thalamus indirectly through the brain stem reticular formation via reticulothalamic tracts
signals from the thalamus released by thalamocortical neurones to limbic areas of the forebrain registers the emotional/motivational component
regulation of pain
- difference between nociception and pain?
- what explains the fact that pain perception is variable ad that pain can be reduced by simultaneous activity in LTMs
- how can this theory be applied?
-pain is awareness of suffering: nociception may occur i the absence of pain and vice versa
-Gate control theory:
some neurones within the substantial gelatinosa project to the spinothalamic tract and can be excited by large diameter sensory axons and unmyelinated nociceptive axons
The projection neurone is inhibited by an interneurone (excited by large sensory axon and inhibited by nociceptive axon)
Activity in the nociceptive axon alone maximally excites the projection neurone, allowing nociceptive signals to arise to the brain
-counter stimulated analgesia
stimulation of non-nociceptive afferents activated inhibitory interneurones which suppress the projection neurone
Thermosensation at the skin
- what are thermoreceptors?
- how does sensitivity change across the body?
- what does this result in?
- specialised neurones that respond to small changes in temp
- temp sensitivity is not uniform accross the body, hot and cold sensitive spots exist
- Separate neurones and their associated receptors/channels must exist to encode between ‘warm’ and ‘cold
