An Introduction To Pain And Thermosensation Flashcards
Name the 3 different forms of pain
Nociceptive, inflammatory and pathological pain
How is acute mild pain effectively treated? (In general)
NSAIDs, paracetamol and in moderate/severe cases the addition of opioids of several classes
Name some alternative drug classes that are not originally designed as analgesics but are used for chronic pain
Antidepressants, anticonvulsants, local anaesthetics
How is pain described when it originates from the skin?
Pricking, stabbing, burning (well localised)
How is pain originating from the muscle described?
Aching, soreness/tenderness, cramping, stabbing, burning (poorly localised)
How is pain originating from the viscera described?
Dull, vague, fullness, nausea (poorly localised)
What are nociceptors?
Specific peripheral primary sensory afferent neurons normally activated preferentially by intense stimuli that are noxious
They are first order neurons that relay information to second order neurons in the CNS by chemical synaptic transmission
What are the subtypes of nociceptor?
A-delta fibres and C fibres
Describe A-delta fibres
They are mechanical/thermal nociceptors that are thinly myelinated - response to noxious mechanical and thermal stimuli. Mediate first, or fast, pain
Describe C fibres
They are nociceptors that are unmyelinated - collectively they respond to all noxious stimuli (they are polymodal). Mediate second, or slow, pain
Describe the afferent function of nociceptors
Afferent - transmit nociceptive information to the CNS via release of glutamate and peptides within the dorsal heron
Describe the efferent function of nociceptors
Efferent - release pro-inflammatory mediators from peripheral terminals - contributes to neurogenic inflammation
What can happen as a result of long term noxious stimulation?
Increases spinal excitability contributing to hyperalgesia and allodynia
Peptides (SP and CGRP) are released from free nerve ending of peptidergic nociceptors due to tissue damage or inflammatory mediators. What does SP cause?
Vasodilation and extravasation of plasma proteins (promotes formation of bradykinin and prostaglandins), release of histamine from mast cells and sensitises surrounding nociceptors
Peptides (SP and CGRP) are released from free nerve ending of peptidergic nociceptors due to tissue damage or inflammatory mediators. What does CGRP do?
Induces vasodilation which causes primary and secondary hyperalgesia and allodynia to occur
What causes neuronal excitation by activating postsynaptic AMPA receptors with NDMA receptor participation?
Glutamate produces a fast e.p.s.p and causes neuronal excitation
Glutamate also participates in neuronal excitation by causing a slow and prolonged e.p.s.p that facilitates activation of NDMA receptors by relieving voltage-dependent block by Mg (T/F)
False - peptides (substance P and CGRP) also participate causing a slow and prolonged e.p.s.p that facilitates activation of NMDA receptors by relieving voltage-dependent block by Mg
Some visceral and skin afferents converge upon the same spinothalamic neurons. This means the brain interprets the nociceptive information arising from the viscera as orginating from an area of skin that may be distant to the internal organ. What is this phenomenon called?
Referred pain
Visceral pain is that perceived at a distance from the affected organ. What are some of the associated autonomic features and where is the area of referral to?
Often associated with symptoms such as nausea, pallor, sweating and vomiting. The area of referral of visceral pain is to the segmental dermatome e.g. gallbladder -> C4
Viscerosomatic pain is sharp and well localised. Give an example of this and describe it
Viscerosomatic pain occurs when inflammatory exudate from a diseased organ contacts a somatic structure e.g. parietal peritoneum. An example of this would be appendicitis - however this classically presents with diffuse visceral pain that then progresses to sharp viscerosomatic pain
Describe the difference between pain and nociception
Pain is awareness of suffering, nociception may occur in the absence of pain and vice versa. Perception of pain is variable; for the same degree of nociceptor activity, depending on the level of concurrent non-painful sensory input and behavioural context more, or less, pain may be perceived
How can pain be reduced in terms of nociceptors and mechanoreceptors?
Pain evoked by activity in nociceptors (C and A-delta fibres) can be reduced by simultaneous activity in low threshold mechanoreceptors (A-beta fibres)
What happens to the gate for painful stimuli to be received by the brain when no input comes in?
When no input comes in, the inhibitory neuron prevents the projection neuron from sending signals to the brain - gate is closed, no pain signal is received by the brain https://s.hswstatic.com/gif/pain-2.gif
What happens to the gate for painful stimuli to be received by the brain when there is excitation of large sensory axons?
Both the inhibitory neuron and the projection neuron are stimulated, but the inhibitory neuron prevents the projection neuron from sending signals to the brain - gate is closed https://s.hswstatic.com/gif/pain-2.gif
What happens to the gate for painful stimuli to be received by the brain when there is excitation of small sensory axons/nociceptive axons?
Nociception happens when there is more small fibre stimulation or only small fibre stimulation. This inactivates the inhibitory neuron and the projection neuron sends signals to the brain informing it of pain - gate is open https://s.hswstatic.com/gif/pain-2.gif
Where do projection neurons of the spinothalamic tract originating from lamina I terminate?
The posterior nucleus of the thalamus
Where do projection neurons of the spinothalamic tract originating from lamina V terminate?
Posterior and ventroposterior nucleus of the thalamus
What is the spinoreticular tract involved in, in terms of pain?
Involved in autonomic responses to pain, arousal, emotional responses and fear of pain
Temperature sensitivity is not uniform across the body surface; separate hot and cold sensitive spots exist and these do not respond to both therefore what must exist?
Separate neurons and their associated channels/receptors must exist to encode between warm and cold
