Psychophysiology of pain Flashcards
Define Pain (IASP definition)
Pain is an unpleasant sensory and emotional experience
associated with actual or potential tissue damage
Mccaffery and Beebe 1989 pain definition
Intensely personal experience with biological, psychological
and social components, existing where a person say it exists
and when a person says it exists.
Why do we feel pain?
-early warning system
-alerts to danger
-warning of actual or potential harm
-actual or potential tissue damage
-elicits changes in behaviour
-to try avoid danger/harm
Describe somatic superficial pain
-caused by tissue damage
-skin
-sharp/fast pain
-localised/brief
Describe somatic deep pain
-caused by tissue damage
-deep layers of skin,muscles,joints
-burning/aching slow pain
-diffuse- long lasting
Describe visceral pain
-caused by distension, lack of oxygen, inflammation
-organs
-dull ache/burning slow pain
-can cause nausea, sweating
-can be referred
Define acute pain
momentary or severe- weeks/ months
-readily resolvable
Define chronic pain
-persistent-remains despite healing processes
-long lasting
-complex emotional effects
-complex social/lifestyle implications
What causes the congenital absence of pain disorder?
central perception of pain mechanisms disrupted
-produced more analgesic neurotransmitters
-mutation in SCN9A gene which sits on specific neurons in the body (these neurons sense pain)
-non functional VG Na+ channels
-no AP
-no nociception
-acute pain sensing missing
Where are nociceptions found?
the neural process of encoding noxious stimuli
What is a nociceptor?
-sensory receptor that responds to pain
-many types of receptor
What types of receptor are found in nociceptors?
-TRPV1(heta, PH, capsaicin)
-mechanoreceptors
CGRP
-histamine
-nerve growth factors
-bradykinin
-prostaglandin
-substance P
How do nociceptors work?
-free nerve ending senses damage
-depolarises, generates AP
-travel along first order neuron
-back to the spine
Define polymodal
The nerve endings can respond to many difference inflammatory mediators- because of all the different protein receptors
Free nerve ending activators
- k+
- H+
- histamine (weak activator)
-serotonin (weak activator)
Free nerve ending sensitization
-prostaglandin (derived of phospholipids, powerful inflammatory mediator, vasodilation)
-bradykinin (released for the blood coagulation cascade)
-nerve growth factors (long lasting effects on the sensitivity of the nerve endings)
What is substance P/ peripheral sensitization?
positive feedback loop, presynaptic 1st order sensory neurons sensitised
-powerful vasodilator
-enhances inflammatory response ( leakiness, dilation of local blood vessels)
-leading to the cardinal signs of inflammation
-directly activates mast cells for degranulation
-more histamine and substance P released so more activation of the free nerve endings
The more you damage the same area, more inflammatory chemicals are released, more sensitive the area
-known as peripheral sensitization
What’s neurogenic inflammation?
a form of inflammation initiated by activation of peripheral nervous system c-fibre neurons rather than by immunological events
Describe mechanical receptors and their fibres/sensation
Aδ
-sharp prickling fast pain
Describe thermal and mechanothermal receptors and their fibres/sensation
Aδ
-slow burning, cold sharp prickling
Describe polymodal receptor and their fibres/sensation
C
-hot and burning sensation, cold, and mechanical stimuli, slow deep pain
What are the two types of nerve fibres?
Aδ
C
What is central sensitization/spinal hyperexcitability?
NMDA receptors activated with strong or repeated activation Post synaptic neurons/ 2nd order sensory neurons sensitised
-between 1st and 2nd order neurons
-AP comes down first order neuron presynaptic cells- releases glutamate
-chemical synapse in the 2nd order neuron and sensed by 2nd order neuron
-2nd order neuron has AMPA and NMDA receptors
-glutamate binds to AMPA or NMDA
2nd order neuron can be sensitized by CGRP or subs P or growth hormones
What is AMPA?
allow sodium ions to enter the cell
(glutamate)
