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)
What is NMDA?
allow calcium ions to enter the cell
(glutamate
What is transient stimulation?
AMPA receptors activated
What is strong stimulation
NMDA receptors activated
calcium entry sensitises the postsynaptic cell
What other factors are involved in spinal hyperexcitability?
-sensitisation of substance P
-changes in number of synapses and connectivity
-changes in cell physiology/number
-AB fibre mediated pain
Describe the indirect spinothalamic tract
-slower C fibres
-limbic system, hypothalamus, reticular formation,recticular activating system
-poorer spatial discrimination
Describe direct spinothalamic tract
-faster ‘Aδ’ fibres
-cortical areas
-better spatial discrimination
-discriminatory sense of pain sensations
3 main functions of the limbic system
-emotional processing
-social processing
-learning
What is referred pain?
pain felt in a part of the body other than the actual source of the pain signals
-happens due to embryology
-as you grow up the parts of your body get further apart from eachother- but the nerve network was layed down first so it is technically sending signals to the same place
Whats the pain gate theory?
-When the gates are open, you feel too much pain for too long. People with chronic pain conditions have gates that stay open even when they should be shut.
Closed gates. If you’ve ever injured two parts of your body at the same time, you understand that pain signals “compete” for our brain’s attention. It’s difficult for your brain to process pain from both areas at the same time.
massaging/’rubbing the area better’ can close pain gates
A- beta fibres can inhibit the 2nd order neurons
How does gently stroking babies provide pain relief?
Subclass of mechanosensory C-fibres involved
C-touch fibres activated by light stroking, 1-10cm/s
In adults – pleasant sensation / affiliative behaviours
Tracked noxious evoked brain activity
~ 60% reduction
Claimed
Similar to topical
anaesthetic
What factors open pain gates ?
Stress
Tension
Depression
Worry
Boredom
Lack of activity
What factors close pain gates?
Relaxation
Contentment
Optimism
Happiness
Distraction
Pro-activity
What is the cognitive modulation of pain?
factors such as attention, experience, expectation and perceived threat can amplify or attenuate pain perception
What is the neuromatrix theory of pain states?
proposed by Ronald Melzack in 1996
-pain is produced by patterns of nerve impulses
-neuromatrix determines how pain is expereinced, we all have an individual neuromatrix
What is the descending inhibitory modulation?
-2 descending pathways
-one from periaqueductal grey matter
-one from the medulla
-serotonergic and noradrenergic (released when the pathways are stimulated)
-release natural endorphins which close pain gates
Beta endorphin overproduction- leads to body wide analgesia- cant feel pain
What factors affect pain experience?
-context(beliefs, expectations)
-cognitive set( hypervigillance, distraction)
-mood
-chemical and structure
(neurodegeneration, maladaptive plasticity, metabolic opiodergic or dopaminergic)
What is pathological pain?
damage to somatosensory system
What can cause peripheral pain?
-physical trauma to nerve
-peripheral sensitization which can become pathological
What can cause central pain?
-stroke
-spinal cord injury
-tumour growth centrally
-central inflammation
-central sesitization- can become pathological
Describe neuropathic pain
lose-neurotrophins
gain-NGF growth factors
-changes in gene expression
-neuronal excitability
-neuronal connectivity
define hyperalgesia
form of increased sensitivity following tissue injury
primary-local to damaged site often linked to peripheral sensitization
secondary-extending to surrounding undamaged areas
What is allodynia?
increased sensitivity to non noxious stimuli
-central mechanism
-microglia-activated during inflammation
-switch inhibitory input to excitability
Describe some effects/ changes of chronic pain
-can become permanent
-often with complete resolution of physical damage
physiological changes- sensitisation mechanisms central or peripheral
Psychological changes- often poorly defined central mechanisms,neuroplastic changes centrally, some evidence of changes to pain neuromatrix
Describe the pain complex and multifactorial
– Peripheral mechanisms
– Spinal mechanisms
– Brain stem mechanisms
– Cortical areas
– Emotional aspects
– Cognitive aspects
– Descending control
– Pain gate theory
– Pathophysiological aspects
