Psychophysiology Of Pain Flashcards
Pain
Unpleasant sensory and emotional experience
Associated with actual or potential tissue damage
IASP
Sharp
Deep
Dull
Acute
Chronic
Bright
Burning
Nagging
Aching
Why feel pain?
Early warning system
Alerts to danger
Warning of actual or potential harm
Actual or potential tissue damage
Elicits change of behaviour
Try and avoid damage/harm
Types of pain
Superficial somatic
Deep somatic
Visceral
Acute
Chronic
Superficial somatic pain
Caused by tissue damage
Skin
Sharp (fast pain)
Localised, brief
Deep somatic pain
Caused by tissue damage
Deep layers of the skin, muscles, joints
Burning, itching, aching (slow pain)
Diffuse, long-lasting
Visceral pain
Caused by distension, lack of oxygen, inflammation
Organs
Dull ache, burning, gnawing (slow pain)
Nausea, sweating, shaking, autonomic responses, can be referred to as
Acute pain
Momentary or severe
Short periods of time - < 3 months
Readily resolvable
E.g. post operative pain
Autonomic response - fight or flight
Psychological component - associated anxiety
Chronic
Persistent
Remains despite healing processes
Long lasting - > 3 months
Complex emotional effects and social implications
Psychological component - increased irritability, depression, somatic preoccupation, social withdrawal, sleep issues, appetite changes
Physiological changes - e.g. sensitisation mechanisms, central and peripheral
Psychological changes - poorly defined central mechanisms, neuroplastic changes centrally
Nociception
Neural process of encoding noxious stimuli
Hard wire neural process
From sensory receptors to the spine then to the brain through the spinothalemic tract
Nociceptor
Sensory receptor that responds to pain
Nociceptor: free nerve endings
When activated it senses damage
Depolarises and sends action potential to spine then brain
Mechanoreceptors - stretch receptors that respond to stretch in the skin
Inflammatory mediators - released when tissue is damaged, CGRP, histamine, nerve growth factor, bradykinin, prostaglandin, substance P
Nociceptor: Polymodal
Free nerve endings
Respond to lots of different inflammatory mediators
Lots of sensory proteins and receptors
Nociceptor: activators
Potassium
Hydrogen ions
Histamine
Serotonin
Nociceptor: sensitisation
Makes the nociceptive nerve endings more sensitive to the inflammatory mediators
Increases the effect
Prostaglandin
Bradykinin
Nerve growth factors
Peripheral sensitisation
Inflammatory mediators activates the free nerve endings
Releases substance P
Substance P - vasodilation; enhanced inflammatory response, activate mast cells; degranulation and release histamine, increases sensitivity of free nerve endings, reactivate which means more substance P is released
Substance P mediated feedback loop
Presynaptic sensitised
Central sensitisation
Postsynaptic neurone sensitised
Presynaptic cell release glutamate
Travels to receptors on postsynaptic cell
Two types of glutamate receptors - AMPA and NMDA
Central sensitisation: AMPA receptors
Small amounts of glutamate released it attaches to AMPA receptors
Allows Na+ to enter the postsynaptic cell
Causing depolarisation and action potential to travel up the spinal cord
Transient stimulation
Central sensitisation: NMDA receptors
Lots of glutamate released it attaches to NMDA receptors
Allows Ca2+ to enter the postsynaptic cell
Causing the cell to become more sensitive
Increase in action potential through the postsynaptic cell
Strong stimulus - more nociceptive signals
Long term potentiation - nociceptive system can remember the sensitivity or pain
Types of nerve fibres
Mechanica;
Thermal and mechanothermal
Polymodal
Types of nerve fibres: mechanical
A delta fibre group
First order neurone
Sharp, pricking, fast pain sensations
Types of nerve fibres: thermal and mechanothermal
A delta fibre group
First order neurone
Slow burning, cold sharp, pricking sensations
Types of nerve fibres: Polymodal
C fibre group
First order neurone
Hot and burning sensation, cold, and mechanical stimuli, slow deep pain sensations
Pathways to the brain: direct spinothalemic
How strong and where the nociceptive signal comes from
Faster A delta fibres - myelinated and fatter axon
Cortical areas - somatosensory cortex
Better spatial discrimination
Discriminatory sense of pain sensations
Pathways to the brain: indirect spinothalemic
How we want to respond to incoming information
Pain experience
Slower C fibres - carry Polymodal information
Frontal cortex
Limbic system - salience of emotional part of pain
Hypothalamus - higher control of autonomic responses
Reticular formation and reticular activating system - autonomy response, feel sick, shaking, change blood flow distribution
Poorer spatial discrimination
Referred pain
Pain felt in a part of the body other than the actual source of the pain signal
Nociceptive signals can manifest as pain in different part of the body
Internal organs
Referred pain: embryology
As the embryo develops the nervous system is developed during early development
Some areas are close together but as you grow and change organs move further from where the nerves originate from
Pain modulation: pain gate - C fibres
Nociceptive signals to the second order neurone
Stimulated second order neurone
Signals are carried up to the brain
Activation leads to inhibition of the inhibitory interneurone means second order neurone is still receiving the signals
Pain modulation: pain gate - A beta fibres
Respond to touch and mechanical information
Activation leads to activation of inhibitory interneurone means second order neurone is inhibited
This stops or limits pain
Closes the pain gait
Fewer nociceptive signals
Pain modulation: pain gate - inhibitory interneurone
Integrates information
Stimulated it inhibits the second order neurone
No signals up to the brain
Releases GABA/enkephalin (inhibitory transmitters
Pain modulation: psychosocial dimensions
Different psychological states seem to gate or affect pain perception
Open the gait - more prone to a larger pain experience
Close the gait - less prone to a larger pain experience
Pain modulation: psychosocial dimensions - open the gate
Stress
Tension
Depression
Worry
Boredom
Lack activity
Feelings of lacking control
Pain modulation: psychosocial dimensions - close the gate
Relaxation
Contentment
Optimism
Happiness
Distraction
Pro-activity
Positive sense of control
Pain modulation: pain perception
Triggered by Nociception
Personalised
Positive outlook/psychology means pain perception can be diminished
Pain modulation: cognitive modulation of pain
Perception of pain is subjective
How we respond to nociceptive signals arriving in the brain
Amplify or attenuate pain perception
Affected by - attention, perceived threat, expectation, experience
Pain modulation: neuromatrix theory of pain states
Roland Melzack (1996)
Different parts of the brain are activated during painful experiences
Find patterns and magnitude of the activation
Not good model as it is difficult to do
Pain modulation: neuromatrix theory of pain states - hippocampus
Memory of pain
Pain modulation: neuromatrix theory of pain states - amygdala
Emotional response to the pain
Pain modulation: neuromatrix theory of pain states - anterior insula
Emotional response to insults
Pain modulation: neuromatrix theory of pain states - primary somatosensory cortices
Where the pain is and the strength
Pain modulation: neuromatrix theory of pain states - primary motor cortex
Response to the pain
Pain modulation: neuromatrix theory of pain states - prefrontal cortex
Decisions about the pain
Pain modulation: neuromatrix theory of pain states - rostral ventromediall medulla and periaqueductal gray
Activate descending pathways
Control the inhibitory interneurone
Pain modulation: descending inhibitory modulation
Two descending pathways - serotonergic and noradrenergic
Serotonin and noradrenaline released at dorsal horn in spine
Release of analgesics onto second order neurone closes the pain gait and reduce pain
Brain stem activated the pathways with release inhibitory neurotransmitters
Neuropathic pain
Pathological damage to somatosensory system
Damage to axon can cause inappropriate signals to the brain which causes a pain response
No nerve endings are activated
Lose - neurotrophins
Gain - nerve growth factors
Changes in gene expression
Neuronal excitability and connectivity
Neuropathic pain: damage to the nervous system - peripheral nervous system
Physical trauma to nerve - damaged nerve
Peripheral sensitisation
Can become pathological
Neuropathic pain: damage to the nervous system - central nervous system
Disrupting communication of the brain
Stroke
Spinal cord injury
Tumour growth centrally
Central inflammation
Central sensitisation
Can become pathological
Neuropathic pain: herniated disk
Pressure or damage to a nerve root coming out of the spinal column
Causes numbness or pain
Neuropathic pain: hyperalgesia
Increased sensitivity and extreme response to pain
Response to noxious stimuli
Exaggerated response to painful stimuli
Primary - local to site of damage, peripheral sensitisation, substance P
Secondary - extending to surrounding undamaged areas, central mediated pain, central sensitisation
Neuropathic pain: allodynia
Increased sensitivity to non-noxious stimuli
Light touch
Central mechanisms, central sensitisation
Microglial - activated during inflammation
Switch inhibitory input to excitatory
