Psychophysiology Of Pain Flashcards by Abi Wareham

Pain

Unpleasant sensory and emotional experience
Associated with actual or potential tissue damage
IASP
Sharp
Deep
Dull
Acute
Chronic
Bright
Burning
Nagging
Aching

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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

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Types of pain

Superficial somatic
Deep somatic
Visceral
Acute
Chronic

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Superficial somatic pain

Caused by tissue damage
Skin
Sharp (fast pain)
Localised, brief

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Deep somatic pain

Caused by tissue damage
Deep layers of the skin, muscles, joints
Burning, itching, aching (slow pain)
Diffuse, long-lasting

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Visceral pain

Caused by distension, lack of oxygen, inflammation
Organs
Dull ache, burning, gnawing (slow pain)
Nausea, sweating, shaking, autonomic responses, can be referred

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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

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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

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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

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Nociceptor

Sensory receptor that responds to pain

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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

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Nociceptor: Polymodal

Free nerve endings
Respond to lots of different inflammatory mediators
Lots of sensory proteins and receptors

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Nociceptor: activators

Potassium
Hydrogen ions
Histamine
Serotonin

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Nociceptor: sensitisation

Makes the nociceptive nerve endings more sensitive to the inflammatory mediators
Increases the effect
Prostaglandin
Bradykinin
Nerve growth factors

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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

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Central sensitisation

Postsynaptic neurone sensitised
Presynaptic cell release glutamate
Travels to receptors on postsynaptic cell
Two types of glutamate receptors - AMPA and NMDA

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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

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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

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Types of nerve fibres

Mechanical
Thermal and mechanothermal
Polymodal

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Types of nerve fibres: mechanical

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A delta fibre group
First order neurone
Sharp, pricking, fast pain sensations

Types of nerve fibres: thermal and mechanothermal

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A delta fibre group
First order neurone
Slow burning, cold sharp, pricking sensations

Types of nerve fibres: Polymodal

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C fibre group
First order neurone
Hot and burning sensation, cold, and mechanical stimuli, slow deep pain sensations

Pathways to the brain: direct spinothalemic

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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

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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

Psychophysiology Of Pain Flashcards

(49 cards)