Psychophysiology of pain Flashcards
What is pain?
Unpleasant sensory and emotional experience associated with or resembling that associated with, actual or potential tissue damage.
International association for the study of pain.
Intensely personal experience where person say it exists and when a person says it exists.
What are the three types of pain?
- somatic - superficial
- somatic-deep
- visceral-deep
What is somatic superficial pain?
- – skin (tissue damage),- sharp and localised (brief fast pain)
What is somatic-deep pain?
- deeper skin, muscles, joints (tissue damage, inflammation), burning, itching, aching, diffuse (slow pain, long-lasting)
What is visceral deep pain?
organs (distension, ischaemic, inflammation), dull ache/ burning, often diffuse (slow pain, Nausea, sweating)
WHat is acute pain?
-Momentary or severe – Weeks to months Less than 3 months
- Ultimately resolvable
- Damage heals and pain goes away
WHat is chronic pain?
-Persistent – remains despite healing processes
- Long-lasting – persists/ recurrent for longer than 3 months
- Complex emotional/psychological effects
- complex social/lifestyles implications
State the different reasons you feel pain?
- Early warning system
- Alerts to danger
- Warning of actual or potential harm
- Actual or potential tissue damage
- Elicits changes in behaviour
Try and avoid danger/harm
WHat is nociception ?
Neural process of encoding noxious stimuli
What is the congential cause of pain disorders?
SCN9A variant
- Ion channel non-functional
- No action potential (lack of neural signalling)
No pain signals arriving at CNS
What are the chemical activators for encoding pain?
Potassium
Hydrogen
Histamine
Serotonin
What are sensitisers chemical of encoding of pain?
Prostaglandin, bradykinin, nerve growth factors
How are free nerve endings activated when tissue is damaged?
- Tissue is damaged
- Inflammatory mediators are released by tissues
- Histamine & serotonin etc. activate the free nerve endings
- Prostaglandin etc. can act as a sensitiser – increasing activation
- The free nerve endings are acting as nociceptors
Free nerve endings send nociceptive signals to the brain via the spinal cord
WHat are the consequences of continued damage/ infection?
Peripheral sensitisation?
Peripheral sensitization:
1.Persistant activation
2. FNE releases substance P (Pain)
3. Powerful vasodilator
4. Powerful mast cell activator
5. Mast cells degranulate
6. More activation of FNEs
7. More release of substance P
Positive feedback loop.
What is central sensitisation?
2nd order neuron sensitisation (possibly long-term changes to excitability
1. 1st order neurone release neurotransmitter glutamate at synapse (in spinal cord)
2. Glutamate activates glutamate receptor on postsynaptic cell (2nd order neurone) – receptors called AMPA receptors – allow sodium to end cell
3. If continued activation of 1st order – too much glutamate which allows uptake by NMDA receptor in postsynaptic cell - allow calcium to enter cell – if they enter then biologically change 2nd order neurone which sensitises them and this can be long term change
4. Summation in receptors make chemical signal fire along 2nd order neurone
What are NMDA receptors?
- Allow Calicum into post-synaptic cell
- Activates 2nd order neurone
- Sensitised this neurone
- Stronger signal sent to the brain
- Make pain experience feel worse
Can biologically change the neurone so long term change or long term pain
What are two types of sensitisation?
Peripheral
Central
Brief
Peripheral sensitisation
- Substance P (pain) mediated feedback loop
- Presynpatic (1st order sensory neurone) sensitised
Brief
Central sensitisation
- NMDA receptors activated with strong or repeated activation
- Post-synaptic neurones (2nd order sensory neurone) sensitised
What are the different types of nociceptors fibre for mechanical ?
- Fibre type A δ – a delta
- Sharp pricking, fast pain
What are the types of nociceptor fibre for thermal and mechanothermal?
- Fibre type A δ – a delta
Slow burning, cold sharp, pricking
What is the type of nociceptor fibre for polymodal sensation?
- C fibre type
Hot and burning sensation, cold and mechanical stimuli, slow seep pain
What is a delta fibre?
nociceptor fibre
Myelinated (insulated) and larger diameter axons
Rapid conduction speed
What is a c fibre?
nociceptor fibre
Unmyelinated (not insulated)
Smaller diameter axons
Slow conduction speed
State the two sides of the spinothalamic pathway
Indirect spinothalemic
direct spinothalemic
Discribe the indirect spinothalemic pathway
Slower C fibres
Limbic system
Hypothalamus
Reticular formation
Reticular activating system
Poorer spatial discrimination
Linked to emotional aspects of pain
Linked to understanding salience / significance
Linked to memory of previous painful experiences
Linked to autonomic responses
Describe the direct spinothalemic pathway
Faster ‘Aδ’ fibres
Cortical areas
Better spatial discrimination
Discriminatory sense of pain sensations
Where on the body the damage or danger is happening
What is referred pain?
Pain felt in a part of the body other than the actual source of the pain signal
In embryonic development this is derived as out diaphragm nociceptors are entering the nervous system in the same area as the neck. You then grow and so there’s some cross over in the neurons fro, the different organs.
What’s the difference between nociception and pain perception?
Nociception
- Warning signal
Pain
- Pain in our brain telling us how important those signals are
- Or brain generates pain experience
- Pain is individual and subjective
What are some psychosocial dimensions (factors) that open the gate of pain experience signals?
Allowing nociceptive signals
Stress, tension, depression, worry, boredom, lack of activity and feelings of lacking control
What Psychosocial dimensions (factors) that Close the gate of pain experience signals – stop nociceptive signals ?
Relaxation, contentment, optimism, happiness, distraction, pro-activity and positive sense of control
Cognitive modulation of pain
4 psychological factors that effect pain perception
- Attention
- Experience
- Expectation
- Perceived threat
Perceptual filtering of incoming nociceptive information – can amplify or attenuate pain perception
What can perceptual filtering of incoming nocicpetive information do?
can amplify or attenuate pain perception
Whats the neuromatric theory of pain?
Different brain areas generates our response. To nociceptive pain signals delivered to the brain.
- Learned responses
- Attitudes and fears
- Perception of danger or safety
- Health beliefs
- Priorities
- Psychological status
What do these area of the brain do?
Amygdala and hippocampus
Primary motor cortex
Frontal cortex
Amygdala and hippocampus – memory
Primary motor cortex – physical response
Frontal cortex – voluntary primary movement
What is the descending inhibitory pathway?
Describe
- Neurones in brain stem send efferent fibres to spine and pass downwards
- Descending modulators fibres release serotonin and norepinephrine
- Powerful endorphins (enkephalins) released
- Signals generated to go up can’t go through
WHAT IS the periaqueductal gray?
propagation and modulation of pain, sympathetic responses as well as the learning and action of defensive and aversive behaviors
brain region
What are enkephalins?
Reduce incoming nociceptive signals and help reduce the central perception of pain
What is the pain gate theory?
-A beta fibres are mechanosensory – encoding touch sensations (not nociceptors)
- Activated they cause enkephalins to be released in the spines (these inhibit transmission of nociceptive signals to the brain)
If harm and you rub the area this activates enkephalin interneurones which shuts down or reduces the sensitivity of pain receptors being sent to my brain.
What is neuropathetic pain? Pathological?
Pathological – damage to somatosensory system
What is neuropathic pain? central damage?
Central damage – stroke, spinal cord injury, tumour growth centrally, central inflammation (central sensitisation)
What is neuropathetic pain? Peripheral damage?
Peripheral damage – physical trauma to nerve, degenerative damage, disease pathologies (peripheral sensitisation)
Explain the example of the neuropathic condition of herniated disks?
(Slipped disk of spinal cord)
Push on to major spinal nerves – cause pain and inflammation and damage to nerves – so can feel pain and discomfort
What is hyper algeria?
Defined – increased sensitivity following tissue injury
Inappropriate involvement of mechanosensory fibres
What are the two types of hyperalgesia?
Primary hyperalgesia – local to site of damage
Secondary hyperalgesia – extending to surrounding unmanaged areas
What is allodynia?
Defined – increased sensitivity to non-noxious stimulus
1. Central mechanism
2. Glial cells microglia – become activated during inflammation
3. Switch inhibitory input to excitatory
