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Applied Health Science > Psychophysiology of pain > Flashcards

Psychophysiology of pain Flashcards

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1
Q

What is pain?

A

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.

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2
Q

What are the three types of pain?

A
  1. somatic - superficial
  2. somatic-deep
  3. visceral-deep
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3
Q

What is somatic superficial pain?

A
  1. – skin (tissue damage),- sharp and localised (brief fast pain)
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4
Q

What is somatic-deep pain?

A
  1. deeper skin, muscles, joints (tissue damage, inflammation), burning, itching, aching, diffuse (slow pain, long-lasting)
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5
Q

What is visceral deep pain?

A

organs (distension, ischaemic, inflammation), dull ache/ burning, often diffuse (slow pain, Nausea, sweating)

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6
Q

WHat is acute pain?

A

-Momentary or severe – Weeks to months Less than 3 months
- Ultimately resolvable
- Damage heals and pain goes away

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7
Q

WHat is chronic pain?

A

-Persistent – remains despite healing processes
- Long-lasting – persists/ recurrent for longer than 3 months
- Complex emotional/psychological effects
- complex social/lifestyles implications

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8
Q

State the different reasons you feel pain?

A
  1. Early warning system
  2. Alerts to danger
  3. Warning of actual or potential harm
  4. Actual or potential tissue damage
  5. Elicits changes in behaviour
    Try and avoid danger/harm
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9
Q

WHat is nociception ?

A

Neural process of encoding noxious stimuli

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10
Q

What is the congential cause of pain disorders?

A

SCN9A variant
- Ion channel non-functional
- No action potential (lack of neural signalling)
No pain signals arriving at CNS

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11
Q

What are the chemical activators for encoding pain?

A

Potassium
Hydrogen
Histamine
Serotonin

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12
Q

What are sensitisers chemical of encoding of pain?

A

Prostaglandin, bradykinin, nerve growth factors

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13
Q

How are free nerve endings activated when tissue is damaged?

A
  1. Tissue is damaged
  2. Inflammatory mediators are released by tissues
  3. Histamine & serotonin etc. activate the free nerve endings
  4. Prostaglandin etc. can act as a sensitiser – increasing activation
  5. The free nerve endings are acting as nociceptors
    Free nerve endings send nociceptive signals to the brain via the spinal cord
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14
Q

WHat are the consequences of continued damage/ infection?

Peripheral sensitisation?

A

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.

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15
Q

What is central sensitisation?

A

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

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16
Q

What are NMDA receptors?

A
  • 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
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17
Q

What are two types of sensitisation?

A

Peripheral

Central

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18
Q

Brief

Peripheral sensitisation

A
  • Substance P (pain) mediated feedback loop
  • Presynpatic (1st order sensory neurone) sensitised
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19
Q

Brief

Central sensitisation

A
  • NMDA receptors activated with strong or repeated activation
  • Post-synaptic neurones (2nd order sensory neurone) sensitised
20
Q

What are the different types of nociceptors fibre for mechanical ?

A
  • Fibre type A δ – a delta
  • Sharp pricking, fast pain
21
Q

What are the types of nociceptor fibre for thermal and mechanothermal?

A
  • Fibre type A δ – a delta
    Slow burning, cold sharp, pricking
22
Q

What is the type of nociceptor fibre for polymodal sensation?

A
  • C fibre type
    Hot and burning sensation, cold and mechanical stimuli, slow seep pain
23
Q

What is a delta fibre?

A

nociceptor fibre

Myelinated (insulated) and larger diameter axons
Rapid conduction speed

24
Q

What is a c fibre?

A

nociceptor fibre

Unmyelinated (not insulated)
Smaller diameter axons
Slow conduction speed

25
Q

State the two sides of the spinothalamic pathway

A

Indirect spinothalemic

direct spinothalemic

26
Q

Discribe the indirect spinothalemic pathway

A

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

27
Q

Describe the direct spinothalemic pathway

A

Faster ‘Aδ’ fibres
Cortical areas
Better spatial discrimination
Discriminatory sense of pain sensations
Where on the body the damage or danger is happening

28
Q

What is referred pain?

A

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.

29
Q

What’s the difference between nociception and pain perception?

A

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

30
Q

What are some psychosocial dimensions (factors) that open the gate of pain experience signals?

Allowing nociceptive signals

A

Stress, tension, depression, worry, boredom, lack of activity and feelings of lacking control

31
Q

What Psychosocial dimensions (factors) that Close the gate of pain experience signals – stop nociceptive signals ?

A

Relaxation, contentment, optimism, happiness, distraction, pro-activity and positive sense of control

32
Q

Cognitive modulation of pain
4 psychological factors that effect pain perception

A
  1. Attention
  2. Experience
  3. Expectation
  4. Perceived threat

Perceptual filtering of incoming nociceptive information – can amplify or attenuate pain perception

33
Q

What can perceptual filtering of incoming nocicpetive information do?

A

can amplify or attenuate pain perception

34
Q

Whats the neuromatric theory of pain?

A

Different brain areas generates our response. To nociceptive pain signals delivered to the brain.

  1. Learned responses
  2. Attitudes and fears
  3. Perception of danger or safety
  4. Health beliefs
  5. Priorities
  6. Psychological status
35
Q

What do these area of the brain do?

Amygdala and hippocampus
Primary motor cortex
Frontal cortex

A

Amygdala and hippocampus – memory
Primary motor cortex – physical response
Frontal cortex – voluntary primary movement

36
Q

What is the descending inhibitory pathway?

Describe

A
  1. Neurones in brain stem send efferent fibres to spine and pass downwards
  2. Descending modulators fibres release serotonin and norepinephrine
  3. Powerful endorphins (enkephalins) released
  4. Signals generated to go up can’t go through
37
Q

WHAT IS the periaqueductal gray?

A

propagation and modulation of pain, sympathetic responses as well as the learning and action of defensive and aversive behaviors

brain region

38
Q

What are enkephalins?

A

Reduce incoming nociceptive signals and help reduce the central perception of pain

39
Q

What is the pain gate theory?

A

-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.

40
Q

What is neuropathetic pain? Pathological?

A

Pathological – damage to somatosensory system

41
Q

What is neuropathic pain? central damage?

A

Central damage – stroke, spinal cord injury, tumour growth centrally, central inflammation (central sensitisation)

42
Q

What is neuropathetic pain? Peripheral damage?

A

Peripheral damage – physical trauma to nerve, degenerative damage, disease pathologies (peripheral sensitisation)

43
Q

Explain the example of the neuropathic condition of herniated disks?

A

(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

44
Q

What is hyper algeria?

A

Defined – increased sensitivity following tissue injury

Inappropriate involvement of mechanosensory fibres

45
Q

What are the two types of hyperalgesia?

A

Primary hyperalgesia – local to site of damage
Secondary hyperalgesia – extending to surrounding unmanaged areas

46
Q

What is allodynia?

A

Defined – increased sensitivity to non-noxious stimulus
1. Central mechanism
2. Glial cells microglia – become activated during inflammation
3. Switch inhibitory input to excitatory

Applied Health Science (11 decks)

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