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Life Control > Physiology of Pain > Flashcards

Physiology of Pain Flashcards

1
Q

What is pain?

A

an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage

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2
Q

What are the 2 components of pain?

A
  • sensory (nociception)

- emotional overlay

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3
Q

What are nociceptors?

A

somatosensory primary afferents

peripheral endings are the sensory receptors

cell body is located in the dorsal root ganglion

synapse onto the second order neuron in the dorsal horn
(within laminae I, II, and V)

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4
Q

What is the difference in location of touch receptors and nociceptors?

A

touch receptors: synapse in brain

nociceptors: synapse in the spinal cord

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5
Q

Where is the cell body of nociceptors (1st order neuron)?

A

in the dorsal root ganglion

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6
Q

In which layers of the dorsal horn do the nociceptors primary afferents synapse?

A

Layer I, II, V

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7
Q

What are the 2 broad classes of nociceptors?

A
  • A-delta fibres

- C fibres

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8
Q

What are A-delta fibres?

A
  • type of somatosensory (nociceptive) primary afferent
  • causes immediate, sharp pain (1st pain)
  • axon is thin and myelinated
  • conducts pain impulses quickly (5-30m/s)
  • NT is glutamate
  • responds to: mechanical trauma and noxious heat
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9
Q

What is noxious heat?

A

> 45C

temperature at which heat starts to become damaging to tissues

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10
Q

What are C fibres/

A
  • type of somatosensory (nociceptive) primary afferent
  • causes delayed aching pain (2nd pain)
  • axon is thin but unmyelinated
  • slower speed of pain transmission (0.5-2m/s)
  • multiple NTs: glutamate, substance P etc
  • responds to inflammatory mediatiors, mechanical trauma, noxious heat/cold (stimuli that don’t change very quickly)
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11
Q

How does activation of A-delta fibres lead to pain perception?

A
  • > Noxious stimuli
  • > activation of A-delta nociceptors
  • > info conducted to spinal cord
  • > Protective segmental reflex (e.g. WITHDRAWAL)
  • > transmission via anterolateral spinal tract to cerebral cortex
  • > perception (sharp pain)
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12
Q

How does activation of C fibres lead to pain perception

A

[secondary/slower response]

  • > damaged tissue releases K+
  • > activation of C fibres, info transmitted to spinal cord
  • > protective reflexes (e.g. IMMOBILISATION)
  • > transmission via anterolateral spinal tract to cerebral cortex
  • > perception of aching pain
  • > informs learning and memory (hippocampus)
  • > aversion memory (won’t do same action in future as associated with fear)
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13
Q

How does infection modulate pain transmission?

A

bacterial release immunogenic chemicals

recruitment of immune cells

  • inflammation
  • can also directly depolarise nociceptors, which indirectly causes inflammation
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14
Q

What problems might having no nociception have?

A

e.g. CIPA (no pain, very rare)
repeated tissue damage due to lack of protective mechanisms

can develop osteoarthritis at early age

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15
Q

What is the lateral pain pathway?

A

controls sensation an perception

SENSATION
awareness event has occurred
“pain”

PERCEPTION
nature of pain
where?
what?
meaning?
response?
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16
Q

What is the course of the ‘main somatosensory/touch pathway’?

A
  • Primary afferent (periphery)
  • enters spinal cord and ascends in dorsal column (ipsilateral side)
  • reaches medulla where it synapses onto 2nd afferent (in dorsal column nuclei)
  • 2nd neuron decussates in medulla
  • ascends to thalamus via medial lemniscus
  • 2nd neuron synapses in the VP nucleus of thalamus
  • 3rd neuron ascends from thalamus to cortex via the internal capsule
  • terminates in the primary SS area (parietal area)
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17
Q

What is the primary SS pathway responsible for?

A

SS = somatosensory

conscious perception and touch

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18
Q

What is the lateral pathway responsible for?

A

pain pathway

=> nociception

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19
Q

What is the course of the ‘lateral pain pathways’?

A
  • primary afferents (periphery)
  • enters spinal cord and synapses in dorsal horn
  • 2nd neuron decussates in dorsal horn and ascends via anterolateral tract (mainly)
  • 2nd neuron travels to the VP nucleus of thalamus where is synapses
  • 3rd neuron travels from VP nucleus to cortex via the internal capsule
  • 3rd neuron terminates in the primary SS area (parietal lobe)
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20
Q

Where do the ‘lateral pain’ and main SS pathways join in their course to the cortex?

A

at the level of the thalamus

[2nd neurons both synapse at the VP nucleus)

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21
Q

Where is the primary SS cortex located?

A

in the homunculus of S1

in parietal lobe

in postcentral gyrus

cortex associated with conscious perception

contains the somatotopic map

22
Q

What creates the somatotopic map in the primary SS cortex?

A

arrival of (tertiary) afferents from various parts of body at the different parts of the SS cortex

23
Q

What sort of pain does direct stimulation of the primary SS cortex create?

A

prickling sensation
(may be perceived as painful)

this area is responsible for pain discrimination

24
Q

What is pain discrimination?

A
  • description of sensation

- localisation of pain

25
Q

What sort of pain does direct stimulation of the VP nucleus create?

A

localised, “sharp, hot/electric” pain

26
Q

How do primary SS lesions impair pain perception?

A

no discrimination of pain

just numbness

afferents are still there working

but lesion impairs perception of this nociception

27
Q

What are recuperative behaviours?

A

e.g. fear, anxiety, fight/flight, aversion

informed by emotional responses to pain previously experienced

  • main cause avoidance and aversion (informs future similar actions)
28
Q

What do the medial pain pathways encompass?

A

SUBCONSCIOUS

  • control of movement
  • ANS
  • emotional and behavioural responses
    e. g. feeding behaviour)
29
Q

What does the ‘CONTROL OF MOVEMENT’ in the medial pain pathway involve?

A

proprioceptor and vestibular input to motor pathways

=> nociceptors: trigger withdrawal and injury immobilisation

30
Q

What does the ‘ANS REPONSES’ in the medial pain pathway involve?

A
  • olfactory input
  • salivation and gastric motility

=> nociceptors activate sympathetic ANS (fight/flight)

31
Q

What does the ‘EMOTIONAL + BEHAVIOURAL RESPONSE’ in the medial pain pathway involve?

A
  • sight/smell of food
  • feeding behaviour

=> nociceptors trigger affective, preventative and recuperative responses

32
Q

What is the course of the MEDIAL PAIN PATHWAYS/SYSTEM?

A

[collection of distinct pathways e.g. spino-amygdala, spina-reticular)

  • primary afferents in periphery
  • travel to the dorsal horn of spinal cord where they synapse
  • 2nd neurones decussate
  • travel via the anteromedial white matter (mainly)
  • as they ascend, multiple branches given off in brainstem (modulatory/autonomic control)
  • reaches the midline nuclei (thalamus) and synapses
  • 3rd neuron gives off a branch to the insular cortex and then travels to the anterior cingulate cortex
33
Q

What structures are present in the anterior cingulate cortex?

A
  • hypothalamus
  • amygdala
  • frontal cortex
34
Q

How do targets in the brainstem help after injury?

A

centre for autonomic and modulatory control

injury -> NA and ACh flood into brain

Increased ALERTNESS and MEMORY lay down

35
Q

What sensation does direct stimulation of the midline nuclei (thalamus) cause?

A

difficult to describe, unpleasant feeling

but no conscious perception, so no discrimination or localisation

36
Q

How do the medial and lateral pain pathways differ in their pain perception?

A

MEDIAL PAIN PATHWAY
distress, fear, protective behaviours, increased alertness and SNS activity

LATERAL PAIN PATHWAYS
conscious perception, localisation and discrimination

37
Q

What is referred pain caused by?

A

usually caused by damage or activation of visceral nociceptors

these synapse onto the same 2nd neurons as SS nociceptors and so pain is ‘felt’ in the same dermatome

visceral nociception therefore ‘piggybacks’ onto the SS pathway

will localise to the parts of the somatoptopic map that those dermatome afferents lead to

38
Q

What determines the characteristic pattern of referred pain?

A

embryonic origin of that organ

“visceral afferents”

39
Q

What is ‘DESCENDING PAIN CONTROL’ pathway involve?

A

MODULATORY PATHWAYS: affect all aspects of brain function
contain axons which travel down the cord and control pain transmission at 1st synapse

Can impact:

  • sleep and wakefulness
    e. g. pain can ruin sleep
  • focusing attention
    e. g. pain disrupts concentration
  • switching attention
    e. g. injury (threatened or actual) is a powerful stimulus
40
Q

What are the main NTs involved in the ‘descending pain control pathway’?

A

NA - binds to alpha-2 adrenoreceptors

SST (5-HT7)

41
Q

How does the descending pain control pathway work?

A
  • direct and indirect inhibitory neurons suppress pain
  • causes loss of pain sensation
  • and loss of negative emotions that overlay nociception

usually will be a balance of facilitatory/excitatory and inhibitory neurones at play

this pathway promotes the action of the inhibitory neurones and suppresses the facilitatory neurons

42
Q

How do opioids work?

A

activation of the descending pain control pathway

by mimicking the action of inhibitory interneurons

can be at the level of the spinal cord
OR
can activate at level of orbito-frontal or periaqueductal centres

43
Q

What is pathological/chronic pain thought to be caused by?

A

imbalance in antagonism/balance between facilitatory/excitatory and inhibitory neurones

stimulated by anxiety, poor expectations and poor coping

can be difficult to overcome this shift

44
Q

What is the course of the descending pain control pathway?

A 
orbitofrontal cortex 
|
anterior cingulate cortex 
|
periaqueductal grey 
|
RV medulla, DL pontine tegmentum
|
spinal cord
45
Q

What is defined by nociceptive pain?

A

“physiological” pain due to tissue damage

stimulated nociceptor nerve endings

46
Q

What is central sensitisation?

A

mechanisms which amplify signalling within pain pathways

makes the response to a given stimulus higher and pain to be perceived as more painful

47
Q

What can inflammation and central sensitisation lead to?

A

HYPERALGESIA
nociceptor activation becomes more painful

ALLODYNIA
touch becomes painful

48
Q

How do nociceptors contribute to inflammation?

A

C-fibres contain specific membrane receptors that can respond to may inflammatory mediators

these cause depolarisation and APs (in the terminal branches of a C-fibre neurone)

mediates release of pro-inflammatory substances from the C-fibre endings
e.g. substance P

cause increased inflammation

AND activation of any adjacent C-fibre neurons that are in the vicinity (with similar receptors)

49
Q

How does diabetic neuropathy cause pathological pain?

A

(= pain resulting from nociceptor response to pathological conditions)

SPONTANEOUS PAIN
micro-injury to nociceptors themselves

HYPERALGESIA and ALLODYNIA occur due to micro-inflammation

=> neuropathy can cause changes to the central pathways (within CNS) leading to neurogenic pain

=> neurogenic pain from abnormal processing may lead to pain without apparent cause

50
Q

Which layers of the spinal cord carry which fibres?

A

[nociceptor activity needs fine control]

layer I, II and V (white matter of spinal cord due to myelin)

Layers I-II: only have nociceptive input (activation here will always be interpreted as pain). But contain inhibitory interneurones to modulate responses to be appropriate to stimuli.

Layer V: both nociceptors and touch receptors. only interpreted as pain when there is high AP firing. If only low AP firing, then interpreted as non-specific touch

51
Q

What causes long-term potentiation?

A

short burst of high frequency APs or persistent activation (due to pathology, e.g. neuropathy, or nerve injury)

  • causing excess axon strengthening
  • future inputs will generate double the pain response to the same stimuli in future
52
Q

How do anti-convulsants help treat long term potentiated neurons?

A

help to dampen down the (hyper stimulated) responses and reduce NT release

Life Control (25 decks)

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