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Week 230 - Pain > Neurology of Pain > Flashcards

Neurology of Pain Flashcards

1
Q

Define pain

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage

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2
Q

What is Congenital insensitivity to pain?

A

Condition with decreased or absent pain sensation caused by:

Na+ channel mutations, other conditions (Genetic usually)

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3
Q

What is nociception?

A

The sensory process that provides the signals triggering pain

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4
Q

What is chronic pain?

A

Pain that persists beyond normal healing time (> 3-6 months)

  • pathological process (involving nervous system)
  • may include biopsychosocial element
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5
Q

Define dysaesthesia

A

Abnormal, unpleasant sensation (not pain itself)

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6
Q

Define hyperalgesia

A

Increased pain response to noxious stimuli

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7
Q

Define allodynia

A

pain response to non-noxious stimuli

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8
Q

Define paraesthesia

A

Pain response in absence of any stumulus

- i.e. paroxysms = spontaneous shooting pains

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9
Q

Define hyperathia

A

Pain threshold actually increased but increased pain response when threshold is passed

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10
Q

Describe the reflex arc

A

Nociceptive fibre (afferent)

  • > interneuron in substantia gelantinosa (dorsal horn)
  • > motor neurone (ventral horn of spinal cord)
  • > impulse travels to effector muscles
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11
Q

Describe the substantia gelatinosa

A

Located in dorsal horn of spinal cord

Sends fibres up to brain via ascending pathways after receiving signal from nociceptive fibres

Send projections to anterior horn (reflex arc)

Synapse with descending pathways which modulate impulse transmission

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12
Q

What are nociceptors?

A

Free nerve endings, i.e. not specialised structures

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13
Q

Give examples of nociceptors

A

TRPV1 (Capsaicin receptor) = temperature receptor

Chemical receptors - inflammation receptors

Mechanical receptors - stretch receptors

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14
Q

What are the main types of 1st-order nociceptive fibres?

A

A-delta fibres (type III fibres)

C fibres (type IV fibres)

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15
Q

Describe A-delta fibres

A

Fast pain fibres (myelinated)

Unimodal (one type of pain = sharp,local)

e.g. muscle spindle, golgi tendon organ pain

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16
Q

Describe C fibres (type IV fibres)

A

Slow pain fibres (unmyelinated)

Polymodal (distinguishable types of pain)

e.g. temp, stretch, inflammation

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17
Q

What are A-beta fibres (Type II)?

A

Transmit crude touch (i.e. non-pain fibres)

  • inhibit pain signals at dorsal horn
    e. g. rubbing sore area relieves pain
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18
Q

Describe 2nd order nociceptive fibres?

  • where they deccusate in ascending pathway
  • which tract they ascend in
  • where they synapse in the brain
A

Decussate at level of entry in spinal cord
Ascend in spinothalamic tract

Synapse in ventro postero-lateral nucleus of thalamus

Send projections to cerebral cortex

  • insula and cingulate
  • primary somatosensory cortex
19
Q

What are the insula and cingulate cortices resposnible for in the cerebrum?

A

Creating unpleasant sensation assoc. with pain

20
Q

What is the role of primary somatosensory cortex?

A

Locate painful stimuli

21
Q

What are the two descending pathways associated with pain?

A

Descending opioid/Serotinergic pathway
- nucleus raphe magnus (medulla)

Descending noradrenergic pathway
- Locus coeruleus (Pons)

22
Q

Describe the nucleus raphe magnus

A

Stimulated by opioidergic projections

Sends serotinergic projections to dorsal horns

23
Q

Describe the Locus Coerulerus

A

Sends noradrenergic projections to dorsal horns of spinal cord

24
Q

Stress induced analgesia occurs how?

A

Stress induces Amygdala to stimulate per-aqueductal grey matter which stimulates opioid release onto Nucleus Raphe Magnus => descending pathway inhibition results

25
Q

How do nociceptors become sensitised to inflammation?

A

Inflammatory mediators act on nociceptors
e.g. prostaglandins, substance P, bradykinin, histamine

Nociceptors also contribute to futher inflammation by release of substance P

26
Q

What are the effects of substance P?

A

Mast cell degranulation
Blood vessel vasodilatation

Increased Na+ channel expression in periphery
Increased interneural connectivity

Causes hypersensitisation

27
Q

Describe how the dorsal horn becomes hypersensitised?

A

By repeated stimulation of C-fibres => increased glutamate release by 1st order nociceptive fibres

=> opening of NMDA receptors => Ca2+ influx through these NMDA gates causes depolarisation of dorsal horn

=? 2nd order fibres more likely to depolarise and cause hyperalgesia

28
Q

How does NO induce opioid resistance?

A

released after Ca2+ influx into post-synaptic fibres

=> stimulates closure of K+ channels o pre-syanptic membrane
- i.e. the opposite to what opioids do (inhibit depolarisation)

29
Q

Why do we get referred pain from internal organs?

A

Since organs have 1st order nociceptive fibres only (no devoted 2nd order fibres) which means brain interprets signals as coming from skin

30
Q

How do NSAIDs work as analgesia?

A

Reduce inflammation and therfore reduce impulses from certain nociceptors

31
Q

How do local anaesthetics work as analgesia?

A

Block transmission of noxious stimulants to spinal cord

32
Q

How do opioids work as analgesia?

A

Act on descending pain pathways - upregulate nucleus raphe magnus

Directly inhibit nociceptive signals at 1st order fibre-dorsal horn neuron synapse

Blunts emotional aspects of pain also

33
Q

What is the difference between opiate and opioids?

A

Opioids generally refer to endogenous substances

Opiates refer to exogenous substances

34
Q

Describe which endogenous opioids target which opioid receptor

A

Endorphins - mu receptor
Enkephalins - delta receptor
Dynorphins - kappa receptor

35
Q

What are the effects of opioids?

A 
Analgesia
Euphoria
Sedation
Cough suppression
Constipation

Respiratory distress
N&V
Miosis

36
Q

What is neuropathic pain?

A

Pain generally caused by neuronal damage

- i.e. anatomical or functional abnormalities of pain pathways

37
Q

What are the causes of neuronal damage?

A

Neuropathies, Nerve avulsions, Cancers, Infections, Amputations

MS, Cord injuries, Stroke

38
Q

What are the mechanisms behind neuropathic pain?

A

Inflammation => Na+ channel abnormalities - increased expression

Increased sympathetic activity

Sensitisation of dorsal horn neurones

Central sensitisation and reorganisation

39
Q

Give a common example of neuropathic pain

A

Trigeminal neuralgia

  • usually due to compression of CN V
  • results in intense episodic pain
40
Q

How should neuropathic pain be treated?

A

With anticonvulsants, e.g.

  • carbamazepine
  • amitryptilline
  • baclofen
  • pregabalin/gabapentin
41
Q

What is phantom limb pain?

A

Perception of pain in a limb that is no longer there (e.g. has been amputated, congenital absence)

42
Q

What percentage of amputees does phantom pain occur in?

A

Up to 80%

43
Q

What is the best treatment for treating phantom limb pain?

A

Mirror visual feedback

  • mirrors used to trick brain into thinking limb is there by providing visual input suggesting it is
  • may provide instant relief

Week 230 - Pain (2 decks)

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