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ETA 5: NERVOUS SYSTEM > 5.1: Neural Basis of Pain and Analgesia > Flashcards

5.1: Neural Basis of Pain and Analgesia Flashcards

1
Q

Define Nociception and Pain

What is the relationship between these?

A

Nociception: non-conscious neural traffic in response to (potential) trauma.

Pain: an unpleasant sensory and emotional experience associated with actual or potential tissue damage.

Nociception leads to pain BUT pain isn’t only nociception

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2
Q

How can pain be good and bad?

A

Pain can be good: stops us from hurting ourself (eg. putting hand on something hot)

Pain is bad because it is unpleasant to live with (eg. chronic pain can be extremely debilitating)

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3
Q

List 4 other factors, in additon to nociception, that can lead to pain

A

1) Cognitive set: attention, distraction, catastrophising
2) Mood: depression, anxiety
3) Context: pain beliefs, placebo, expectation
4) Chemical and structure: neurodegeration, metabolic

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4
Q

Which gender and age group is most commonly affected by chronic pain?

A

Women and elderly

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5
Q

List 3 things chronic pain is associated with

A

1) increased mortality
2) worsening mental health
3) social deprivation

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6
Q

What parts of the brain are responsible for the following?

a) perception of pain
b) fear
c) memories
d) planning and reaction

A

a) somatosensory cortex
b) amygdala
c) hippocampus
d) prefrontal cortex

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7
Q

What type of nerves are pain nociceptors?

Give 3 stimuli they are sensitive to

A

They are free nerve endings

Sensitive to mechanical, thermal and/or chemical stimulation

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8
Q

What kind of channels do pain nociceptors contain?

Name five factors that may potentially trigger these channels

A

TRP channels- cation channels (resemble voltage gated K+ channels but more unspecific)

Triggered by:

  1. Inflammation
  2. Injury
  3. Injury to CNS
  4. Nerve invasion (i.e cancer)
  5. Abnormal activity (i.e chronic regional pain syndrome)
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9
Q

What is complex regional pain syndrome (CRPS)

A

A condition that causes severe pain which won’t go away

Eg. a minor injury such as a sprained ankle, where pain persists even after the injury has healed. This is because of abnormal healing processes

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10
Q

What are the spinothalamic tracts responsible for?

A

Pain, temperature and crude touch

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11
Q

Define the sensation of crude touch

A

Being able to sense the feeling of touch without being able to localize where you were touched

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12
Q

What 2 fibre types transmit pain?

Compare these fibres

A

Pain is transmitted via Aδ and C fibres

Aδ fibres are myelinated and transmit fast, sharp and well localized pain

C fibres are unmyelinated and transmit slow, diffuse and dull pain

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13
Q

Describe the sensation of visceral organ pain and state 2 reasons why

A

Visceral/organ pain is diffuse and poorly localised

1) Organs have relatively few pain sensors
2) Enter the spinal cord at many levels, leading to potential crossing over of signals. This which is what results in ‘referred pain’

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14
Q

Give 3 examples of reffered pain

A

1) Appendix pain: reffered from peri-umbilical area to RLQ
2) Flank pain from the kidney and/or radiating down the lower abdomen from the ureter
3) MI: pain presents in the upper chest, left arm, neck and lower jaw

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15
Q

What theroy describes how the spinal cord modulates pain?

A

The gate theory of pain: suggests that stimulation of non-nociceptive receptors can inhibit transmission of nociceptive information in the dorsal horn.

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16
Q

Explain the Gate theory of pain (use the example of stubbing toe)

A

1) Painful stimuli (eg. stubbing toe) will stimulate first order nociceptor C fibres and Aδ fibres
2) These will synaps with the second order fibres in the substantia gelatinosa of the dorsal horn and carry the signal to the brain via the spinothalamic tract (perception of pain)
3) If we rub the area, we stimulate touch/pressure fibres
4) The touch pathway neurons activate an inhibitory interneuron which reduces ascending pain signals from the C fibres and Aδ fibres
5) This therefore reduces the sensation of pain

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17
Q

Name two ways the CNS can modulate pain

A

1) Endogenous opioids in brain and spinal cord
2) Central modulation/ descending signals from the brain

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18
Q

Explain the mechanism of central modulation of pain

A

Central modulation of pain involves descending analgesia producing pathways from the brain stem to the spinal cord

1) This starts at the Periaqueductal grey matter (PAG) of the midbrain in the brain stem
2) Passes down through the rostroventromedial medulla (RVM) into the spinal cord
3) As it does this it receives inputs from other areas of the brain (eg hippocampus, PFC, amygdala etc…) as part of regulatory processes
4) These travel down to the dorsal horn where they release Serotonin and NA
5) These NT’s stimulate interneurons to release Enkephalins, beta-endorphins and/or dynorphin which bind to opioid receptors
6) This has an inhibitory affect on the synapses between the first and second order neurones of the nociceptive pathways, thus modulating pain

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19
Q

Explain why we encourage patients with chronic pain (ie. Trigeminal neuralgia) to exercise?

A

Targeting the central modulation of pain! Excersise releases endorphins which can bind to the opioid receptors and help relieve pain

20
Q

Give 3 substances which bind opioid receptors

Give 2 substances which bind non-opioid receptors

A

Opioid: Enkephalins, beta-endorphins, dynorphin

Non-opioid: Serotonin and noradrenaline

21
Q

Define chronic pain and list 3 influential factors?

A

Any pain that lasts for more that 3 months past the normal healing time for an injury or disease

Has extensive psychological, social and economical factors

22
Q

List 3 broad catagories that may cause chronic pain and give 2 examples of each

A

1) Nociceptive/inflammatory

  • Osteoarthritis and Rheumatoid arthritis
  • Post-op pain

2) Neuropathic

  • Trigeminal neuralgia
  • Nerve injuries/ neuropathies

3) Idiopathic

  • Fibromyalgia
  • Irritable bowel disorders
23
Q

List 2 reasons we may have increased sensitisation to pain

A

1) increased activity of nociceptors
2) lower threshold of nociceptors

24
Q

Hyperalgesia and Allodynia are both examples of sensitisation, define and expalin each of these

A

Hyperalgesia: Increased pain from a stimulus that normally provokes pain due to an increased response at a normal threshold

  • Eg. a stimulus that would normally be perceived as slightly painful is perceived as significantly more so

Allodynia: Pain due to a stimulus that does not normally provoke pain due to increased excitability of neurons in the dorsal horn of the spinal cord (CNS)

  • Eg. perception of pain from something that is normally an innocuous stimulus (such as a feather)
25
Q

What is central sensitisation and what does this lead to?

A

Increased excitability of neurons in the dorsal horn of the spinal cord (CNS)

Leads to allodynia: perception of pain from something that is normally an innocuous stimulus

26
Q

Compare nociceptive vs neuropathic pain

A

Nociceptive pain is pain elicited by an INTACT nervous system

  • Pain pathways is acting normally, it is an actual stimulus affecting the nerve endings

Neuropathic pain is pain caused by a lesion or disease of the somatosensory nervous system.

  • Can occur anywhere along the pain pathway
27
Q

Why can neuropathic pain be difficult to treat?

What 2 things commonly occur alongside neuropathic pain

A

Cannot be explained by a single disease process or specific location of damage

Neuropathic pain commonly occurs alongside hyperalgesia and allodynia

28
Q

Name 4 examples of neuropathic pain

A
  1. cancer
  2. phantom limb
  3. diabetes (diabetic neuropathy)
  4. MS
  5. spinal injury
  6. postherpetic neuralgia
29
Q

What causes postherpetic neuralgia and what is it?

A

Most common complication of shingles, it’s a condition affecting the nerve fibres on the skin which causes burning and pain lasting long after the shingles have disappeared

30
Q

Name 2 potential causes of neuropathic pain for each of the following locations:

a) thalamic/cortical level
b) brainstem
c) spinal level
d) peripheral level

A

a) Infarctions, tumors, MS
b) Infarctions (Wallenberg’s syndrome), tumors, MS
c) spinal cord injuries, MS
d) diabetic neuropathies, peripheral trauma, plexus avulsion, herpes zoster

31
Q

What is Wallenberg’s syndrome?

A

When an infarction or stroke occurs in the lateral medulla (part of the brainstem)

32
Q

Pathophysiology of neuropathic pain:

After a peripheral nerve injury sensitization occurs, give 6 things this can lead to:

A

1) decreased threshold of the nociceptor to activation
2) Increased receptive field of nociceptors
3) Allodynia and/or Hyperalgesia
4) Prolonged post stimulus sensations – hyperpathia
5) Emergence of spontaneous activity/increased excitability
6) Damaged peripheral nerves can develop abnormal Na+ channels which fire dysfunctionally and demonstrate different depolarisation properties

33
Q

Give 3 symptoms of neuropathic pain

A

1) Shooting and burning
2) Tingling and numbness
3) Unpredictable

34
Q

Give 2 treatments of neuropathic pain and explain the MoA of these

A

Amitriptyline: Tricycline which is an antidepressant

Duloxetine: NA/ Serotonin re-uptake inhibitor

Both of these increase the amount of Serotonin and NA that is available in the dorsal horn. This activates the inhibitory interneurons thus reducing the pain signals sent up the spinothalamic tract

(Non-pharmacological treatments must also be considered: eg psychological therapies)

35
Q

Explain the pathophysiology of chronic pain

A

1) Tissue injury (nociceptive pain) or nerve damage (neuropathic pain) may cause persistent activation of the pain pathway
2) This leads to excess Glutamate release and thus excess excitation of the NMDA receptor
3) This leads to excess activation of 2nd order neurone firing, continued stimulation is known as ‘wind up’
4) This results in long term changes in the second order nociceptive neurones which become hyper-excitable (respond at lower stimulus intensity)… ‘hyperalgesia’
5) Wind up can also lead to receptive field expansion at the peripheral site or allodynia

36
Q

Explain how wind up leads to receptive field expansion at the peripheral site

A

There is a certain amount of cross-over at the dorsal horn, so there is link between the second order neurones.

Normally a first order neurone will predominantly link to one second order neurone. However, with wind up stronger links form between first order neurones synapsing with two or three second order neurones

This causes expansion of the receptive field, making the location of pain perceived more diffuse

37
Q

Pain relief is multifactoral, not simply pain reduction

Give 4 other considerations we must make when treating pain

A

Context, cognition, mood, personality

38
Q

Give 5 types of analgesia

A
  1. Paracetamol
  2. NSAIDS
  3. Opioids
  4. Adjuvants
  5. Placebo
39
Q

Compare paracetamol vs NSAIDS

A

Both are COX enzyme inhibitors which block the formation of prostaglandins (trigger pain pathways at nerve endings) and thromboxane from arachidonic acids.

Paracetamol:

  • Main action is in the CNS
  • Has an analgesic and anti-pyretic effect (reduce temperature)

NSAIDS:

  • Main action is in the PNS
  • Has an analgesic, anti-pyretic AND anti-inflammatory effect
40
Q

Give 3 examples of an NSAID

A

Ibuprofen, naproxen and aspirin

41
Q

What is an Adjuvant?

Give an example

A

Adjuvants are drugs that have few or no pharmacological effects by themselves, but may increase the efficacy or potency of other drugs when given at the same time.

Eg. patients with arthritis may be given pain relief meds alongside corticosteriods (to reduce inflammation)

42
Q

Give 2 examples of the following analgesia:

  • Non-opioids
  • Weak opioids
  • Strong opioids
A

Non-opioid: Paracetamol, NSAIDs

Weak opioids: Codeine, Tramadol

Strong opioids: Morphine, diamorphine, fentanyl, alfentanyl

43
Q

Give 4 examples of an adjuvant

Give 4 examples of non-pharmacological analgesia

A

Adjuvants: Antidepressants, anticonvulsants, steroids, muscle relaxants, bisphosphonates, radiotherapy, nitrous oxide

Non-pharmacological: TENS, CBT, meditation, acupuncture, massage, hypnosis

44
Q

Explain how exogenous opioids work as an analgesia

A

1) Exogenous opioids interact with specific receptors:

  • μ (mu)
  • δ (delta)
  • ƙ (kappa)

2) This has an inhibitory effect on pain pathways
3) It also has an central effect of creating a feeling of euphoria, which helps the patients short-term dealing with pain (this is a side effect)

45
Q

Give 4 side effects of exogenous opioids

A

Euphoria, sedation, respiratory depression, tolerance, miosis, nausea and vomiting, cough suppression, constipation, dependence, addiction

46
Q

Compare codeine vs morphine

Briefly explain how morphine works

A

Codeine: partial/weak mu-opioid receptor agonist

Morphine: full agonist at mu-opioid receptors in the CNS

  • Binds receptors in CNS involved in transmission and modulation of pain and dampens nerve signals transmitting pain
47
Q

What ‘effect’ demonstrates the higher brain functions and the complexity of pain in an individual

Give 2 examples of studies demostrating this effect

A

The placebo effect

Numerous studies:

  • Students and stimulants vs sedatives
  • Alcohol vs non-alcohol
  • Post-operative pain

ETA 5: NERVOUS SYSTEM (18 decks)

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