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Jess Nervous > 5.1: Neural Basis of Pain and Analgesia > Flashcards

5.1: Neural Basis of Pain and Analgesia Flashcards

1
Q

Define nociception and pain and describe the relationship between the two

A

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

Pain: complex and unpleasant awareness of a sensation. Pain isn’t only nociception.

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2
Q

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

A

Women and elderly

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3
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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4
Q

Which stimuli are pain nociceptors sensitive to?

A

They are free nerve endings sensitive to mechanical, thermal and/or chemical stimulation

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5
Q

What kind of channels do pain nociceptors have? What happens when they’re triggered? Name five factors that may potentially trigger these channels

A

TRP channels (cation channels - activation stimulates an AP)

Triggered by

  1. Inflammation
  2. Injury
  3. Injury to CNS (scar tissue)
  4. Nerve invasion (i.e cancer)
  5. Abnormal activity (i.e chronic regional pain syndrome)
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6
Q

How does an AP fired by a TRP nociceptor channel reach the brain?

A

AP ascends through spinothalamic tracts

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7
Q

What are the spinothalamic tracts responsible for transmitting?

A

Pain
Temperature
Crude touch: being able to sense the feeling of touch without being able to localize where you were touched

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8
Q

What are the two types of peripheral nociceptive fibres? Compare them

A

Adelta 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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9
Q

Which type of pain is always diffuse and poorly localized? Provide 5 reasons as to why

A

Visceral pain

  1. Organs have relatively few sensory receptors (compared to those of somatic origin)
  2. There is a lack of separate visceral sensory pathways
  3. Signals get mixed in with peripheral sensory pathways in the spinal cord (often at spinal cord levels away from their origin)
  4. Neurons from viscera move extensively above and below the spinal cord entry point in Lissauer’s tract; adding to the diffuse nature of the pain
  5. Signals can cross over and lead to referred pain
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10
Q

How does the spinal cord modulate pain? Describe this concept in detail

A

Through the gate theory of pain, which suggests that stimulation of non-nociceptive receptors can inhibit the transmission of nociceptive information in the dorsal horn

Both first order C and A fibres synapse with second order fibres, which then transmit the nociceptor signal to the spinothalamic tract. In the middle is an interneuron, which inhibits the transmission of signals between the 1st and 2nd order fibres. C fibres inhibit the interneuron, but A fibre excite the interneuron. Therefore, a painful stimulus will be relieved (prevented from transmitting) by stimulating your touch A fibres, which is why rubbing a painful area can reduce the sensation of pain.

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11
Q

Which area of the spinal level is involved in the modulation of nociception in the gate theory?

A

The substantia gelatinosa of the dorsal horn

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12
Q

Name two ways the CNS can modulate pain

A
  1. Endogenous opioids produced by the brain and spinal cord

2. Central modulation/ descending signals from the brain

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13
Q

Which neurotransmitters are released from A and C fibres?

A

Glutamate and substance P (excitatory).

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14
Q

Name three peptides which bind to the same receptors as opioids and two neurotransmitters which bind to non-opioid receptors

Where are all these receptors located?

A

Peptides: Enkephalins, beta-endorphins (exercise) and dynorphin.

Neurotransmitters: Serotonin and NA

In the dorsal horn of the spinal cord

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15
Q

Describe the descending pathway used by the CNS to modulate pain

A

Signals are received in the periaqueductal grey matter of the midbrain and project into the dorsal horn of the spinal cord. They then pass through the ventromedial medulla and are carried down descending pathways to serotonergic and noradrenergic neurons.

These neurons release serotonin and NA, which activate interneurons producing endogenous opioids (such as enkephalins). These inhibit pain signals from the PNS from ascending up the spinothalamic tracts.

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16
Q

Define acute and chronic pain. What are three factors which may be influenced by chronic pain?

A

Acute: Completely resolves on removal of the provoking stimulus

Chronic: Pain that lasts for over 3 months past the normal healing time (for injury or disease)

Has psychological, social and economical factors

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17
Q

Describe how sensitization of pain can increase

A

Increased sensitization means there is a lower threshold for activation and an increased activity (therefore displaying hyperalgesia)

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18
Q

Define hyperalgesia and allodynia, which is more associated with the peripheries vs CNS?

A

Hyperalgesia: Though the threshold for pain stays normal, there is increased sensitivity - and therefore a stimulus which normally invokes prain will invoke an increased amount of pain: Peripheries

Allodynia: pain due to a stimulus that doesn’t normally provoke pain due to the increased excitability of neurons - the CNS (i.e normal touch fibres abnormally interact with the nociceptive pathway)

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19
Q

The CNS displays a(n) _____ excitability of neurons in the _____ of the ___ which leads to ____ ;)

A

The CNS displays an increased excitability of neurons in the dorsal horn of the spinal cord which leads to allodynia

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20
Q

What are the two main types of chronic pain? Describe their primary difference

A

Nociceptive pain is pain elicited by an INTACT nervous system, and is generated by the interaction between the skin and first order neuron.

Neuropathic pain is pain caused by a lesion or disease of the somatosensory nervous system, which can occur anywhere along the pathway from the first-third order neuron.

21
Q

Which abnormal nerve symptoms are commonly experienced in neuropathic pain?

Name six examples of neuropathic pain

A

Hyperalgesia or allodynia are common

Cancer, phantom limb, diabetes, MS, spinal injury, postherpetic neuralgia

22
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 has disappeared.

23
Q

Name two potential causes for neuropathic pain at each of the following locations

a) thalamic/cortical level
b) brainstem
c) spinal level
d) peripheral level - name four for this one!

A

a) /b) MS, infarctions
c) spinal cord injuries, MS
d) Diabetic neuropathies, peripheral trauma, plexus avulsion (nerve roots torn from spinal cord), herpes zoster

24
Q

What is Wallenberg’s syndrome?

A

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

25
Q

Describe the pathophysiology of neuropathic pain

including longer term changes

A

Tissue injury (nociceptive pain) and nerve damage (neuropathic pain) may cause sensitization to occur - this results in excessive glutamate release on the NMDA receptor

The continual activation of second order neurons (second order firing or wind up) can lead to allodynia (pain in response to non painful stimulus) and hyperalgesia (responding at lower stimulus). This can cause..

  1. Increased receptive field of nociceptors
  2. Hyperexcitable neurons: Decreased threshold of activation for the nociceptor, can result in spontaneous activity
  3. Hyperpathia: prolonged post stimulus sensations

Damaged peripheral nerves can also develop abnormal sodium channels which fire APs dysfunctionally and demonstrate different depolarisation properties, therefore signalling pain without proper stimuli

26
Q

How does the sensation of neuropathic pain differ from nociceptive pain?

Name three possible ‘sensations ‘ of neuropathic pain

A

Neuropathic pain is LESS localized than nociceptive pain

  1. Shooting and burning (i.e sciatica)
  2. Tingling and numbness (i.e glove and pattern stockings)
  3. Unpredictable
27
Q

Name two drugs you might offer as initial treatment for neuropathic pain, what are their mechanisms of action?

What other general anaesthesia is usually required as part of management for neuropathic pain? How are opioids often used?

A

Amitriptyline, duloxetine: These increase the amount of NA and serotonin available in the dorsal horn

Generally requires adjuvant analgesics like antidepressants, antiepileptics, TENS, etc. Opioids rarely used in isolation to control neuropathic pain

28
Q

Name four factors that can influence the effectiveness of analgesics

A

Multifactorial: context (that they’re feeling the pain), cognition, mood, personality

Types: paracetamol, NSAIDS, opioids, placebo, adjuvants

29
Q

Name two examples of the following

a) non-opioid analgesia
b) weak opioid
c) strong opioid
d) adjuvants - name 6 of these
e) Non-pharmacological - name 4 of these

A

Non-opioid: paracetamol and NSAIDS

Weak opioid: codeine and tramadol

Strong opioid: morphine, fentanyl

Adjuvants: antidepressants (tricyclic or SSRIs), anticonvulsants, muscle relaxants, steroids, bisphosphonates, radiotherapy

Non-pharmacological: TENS, CBT, acupuncture, hypnosis

30
Q

Name two types of NSAIDS

A

Naproxen and ibuprofen

31
Q

Briefly describe the WHO analgesic ladder

A

Step 1 for Mild pain: non-opioid (i.e NSAID, paracemetol) +/- adjuvant

Step 2 for Moderate pain: weak opioid +/- non-opioid and +/-adjuvant

Step 3 for Severe pain: strong opioid +/- non-opioid and adjuvant

32
Q

Describe the basic mechanism of action for opioids, which receptors do opioids act on?

A

Opioids bind to specific opioid receptors in the CNS to produce effects that mimic the actions of endogenous peptide neurotransmitters (i.e endorphins, enkephalins, etc)

mu, delta, kappa

33
Q

Describe the mechanism of action for codeine and morphine

A

Codeine: partial/weak mu opioid receptor agonist

Morphine: full agonist at mu-opioid receptors in the CNS, these activate the interneurons which dampen nerve signals for pain from synapsing with the second neuron

34
Q

Name 8 side effects for opioids!

A
  1. Euphoria
  2. Sedation
  3. Rep depression
  4. Cough depression
  5. Nausea and vomiting
  6. Tolerance
  7. Constipation
  8. Dependence/addiction
35
Q

Describe the mechanism of action for paracetamol and NSAIDS, where does the main action for paracetamol seem to be?

A

COX inhibitor; blocks formation of prostaglandins (which can trigger pain pathways from nerve endings) from arachidonic acid, main action in the CNS

36
Q

What is the added advantage of taking NSAIDs over paracetamol?

A

Also has anti inflammatory properties.

37
Q

Why is codeine so potentially addictive despite being a weak opioid?

A

It’s broken down into morphine (a strong opioid)

38
Q

What are the two major nerve routes for transmission of pain from the body and face to the brain?

A

Spinothalamic and trigeminal nerve pathways

39
Q

Where do pain (and temperature) fibres synapse and where do the ascending fibres cross over?

A

They synapse in the dorsal horn of the spinal cord and the ascending fibres cross over at the segmental level to travel to the brain in the anterolateral spinothalamic tract/

40
Q

Where might pain fibres join and “peel off” to as they ascend?

A

Most join the spinothalamic tract to enter the thalamus on their way to the sensory cortex

On their way, some will peel off to

a) activate the reticular formation
b) enter the periqueductal grey matter (PAG) of the midbrain

41
Q

Where do pain fibres from the face and front of the head go?

A

They enter the trigeminothalamic system

42
Q

What concept is the gate control theory similar to?

A

Descending pathways using serotonergic signalling; these synapse on the dorsal horn and show a higher more emotionally controlled level of pain interpretation

I.e; an injury may not be as painful until one stops and considers its full effects (battlefield injuries)

43
Q

What is thalamic pain and how might it be caused? How responsive is it to treatment?

A

Damage to the thalamus (i.e from a stroke) can disrupt pain transmission pathways (afferent and efferent), which gives rise to a form of chronic pain called thalamic pain. Can be severe and appears to be largely unresponsive to treatment

44
Q

The analgesic properties of opioids are primarily mediated by which receptor?

A

Mu which mediates response to thermal, mechanical and chemical nociception

45
Q

What is the main analgesic drug contained in crude opium?

A

Morphine

46
Q

Put these opioid agonists in order of power from weakest-strongest; fentanyl, codeine, morphine, tramadol, alfentanyl

A

Codeine, tramadol, morphine, fentanyl, alfentanyl

47
Q

What is a mixed spinal nerve? Name one example

A

Often contains efferent and afferent axons, and can thus conduct sensory and motor information within the same bundle

I.e Median nerve

48
Q

What is the mechanism of the analgesic action of aspirin?

A

Damaged/inflamed tissues produces prostaglandins (and a number of other substances, i.e; bradykinin, histamine). These excite nociceptive fibres and give rise to the sensation of pain. Aspirin is a COX inhibitor, and therefore inhibits prostaglandin synthesis from arachidonic acid

Jess Nervous (16 decks)

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