Lecture 5.1 The Neural Basis of Pain and Analgesia Flashcards

1
Q

What is Nociception?

A

Non-conscious neural traffic in response to (potential) trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is Pain?

A

Complex and unpleasant awareness of a sensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What Factors influence Pain? (7)

A
  • Experience
  • Expectation
  • Context
  • Culture
  • Mood
  • Cognitive Set
  • Injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is IASP definition of Pain?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the link between pain and nociception?

A
  • Nociception leads to pain
  • But pain isn’t only nociception
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the Neural basis of Pain?

A
  • Unclear
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What parts of the brain are though to be involved in the Neural basis of Pain? (5)

A
  • Ascending & Descending Pathways
  • Somatosensory Cortex – perception of pain
  • Amygdala – fear
  • Hippocampus – memories
  • Prefrontal Cortex – planning and reaction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do Pain Receptors (Nociceptors) work?

A
  • Free nerve endings sensitive to mechanical, thermal,
    and/or chemical stimulation
  • Contain TRP channels (cation channels)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What can trigger TRP channels? (5)

A
  • Inflammation
  • Injury
  • Nerve invasion e.g. cancer
  • Injury to CNS
  • Abnormal activity (eg chronic regonal pain syndrome)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What do the Spinothalamic Tracts detect? (3)

A
  • Pain
  • Temperature
  • Crude Touch
  • Carries information from the skin to the thalamus
    where it is processed and transmitted to the primary
    sensory cortex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What fibres is pain is transmitted via? (2)

A

and C Fibres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the structure and function of Aδ Fibres?

A
  • Myelinated
  • Transmit fast, sharp, well localised pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the structure and function of C Fibres?

A
  • Unmyelinated
  • Transmit slow, diffuse, dull pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is Visceral/Organ Pain?

A
  • It is diffused and poorly localised
  • Organs have relatively few pain sensors
  • Enter spinal cord at multiple levels
  • No cortical mapping
  • Referred pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Modulation of Pain: Spinal Cord (1)

A

Gate Theory of Pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Modulation of Pain: Central (2)

A
  • Endogenous neuromodulatory systems (opioids,
    endocannabinoids) in brain and spinal cord
  • Central modulation/descending signals from the brain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the Gate Theory of Pain?

A
  • Modulation of nociception at the spinal level in the
    substantia gelatinosa of the dorsal horn
  • Rubbing a painful area reduces the sensation of pain =
    Gate Theory
  • The touch pathway neurons– activate an inhibitory
    neuron reducing ascending pain signals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does PAG stand for?

A

Periaqueductal Grey

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does RVM stand for?

A

Rostroventromedial Medulla

20
Q

Central Modulation of Pain

A

Descending analgesia producing pathways descend from the brain stem to the spinal cord

21
Q

What is Chronic Pain?

A

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

22
Q

What is Hyperalgesia?

A

A stimulus that would normally be perceived as slightly painful is perceived as significantly more so

23
Q

What does increased excitability of neurones in the dorsal horn of the spinal cord lead to?

A

It leads to allodynia, perception of pain from something that is normally an innocuous stimulus

24
Q

What is Neuropathic Pain?

A

Pain caused by a lesion or disease of the somatosensory nervous system

25
Q

What can cause Neuropathic Pain? (6)

A
  • Cancer
  • Post Herpetic Neuralgia
  • Phantom Limb
  • Diabetes
  • MS
  • Spinal Injury
26
Q

What can cause Neuropathic Pain on a Thalamic/Cortical Level? (3)

A
  • Infarctions
  • Tumours
  • Multiple Sclerosis
27
Q

What can cause Neuropathic Pain on a Brainstem Level? (3)

A
  • Infarctions (Wallenberg’s Syndrome),
  • Tumours
  • Multiple Sclerosis
28
Q

What can cause Neuropathic Pain on a Spinal Level? (2)

A
  • Spinal Cord Injuries
  • Multiple Sclerosis
29
Q

What can cause Neuropathic Pain on a Peripheral Level? (5)

A
  • Diabetic Neuropathies
  • Peripheral Trauma
  • Plexus Avulsion
  • Dorsal Rhizotomy
  • Herpes Zoster
30
Q

After a peripheral nerve injury sensitisation occurs it can lead to….? (7)

A
  • Decreased threshold of the nociceptor to activation
  • Increased receptive field of nociceptors
  • Allodynia
  • Hyperalgesia
  • Hyperpathia
  • Emergence of spontaneous activity / increased
    excitability
  • Damaged peripheral nerves develop abnormal sodium
    channels which fire dysfunctionally and demonstrate
    different depolarisation properties
31
Q

What is Hyperpathia?

A

Prolonged post stimulus sensations

32
Q

Symptoms of Neuropathic Pain (3)

A
  • Shooting and Burning Sensation
  • Tingling and Numbness
  • Unpredictable
33
Q

Treatment of Neuropathic Pain (4)

A

Offer a choice of amitriptyline, duloxetine, gabapentin or pregabalin as initial treatment for neuropathic pain

34
Q

Types of Analgesia (5)

A
  • Paracetamol
  • NSAIDS
  • Opioids
  • Adjuvants
  • Placebo
35
Q

WHO Analgesic Ladder (3)

A
  • Step 1: Non-Opioids
  • Step 2: Weak Opioids
  • Step 3: Strong Opioids
  • Ajduvants
36
Q

Examples of Non-Opioids (2)

A
  • Paracetamol
  • NSAIDs – ibuprofen, diclofenac, naproxen
37
Q

Examples of Weak Opioids (2)

A
  • Codeine
  • Tramadol
38
Q

Examples of Strong Opioids (4)

A
  • Morphine
  • Diamorphine
  • Fentanyl
  • Alfentanyl
39
Q

Examples of Adjuvants (9)

A
  • Antidepressants
  • Anticonvulsants
  • Antispasmodics
  • Steroids
  • Muscle Relaxants
  • Local Anaesthetics
  • Bisphosphonates
  • Radiotherapy
  • Nitrous Oxide
40
Q

Non-Pharmacological ways to manage Pain (6)

A
  • TENS
  • CBT
  • Meditation
  • Acupuncture
  • Massage
  • Hypnosis
41
Q

What Opioid Receptors are there? (3)

A
  • µ (mu)
  • δ (delta)
  • ƙ (kappa)
42
Q

What Opioid Receptors is Codeine an agonist to?

A

Partial/weak (µ) mu-opioid receptor agonist

43
Q

What Opioid Receptors is Morphine an agonist to?

A

Full agonist at mu-opioid receptors in the CNS

44
Q

How does Morphine work?

A
  • Bind receptors in regions of the CNS involved in
    transmission and modulation of pain
  • Dampen nerve signals transmitting pain
45
Q

Side-Effects of Opioid use (10)

A
  • Euphoria
  • Sedation
  • Respiratory Depression
  • Tolerance
  • Miosis
  • Nausea & Vomiting
  • Cough Suppression
  • Constipation
  • Dependence
  • Addiction
46
Q

How do Cannabinoids work?

A
  • Cannabinoids inhibit excitatory synaptic transmission
    in substantia gelatinosa cells
  • Cannabinoid (CB1) receptors are expressed
    presynaptically, where they inhibit transmitter release
    from nociceptive primary sensory neurones
  • Cannabinoids act to reduce experimental models of
    pain – non-opiate based analgesia
47
Q

How is Acupuncture theorised to work?

A
  • Acupuncture involves the insertion of extremely fine
    needles into the skin at specific acupoints
  • This may relieve pain by releasing endorphins, the
    body’s natural pain-killing chemicals
  • They also affect the part of the brain that governs
    serotonin, a brain chemical involved with mood