Neural basis of pain. Flashcards

1
Q

What is pain?

A

An unpleasant sensation and emotional experience with actual or potential tissue damage

It has visceral and somatic origin
Elicits sensation with autonomic, somatic, endocrine and emotional responses

(So it is both sensory - discriminative - and subjective - affective, behavioural processes)

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2
Q

Define nociception

A

Non-conscious neural traffic originating with trauma or potential trauma tissue

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3
Q

What is the difference between threshold for pain and tolerance to pain?

A

Stimulus threshold
- Is the same in each of us

Tolerance
- Is our variable reaction to a painful stimulus
(environment, situation, psychological/emotional factors, increases with age, ongoing pain, placebo effect)

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4
Q

What tracts are used for pain?

A

Anterolateral system

  • Spinothalamic tract is the only conscious pain pathway
  • Lateral spinothalamic tract is pain

There is also the routes to the Cerebellum that transmit pain, but that is unconscious

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5
Q

What are the two different type of pain sensations in terms of time cale?

A

Direct (fast) lateral STT

  • Discriminative pain (quality, intensity, location)
  • Somatotopic organization
  • Contralateral
  • No sub-cortical target
  • Cortical locatin - Parietal lobe
  • Other functions of temperature and crude touch
  • Dorsal horn origin of lamina I, IV, V

Indirect (slow) Lateral STT
- Affective - arousal
- Bilateral
- Synapses in brain
- Sub-cortical targets - hypothalamus, RF, limbic
structures, autonomic centres.
- Dorsal horn origin - Lamina I, IV and V (VII,VIII)

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6
Q

Name the indirect pathways of pain sensation.

What sensations are they responsible for?

A
Spinoreticular fibres
- Arousal, wakefulness
Spinomesencephalic fibres
- Contributes to activation of descending pain inhibition
- Emotion
Spinotectal fibres
- Reflex eye, upper body and head turning
Spinoghypothalamic fibres
- Autonomic and reflex responses
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7
Q

What are the stages of nociception?

A

Transduction
- Activation of nociceptors by a stimulus
Transmission
- Relay of action potentials along nociceptive fibres to
CNS
Modulation
- By other peripheral nerves or CNS mechanisms
Perception (where pain is felt)
- The interpretation by the brain of the sensation as
painful

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8
Q

What are the two different types of nociceptors?

A
A-delta
- Mechanical
C
- Mechanical 
- Thermal
- Chemical
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9
Q

What are some analgesics acting at site of injury?

A

NSAID

Steroids

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10
Q

What are some of the things that happen in transduction of a pain stimulus?

A

A lesion of the skin would then:
- Cause increases of K+, prostaglandin, serotonin and
bradykinin levels, thus activating nociceptor.
- Substance P is the released from nerve endings,
increasing capillary permeability and contributing to
inflammation.
- Substance P also causes mast cells to release
histamine, which in turn activates nociceptor endings

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11
Q

Tell me about the two types of nociceptive fibres.

A
A-delta
Sharp, stabbing pain
Well localized
First pain / phase 1
Lower threshold
Initiates withdrawal reflex
C
Dull, throbbing pain
Poorly localised
Second pain / phase 2
Higher threshold
Tissue damage occurring
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12
Q

How do local anaesthetics work? (Very simple)

A

They inhibit voltage dependant sodium channel activity, thereby stopping the propagation of an action potential along a nociceptive fibre

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13
Q

Where do nociceptive afferents terminate in the spinal cord?

A

A-delta fibres to I and V
C fibres to I, II(substantia gelatinosa) and V

(A-beta branches to II, IV and V)

STT origin in I, IV to VII

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14
Q

How does visceral and referred pain work?

A

Visceral fibres converge on the same second order neurones shared by somatic nociceptive fibres (lamina V)

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15
Q

What is analgesia?

A

Inability to perceive pain when tissue damage is occurring

Can be caused by:
Hypnosis
Morphine
TENS
Natural childbirth techniques
Placebos
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16
Q

Describe central modulation.

A

Inherent modulatory system via inhibition in spinal cord

  1. The gate control theory of pain
    - Could be how massages, TENS and acupuncture work
  2. Central and descending spinal system, employing endogenous opioid peptide analgesics and other neurotransmitters
17
Q

Name some endogenous analgesics.

A

Opioid neuropeptides:
Enkaphalins, endorphins, dynorphins, endomorphins

Opiate receptors: μ(mu), delta, k(kappa) and nociception
Agonist: Morphine codeine, heroin
Antagonist: Naloxone

18
Q

What are the different pathways of central modulation of pain?

A

Pain fibres synapse in the dorsal horn of the spine
Then they travel up and act on both the thalamus (Direct pathway) and nucleus reticularis paragigantocellularis (NRPG)

The thalamus then has fibres to the cortex (direct) and some excitatory fibres to periaqueductal grey matter
The cortex has inhibition and excitatory pathways to the periaqueductal grey matter
This then has excitatory fibre to the nucleus raphe magnus (NRM)
Which has inhibitory fibres to the dorsal horn to reduce pain

The pathway to the NRPG then has excitatory to the NRM as well

There is also fibres from the hypothalamus to:

  • Periaqueductal grey matter
  • Locus ceruleus

Locus ceruleus the has inhibitory fibres to the dorsal horn

19
Q

What are some other transmitters for pain analgesia or therapies in that area?

A

Analgesia in morphine tolerant patients:
- Baclofen (GABA agonist), anti-depressants, anti-
convulsants
- Somatostatin

Potential drug therapies:
- NMDA receptors, ion channels, neurotrophins (NGF)

20
Q

How are the thalamus and cortex involved in perception of pain?

A

Thalamocortical projections carry information on location intensity and nature of pain.

Primary and association areas, secondary somatosensory cortex

Emotional response via the limbic system
Stress response via hypothalamus