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Brain and Behaviour Year 2 > Anatomy and Physiology of Pain > Flashcards

Anatomy and Physiology of Pain Flashcards

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1
Q

Name the 4 steps that are involved in the physiological mechanisms of pain

A
  1. Transduction
  2. Transmission
  3. Perception
  4. Modulation
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2
Q

describe the 4 steps that are involved in the physiological mechanisms of pain

A
  1. TRANSDUCTION
    - Noxious (potentially harmful) stimuli translated into electrical activity at sensory nerve endings
  2. TRANSMISSION
    - Propagation of impulses along pain pathways
  3. PERCEPTION
    - Descrimination/ affect / motivation
  4. MODULATION
    - Stages 1-3 are modified (positive and negative modulation occurs) - this is the idea that you can down regulate pain as we don’t want to be in pain all the time
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3
Q

describe the definition of pain

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage

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4
Q

pain is a ….

A

…pain is a perception usually but not always associated with tissue-damaging stimuli (nociceptive information)

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5
Q

what does acute pain result form

A
  • this results from the activity of a nociceptor
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6
Q

What is a nociceptor

A
  • a sensory neuron transducing potentially harmful stimuli
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7
Q

Name the two nociceptors

A
  • A delta fibres (myelinated) = these transmit fast pain

- C fibres (unmyelinated) = these transmit slow pain

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8
Q

What do nociceptors cause to happen

A
  • they give signal transduction and transmit across pain pathway
  • these leads to withdrawal behaviour via reflexes or perception behaviour which includes pain, avoidance, and emotional reaction
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9
Q

what gene defects can cause a life without pain

A

Loss of Tranduction/Transmission
Loss of NaV1.7
= (sodium channel subunit)
= Congenital indifference to pain

Loss of C fibres
= trkA - NGF receptor mutation
= Congenital insensitivity to pain with anhydrosis CIPA

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10
Q

What does life without pain result in

A
  • results in shortened life span

- death is often due to secondary consequences of injury such as infections

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11
Q

describe A delta fibres

A
  • Sharp pricking fast pain – thermal and mechanical
  • precise localisation of insult/stimulus
  • reflex withdrawal
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12
Q

Describe C fibres

A

Slow burning pain, affect, misery; autonomic effects

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13
Q

what are the two types of C fibres

A
  1. ‘peptidergic’ C fibres release peptides peripherally e.g., Substance P / CGRP
    = this leas to Vasoactive, promote inflammatory responses (neurogenic inflammation) and healing; thermal nociception
  2. ‘Peptide-poor’ C fibres have distinct receptors (e.g., P2X3 ATP receptors) and projections
    = these leads to mechanical nocicpetion
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14
Q

what lamina does central termination of A delta and C fibres occur

A

C fibres = lamina I and II (they also innervate lamina V through these interneurons)

A delta fibres = Lamina I and lamina V and more deeply into the dorsal horn

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15
Q

where do the axons of nociceptive receptors decussate

A
  • they ducat close to where the nociceptors enter the spinal cord and form the spinothalamic tract
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16
Q

describe the pathway of the anterior spinothalamic (or neospinothalamic) tract

A
  1. Primary afferent: Aδ fibres as well as input from C (indirect via interneurons) and Aβ fibres innervate →
  2. Projection neurones in Lamina V – ‘wide dynamic range cells’. After decussating axons travel in the anterior spinothalamic tract
  3. innervate ventral posterior lateral (VPL) and ventral posterior medial (VPM) – somatosensory thalamus; and ventral posterior inferior (VPI) and central lateral (CL) nuclei of the thalamus (reticular and limbic associated areas).
  4. The main projection is to the primary somatosensory cortex (SI) from
    VPL/ VPM →; localisation & physical intensity of noxious stimulus
    - input to SII (secondary somatosensory cortex) via VPI
    - and ACC (anterior cingulate cortex; emotion) and prefrontal cortex and striatum via CL (sites for cognitive function/ strategy)
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17
Q

what fibres mainly enter the anterior spinothalamic (or neospinothalamic) tract

A

mainly from A delta fibres

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18
Q

describe the pathway of the lateral spinothalamic (or paleospinothalamic) tract

A
  1. Primary afferent: C fibres but also some Aδ fibres innervate →
  2. Projection neurones in Lamina I –After decussating axons travel in the lateral spinothalamic tract
  3. innervate the more posterior/ medial parts of the thalamus
    Mediodorsal nucleus (ventrocaudal) (MDvc)
    ‘Posterior thalamus’ – posterior nucleus (medial subnucleus) (POm) and ventral medial nucleus (posterior) (VMpo)
    (also some projections to the VPL, VPM and CL)
  4. Projections to Cortex MDvc → anterior cingulate cortex (ACC); (emotion/ motivation) Posterior thalamus (POm and VMpo) → anterior or rostral insula (emotion, quality i.e. ‘pain’, autonomic integration)
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19
Q

what system lateral or anterior spinothalamic tract is earlier

A

Lateral or paleo spinothamaic tract

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20
Q

what does the lateral Lateral or paleo spinothamaic tract receive its main input from

A

C fibres

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21
Q

what is the difference between the cortical targets of the anterior and lateral spinothalamic tract

A

Anterior or ‘neo’spinothalamic tract to primary and secondary somatosensory cortex

Lateral or ‘paleo’spinothalamic tract’: anterior cingulate and rostral insular cortex

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22
Q

the axons of the lateral spinothalamic tract also synapse in ….

A

Axons of the lateral spinothalamic tract synapse in several sites in the brainstem- as well as the thalamus (mainly the posterior, medial nuclei

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23
Q

name three other areas that the lateral spinothalamic tract projects to

A
  • the limbic system
  • midbrain reticular formation
  • intralaminar(reticular) nuclei of thalamus
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24
Q

describe the three other areas that the lateral spinothalamic tract project to

A

the limbic system

  • subjective sensations of pain
  • goes via the brainstem and posterior medial thalamus

Midbrain reticular formation
- pain - induced arousal and descending control of nociceptor input

Intralaminar(reticular) nuclei of thalamus
- alerting cerebral cortex and focus of attention of pain

25
Q

what is the unpleasant painful character of pain mediated by

A
  • projects of the lateral spinothalamic tract going towards the limbic system
26
Q

describe the other collateral projections of the lateral spinothalamic projections

A

Spinal circuitry– Reflexes, integration of information

Reticular formation (and reticular thalamus)- arousal and alerting cortex

Periaqueductal grey (PAG) in midbrain: descending pain modulation

Parabrachial nucleus in pons- from there onward to the amygdala

27
Q

what do these areas do in terms of pain

  • anterior cingulate cortex
  • pre-frontal cortex
  • insula
  • amygdala
  • primary sensory cortex
A
  • anterior cingulate cortex = emotional reaction and motivation
  • pre-frontal cortex = evaluation and cognition
  • insula = pain map, interception, homeostatic adjustment and emotion
  • amygdala = aversion, emotional memory and response
  • primary sensory cortex = somatosensory, discrimination- location, intensity
28
Q

describe actue pain

A

is of sudden onset, usually the result of a clearly defined cause such as an injury. It resolves with the healing of its underlying cause.

29
Q

describe fast pain

A

sharp pain conveyed by Aδ elicits reflexive withdrawal to prevent further injury

30
Q

describe slow pain

A

burning, lingering, emotionally charged

31
Q

what are the 4 signs of inflammation

A

Calor (heat)
Rubor (redness)
Dolor (pain)
Tumor (swelling)

32
Q

what is peripheral sensitisation

A

= this is when the area that was damaged becomes sensitised
= this results in hyperalgesia, allodynia, spontaneous pain
= this enables protection and facilitates healing without further damage

  • this resolves with healing of the underlying cause
33
Q

How does peripheral sensation resolve itself

A
  • this resolves with healing of the underlying cause of the pain
34
Q

What is peripheral sensation caused by

A

Due to effects of inflammatory mediators (from inflammatory cells and damaged tissue) nociceptors show
= reduction in activation threshold
= increase in responsiveness

35
Q

what plays a key role in inflammatory pain

A

= prostaglandins

36
Q

What targets prostaglandins

A

NSAIDS

37
Q

describe how prostaglandins are made

A
  1. Phospholipase A2 releases arachidonic acid from cell membranes (driven by inflammatory mediators)- targeted by steroids
  2. Cyclooxygenase 1 (COX-1) and COX-2 enzymes use arachidonic acid as a substrate for prostaglandin (PG) synthesis
38
Q

when and where are COX 1 and COX 2 present

A
  • COX-1 normally present in tissue at low levels

- COX-2 induced during inflammation

39
Q

How do prostaglandins lead to inflammatory pain

A

PGs sensitise C-fibres by increasing numbers of other receptors and increasing the number of open sodium channels. There are also central (i.e. spinal cord) sensitising effects

40
Q

What produces central sensitisation

A

Prolonged nociceptor input onto dorsal horn neuron projection neurons produces

41
Q

What are the two types of modulation

A

central sensitisation

peripheral sensitisation

42
Q

describe how central sensitisation works

A
  • there is prolonged nociceptor input
  • the activity dependent increase in excitability of dorsal horn projections outlast the stimulus which caused it in the first place
  • this leads to modified responsiveness, the projection neurones show enhanced responses and low leave inputs produce a response and pain, therefore the threshold has been lowered
  • this leads to pain such as allodynia, 2nd degree hyperalgesia and spontaneous pain
43
Q

What is allodynia

A

Allodynia refers to central pain sensitization (increased response of neurons) following normally non-painful, often repetitive, stimulation.

44
Q

What is hyperalgeisa

A

yperalgesia is a condition where a person develops an increased sensitivity to pain.

45
Q

what do nociceptor afferents release

A

glutmate and peptides

46
Q

what can chronic pain arise form

A

nociceptive pain

47
Q

describe the definition of chronic pain

A

Defined as pain of more than 12 weeks by British Pain Society, normally associated with an underlying condition

48
Q

name the two types of maladaptive chronic pain

A 
Neuropathic pain (due to injury in PNS or CNS)
Dysfunctional pain (no known lesion or inflammation
49
Q

what is maladaptive chronic pain characterised by

A

Characterised by hyperalgesia, allodynia, spontaneous pain i.e., central sensitisation effects

50
Q

What are the causes of chronic maladaptive pain

A

injury, stroke, infection i.e. post-herpetic neuralgia, drug treatments, diabetes, chronic alcoholism, hereditary conditions

51
Q

where does pain modulation occur

A

= In the cortex
= From the brain/ brainstem
= In the spinal cord (central sensitisation)
= In the periphery (inflammation)

52
Q

What theory is at the spinal level that is a modulation theory

A

gate control theory

53
Q

describe gate control theory

A

If you hit your hand painful than if you rub it adds another stimulus and this reduces the painful stimulus going up to the CNS
- this has a role of TENS, lamina II interneurones

54
Q

describe what the midbrain periaqueductal gray does

A
  • this is a descending system that modulates the transmission of ascending pain signals
  • it is inhibitory or facilitating
  • this effects the parabrachial nucleus, medullary reticular formation, locus coeruleus, and raphe nuclei
55
Q

describe how acupuncture works

A
  • activates A delta fibres
  • this stimulates the periaquaductal grey through diffuse noxious inhibitory control (DNIC) of pain
  • this pain can inhibit pain
56
Q

what are key mediators of endogenous analgesic mechanisms

A

lamina II interneurons are key mediators of endogenous analgesic mechanisms.

57
Q

what causes the intensity of the pain

A
  • superior parietal lobe and insula and amygdala pathway
58
Q

What feeling causes the unpleasantness of pain

A

ACC - PFC - PAG path emotion/ placebo control– unpleasantness
= Sensitive to μ opioid antagonist - naloxone

Brain and Behaviour Year 2 (36 decks)

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