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Case 2 > Pain > Flashcards

Pain Flashcards

0
Q

What are nociceptors

A

Free nerve endings, found everywhere except brain and bones.
Ply modal so responds to several different types of stimuli - chemical, temp, mechanical

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1
Q

Types of pain

A

Nociceptive (acute) - provoked by stimulus. Flexion withdrawal in response. Adaptive to protect body from injury.
Prolonged (sunburn) - pain to prevent any further injury. Caused by decreased activation threshold of nociceptors, peripheral sensitization
Chronic (neuropathic) - pain present for 2-3 months. Results from damage to cns or pns. Pain in absence of initial injury due to abnormal sensitivity of nociceptors. Greatest concern

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2
Q

2 categories of pain sensation

A

Fast: stabbing, sharp, bright sensations. Meidated by A-delta fibres.

Slow: dull, throbbing, aching sensations. Mediated by C fibres. These fibres selective for histamine and so itch

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3
Q

Slow pain

A

Slow pain mediated by c fibres and signals emotional aspect of pain.
Reaches thalamus indirectly via connections with brainstem reticular formation.

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4
Q

What parts of brain associated with different types of pain

A

Discriminative (where and how much it hurts) - somatosensory cortex

Affective motivational (i dont like it, stop it!) - limbic regions, cingulate cortex

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5
Q

Receptors on nociceptors involved in signal transduction

A

P2X (purinergic ATP)
ASIC (acid sensing ion channels)
TRP (transient response potential heat)

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6
Q

Receptors on nociceptors involved in membrane excitability

A 
Voltage gated Na+
Voltage gated Ca+
Voltage gated K+
Glutamate receptors
GABA receptors
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7
Q

Receptors on nociceptors involved in peripheral sensitisation

A

H1 (histamine)
IL-1R (interleukin 1)
BK2 (bradykinin)
CB1 (canaboid)

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8
Q

Hyperalgesia

A

Example of peripheral sensitization. Results from interaction of nociceptors with inflammatory chemicals released when tissue is damaged (histamine, bradykinin, arachidonic acid, serotonin, prostaglandins, nucleotides). These amplify sensory signals. When damaged area hypersensitive - primary hyperalgesia.
Secodnary hyperalgesia - surrounding area hypersensitive due to secretion of substance P by axon when activated primarily. Substance p causes vasodilation and release of mast cells

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9
Q

Allodynia

A

Induction of pain by a normally innocuous stimuli.
Result of central hypersensitisation - increased excitability of neurones in dorsal horn of spinal cord
Can last several hours

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10
Q

Pain pathways

A

All reside in ventro-lateral region of SC.
Signals transmitted to the:
- brain stem: spinoreticular tract
- hypothalamus: spinoparabrachial tract
- thalamus: spinothalamic tract

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11
Q

Spinothalamic pathway

First neurone

A

First neurone enters spinal cord through dorsal root.
Cell body lies in DRG
Main fibre remians on ipsilateral side and synapses in dorsal horn of spinal grey matter at substantia gelatinosa

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12
Q

Spinothalamic pathway

Second neurone

A

Has cell body deeper in dorsal horn
Its axon decussates either immediately or further up a few spinal segments (ventral) and ascends.
Synapses at ventral posterolateral nucleus of thalamus

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13
Q

Spinothalamic pathway

Third neurone

A

Cell body in the ventral posterolateral nucleus of thalamus
Project through posterior limb of internal capsule
Terminates in somatosensory cortex of pariteal lobe

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14
Q

Pain and temp sensations from limb and trunk?

A

Lateral spinothalamic tract

FAST PAIN

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15
Q

Crude touch and pressure sensations from limbs and trunk?

A

Ventral spinothalamic tract

Carried by Adelta and C fibres

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16
Q

Proprioception, discriminative touch and vibratory sensations from limb and trunk?

A

Dorsal column medial lemniscus

Carried by Aalpha and Abeta fibres

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17
Q

Dorsal column medial lemniscus

First neurone

A

Receptor at meissners corpuscle, panicuan corpuscles, muscle spindles.
Cell body in DRG. Goes up the spinal cord ipsilaterally.
Synapses at gracile nucleus and cuneate nucleus of medulla.

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18
Q

Dorsal column medial lemniscus

Second neurone

A

Nerve cell body in gracile nucleus and cuneate nucleus of medulla.
Internal arcuate fibres decussate in caudal medulla
Synapses at ventral posterior nucleus of thalamus.
Third neurone same as STT pathway

19
Q

Decussation of touch and pain neurones.

A

Info about touch ascends ipsilaterally and decussates in brainstem.
Info about pain and temp decussates earlier in spinal cord.

22
Q

Peripheral mechanisms for neuropathic pain

A
  • increased expression of sodium channels at peripheral site of injury, damaged spinal ganglion or dorsal roots. Leads to spontaneous activity.
  • ephatic connections between injured and uninjured nerve fibres with injured one causing spontaneous activity in uninjured.
  • primary afferents becoming sensitive to substances that they were not initially responding to (like cathecolamines)
23
Q

Central mechanisms for neuropathic pain

A
  • central sensitixation of spinal cord due to ongoing spontaneous activity in injured and non injured afferents and release of neuroactive substances in glial cells.
  • disinhibition of spinal cord cells due to afferent cell death, atrophy or loss of inhibitory transmitters like GABA
  • CNS plasticity
24
Q

Neurotransmitter for pain

A

Is glutamate.

Synaptic transmission is mediated by substance P for moderate to intense pain (released by high frequency AP)

25
Q

What does release of glutamate cause

A

Evokes fast synaptic potentials in dorsal horn neurones by activating AMPA-type glutamate receptors

26
Q

Spinomesencephalic tract

A

Projects to midbrain periaqueductal grey (PAG) matter and superior colliculi. PAG has reciprocal connections to limbic system and recieves input from hypothalamus and cortex.
Projections to superior colliculus thought to influence eye movements and direct our gaze to site of injury.

27
Q

Spinoreticular tract

A

Terminates on medullary-pontine reticular formation, which then projects to intralaminar thalamic nucleus.
This then projects diffusely to entire cerebral cortex and is thought to be involved in behavioural arousal.
Conveys emotional and arousal aspects of pain and transmission of slow pain.

28
Q

Trigeminal pain pathway

A

First order axons get info from facial nociceptors and thermoreceptors and transmit to brainstem. Enter pons, descend to medulla, forming spinal trigeminal tract. Then becomes2 subdivisons the pars interpolaris and pars caudalis.
These then cross midline and ascend to contralateral thalamus in trigeminothalamic tract. This then terminates in ventral posterior medial nucleus of thalamus.

29
Q

Gate control theory

What are large fibres

A

Non-nociceptive A alpha and beta fibres

30
Q

Gate control theory

What are small fibres

A

Nociceptive Adelta and C fibres

31
Q

With no simulation

A

Without stimulation the gate is closed, as both sets of nerves inactive.
Therefore the inhibitory neurone blocks any signal that feeds into projections neurone.

32
Q

With non painful stimulation

A

Abeta fibres activated, activating projection neurone.
However it also activates the inhibitory neurone which blcoks the signal in projection neurone.
So gate is still closed, pain is not felt.

33
Q

Painful stimulus

A

With painful stimulus, the nociceptive Adelta and C fibres become active. These activate substance P, but also by original theory they block P. This allows sensation to be felt by the brain.
So activate projection neurone, and DO NOT activate the inhibitory interneurone.

34
Q

TENS machine

A

Uses the principle of gate control theory. Same as rubbing a bruise.
Rubbing the bruised area/ TENS machine stimulates the non-nociceptive nerve fibres that will send impulses to spinal cord, and then activate lamina 2 inhibitory neurones, inhibiting the action of projection neurones, therefore shutting he gate. This relieves pain to an extent.

Useful in acute pain, but not in chronic as some forms of chronic pain cause low threshold fibres to become nociceptors, making TENS machine increase pain!

35
Q

Areas of brainstem involved in pain reduction/ analgesia

A

Periaqueductal grey PAG
Locus coerulus LC
Nucleus raphe magnus NRM

36
Q

How does PAG neurones excite amine containing cells in NRM and LC?

A
  • direct presynaptic inhibition of neurotransmitter release from 1st afferent terminals, by activating G protein coupled receptors that cause closure of Ca2+ channels
  • direct postsynaptic inhibition of projection cells causing hyperpolarisation due to activation of G receptors that cause K+ channels to open
  • indirect inhibition vis activation of local enkephalin of GABA inhibitory interneurones by descending axons.
37
Q

How does NRM help cause analgesia?

A

NRM sends inhibitory enkephalins and serotonergic (5-HT) axons via dorsolateral funiculus to the dorsal horn to inhibit substantia gelatinosa cells and nociceptors.

38
Q

How does LC help cause analgesia?

A

LC sends separate noradrenergic inhibitory inputs to the dorsal horn via the dorsolateral funiculus.

39
Q

What is the receptive field?

A

Area of skin surface over which stimulation results in significant change in rate of action potentials.

40
Q

Two point discrimination

A

Minimum interstimulus distance required to perceive two simultaneous stimuli as different.

41
Q

Substance P

A

Expressed by nociceptive afferent neurones and released at peripheral and central terminals

42
Q

Glutamate

A

Released from promary afferent neurones and act on AMPA recpetors. Responsible for fast transmissions at first synapse of dorsal horn.
There also is a slower NMDA receptor mediated response

43
Q

GABA

A

Released by spinal interneurones and inhibits transmitter release from primary afferent terminals in the dorsal horn

44
Q

5-HT

A

Tranmitter of inhibitory neurones running from NRM to dorsal horn

45
Q

Noradrenaline

A

Trabsmitter of inhibitory neurones from LC to dorsal horn

46
Q

Adenosine

A

Activation of A1 receptors can cause analgesia by acting on peripheral nerve terminals and dorsal horn neurones.
Activation of A2 receptors in periphery does reverse.

Case 2 (5 decks)

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