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Scenario 26 > L2 Somatosensation 2 > Flashcards

L2 Somatosensation 2 Flashcards

1
Q

A - beta

A
  • big
  • fat
  • myelinated

e.g. discriminative touch

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2
Q

A- delta

A
  • small
  • myelinated
  • free nerve endings

e.g. fast pain localised, crude localisation of touch

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3
Q

C fibres

A
  • unmyelinated
  • non-localising
  • slow pain
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4
Q

What does fast pain depend upon?

A
  • Small myelinated axons - A delta
  • esp high-threshold mechanoreceptors that
    • respond selectively to cutting or pinching
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5
Q

What does slow pain depend on?

A
  • signals in unmyelinated axons - C fibres
  • usually Polymodal
    • respond to warmth and touch as wel as noxious stimuli
    • some respond to chemicals released in trauma
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6
Q

What are nociceptors?

A

Specialised high-threshold detectors of damagins stimuli

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7
Q

Multi modal nociception

Mechanical

A

High threshold mechanoreceptors, Aδ

– Tissue damage

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8
Q

Multi-modal Nociception

Thermal

A
  • Extreme cold, C-fibres
  • Extreme heat, Aδ
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9
Q

Multi-modal Nociception

Chemical

A
  • ATP, purinergic receptors (PTX3)
  • Reduction in pH
  • Bradykinin
  • Direct and indirect effects
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10
Q

Multi-modal Nociception

another type?

A

axon reflexes

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11
Q

Multi-modal Nociception

TTX-insentive Na+ channel

what does this cause?

A

No or extreme pain

Mutations in SCN9A cause this

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12
Q

Why are chillies hot and painful?

A

Activate Capsaicin and TRP channels

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13
Q

What can TRP channels respond to?

A

Temperatur AND Chemicals

  • TRPV1 specific to nociceptors:
    • capsaicin and heat , current enhanced by reduction in pH
  • TRPV2 found in A δ:
    • high temperature
  • TRPM8:
    • menthol and low temperature
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14
Q

What does Capsaicin activate

A

A depolarizing ion-channel that is also activated by noxious heat

TRP is a type of depolarizing channel

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15
Q

Nociception

Dorsal Horn Inputs

Differential laminar inputs define physiology of dorsal horn laminae

There is lots of capacity for modulating receptors!

A
  • Lamina 1
    • Nociception-specific neurons specific neurons
    • Cold-specific
    • Wide-dyanmic range neurons
  • Lamina II
    • Variety of interneuons
  • Lamina III/IV
    • Interneurons and supraspinal projection neurons: innocuous
  • ​Lamina V
    • Projection neurons: innocuous and nociceptive
      *
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16
Q

Nociception

Dorsal Horn Projections

where do they arise/cross/ascend to?

A
  • arise from superficial and deep laminae
  • cross the midline
  • ascend in white matter to terminate subcortically
17
Q

What are the important targets for Dorsal horn Projections?

A
  • Thalamus
  • Periaqueductal Grey (PAGP)
    • important! crucial in modulating pain transmission
  • Reticular formation
    • ​activates attention, awareness
    • nociception information goes here
18
Q

What do nociceptor afferents co-release?

What other information is there?

A

GLUTAMATE AND PEPTIDES

  • Substance P, CGRP , somatostatin
  • Dense-cored vesicles
  • Long range diffusion
  • Substance P via NK1: slow epsps
19
Q

What do some interneurons release?

A

Enkephalin - endogenous, naturally occurring opiate

  • µ-opiod recceptor on dorsal horn neurons and sensory afferent terminals
  • Presynaptic action reduces transmitter release
20
Q

Where does the Spino-thalamic pathway decussate?

A

Immediately upon entry to the spine

21
Q

WHere does the DCML pathway decussate?

A

At the medulla

22
Q

Why does referred pain occur?

A

Nociceptors from the vicera converge on the dorsal horn neurons that also receive input from cutaneous nociceptors

Hence the brain gets confused and perceives pain from the organs as being from the skin

hence why referred pain symptoms from the heart are at T1-4 dermatomes etc

23
Q

nociceptive aspect of pain goes via?

A

SPINOTHALAMIC TRACT

  • Goes to VP thalamus
  • And then to Somatosensory cortex (s1,s2)

(more info):

  • Inputs to somatosensory cortex
  • Localisable pain
  • Lesions and pain
  • Phylogenetically recent
24
Q

The affective/emotional side of pain goes via the:

A

MIDLINE THALAMIC NUCLEI
to the ACC and Insular cortex

(more info):

Projection to medial nucleus of thalamus

  • Input from deep dorsal horn laminae
  • Projection to basal ganglia and cortex
  • Phylogenetically old
25
Q

What is Placebo?

A

amelioration of pain with false agent

26
Q

What is Nocebo?

A

sensation of pain with false element

27
Q

What is the pain matrix?

A

A collection of brain regions accessed during nociceptive processing

28
Q

What can stimulate nociception?

A

­Noxious temperature

  • ­Extreme heat = A-delta, Extreme cold = C-fibres
  • ­TRP channels (all for heat except TRPM8)
  • ­These also respond to chemical stimuli (e.g. capsaicin) and pH changes

­Peptides

  • ­ATP (PTX3 receptor)
  • ­Bradykinin
  • ­Substance P, Somatostatin, CGRP
  • ­[note these have no reuptake mechanism so spread far and wide and activate other neurones – this could contribute to the poorly localised nature of many pain conditions]

­Low pH

  • ­Due to release of H+
29
Q

What is allodynia?

what causes it?

A

perception of pain when there is no painful stimulus
­

caused by: Uncontrolled activation of nociceptors

30
Q

What is the gate theory in terms of modulation?

A

An Ascending modulatory circuit

31
Q

Descending Modulation

A

Many pathways for descending modulation

Many also receive direct ascending nociceptive inputs

Common target:

  • encephalinergic local circuit neurons,
  • activation of which inhibits transmitter release from C-fibres
32
Q

What is Hyperaesthesia?

A

oversenstivity of mechano- and thermo-sensitive systems to non-noxious stimuli

33
Q

What is Hyperalgesia?

A

oversensitivity of nociceptive system to noxious stimuli

34
Q

What is Analgesia?

A

complete absence of pain in response to noxious stimuli

Scenario 26 (6 decks)

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