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303: Neurology > Temperature And Nociception > Flashcards

Temperature And Nociception Flashcards

0
Q

How do thermal receptors perceive temperature?

A

Separate receptors for cold to hot

43 degrees is perceived as pain (tissue damaging)

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1
Q

What type of receptors respond to temperature in the skin?

A

Free nerve endings

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2
Q

What is the minimum temperature not perceived as pain?

A

15 degrees

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3
Q

What is the maximum temperature not perceived as pain?

A

43 degrees

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4
Q

What type of thermal receptors are most superficial and are in greater distribution?

A

Cold receptors

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5
Q

Is the distribution of thermal receptor in the skin uniform or not uniform?

A

Not uniform

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6
Q

What are the 6 temperature activated transient receptor potential ion channels?

A 
TRPA1
TRPM8
TRPV4
TRPV3
TRPV1
TRPV2
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7
Q

Which temperature activated transient receptor potential ion channels respond to nociceptive stimuli?

A

TRPA1, TRPV1, TRPV2

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8
Q

Which temperature activated transient receptor potential ion channels respond to heat stimuli?

A

TRPV1-4

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9
Q

Which temperature activated transient receptor potential ion channels respond to cold stimuli?

A

TRPM8, TRPA1

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10
Q

Describe the first and second pain.

A

Early, sharp pain carried by Ad(delta) fibres followed by a later, dull burning pain carried by C-fibres

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11
Q

What are the afferent axon types of free nerve endings in nociception?

A

Ad(delta) fibre mechano-heat sensitive

C fibre mechano-heat sensitive

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12
Q

What are the characteristics of C-fibres?

A

Slow conduction

Unmyelinated (thinner)

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13
Q

What are the characteristics of A fibres?

A

Rapid conduction

Myelinated

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14
Q

What can activate nociceptors?

A 
High intensity and thermal stimuli
Chemical stimuli (inflammation)
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15
Q

What are the three modalities mediated by the spinothalamic tract?

A

Non-discriminative touch
Innocuous temperature sensation
Nociception

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16
Q

What modalities are mediated by Ad(delta) fibres?

A

Non-discriminative touch
Innocuous temperature sensation
Nociception

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17
Q

What modalities are mediated by C fibres?

A

Innocuous temperature sensation

Nociception

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18
Q

What activates TRPV1?

A 
Noxious temperatures (>43 degrees)
Capsaicin
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19
Q

In what afferent fibres are TRPV1 expressed in?

A

Both Ad(delta)and C fibres

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20
Q

Describe the pathway of the afferent fibres from when they enter the spinal cord to the formation of spinothalamic tract

A

Delta and C fibres enter dorsal roots
Passes through Lissauer’s tract (zone) in grey matter
Travel 1-2 levels before entering dorsal horn
Synapse with 2nd order neurons in Rexed’s laminate I-V (anterolateral system)
Ascend spinal cord contra laterally via spinothalamic tract

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21
Q

Which lamina in Rexed’s lamina contains substantia gelatinosa?

A

Lamina II

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22
Q

What is the relevance of Rexed’s lamina II to temperature and nociception?

A

It contains substantia gelatinosa which modulates temperature and nociceptive afferents

23
Q

Decribe the segmental organisation of the spinothalamic tract.

A

From anterior to lateral

Pressure - touch - pain - temperature

24
Q

What are the pain pathways for visceral innervation?

A 
Vagus nerve
Splanchnic nerves (ganglion)
25
Q

What type of stimuli do visceral nociceptors respond to?

A

Stretch

Various chemicals

26
Q

What type of fibres receive visceral nociceptive stimuli?

A

C fibres

27
Q

What are the three categories of pain?

A

Nociceptive
Inflammatory
Neuropathic

28
Q

What are the characteristics of nociceptive type pain?

A

Brief pain
Normal response to acute tissue injury
Stimulus-dependent
Protects by signalling potential tissue damage

29
Q

Where does the spinothalamic and trigmeniothalamic terminate?

A

Thalamus ventral posterior nuclei

30
Q

From where does sensory information terminate in the VPL?

A

Information from the body

31
Q

From where does sensory information terminate in the VPM?

A

Information from the face

32
Q

Where does the spinothalamic tract project to other than the thalamic VPN?

A

Reticular formation and parabrachial nucleus
Cingulate and insula cortex
Amygdala and hypothalamus

33
Q

What are projections of the spinothalamic tract to the Reticular formation and parabrachial nucleus associated with?

A

Arousal component of pain

34
Q

What are projections of the spinothalamic tract to the cingulate and insula cortex associated with?

A

Signalling unpleasant and autonomic components of pain response (respectively)

35
Q

What are projections of the spinothalamic tract to the amygdala and hympothalamus associated with?

A

Amygdala: Fear and anxiety response
Hypothalamus: Autonomic response to pain

36
Q

What are the nerve fibre(s) associated with low intensity, non-noxious stimuli?

A

Aß fibres

37
Q

What are the nerve fibre(s) associated with high intensity, noxious stimuli?

A

Ad(delta) and C fibres

38
Q

What part of the spinal cord do Aß, delta and C fibres transverse?

A

Dorsal horn via peripheral nerve and dorsal root ganglion

39
Q

What are the characteristics of inflammatory type pain?

A

Active inflammation is present
Spontaneous/stimulus dependent (low and high intensity)
Long term (persistent) but reversible
Protects by producing pain hypersensitivity during healing (peripheral
/central sensitisation)

40
Q

What are the overall mechanisms/processes involved in inflammatory pain?

A

Peripheral sensation
Central sensitisation and wind up
Long term potentiation

41
Q

Describe the process of peripheral sensitisation of nociceptors

A

Activation/augmentation of nociceptor fibres (by inflammatory mediators eg platelets, bradykinin, histamine)
Release of neuropeptides substance P and Calcitonin Gene-Related Peptide (CGRP)
Causes histamine release from mast cells, vasodilation and plasma extravasation
Histamine decreases threshold for nociceptive activation - hyperalgesia (increased sensitivity of pain)

42
Q

What does the release of substance P and CGRP cause?

A

Plasma extravasation
Histamine release
Vasodilation

43
Q

What process is associated with hyperalgesia?

A

Histamine release that decreases the threshold for nociceptive activation in peripheral sensitisation

44
Q

What is central sensitisation?

A

Enhancement, potentiation or facilitation of synaptic activity in dorsal horn to generate AP’s in 2nd order neurons

45
Q

What is central sensitisation typically associated with?

A

Chronic tissue damage/inflammation

46
Q

What are two possible responses of central sensitisation of nociceptors?

A

Hyperalgesia: increased pain sensitivity
Allodynia: pain due to stimulus that does not normally provoke pain

47
Q

Describe the process of wind up and central sensitisation.

A

Repeated high intensity noxious stimuli
C-fibre stimulation (increased synaptic activity in dorsal horn)
“Wind up”: release of glutamate, substance P and CGRP (neurotransmitters)
Increases duration of post synaptic depolarisation of 2nd order neuron by decreased threshold/increasing sensitivity (summation) and increased receptor fields
Removal of voltage-dependant Mg2+ block from NMDA receptors
Increase influx of Ca2+ triggers long term potentiation/increased release if glutamate

48
Q

Describe the process of long term potentiation.

A

Influx of Ca2+ due to opening of NMDAR channels
Enhances glutamate release (protein kinases in post synaptic neuron)
Results in insertion of new AMPA receptors into post synaptic membrane
Increased sensitivity to glutamate

49
Q

What are the characteristics of neuropathic pain?

A

Nervous system lesion or disease present
Spontaneous/stimulus dependent (low and high intensity)
Long term (persistent)but reversible
Protects by producing pain hypersensitivity during healing (peripheral
/central sensitisation)

50
Q

How are pain signal modulated as they travel along sensory pathways?

A

The gate control theory

51
Q

Describe the gate-control theory.

A

Neural gating mechanism
Increased touch/skin mechanoreceptor stimulation (rubbing injured area) - Aß fibres
Increase afferent signals from mechano receptors to dorsal horn
Blockage of noxious afferents (C fibres) at same spinal cord level due to increased touch afferents

52
Q

Describe the mechanisms of pain modulation by descending pathways?

A

Somatic sensory cortex sends impulses to the hypothalamus
Hypothalamus stimulates periaqueductal grey matter in brain stem to initiate an analgesic impulse
Analgesic impulse to raphe nucleus in brain stem then down spinal cord in dorsolateral tracts
At spinal cord level, analgesic neurons release endogenous opioids (enkephalins) to inhibit release of substance P from presynaptic neuron and inhibits stimulation of 2nd order neuron (block nociceptive pathway)

53
Q

Where is the periaqueductal grey matter located?

A

Brainstem - surrounding cerebral aqueduct in midbrain

54
Q

What is the function of the periaqueductal grey matter?

A

Relay/coordination centre for analgesic system (descending pain modulation pathway)

55
Q

What neurotransmitter is involved in the inhibition (modulation) of nociceptive transmission in the descending pathway.

A

Endogenous opioids - enkephalin

303: Neurology (7 decks)

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