Neuroscience > Pain > Flashcards

Pain Flashcards

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1
Q

What is Pain?

A

Unpleasant sensory and emotional experience associated with actual or potential tissue damage,

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2
Q

What is nociception?

A

Series of neural and chemical pathways that process pain.

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3
Q

What fibres detect pain?

A

Free nerve endings of Aδ and C fibres

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4
Q

Where is pain information in Adelta and C fibres carried to?

A

Dorsal horn of the spinal cord

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5
Q

What tract do pain fibres form when they reach the dorsal horn?

A

Tract of Lissauer

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6
Q

Where do pain fibres travel in the tract of Lissauer?

A

Run up for one or two spinal cord segments before grey matter of the dorsal horn is penetrated

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7
Q

What rexed lamina do both Adelta and C fibres send branches to?

A

Rexed lamina 1 (marginal zone)

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8
Q

What is rexed lamina 1 known as?

A

Marginal zone

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9
Q

What is rexed lamina II known as?

A

Substantia gelatinosa

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10
Q

How do Adelta fibres send signals to the marginal zone?

A

Directly

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11
Q

What are the two pain sensations felt, how are they distinctive?

A

A fast ‘sharp’ sensation transmitted by faster Aδ fibres and a slow ‘dull’ pain that C fibres carry.

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12
Q

How do C fibres send signals into the marginal zone?

A

Indirectly, via interneurons in lamina II (substantia gelatinosa)

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13
Q

Where is information from rexed lamina I/II sent?

A

Second-order projection neurons in laminae IV, V, and VI (nucleus proprius),

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14
Q

What laminae makes up the nucleus proprius?

A

IV, V, VI

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15
Q

What happens to the second order neurons in the spinal cord?

A

Decussate immediately and ascend in anterolateral system

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16
Q

Why does lesion of anterolateral pathway nearly always result in contralateral loss of pain/temp/crude touch?

A

Decussation so early (in spinal cord)

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17
Q

Where may a lesion produce ipsilateral loss of pain and temp?

A

Tract of Lissauer

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18
Q

What synapses are formed between 1st and 2nd order neurons?

A

Excitatory sub P/glutamate synapses in the dorsal horn

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19
Q

What tracts make up the anterolateral system?

A

Spinothalamic, Spinoreticular, Spinomesencephalic

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20
Q

Is there lateral inhibition in pain system?

A

No, convergent excitation

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21
Q

What is peripheral sensitization?

A

Reduction in threshold and an amplification in the responsiveness of nociceptors exposed to inflammatory mediators and damaged tissue.

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22
Q

What are types of peripheral sensitization?

A

Allodynia

Primary hyperalgesia

Spontaneous pain

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23
Q

What is allodynia?

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A

Pain response to previously innocuous stimuli e.g. joint movement in rheumatoid arthritis

24
Q

What is primary hyperalgesia?

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A

Exaggerated response to noxious stimuli

25
What causes peripheral sensitization?
Persistent activation by inflammatory mediators - upregulation of cell surface receptors involved in nociception - Increased release and increase in channels - increased open probability - decrease threshold for nociceptive activation
26
Old spinothalamic tract
A delta/C fibres with large receptive fields - WDR neurones in nucleus proprius - central lateral nucleus of thalamus (e.g. anterior insula, cingulate decision making + emotional consequences region)
27
New spinothalamic tract
A delta fibres with small receptive fields - nociceptive specific neurones in lamina 1 - VPL nucleus of thalamus - S1 for localisation and immediate sensory perception.
28
Spinoreticular tract
Terminates in Pontine/medullary reticular formation - projects to higher centres i.e. alerts cerebral cortex. Central lateral nucleus of thalamus - S1, and along reticulospinal tract - increase stretch and reflex activity.
29
What is the key difference between old and new spinothalamic divisions?
Old - emotional/decision making pain response | New - location and perception
30
Spinomesencephalic tract
Pain control centre (PAG), midbrain reticular formation (inputs to limbic system e.g. amygdala), superior colliculus (influences tectospinal tract).
31
What is the gate control theory of pain?
Relay of nociceptive signals to projection neurone (WDR neurone) gated by activity of inhibitory interneuron, which is inhibited by C and excited by A beta fibres.
32
What effect do A beta fibres have on the inhibitory interneuron?
Excite - promote inhibition of projection neuron
33
What effect to C fibres have on the inhibitory interneuron?
Inhibit - prevent inhibition of the projection neuron
34
What is central sensitization?
Altered central processing due to enhanced responsiveness of secondary nociceptive neurones in dorsal horn - threshold for activation falls.
35
Why is central sensitization beneficial?
Enhances the protective function of pain (hyperalert when further risk to damage is high) and occurs after repeated or particularly intense noxious stimuli
36
What causes central sensitization?
Increased nociceptive input
37
What is one mechanism of central sensitization
With each response - potentiation of the synapse and the dorsal horn responds progressively more excitably each time - form of plasticity
38
How is referred pain generated?
Convergence of sensory information from different body parts onto the same second order neurones - may provide ambiguous information as to the exact location of the noxious stimulus.
39
What is the lateral thalamus implicated in?
Lateral region is involved in the processing of precise location to injury – conveyed to consciousness as acute pain.
40
What is the medial thalamus implicated in?
Process nociceptive input relevant for affective and motivational aspects of pain.
41
What areas of the cortex have been implicated in pain?
Cingulate and insula
42
What processing of pain occurs in the cingulate?
Processing emotional and behavioural states of pain.
43
What processing of pain occurs in the insula?
Cognitive input is integrated here
44
What does the descending pain modulatory system control?
Regulates dorsal horn processing
45
Where receives descending input of pain information?
PAG
46
What nuclei does the PAG signal via?
Raphe 5HT cells of medulla and locus coeruleus NA cells of pons.
47
What are the two effects of the descending 5-HT system? What receptors?
5HT inhibits via 5HT1 - descending inhibition or activates via 5HT 2/3 - descending facilitation
48
What are is the effect of the descending NA system? What receptors?
NA inhibits via Alpha 2 directly on second order neurones and via alpha 1 on enkephalinergic interneurons.
49
Why are tricyclic antidepressants used as pain relief?
Amilyptyline inhibits 5HT/NA uptake - enhance descending inhibition
50
How else does the PAG provide analgesia?
Endogenous opioid release by CNS - PAG has many opioid receptors
51
Where are opioid receptors and what effects does binding at different sites have?
Opioid receptors in periphery, dorsal horn and brainstem - analgesia. Also bind receptors in PAG and higher centre e.g. frontal cortex - altered emotional response to pain.
52
How is opioid effect produced?
Enkephalin binding to mu opiate receptors inhibits nociceptive transmission to higher brain areas by inhibitory presynaptic glutamate release and hyperpolarizing post synaptic membrane
53
What is codeine, what receptor does it bind?
Codeine is an opioid. It is a selective agonist of the μ-opioid receptor (MOR). Acts on CNS for analgesic effect
54
What is morphine, what receptor does it bind?
Morphine an opioid. It interacts predominantly with the μ–δ-opioid (Mu-Delta) receptor heteromer. Most powerful pain medication.
55
What is tramadol, what receptor does it bind?
Opioid pain medication used to treat moderate to moderately severe pain. Agonist of the μ-opioid receptor (MOR) and to a far lesser extent of the δ-opioid receptor (DOR) and κ-opioid receptor (KOR) Serotonin reuptake inhibitor (SRI) and norepinephrine reuptake inhibitor; hence, an SNRI
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