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Neuroscience > Pain > Flashcards

Pain Flashcards

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?

A

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

24
Q

What is primary hyperalgesia?

A

Exaggerated response to noxious stimuli

25
Q

What causes peripheral sensitization?

A

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
Q

Old spinothalamic tract

A

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
Q

New spinothalamic tract

A

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
Q

Spinoreticular tract

A

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
Q

What is the key difference between old and new spinothalamic divisions?

A

Old - emotional/decision making pain response

New - location and perception

30
Q

Spinomesencephalic tract

A

Pain control centre (PAG), midbrain reticular formation (inputs to limbic system e.g. amygdala), superior colliculus (influences tectospinal tract).

31
Q

What is the gate control theory of pain?

A

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
Q

What effect do A beta fibres have on the inhibitory interneuron?

A

Excite - promote inhibition of projection neuron

33
Q

What effect to C fibres have on the inhibitory interneuron?

A

Inhibit - prevent inhibition of the projection neuron

34
Q

What is central sensitization?

A

Altered central processing due to enhanced responsiveness of secondary nociceptive neurones in dorsal horn - threshold for activation falls.

35
Q

Why is central sensitization beneficial?

A

Enhances the protective function of pain (hyperalert when further risk to damage is high) and occurs after repeated or particularly intense noxious stimuli

36
Q

What causes central sensitization?

A

Increased nociceptive input

37
Q

What is one mechanism of central sensitization

A

With each response - potentiation of the synapse and the dorsal horn responds progressively more excitably each time - form of plasticity

38
Q

How is referred pain generated?

A

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
Q

What is the lateral thalamus implicated in?

A

Lateral region is involved in the processing of precise location to injury – conveyed to consciousness as acute pain.

40
Q

What is the medial thalamus implicated in?

A

Process nociceptive input relevant for affective and motivational aspects of pain.

41
Q

What areas of the cortex have been implicated in pain?

A

Cingulate and insula

42
Q

What processing of pain occurs in the cingulate?

A

Processing emotional and behavioural states of pain.

43
Q

What processing of pain occurs in the insula?

A

Cognitive input is integrated here

44
Q

What does the descending pain modulatory system control?

A

Regulates dorsal horn processing

45
Q

Where receives descending input of pain information?

A

PAG

46
Q

What nuclei does the PAG signal via?

A

Raphe 5HT cells of medulla and locus coeruleus NA cells of pons.

47
Q

What are the two effects of the descending 5-HT system? What receptors?

A

5HT inhibits via 5HT1 - descending inhibition or activates via 5HT 2/3 - descending facilitation

48
Q

What are is the effect of the descending NA system? What receptors?

A

NA inhibits via Alpha 2 directly on second order neurones and via alpha 1 on enkephalinergic interneurons.

49
Q

Why are tricyclic antidepressants used as pain relief?

A

Amilyptyline inhibits 5HT/NA uptake - enhance descending inhibition

50
Q

How else does the PAG provide analgesia?

A

Endogenous opioid release by CNS - PAG has many opioid receptors

51
Q

Where are opioid receptors and what effects does binding at different sites have?

A

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
Q

How is opioid effect produced?

A

Enkephalin binding to mu opiate receptors inhibits nociceptive transmission to higher brain areas by inhibitory presynaptic glutamate release and hyperpolarizing post synaptic membrane

53
Q

What is codeine, what receptor does it bind?

A

Codeine is an opioid. It is a selective agonist of the μ-opioid receptor (MOR).

Acts on CNS for analgesic effect

54
Q

What is morphine, what receptor does it bind?

A

Morphine an opioid. It interacts predominantly with the μ–δ-opioid (Mu-Delta) receptor heteromer. Most powerful pain medication.

55
Q

What is tramadol, what receptor does it bind?

A

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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