Somatosensation and Pain Flashcards

1
Q

What does the limbic system play a key role in?

A

regulating emotions, memory and behaviour

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2
Q

What does the limbic system include?

A
  • amygdala
  • hippocampus
  • hypothalamus
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3
Q

What is the role of the amygdala?

A
  • processes emotions like fear, anger and pleasure
  • helps recognise emotional cues
  • triggers fight or flight response
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4
Q

What is the role of the hippocampus?

A

declarative memory i.e. crucial for forming and retrieving memories linked to emotions to contextualise emotional experiences based on past events

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5
Q

What is the role of the hypothalamus?

A

regulates emotional responses by controlling autonomic functions like heart rate, blood pressure, and hormone release, which are linked to emotional states

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6
Q

How does pain serve as a critical protective mechanism?

A

it alerts the body to potential or actual harm

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7
Q

What are the 3 main components of pain?

A
  1. sensory-discriminative aspect
  2. affective-motivational aspect
  3. cognitive-evaluative aspect
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8
Q

What does the sensory-discriminative aspect of pain involve?

A

the physical sensation of pain, including its intensity, location, quality and duration

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9
Q

What is the mechanism of the sensory-discriminative aspect of pain?

A

pain signals are initiated by nociceptors and are transmitted through peripheral nerves to the spinal cord and then to the brain, where they are processed primarily in the somatosensory cortex, allowing the individual to localise and describe the pain

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10
Q

What does the affective-motivational aspect of pain refer to?

A

the unpleasant emotional and psychological responses associated with pain, such as fear, anxiety, and the urge to escape the painful stimulus regulated by the limbic system

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11
Q

What does the cognitive-evaluative aspect of pain involve?

A

the interpretation and meaning assigned to the pain experience, including beliefs, attitudes, and expectations about pain, as well as coping strategies

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12
Q

What is nociceptive pain?

A

pain that results from actual or potential tissue damage, typically protective in nature, often described as sharp, aching, or throbbing

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13
Q

Give an example of nociceptive pain

A

pain from a cut, burn, or broken bone

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14
Q

What is neuropathic pain?

A

(often chronic) pain caused by damage to or dysfunction of the nervous system itself, described as burning, shooting, or electric shock-like

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15
Q

Give an example of neuropathic pain

A

pain from diabetic neuropathy, shingles or nerve compression

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16
Q

What is inflammatory pain?

A

pain associated with inflammation, which occurs when the body’s immune response triggers the release of chemicals that sensitise nociceptors

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17
Q

Give an example of inflammatory pain

A

pain from rheumatoid arthritis

18
Q

What is chronic pain?

A

pain that persists for longer than 3-6 months, often resulting from ongoing tissue damage, nervous system dysfunction, or sensitisation

19
Q

Give an example of chronic pain

A

chronic back pain, fibromyalgia, migraine headaches

20
Q

What is pain intensity?

A

the sensory dimension of the pain experience, which often translates into the quantity of the pain experienced

21
Q

What is pain unpleasantness?

A

the emotional dimension of the pain experienced, or the extent to which the pain is considered uncomfortable or bothering

22
Q

What happened to neural activity in the ACC when pain unpleasantness was decreased via hypnosis?

A

it also decreased

23
Q

What happens when pain signals reach the ACC?

A

they trigger emotional and behavioural responses aimed at avoiding or escaping the painful stimulus

24
Q

What does activity in the ACC correlate to?

A

the subjective feeling of how unpleasant the pain is, rather than just the intensity of the pain stimulus

25
Q

What is allodynia?

A

pain to a normally non-painful stimulus

26
Q

What are possible mechanisms of touch allodynia?

A
  • peripheral sensitisation
  • central sensitisation
  • disinhibition
  • aberrant sprouting
  • altered brain processing
  • involvement of glial cells
27
Q

When does peripheral sensitisation occur?

A

when PNS nociceptors become more sensitive and responsive to stimuli

28
Q

What is the mechanism of peripheral sensitisation?

A

after tissue injury or inflammation, nociceptors can lower their threshold for activation, meaning that even light touch can activate them and send pain signals to the brain (inflammatory mediators can also contribute to this)

29
Q

What is the result of peripheral sensitisation?

A

increased sensitivity of primary afferent neurons (especially Aδ and C-fibres)

30
Q

What is central sensitisation?

A

increased responsiveness of CNS neurons, particularly in the dorsal horn of the spinal cord, to normal or subthreshold sensory input

31
Q

What are the 3 mechanisms of central sensitisation?

A
  • increased synaptic efficiency (repeated stimulation of nociceptors → increased neurotransmitter release and activation of NMDARs in dorsal horn neurons → LTP)
  • loss of inhibitory control (inhibitory interneurons become less effective through loss of GABA or glycinergic inhibition)
  • spinal cord rewiring (Aβ fibres synapse on neurons that normally transmit pain signals)
32
Q

What is disinhibition?

A

a reduction in the inhibitory control that normally prevents non-painful stimuli from being perceived as painful

33
Q

What is the mechanism of disinhibition?

A

destruction of inhibitory interneurons, such as those in lamina II of the dorsal horn, leads to a loss of inhibition on pain-processing neurons

34
Q

Give an example of disinhibition

A

the loss of dynorphin-expressing neurons, which inhibit pain pathways, can result in increased excitability of pain-transmitting neurons → touch allodynia

35
Q

What is aberrant sprouting?

A

abnormal growth of CNS nerve fibres e.g. after injury, Aβ fibres may sprout and form new synaptic connections with neurons in the dorsal horn that usually receive input from nociceptive fibres

36
Q

How can altered brain processing cause touch allodynia?

A

brain regions e.g. somatosensory cortex and ACC may become hyperactive or reorganised which amplifies the perception of touch leading to the sensation of pain even in response to light touch

37
Q

How can glial cells cause touch allodynia?

A

after injury or inflammation, glial cells can become activated and release pro-inflammatory cytokines and chemokines that enhance the excitability of pain-processing neurons and enhance the central sensitisation

38
Q

What is LTP?

A

a form of synaptic plasticity that makes these neurons more responsive to incoming signals

39
Q

What are the 6 steps of long-term modulation of spine plasticity?

A
  1. nociceptive afferent, on intense activation by peripheral damage, releases relative excessive glutamate at glutamatergic synapse on 2nd order neurons
  2. glutamate combines with NMDARs, which facilitates the rise in calcium in the 2nd order neurons
  3. calcium phosphorylates AMPARs which increase the excitability of the receptor
  4. elevated calcium also triggers translocation of AMPARs to the membrane, which increases the excitability of the 2nd order neurons
  5. postsynaptic messengers travelling from the synapse to the nucleus of the 2nd order neuron trigger calcium signalling in the nucleus and activation of CREB-dependent genomic programmes
  6. this about long-term modulation of spine structure and density
40
Q

Give examples of touch allodynia

A
  • sprained ankle
  • sunburn
  • neuropathy