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Neuroscience > Lecture 21 > Flashcards

Lecture 21 Flashcards

1
Q

What can loss of pain sensation (due to nerve damage) be a feature of?

A

Diabetes mellitus and leprosy

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2
Q

How does pain differ from the classical senses?

A

It is both a discriminitive sensation and a graded motivation (or behavioral drive)

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3
Q

What is allodynia?

A

Sensitization to normally innocuous stimuli

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4
Q

What is hyperpathia?

A

Hysterical responses

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5
Q

What is specifity?

A

Theory holds that pain is a distinct sensation, detected and transmitted by specific receptors and pathways to distinct “pain areas” of the brain

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6
Q

What is convergence?

A

Theory suggests that pain is an integrated, plastic state represented by a pattern of convergent somatosensory activity within a distributed network (a so-called “neuromotion”)

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7
Q

How are afferents with free nerve endings (nociceptors?) classified?

A

Classified according to activating stimulus, fiber-type and conduction velocity

  • lightly myelinated A-delta fibers, FAST 20 m/s
    • mechanosensitive
    • mechanothermal - sensitive
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8
Q

Nociceptors repond specifically to pain and are a subset of afferents with free nerve endigs. How is this easly demonstrated for?

A

Heat responses
i.e. Can find afferents whose activity correlates with pain perception
Clear that thermoreceptor activation has already saturated before pain is perceived
i.e. pain is not due to “ramping up” of normal receptors

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9
Q

What is Fast pain?

A

“first” pain
Sharp and immediate
Can be mimicked by direct stimulation of A-delta fiber nociceptors

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10
Q

What is Slow pain?

A

“second” pain
More delayed, diffuse and longer-lasting
Mimicked by stimulation of C fiber nociceptors

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11
Q

How can specifity be demonstrated?

A

Selectively blocking the fibers in turn

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12
Q

Which fiber is proprioceptive and which fiber is mechanoceptive?

A

A-delta

A-beta

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13
Q

What are molecular pain receptors?

A

Specific molecular receptors associated with nociceptive nerve endings are activated by heat (and hot chillis)

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14
Q

How are capsaicin receptors (TRPV1) activated?

A

Activated in nociceptive A-delta and C fibers at 45 degrees

Activated by capsaicin (a vanilloid which is the active component in chillis)

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15
Q

What are TRPV1 related other TRP receptors activated in?

A

A-delta fibers alone at even higher thresholds (52 degrees)

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16
Q

What are TRPs?

A

Respond directly to heat

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17
Q

What does capsaicin mimic?

A

Endogenous vanilloids released by stressed tissues

- nociceptors may also work by detecting release of chemicals from stressed cells

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18
Q

What are the two components of the central pain pathways?

A
  1. Sensory discriminative
    - signals location, intensity and type of stimulus
  2. Affective-motivational
    - signals “unpleasantness”, and enables autonomic activation, classic fight-or-flight response
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19
Q

What tract does the discriminative pathway use?

A 
Spinothalamic tract (also called anterolateral system)
 - pain goes through different pathways to reach different tissues
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20
Q

What do spinothalamic projections also preserve?

A

topography

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21
Q

What does the measurement of activity in the somatosensory cortex indicate?

A
  1. That this region does indeed respond to painful stimuli and that response correlates to intensity of pain
  2. Spatially mapped…
22
Q

What does the comparison of cortical activation by painful (c fiber) or innocuous mechanical stimuli to skin demonstrate?

A

Painful stimuli activate the same region of the somatosensory cortex as the non-painful mechanical stimulation applied to the same region of skin

23
Q

What does the activation of the insula and the cingulate cortex imply?

A

These regions are connected to the limbic system and known to be involved in the activation of emotional response
Part of the affective-motivational response to pain…

24
Q

What does the affective-motivational pathways share some paths with?

A

Anterolateral (spinothalamic) system

25
Q

Does affective-motivational pathways have topographic mapping?

A

no

26
Q

Neurons from which nucleus can respond to painful stimuli from anywhere on the body’s surface?

A

parabrachial nucleus

27
Q

Which two systems share a number of points of input?

A

Limbic and hypothalamic (emotional and homeostatic)

28
Q

Which cortex has a strong correlation of painful “experience”?

A

cingulate cortex

29
Q

Which cortex is activated by the intensity of pain?

A

Somatosensory cortex via the discriminative pathway

30
Q

How does pain comply to the specifity theory?

A
  1. There are receptors, both cellular and molecular, that respond specifically to pain ( subset of A-delta, and c fibers; TRPV1)
  2. There are specific pathways that convey pain messages
  3. There are regions of the CNS that are specifically and distinctly activated in response to pain
31
Q

How does pain not comply to the specifity theory?

A

Pain perceived is not always proportional to intensity of stimulus
Perception of pain in severed limbs (phantom limbs)
Modulation by other stimuli (acupuncture)
Referral of pain from viscera to skin
Placebo effect

32
Q

What is hyperalgesia?

A

Increased response to a painful stimulus

- hypersensitivity of damaged skin to a normally tolerable painful stimulus

33
Q

What do prostaglandins do?

A

Lower the threshold for axon potential generation

34
Q

What does bradykinin do?

A

Directly affects the function of nociceptive molecular receptors such as TRPV1

35
Q

What are some examples of painkillers (analgesics)?

A

Aspirin and ibuprofen

36
Q

What do analgesics act on?

A

COX; an enzyme important in prostaglandin biosynthesis

37
Q

What is hyperalgesia a result of?

A

Lowered nociceptor thresholds which heightens pain response

38
Q

What can central sensitization result from?

A

Activity-dependent local release of substances like prostaglandins from nociceptive dorsal horn neurons

39
Q

What can prostaglandin release from nociceptive dorsal horn neurons do?

A

As in the periphery, this can lower the thresholds for action potential generation for neurons relaying nociceptive information, also giving rise to hyperalgesia

Can also sensitize neurons to non-nociceptive inputs

40
Q

When does hyperpathia occur?

A

When there is fiber/axonal loss (either centrally or peripherally) that results in a raising of the detection threshold

41
Q

What happens when the detection threshold is exceeded in hyperpathia?

A

Subsequent excitability is much greater and patients report “explosive” pain

42
Q

What diseases can cause central sensitization?

A

Diabetes, shingles, multiple sclerosis, or after stroke

43
Q

What does phantom limb pain imply?

A

Central representation of the body isn’t passive

i.e. that it persists in the absence of peripheral input

44
Q

What has leaded to suggest that central maps may be partly pre-formed?

A

Children born without limbs can also have phantoms

45
Q

What is Referred pain?

A

Pain due to damage in the viscera is often perceived as coming from specific locations in the skin according to what organ is affected
e.g. heart attack is often preceded by pain in the left shoulder and arm

46
Q

What is referred pain though to reflect?

A

Convergence of visceral afferents onto the same pathways as cutaneous afferents in the CNS

47
Q

What is referred pain useful for?

A

Aiding clinical diagnosis of organ dysfunction

48
Q

What does the placebo effect imply?

A

That voluntary and involuntary mechanisms exist to overcome severe pain

49
Q

What does the stimulation of the periaqueductal gray activate?

A

Brainstem nuclei that modulate the activity of dorsal horn neurons

50
Q

In the dorsal horn, what do descending inputs activate?

A

Enkephalin-releasing interneurons which presynaptically inhibit nociceptive fibers

51
Q

What are enkephalins?

A

Member of a family of endogenous opioid peptides that also include endorphins, and dynorphins

52
Q

Why is it that rubbing an injury can relieve pain?

A

Thought to be due to local inhibition by mechanoreceptors (A-beta fibers) of nociceptive (C fibers) inputs in the spinal cord

Neuroscience (28 decks)

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