lecture 21 Flashcards

1
Q

define somatosensation

A

mechanosensation + pain/temp sensation

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2
Q

what is thermoreception?

A

sensation of temperature in environment/body

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3
Q

what is nociception?

A

sensation of pain

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4
Q

what are nociceptors?

A

specialized sensory neurons that responf to noxious stimuli by sending signals to the brain

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5
Q

define “noxious”

A

damaging to tissue

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6
Q

describe the relationship between stimulus intensity and pain intensity

A

slow build to steep curve then plateau

increases but I dont think proportionally..

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7
Q

what are the 4 major types of pain?

A
  • nociceptive (noxious stimuli - high threshold) (normal)
  • inflammatory (lower threshold) (normal)
  • neuropathic (nerve pain - lower threshold) (abnormal)
  • dysfunctional (no obvious cause) (abnormal)
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8
Q

define pain

A

unpleasent discriminative and emotional (affective) sensation assoicated with tissue damage

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9
Q

explain TRP receptors

A
  • nerve endings have channels with receptors that open in response to temperature change, depolarizing the nerve
  • certain plants can bind teh receptor and open the associated channel (hot peppers - capsaicin)
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10
Q

explain nociceptors

A

open due to deformation or inflammation, but can detect higher temperatures as well, cause pain

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11
Q

what is first pain?

A

relatively fast conducting A(gamma) fibers mediate fast, sharp and localized pain

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12
Q

what is second pain?

A

relatively slow conducting C fibers mediate a delayed, diffuse and longer-lasting pain

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13
Q

describe the difference between fast and slow conducting fibers

A

slow conducting fibers are typically unmyelinated and more narrow in diameter

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14
Q

how are action potentials more easily blocked along A fibers?

A

by crushing the nerve

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15
Q

how are action potentials more easily blocked along C fibers?

A

by Na+ channel antagonists

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16
Q

describe inflammatory pain (generally)

A

pain that occurs over the long term (mins-days) due to inflammation - which promotes constant traffic along second pain pathways (mainly C fibers)

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17
Q

describe the inflammatory pain that results after damage

A
  • substances, such as K, serotonin, histamine, etc., are released into damaged tissues
  • these make nociceptors more sensitive
  • thus, non-painful stimuli can become painful, leading to hyperalgesia and sensitization
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18
Q

where is affective pain perceived?

A

percieved by neocortex that is not primary somatosensory cortex

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19
Q

affective pain is mainly carried by ___ fibers?

A

C

20
Q

describe the sensation of affective pain

A

dull, throbbing, porrly localized, may be unremitting

21
Q

provide an example of affective pain

A

psycological pain of serious depression

22
Q

what is gate theory of second pain?

A
  • there is interaction btwn pain reception and mechanoreception
  • helps to rub toe after stub it
  • essentially, nonpainful stimuli stops (closes gates for) painful stimuli
  • due to inhibitory local circut neuron
23
Q

where do the first pain signals ascend to?

A

primary somatosensory cortex

24
Q

where do the second pain signals ascend to?

A

cingulate cortex and insular cortex

25
Q

summary - describe the anterolateral system pathways

A

sensory (discriminative):
spinothalamic tract –> ventral posterior nucleus –> somatosensory cortex (S1, S2)

affective (motivational):
spinothalamic tract –> midline thalamic nuceli –> anterior cingulate cortex/insular cortex
OR
spinothalamic tract –> amygdala, hypothalamus, periaquaductal gray, superior colliculus, reticular formation

26
Q

define hyperalgesia

A

heightened sense of pain to noxious stimuli

27
Q

define allodnyia

A

pain resulting from normally painless stimuli

28
Q

what does allodnyia result from?

A

(hypothesized to be) the development of altered central pathways being activated by the surviving afferent nerves

29
Q

what does neuropathic pain result from?

A

complete or partial nerve transection or compression

30
Q

phantom limb is an example of which type of pain?

A

neuropathic

31
Q

explain how phantom limb arises

A

when arm or leg has been removed bc of illness/injury, but the brain still gets pain messages from the pathway that origionally carried impulses from the missing limb
-i.e., altered proprioceptiv/pain pathways and cortical reorganization are the cause

32
Q

what are some common causes of neuropathic pain?

A

diabetes, injury or trauma to PNS/CNS, MS, HIV infection, chemotherapy

33
Q

patients with congenital limb deficiency may also experince phantom limb sensations, what does this suggest?

A

there is an innate central representation of the limbs in the primary sensory cortex

34
Q

what is reffered pain?

A

pain perceived on the body’s surface at a site distant from the actual site of injury/inflammation

35
Q

pain from viscera is commonly reffered where? explain why.

A
  • to the surface of the body
  • dorsal horn neurons receive input from primary afferent neurons from both the surface and viscera
  • by some unclear mechanism, the visceral input is transferred to the somatic pathway
36
Q

describe some remedies for pain relief

A
  • drugs
  • rhizotomy (snip dorsal root)
  • chordotomy (snip spinal tracts for pain)
  • cingulotomy (remove anterior cingulate cortex)
  • spinal cord stimulation
37
Q

recap - axon input from pain goes where?

A

spinothalamic tract to periaquaductal gray (PAG) and reticular formation (RF)

38
Q

describe central regulation of ascending pain

A

descending pathways from the cortex, hypothalamus and amygdala send relays through PAG and raphne nuclei in the RF - which dampens ascending pain activity in the spinothalamic tract

39
Q

describe the role of endogenous opiods in the central regulation of pain

A
  • endogenous opiods (codeine, morphine, heroin)
  • bind g-coupled protein receptors (opiod receptors) to releive pain
  • involved in gating
40
Q

is the placebo affect a real physiological procces? why or why not?

A

yes - placebo pills can reduce pain and can be blocked by naloxone (comp. agonist of opiod receptors)

41
Q

how is the right prefrontal cortex involved in placebo?

A
  • RPRC is associated with the inhibition of affective thought and behaviour
  • placebo increases RPRC response to pain, & improves symptoms
42
Q

how is the anterior cingulate cortex involved in placebo?

A
  • associated with sensing affective pain

- placebo decreases ACC reactivity to pain, & improves symptoms

43
Q

describe the relationship btwn the right prefrontal cortex and the anterior cingulate gyrus with respect to the placebo effect

A

negatively correlated (one increases, other decreases)

44
Q

summarize the placebo pathway

A
  • cortical beleif caused by placebo activates right prefrontal cortex
  • rpfc is though to inhibit anterior cingulate cortex
  • reduced acc means increased descending control of ascending pain
  • results in symptom improvement
45
Q

explain reflexology

A
  • whole body is mapped to feet

- pressure is applied to feet to releive pain

46
Q

explain magnet therapy

A

magnets applied to body to reset the magnetic field

47
Q

explain homeopathy

A

tiny amounts of natural substances (herbs, etc.) or drugs are used to promote healing