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?

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
summary - describe the anterolateral system pathways
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
define hyperalgesia
heightened sense of pain to noxious stimuli
27
define allodnyia
pain resulting from normally painless stimuli
28
what does allodnyia result from?
(hypothesized to be) the development of altered central pathways being activated by the surviving afferent nerves
29
what does neuropathic pain result from?
complete or partial nerve transection or compression
30
phantom limb is an example of which type of pain?
neuropathic
31
explain how phantom limb arises
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
what are some common causes of neuropathic pain?
diabetes, injury or trauma to PNS/CNS, MS, HIV infection, chemotherapy
33
patients with congenital limb deficiency may also experince phantom limb sensations, what does this suggest?
there is an innate central representation of the limbs in the primary sensory cortex
34
what is reffered pain?
pain perceived on the body's surface at a site distant from the actual site of injury/inflammation
35
pain from viscera is commonly reffered where? explain why.
- 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
describe some remedies for pain relief
- drugs - rhizotomy (snip dorsal root) - chordotomy (snip spinal tracts for pain) - cingulotomy (remove anterior cingulate cortex) - spinal cord stimulation
37
recap - axon input from pain goes where?
spinothalamic tract to periaquaductal gray (PAG) and reticular formation (RF)
38
describe central regulation of ascending pain
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
describe the role of endogenous opiods in the central regulation of pain
- endogenous opiods (codeine, morphine, heroin) - bind g-coupled protein receptors (opiod receptors) to releive pain - involved in gating
40
is the placebo affect a real physiological procces? why or why not?
yes - placebo pills can reduce pain and can be blocked by naloxone (comp. agonist of opiod receptors)
41
how is the right prefrontal cortex involved in placebo?
- RPRC is associated with the inhibition of affective thought and behaviour - placebo increases RPRC response to pain, & improves symptoms
42
how is the anterior cingulate cortex involved in placebo?
- associated with sensing affective pain | - placebo decreases ACC reactivity to pain, & improves symptoms
43
describe the relationship btwn the right prefrontal cortex and the anterior cingulate gyrus with respect to the placebo effect
negatively correlated (one increases, other decreases)
44
summarize the placebo pathway
- 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
explain reflexology
- whole body is mapped to feet | - pressure is applied to feet to releive pain
46
explain magnet therapy
magnets applied to body to reset the magnetic field
47
explain homeopathy
tiny amounts of natural substances (herbs, etc.) or drugs are used to promote healing