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Neuro > Pain and temperature - anterolateral system > Flashcards

Pain and temperature - anterolateral system Flashcards

1
Q

Cool receptors are geared to what temperature?

A
  • 10-37 degrees C

* Way more of these (10X) than warm receptors

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2
Q

Warm receptors are geared to what temperature?

A

• 30-48 degrees C

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3
Q

How do temperature receptors encode intensity?

A

• Intensity of temperature sensation is encoded in the frequency in which the receptors fire action potentials

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4
Q

At what temperature do cold and warm receptor afferents have similar firing rates?

A

• 33 degeres celsius, or the thermoneutral point

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5
Q

How does the body both recognize a change in temperature and absolute, steady temperature?

A
  • Change in temperature is encoded in the transient frequency of warm and cold receptors
    • After a new steady state is reached there is a consistent frequency of afferent firing which gives us the sense of absolute temperature
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6
Q

Typically, warm and cool receptor afferents are associated with what class of fibers?

A
  • Warm - C fibers

* Cool - a-delta

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7
Q

Temperature afferents synapse where first?

A
  • DRG and trigeminal neurons send axons into the CNS and form a first synapse in the dorsal horn of the spinal cord and the spinal trigeminal nucleus, respectively
    • The sensory neurons in the periphery are considered first-order neurons and the contacted neurons in the CNS 2nd order
    • 2nd order neurons synapse in thalamus
    • 3rd order neurons from thalamus to cortex
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8
Q

The spinothalamic tract is what?

A
  • Conscious appreciation of skin temperature

* Follow the temperature afferents from skin to cortex and that’s the spinothalamic tract

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9
Q

What is the spinoreticular tract?

A
  • Conveys information via the reticular formation to the hypothalamus
    • Information important for control of body temperature (ANS)
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10
Q

What tracts does the anterolateral system contain?

A
  • Spinothalamic, spinoreticular and spinomesencephalic tracts
    • That’s ANS thermoregulation and temperature sensation
    • Describes the midline switching of these fibers and anterolateral spinal cord localization
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11
Q

The spinothalamic tract carries what where?

A
  • A Principal pathway and conveys pain information to the thalamus
    • Projects to the nuclei of the ventrobasal thalamus, including VPL
    • Neurons in these nuclei process information related to localization of pain and project to somatosensory cortex
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12
Q

The spinomesencephalic tract projects what where?

A
  • Projects to midbrain periaqueductal gray region (PAG)

* Important for descending control of pain

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13
Q

The spinoreticular tract projects what where?

A

• Conveys pain inputs that lead to forebrain arousal and elicits emotional/behavioral responses via connections to the emotional circuits of the brain
○ Limbic system
• Terminates in the medulla and pons, the site of the reticular formation

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14
Q

What cortical regions are involved in pain sensation and control?

A
  • Cingulate gyrus and insular cortex
    • Cingulate is part of limbic system and is involved with emotional component of pain
    • Insular cortex is a processing center for the autonomic component of pain
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15
Q

How are pain receptors classified?

A

• Based on the stimuli that activate them

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16
Q

Extreme cold temperatures are typically associated with what classificaiton of fiber?

A
  • C fibers
    • Polymodal nociceptors that are activated by high intensity mechanical, chemical or thermal stimuli are in this category too
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17
Q

Extreme hot temperatures are typically associated with what classificaiton of fiber?

A
  • A-delta

* Intense pressure and mechanical nociceptors are also A-delta

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18
Q

Thermal nociceptors are activated when?

A

Thermal nociceptors are activated when?
• Extreme temperatures
• Less than 5 degrees celsius
• More than 43 degrees celsius

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19
Q

What is the vanilloid receptor?

A
  • Vanilloid moiety-containing compounds activate it, and thus the name
    • Type of molecular receptor for pain
    • VR-1 = capsaicin receptor
    • Strongly activated by capsaicin and weekly by acid
    • Also activated by moderate heat (43 degrees C)
    • Expressed on polymodal nociceptors
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20
Q

What do acids and ATP have to do with nociceptors?

A
  • They are ligands for NSC’s on nociceptors
    • ATP opens ionotropic P2X receptors
    • Acid-sensing channels are known as ASICs, 4 different ones expressed in C fiber nociceptors
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21
Q

Difference between A-delta and C fibers?

A

• Both are small and not fully myelinated
• C are smaller and slower and have no myelination
• A-delta are still small but lightly myelinated
• A-delta have smaller receptive fields
○ Leads to spatial discrimination

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22
Q

Pain is sensed as 2 types separated by time

A

• First comes a tolerable localized pricking pain
○ A-delta fiber
• Then comes a burning intolerable, diffusely localized pain
○ Burning pain is C fiber pain

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23
Q

Why, with increasing pressure does the sensation profile change?

A

• Has to do with metabolically active (related to size) of the fibers
• A-alpha and A-beta fibers are cut-off by pressure first because they are faster to respond to hypoxia
○ Lost proprioception, light touch, vibration and motor
• A-delta fibers are next, leaving only C fibers and purning pain is left

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24
Q

Describe the dose-related effect of anesthetics

A
  • Lower doses are preferential for smaller fibers
    • Burning pain first
    • Pricking pain second
    • Motor last with high doses
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25
Q

What molecules are activators of pain receptors?

A
  • Bradykinin is the classic example
    • Comes from cleavage of inactive precursor that only happens with necrosis and cytoplasmic enzymes being spewed out
    • Potassium, acid and serotonin are also activators
    • Bradykinin activates directly A-delta and C nociceptors (pricking and burning pain)
26
Q

Describe the process of sensitization

A
  • Lowers the threshold for a nociceptor to fire an action potential
    • Makes it easier to feel pain in an injured area
    • Substance P is released by C fibers that are activated for long periods of time
    • ATP, ach and 5-HT are sensitizers separately or together
    • Activators and sensitizers are often present together
27
Q

How does aspirin help with pain?

A

• By inhibiting the production of prostaglandins, it inhibits the sensitization of nociceptors

28
Q

Hyperalgesia?

A
  • Sensitiaztion of nociceptors is known as primary hyperalgesia
    • Mechanism leading to the increased sensitivity to pain occurs at the first site of the pathway
    • Allodynia is such a sensitization that non-noxious stimuli trigger pain
29
Q

Reddening, wheal and flare come together to form…

A

• The triple response
• Bradykinin plays an important role
• Tissue damage leads to local production of bradykinin
• Bradykinin is both vasodilator and activator
○ Heat and redness
• Also increased capillarly permeability, leading to the edema in a wheal
• Around the inflamed area is the pink-colored flare
• Remember that C fibers have large receptive fields and poorly localized signals and that is largely from a large and complex network of terminals
• C fiber action potential goes toward cell body but also to the collateral terminals in ever-peripheral locations
• Substance P produces vasodilation but lesser extent than bradykinin
• “axon reflex”

30
Q

Describe how the “axon reflex” creates the flare in an injured skin location.

A
  • Remember that C fibers have large receptive fields and poorly localized signals and that is largely from a large and complex network of terminals
  • C fiber action potential goes toward cell body but also to the collateral terminals in ever-peripheral locations
  • Substance P produces vasodilation but lesser extent than bradykinin
  • “axon reflex”
31
Q

Why does the flare hurt, even though its pretty far away from the injury site?

A
  • The flare is created by vasodilation by substance P
    • Substance P is a sensitizer of nociceptors
    • Thus, less stimulus is needed to activate a nociceptor in the flare
32
Q

What’s up with modality segregation in pain sensation?

A
  • C fibers terminate in the supstantia gelatinosa in the dorsal part of the spinal cord
    • Nociceptive afferent fibers form synapses in the dorsal horn of the spinal cord, bu they are organized based on modality
    • There is preservation of a certain modality signal all the way to the cortex
    • They segregate into different regions of the dorsal horn (laminae)
    • C fiber afferents terminate in the Rexed’s laminae
33
Q

In general, when thinking about a 2nd order neuron in the pain pathway we are talking bout

A

• Neuron with cell body in substantia gelatinosa that recieves input from C fibers

34
Q

Substantia gelatinosa is also known as

A

• Rexed’s lamina II

35
Q

Describe: “there is a convergence of inputs at the level of the dorsal horn neuron”.

A
  • Some pain-activated dorsal horn neurons receive inputs from cutaneous as well as visceral pain afferents
    • The mixing of signals is the basis of referred pain
    • Few if any dorsal horn neurons are dedicated to visceral pain alone
36
Q

What are some common referred pain examples?

A
  • Anoxia in heart muscle is referred to upper chest wall, left arm and hand
    • Gallbaldder pain is referred to the scapula
    • Uretral pain (nephroliathisis) referred to lower abdominal wall
    • Bladder pain is referred to perineum
    • Inflamed appendix gives rise to referred pain in the periumbilical anterior abdominal wall
37
Q

If a dorsal horn neuron shares pain information between visceral and cutaneous, and both are firing, which one wins?

A
  • Cutaneous has greater representation and smaller receptive fields
    • Few if any dorsal horn neurons are dedicated to visceral pain
    • Thus, cutaneous pain wins out
38
Q

Why can glutamate evoke two different types of potentials in the dorsal horn neurons?

A
  • AMPA and NMDA receptors both

* AMPA is fast, NMDA is slow

39
Q

What does NMDA receptor activation in nociceptors lead to in the long term?

A
  • Long lasting changes in excitability
    • Phosphorylation by PKC and tyrosine kinases
    • Removes requirement for depol. To activate
    • They essentially become AMPA at that point
    • Central sensitization
40
Q

What’s the “wind-up” in C fibers?

A

• Glutamate at first just opens AMPA
• If there is a prolonged and intense stimulus, NMDA will open too
• The result is a larger post-synaptic response which is the wind-up
○ Form of central sensitization

41
Q

In the dorsal horn, what neurotransmitters are being used to convey painful stimuli?

A

• The pre-synaptic nociceptor will release glutamate
• It will also release substance P in a prolonged stimulation
• Substance P blocks potassium channels
• Central sensitization
*this form of sensitization is broader and lasts longer because substance P is not taken up into glial cells like glutamate

42
Q

Trace the nociceptors through the trigeminal system.

A
  • Pain and temperature inputs from head and neck
    • Trigeminal ganglion neurons with central axons entering CNS at level of pons and descent to a caudal position before forming firs synapses
    • Spinal trigeminal nucleus is site of first synapse
    • Functionally analogous to dorsal horn of spinal cord
    • From there they cross the midline and go to thalamus
43
Q

Why does rubbing an owie help with pain?

A

• At the level of dorsal horn synapse
• When rubbing, activating non-nocieptive afferent pathways
○ Touch and a-beta fibers
• This leads to activation of dorsal horn interneurons that inhibit the inputs of nociceptive fibers

44
Q

What does the condition tabes dorsalis show?

A
  • Tabes dorsalis is a symptom of advanced syphilis
    • Characterized by damage to large diameter myelinated primary afferents
    • The result is hyperalgesia
    • The converse of TENS, shutting down a-beta fibers will lead the dorsal horn neurons to listen to nothing but nociceptor inputs
    • Illustrative as gate control theory
45
Q

What therapy modality claims it is stimulating A-beta fibers preferentially to suppress pain?

A
  • TENS - transcutaneous electrical nerve stimulation
    • Selective activation of a-beta fibers
    • This leads to activation of dorsal horn interneurons that inhibit the inputs of nociceptive fibers
46
Q

Stimulation produced analgesia involves what area of the CNS?

A
  • Periaqueductal gray region - PAG (midbrain)
    • Example of DESCENDING control of pain
    • The gate control theory is ascending control pain
    • The only information getting through is touch pressure and temp, only pain is attenuated
47
Q

How does PAG stimulation result in analgasia? (trace the pathway)

A

• PAG - periaqueductal gray region - midbrain
• Neurons project to nucleus raphe magnus in medulla
• Neurons in medullar region are serotonergic and project to spinal cord via the dorsal lateral funiculus
• In spinal cord, serotonin leadst o inhibition of 2nd order neurons of dorsal horn
• Excites inhibitory interneurons that use enkaphalin
• Enkaphalin is an endogenous opiate
• Blocks voltage gated calcium current in pre-synaptic cell and opens potassium channels in post-synaptic cell
○ In the dorsal horn pain pathway that is
• Thus SSRIs are sometimes used to treat chronic pain conditions

48
Q

Sometimes depression and chronic pain are treated with the same drug. What’s up with that?

A

*the main concept is that descending pain control is serotonin-mediated. keeping serotonin around longer means more downward suppression of pain in dorsal horn spinal cord neurons
• PAG - periaqueductal gray region - midbrain
• Neurons project to nucleus raphe magnus in medulla
• Neurons in medullar region are serotonergic and project to spinal cord via the dorsal lateral funiculus
• In spinal cord, serotonin leadst o inhibition of 2nd order neurons of dorsal horn
• Excites inhibitory interneurons that use enkaphalin
• Enkaphalin is an endogenous opiate
• Blocks voltage gated calcium current in pre-synaptic cell and opens potassium channels in post-synaptic cell
○ In the dorsal horn pain pathway that is
• Thus SSRIs are sometimes used to treat chronic pain conditions

49
Q

Activation of an opiate receptor in the CNS will generally do what?

A
  • Inhibit that’s neurons firing

* If they are on a neuron, they play an inhibitory role

50
Q

Naloxone does what?

A
  • Blocks opiates binding opiate receptors in CNS

* Blocks analgesia produced by PAG or central opiate admin

51
Q

What are endogenous opiates?

A
  • Enkephalins
    • Beta-endorphin (endorphins)
    • Dynorphins (endorphins)
52
Q

What happens if you cut the dorsal lateral funiculus bilaterally?

A
  • This is the tract of neurons from PAG to dorsal horn interneurons
    • If cut bilaterally both stimulation-produced and systemic opiate-induced analgesia re blocked
    • Thus PAGE simulation and systemic opiate admin involve the same descending pathway
53
Q

What do cannabinoids do?

A
  • Endogenous version of THC
    • Endocannabinoids interact with cannbinoid receptors
    • Modulate a wide variety of synapses leading to analgesic and psychosis-inducing effects
    • Also interact with opiate system and thus modulate pain
54
Q

What is the theory behind stress-induced analgesia

A
  • Under stress, hyperactivity of limbic system activates PAG
    • Leads to inhibition of 2nd order neurons in dorsal horn pain pathway
    • But naloxone blocks some, not all of stress-induced analgasia
    • Thus there is opiate receptor AND something else
55
Q

The placebo effect is blocked by what?

A
  • Naloxone, which blocks opiate receptors

* Thus, placebo effect is limbic system - PAG invovled

56
Q

Sodium channel blockers can be used in cases of neuropathic pain. What’s up with that?

A

• Part of the process of neuropathic pain is sodium channel-dependent
• TTX and TTX-resistant sodium channel types
• ATP will lead to activation of the TTX-resistant sodium channels preferentially
○ Leads to sensitization and more pain in injured area
• After nerve injury the expression profile of sodium channels goes haywire and there can be stimulus-INDPEDENDENT opening of channels and firing of pain action potentials
• Blocking all sodium channels helps, but there are obvisoulsy cross over side effects

57
Q

The human disease familial primary erythermalgia is a problem with what?

A
  • Neuropathic pain because of a sodium channel problem

* Mutation in SCN9A gene, TTX-resistant sodium channel

58
Q

In terms of GABA, what happens in some cases of injury turning into neuropathic pain?

A
  • Injury to C fibers will result in GABA supply going silent
    • Without post-synaptic modulation or “signal” the neurons will start atrophying
    • In the dorsal horn this results in neuronal loss, a reduction in GABA content and ecreased numbers of GABA and opiate receptors
    • Such changes will lead to a reduction in inhibtion of dorsal horn neurons
    • Treat this problem with opiates and GABA-A receptor agonists
59
Q

What’s up with sprouting and rewiring in neuropathic pain?

A
  • Normally substantia gelatinosa is dedicated to C fibers (nociceptors)
    • There is also an inhibitory interneuron circuit in place for gate control and descending control
    • Damage to C fibers means that A-beta fibers (non-nociceptors) will sprout and fill in the vacuum of dying C fibers
    • End result is non-noxious stimuli tell the dorsal horn neurons there is pain (when there isnt’)
60
Q

How can immune cells and glia maintain and worsen neuropathic pain?

A

• In the context of injury, macrophages will mediate inflammatory response in DRG
• Release of TNF binds TNFR1
○ Preferentially modulates TTX-resistant sodium channel, linked to pain sensitization
• Also, ATP (from cell damage) will modulate astrocytes to release BDNF
○ Change in chloride reversal potential
○ Now GABA activation (inhibition normally) leads to excitation
• End result is decreasing inhibition of pain pathway

Neuro (59 decks)

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