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| Question | Answer |
| Differences between mechanoreceptors and nociceptors. | Mechanoreceptors have their ending encapsulated and tuned to stretch stimuli. Once the skin is stretched, ion channels will open, allowing depolarization. Nociceptors are free nerve endings embedded within the skin and viscera. |
| Main type of neuron fibers for pain. | A-delta C |
| What are the ion channels for nociception called? | Transient receptor potential vanilloid (TRPV) |
| What type of signals are recognized by TRPVs? | heat (thermal) chemicals pH |
| T/F: TRP channels are polymodel. | T |
| _____ fibers relay the first, sharp pain while ______ fibers relay the second, dull pain. | First pain: A-delta (thinly myelinated) Second pain: c fibers (unmyelinated) |
| T/F: it is impossible to block pain. | F. First pain can be blocked by selective blocking of A-delta fibers. Second pain can be blocked by a selective blocking of C fibers. |
| A-delta fiber terminates in lamina _____, _____ and _____ of the spinal cord. C fiber terminates in lamina _______ and _______ of the spinal cord. | A-delta: I, II, V C: I, II |
| Both A-delta and C fibers synapse with ________ cell in lamina V of the spinal cord. | Wide dynamic range cells |
| The pain signal is related to _________ after leaving the spinal cord. | Thalamus. |
| Another type of afferents that share the WDR cell with nociception signal is _________. | Mechanoceptor afferents. |
| Nociceptive-specific neurons have cell bodies in lamina ___. | I |
| What causes referred pain? | Viscera does not have its own somatosensory map. It shares the same WDR neuron as regions of skin. |
| T/F: Pain is proportional to the probability of tissue damage. | F. Not always. This is the ideal situation. |
| What is peripheral hyperalgesia? | Tissue damage in a localized area will cause lower pain thresholds in adjacent tissue. |
| Mechanism of peripheral hyperalgesia: 1. damaged area releases _____. 2. this causes the release of _____, which directly stimulates adjacent nociceptors to release ____________ and _______. 3. ______ causes dilation of peripheral blood vessels, and liberates additional ________ which spreads to nearby locations. | 1. damaged area releases [bradykinin and prostaglandins] 2. this causes the release of [histamine], which directly stimulates adjacent nociceptors to release [calcitonin gene releasing peptide CGRP]and [substance P]. 3. [substance P] causes dilation of peripheral blood vessels, and liberates additional [histamine] which spreads to nearby locations. |
| Wind-up is a phenomenon that happens to the _____ fiber. | C fibers. |
| In servere or persistene injury, the ___ fibers fire repetitively and the synaptic strength onto ________ increases progressively. This is referred to as ________ or ________. | C fibers. Synaptic strength onto dorsal horn increases. Wind-up. Central sensitization. |
| Which of the neurotransmitters have specific reuptake mechanism? Substance P or glutamate? | Glutamate |
| At the synapse, post-synaptic receptors of A-delta fibers have receptors such as ______ and ______. | AMPA and NMDA |
| In addition to AMPA and NMDA receptors, the post-synaptic receptors of C fibers also have _____ and ________ receptors. | NK1 and ion channels |
| T/F: There are less NMDA receptors but more NK1 receptors on post-synaptic neuron of C fibers. | F. More NMDA receptors. |
| Build-up of ______ increases the NMDA response to glutamate. | Ca2+ |
| The 5 pain pathways in the body are: | 1. spinothalamic tract 2. spinoreticular tract 3. spinomesencephalic tract 4. cervicothalamic tract 5. spinohypothalamic tract |
| Localization of pain is accomplished by the ______ tract. | Spinothalamic tract |
| the sensory-discriminative pain processing pathway | somatosensory cortex | ventral posterior nucleus | anterolateral system |
| Pathway of the affective/ motivational pain processing pathway | anterior cingulate cortex/ insular cortex | midline thalamic nuclei | anterolateral system |
| Other non-cortex regions involved in pain processing. | 1. periaquiductal grey 2. amygdala 3. hypothalamus 4. superior colliculus 5. reticular formation |
| PET scan demonstrated that the thermal grill illusion activates ________ for all conditions, and ______ only in noxious stimuli and grill. | all conditions: insula. Noxious and grill only: anterior cingulate |
| The hypothesis for thermal grill is similar to that of | lateral inhibition |
| What are some changes that occur in the brain when acute pain becomes chronic? | 1. reduction in grey matter volume in nucleus accumbens 2. changes in connectivity in frontal-striatal circuits 3. SBP |
| Spinal pain gating: 1. both C fiber and A-beta fibers synapse with the ___________ neuron. 2. They also both synapse with ________ interneuron which inhibits the projection neuron. 3. However, C fiber (excites/inhibits) the inhibitory neuron while A-beta fibers do the opposite. 4. Therefore, when there is an increased mechanoceptor input, the inhibitory neuron is (more/less) active, resulting in (increased/decreased) inhibition of the projection neuron, hence less pain. | 1. both C fiber and A-beta fibers synapse with the [projection] neuron. 2. They also both synapse with [inhibitory] interneuron which inhibits the projection neuron. 3. However, C fiber [inhibits] the inhibitory neuron while A-beta fibers do the opposite. 4. Therefore, when there is an increased mechanoceptor input, the inhibitory neuron is [more] active, resulting in an [increased] inhibition of the projection neuron, hence less pain. |
| There can also be pain mitigation happening at the _______ level, from __________ or ________. | supraspinal level. periaqueductal grey or locus ceruleus |
| T/F: Motor activity cannot mitigate pain. | F. Motor cortex has a profound and necessary influence on PAG. |
| Pt. with chronic low back pain demonstrates (anterior/posterior) shift in CoG. | Posterior |
| Conditions with recently-recognized motor cortex dysfunction: | 1. interstitial cystitis 2. chronic prostatitis/ chronic pelvic pain 3. vulvodynia 4. temporomandibular disorder |
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