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Med Neuro2 Lect4
Med Neuro2 Lect4 Nociception and Spinal Facilitation
| Question | Answer |
|---|---|
| When we sense pain, what are we actually sensing? | WDR cell activation. |
| What are the main afferents converging on the WDR neurons? | DEEP SOMATIC CELLS: 1.bone. 2.Joint. 3.Muscle. 4.Gut. |
| Describe the process of central sensitization as it applies to WDR cells | receptors on the membrane of WDR cells will alter the capabilities of NMDA receptors which will open allowing excessive Ca+ influx. **this causes the cell to be activated much more easily. |
| Summarize central Sensitization | Making the spinal cord more receptive/sensitive to PANs. |
| Describe the process of "Walking it off" | moving or rubbing the area will activate large Aalpha & beta fibers which will gait/block the WDR cell from being activated by the small nociocetive fibers as they enter the dorsal horn. |
| Mechanism behind the gaiting/blocking that large fibers exhibit on small fibers | 1.Rubbing skin triggers Abeta fibers. 2.Synapse on Inh interneurons in dorsal horn. 3.Inh interneurons inactivate the WDRs. **C-fibers usually inhibit these inh interneurons. |
| Can the inhibitory interneurons acting in the gaiting/blocking process become overstimulated? what happens? what does this cause? | YES, if there is too large of Ca+ influx the interneuron will become cytotoxic and undergo apoptosis. **Light touch will then stimulate WDR cells and thus pain: allodynia |
| What is occuring in spinal facilitation which allows for easy onset of muscle spasms? | 1.Inflammed joint activates motor neurons to surrounding muscles & joints. 2.They send nocioceptive signals back to the same interneuron. 3.Interneuron gets overstimulated, cytotoxic, & apoptosis occurs. **now the muscle spasm is very easily trigger |
| The loss of what will take away our ability to localize pain? | Primary somatosensory region of the postcentral gyrus. |
| 4 key areas in the cerebrum in reception and integration of nocioceptive signals/stimuli? | 1.Amygdala. 2.Insula. 3.Primary Somatosensory Cortex. 4.Anterior cingulate cortex/limbic system. |
| What happens if a patient loses their amygdala in an infarct? can the patient still feel pain? | NO FEAR off pain. There will be no conditioned/learned response to pain. **Yes they still feel pain, but there is no developed response from it. |
| What happens if a patient loses their cingulate gyrus in an infarct? Can the patient still fell pain? | The pateint will still feel pain, but there will be no apprehension to it, pain won't bother them. |
| What are 2 very important regions inolved in the anticipation of pain? | 1.amygdala. 2.Cingulate gyrus. |
| List the main components of the Descending Endogenous Pain Control Systems | 1.Limbic forebrain. 2.Hypothalamus. 3.Periaquaductal Gray (PAG or Central Grey). 4.Raphe Nuclei in the medulla. 5.Spinal cord. **3 controls 4. |
| What inhibits the descending endogenous pain control systems at the level of the hypothalamus and PAG? | Neuropeptides |
| What inhibits the descending endogenous pain control systems at the level of the Rostral Medulla? | Opioids |
| What inhibits the descending endogenous pain control systems at the level of the Medullary or spinal dorsal horn? | 1.Serotonin. 2.Norepinephrine (atheles can temporarily not feel pain). **Depression can cause a hightened sense of pain so small pain triggers larger response. |
| What could really be the cause of an overwhelming fear of pain? | Sensitization of forebrain structures like the Amygdala. |
Created by:
WeeG
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