sometosensry lecture 3
Terms
undefined, object
copy deck
- How do we know that post central gyrus area is responsible for sometosensory?
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1.clinical experiment-structural injuries, tumors, strokes
2.Stimulate the cortex directly and measure the patient's sensation
3.Stimuate different body parts and record the neurons' activities - Most complex levels of somatosensory processing occur in the cerebral cortex
- cerebral cortex
-
True/False
Most somatic sensory inputs targeted to the cortex are received in the postcentral gyrus in parietal lobe - T
- What is somatotopy?
- The mapping of body's surface sensations onto a structure in brain; spatial representation of body onto cortex
- What are 4 spatial organization of body surface?
-
1.not continous
2.not scaled proportionally becauses of # of sensory receptors
3.multiple maps
4.malleable map-borders are dynamic, regulated by experience - What is phantom limb sensation?
- amputees will feel sensations in missing limv if stroke face because afferents from face will take over somatosotpic representation of arm/hand
- S1 reagion recieves dense inputs from _______
- thalamus (VPM, VPL, intralaminar nuc.)
- What is homunculus?
- little man in the brain
- Cells reponsive to same stimulus were arranged __________
- vertically
- What are Cortical barrels?
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vertical columns containing neurons specialized for one sensation
-found in other primary somatosensroy cortices-auditory and visual -
True/Fase
Receptive fields enlarge as info passes through cortex. Stimuli that neurons prefer becomes increasingly complex - T
-
What are 4 distinct areas of S1 region?
funct? -
Broadman's areas 1,2, 3a, 3b
-recieve info about size, shape and texture of object and direction of stimulus movement - What is the function of S2?
- S1 send info to S2 (secondary somatosensory cortex) which interprets meaing of stimuli
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What is Lesions?
and what does it cause -
ablation of S1
-cause astereoagnosia-inability to judge shapes, size, texture of tactile stimuli, stimulus localization)
-also loss of position sense
-loss is contralateral
-pain and temp will not be lost completely - What does ablation of S2 (or pareital cortex area 5,7)cause?
- amorphosynthsis-inability to recognize objects by feeling
- What happens if there are lesions in S1?
- impair somatic tactile sensation (not so much pain and temp)
- What is Neglecct syndrome and what area of cortex is damaged?
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-posterior-pareital cortex damaged
-patints ignore part of their spatial world - What is nociception?
-
The sensory process that PROVIDES the SIGNAL that TRIGGER pain
-pain may or may not follow - What is Pain?
- the feeling or perception of irritating, sore, stinging, aching, throbbing, miserable, or unbearable sensations arising from a part of body
-
True/False
More than any other sensory modality, the cognitive qualities of nociception can be controlled from within, by the brain itself - T
- Transduction of painful stimuli
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-damaged cells at the injury release proteases->convert kininogen to bradykinin,ATP and K+ions. bradykinin and ATP bind to specific receptors that depolarize nociceptors. K+m can do this directly.
-muscles buildup lactic acid, leads to an excess of H+ ions -->activate H+gated ion channels on nociceptors
-Mast cells repond to foreign bodies penetrating the skin by releasing histamine. Histamine binds to receptors and depolarize nociceptors. Histamine increase the permeability of nearby blood vessels leading to swelling and redness. Antihistamine creams reduce swelling and pain - What are the types of nociceptors?
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mechanical
thermal
chemical-capsacin
polymodal
itch-smallest C fibers respond to histamine - What is Hyperalgesia?
-
Reduced threshold for pain, spontaneous pain, or increased intensity of painful stimuli
-mechanism: modulation of nociceptor excitability by substances released by damaged skin - What are the examples of sensitizing chemicals released by damaged skin and what do they do?
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increase the sensitivity of nociceptors to other stimuli
-bradykinin, prostaglandins, substance P - Describe Substance P
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Substance P is produced and released by activated nociceptors themselves
-causes vasodilation (swelling of capillaries)
-release of histamine from mast cells
-this sensitizes other nociceptors and is one cause of secondary hyperalgesia - Explain Melzack & Wall's Gate Theory of Pain
-
rubbing makes feel better
-at the level of spinal cord
- C fibers(nociceptive signals) from nociceptor enters spinal cord and activates projection neuron. Then projection neuron crosses midline and goes up the spinal cord.
-It can be modulated by non-nociceptive mechanoreceptor (Aalpha, Abeta axons)by touching and rubbing. Then it inhibits the processing of nociceptors. Inhibits the projection neuron. - Explain Descending Brain Control of Nociception
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-modulation of nociceptor
-In Midbrain, Periaquaductal gray descends efferet (Endorphins & Opioid receptors released) to Raphe nuclei in Medulla. Then it activates inhibition neuron in Dorsal horn of spinal cord by releasing serotonin. - What is Referred Pain?
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ex. during heart attack, feel chest hurting, NOT heart.
-Brain dosn't recognize internal organs
-involves visceral nerve fibers and skin nerve fibers. They enter the spinal cord by parellel then come together.