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18 Cards in this Set

  • Front
  • Back
Relay Nuclei
1. what are they the homes of?
2. what are their receptor fields like? why?
1. secondary and tertiary neurons
2. larger and more complex than those of primary sensory neurons (b/c they receive input from more than one primary neuron)
Inhibitory interneurons
1. feedback inhibition
2. feedforward inhibition
1. send signals back to relay neurons to modify their output
2. send signals to thalamus modifying its output
How does the complexity of receptors fields change amongst relay nuclei?
-where are they most complex?
complexity increases which each successive relay nucleus
-primary sensory cortex is most complex
Ventrobasal complex consists of severeal nuclear subdivision that project to both S1 and S2
-what are they and what do they receive?
1. VPL: ALS (pain/temp), DCMLS (vib), a little prop
2. VPM: ventral trigeminothalamic tract (face pain/temp), a little prop
3. VPS: most propriception from both face and body
4. VPI: mixed sensations projectin gto S2
What does these primary sensory areas receive from the thalamus?
1. 3a
2. 3b
3. 1
4. 2
1. prop from deep muscle receptors
2. highly conserved projections from skin mechanoreceptors (both RA and SA); ex: reading braile
3. RA skin receptors
4. deep pressure and joint position receptors
In terms of complexity, what type of stimuli do areas 3a and 3b respond to?
areas 1 and 2?
3a/3b: point stimuli (most focused of cortical sensory neurons)
1/2: stimulus moving across skin, different textures (more abstract)
Primary Sensory Cortex
1. brodmann's areas
2. location
3. lesions
1. 3, 1, 2
2. postcentral gyrus, posterior paracentral lobule
3. impair finer aspect of somatic sensations (judging location/intensity) and senses of body position; little or no impact on pain
Secondary Sensory Cortex
1. receives input from...
2. location
3. receptor fields
4. plays a role in..
1. S1 and a little from VPI
2. parietal operculum (upper border of lateral fissure), extends onto insula
3. bilateral receptive fields
4. pain perception and memory/recall of somatosensory events
Most of the cerebral cortex contains 6 layers, known as (1)...more primitive areas consisit of fewer than six layers (ex: hippocampus) and are called (2)...or (3)...
1. neocortex
2. archicortex
3. paleocortex
What two fiber types convey pain to CNS? What type of pain does each of them carry? to where? Via what tract?
1. A delta fibers: rapid, transient pain to thalmus via spinothalamic tract of ALS
2. C fibers: longer lasting, deep pain to brainstem via spinoreticular tract of ALS
What pathways make up the ALS?
-which is the smallest?
-where do most pain and temp pathways project?
1. spinothalamic (smallest)
2. spinoreticular
3. spinotectal
4. spinohypothalamic
5. spinoreticulothalamic
-subcortical structures
What is an alternative pain pathway?
-what problems does it cause
the dorsolateral tract
-can frustrate attempts to abolish pain by tractotomy of ALS
What else enters the dorsal horn along with A-delta and C pain fibers?
A-beta fibers: large-diameter nonpain sensory axons
Chronic Pain
1. what does it usually accompany?
2. usually the result of...
1. inflammation
2. temporary changes in peripheral receptors (increase #) or central tract neuron (begin to fire at tonic rates due to removal of Mg++ that usually block NMDA receptors)
6 pathways leading to feedback inhibition of pain
1. ALS
2. PAG (periaqueductal gray)
3. ENK (enkephalinergic)
4. 5-HT (serotonin)
5. NRM (nucleus raphe magnus)
6. NRPG (nucleus reticularis paragigantocellularis)
3 pathways leading to feedback inhibition of pain at level of dorsal horn
1. NA (noradrenergic)
2. SER (serotonergic)
3. ENK (enkephalinergic)
Neuropathic pain
1. caused by...
2. what is allodynia?
1. permanent changes in architecture of central neural paths
2. after neuronal damage, small fibers (pain) less likely to regenerate, so large fibers (touch) synapse on the vacated relay nuclei (touch is now transmitted as pain)
Neuropathic pain
1. peripheral nerve injury
2. central lesions
1. entrapment, neurotmesis, amputation (if amputation leads to allodynia = phantom pain)
2. occlusion of thalamogeniculate branch of PCA causing thalamic pain (constant, agonizing pain with no sensory input)