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178 Cards in this Set
- Front
- Back
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what layer of cortex do CST and CBT fibers leave from?
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layer 5
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giant cells of betz
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giant pyramidal cells
- only make up CST fibers (only 3% of them), in layer V of primary motor cortex - synapse directly onto LMN w/o interneuron |
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What are lesions of M1 and possible consequences?
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1. irritative --> Jacksonian epileptic seizure, because lesion could trigger M1 to polarize
2. Destructive --> contralateral paralysis |
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What are the inputs of the association cortices? Where do they project?
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1. thalamus (pulvinar and dorsal medial nucleus, to layer 4)
2. other cortical areas (all layers) --> reverberating circuits 3. brainstem nuclei modulating areas (DA, NE, 5HT, Ach) |
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What are possible lesions of cortical area 5,7?
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1. deficits in attention
2. contralateral neglect |
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contralateral neglect syndrome
what happens in right hemisphere lesion? in left? |
often due to right parietal lobe lesion
- results in patient ignoring everything in visual field opposite the lesion R lesion = severe left neglect L lesion = minimal right neglect (right hemisphere projects a little to right side too, so compensates) |
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What is the dominant side in somesthetic area?
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Right side lateralization
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What are the different parts of the visual association cortex? (18,19)
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1. temporal association areas - analysis of form and color; what is seen, what is moving?
2. parietal association areas: analysis of motion and spatial relations; where is it, where is it moving? |
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What is the dominant side in visual association areas?
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Left side
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Possible lesions of 18,19?
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On dominant side (left)
1. visual agnosia (have no idea what we see) 2. Psychic blindness - whatever we see makes no sense |
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What association areas exhibit lateralization, and what side is dominant?
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1. somesthetic (5,7) - Right side
2. visual assoc (18,19) - left 3. posterior temporal lobe assoc - left (language) |
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Where are multimodal association areas most commonly found?
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parietal and pre-frontal regions
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What makes up the posteiror temporal lobe assoc area?
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1. Broca's (44/45)
- affilitated w/ motor fn for expressing a thought or word by saying/writing it 2. Wernicke's (22) - comprehending what is seen/heard (near auditory cortex) 3. Arcuate fasiculus - passes info from wernicke--> broca |
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What is the blood supply of wernicke and broca's areas?
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1. Broca (superior operculum) - Middle cerebral artery (superior division)
watershed = anterior cerebral 2. Wernicke (inferior operculum) - middle cerebral artery (inf division) watershed = posterior cerebral |
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How does the flow of language and execution of speech, etc, occur?
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Left-side wernicke's gets auditory/visual info (comprehends it)
- passes info to right side wernicke's (via corpus callosum splenium) - passes info to left side Brocas (arcuate fasiculus) Left side Brocas passes info to right side Brocas (via corp callosum) can also have reciprocal connections from right to left side |
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What would be the result of a left posterior cerebral artery infarct on Language?
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- damages left visual cortex --> literally blind on that side
- no input to wernicke's for vision - lesion includes corpus callosum so info can't get over from right Symptom = can't read own handwriting, but can physically write it (Broca's intact) |
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Left hand apraxia
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due to left MCA superior division infarct
- affects Broca's area - Left hand can function, has sensation, etc., but can't do anything that makes sense for language - Right hand paralyzed (whole left side of head, including motor region is damaged) |
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what is large fiber sensory neuropathy characterized by?
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degradation of fibers carrying proprioceptive and tactile info
- no sense of where their limbs are in space if they can't see them - show deficits of both feedback and feed forward control of movement |
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What are the differences in the functions of cerebellum vs. basal ganglia
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BG - more involved w/ predictive control of movements
cerebellum - more invovled w/ regulating moment-to-moment execution of movements --> by acting on brainstem and cortical systems that project directly to SC |
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what are the 2 great loops of hierarchal motor organization?
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1. output from motor cortical areas --> basal ganglia (corticostriatal) --> thalamus (pallidothalamic) --> motor cortical areas
2. cerebral cortex --> cerebellum (to brainstem too, but not in feedback) --> thalamus --> cerebral cortex 2. |
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What is the SC topography of motor neurons in regards to muscle location?
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1. MN's innervating proximal/axial muscles are located more medial (input from medial descending systems)
2. MN'S innervating distal muscles are located progressively more laterally (input from lateral descending system) |
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What is the SC topography of motor neurons in regards to flexors/extensors?
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Extensors more ventrally located than flexor neurons
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Interneuron innervation in SC
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- tend to innervate larger groups of motoneuron pools (more muscles)
- medial motoneuron (proximal) interneurons --> inervate bilaterally - lateral motoneuron (distal) interneurons --> innervate ispilateral |
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Propriospinal interneurons
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ones that innervate the most axial motoneurons
- span many segments cuz tend to be utilized together |
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What is the only medial brainstem pathway to cross the brain?
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tectospinal
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What descending brainstem pathways stimulate extensor muscle motoneurons?
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1. lateral vestibulospinal
2. medial reticulospinal (pontine) |
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What descending brainstem pathways stimulate flexor muscle motoneurons
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1. rubrospinal
2. possiblly lateral reticulospinal |
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What descending brainstem pathways inhibit extensor MN function?
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Lateral reticulospinal
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"chin limb extends" rule
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whatever side the chin is tilted/turned towards, the muscles in that area extend
- ex. head turns to the right --> flexion on left side and extension on right side |
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What neck and vestibular reflexes are synergisitc?
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vestibulocolic and cervicocolic
- contract muscles that are stretched when head is rotated/tilted |
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What vestibular and neck reflexes are antagonistic?
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vestibulospinal and cervicospinal (limbs)
1. vestibulospinal = tilting body forward --> extension of arms and flexion of legs (prepare for landing) 2. cervicospinal --> tilting body forward --> flexion of arms and legs |
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Decerebrate rigidity
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transection of brainstem above vest nuclei but below red nucleus
- result = extension of all 4 limbs due to 1. decreased activity in rubrospinal pathway (flexors inhibited) 2. tonic activity of vestibulospinal and pontine reticulospinal (activate extensors) --> nuclei are below the cut |
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Decorticate rigidity
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due to large cerebral lesions (brainstem is left intact, but cortical activity can't reach brainstem nuclei)
result = flexed arms (rubrospinal intact) with extensor rigidity in legs |
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anterior cerebellar lobe ablation
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enhancement of extensor rigidity
due to removal of inhibitory action on lateral vestibulospinal tract |
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Spasticity
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from supraspinal lesions
- increased muscle ton in leg extensors and arm flexors - hyperactive stretch reflexes - greater resistance to rapid movement - steady movement results in melting of resistance (clasp knife effect) |
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What is the organization of the reticular formation areas?
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1. raphe = midline
2. large/giganto/m cells = medial 3. parvocellular = lateral |
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Regulation of posture and tone by reticular formation in what regions?
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M cell regions in pontine and medullary reticular formation
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Control of pain is via spinal projections from what RF area?
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raphe
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What RF area neurons regulate horizontal gaze and how?
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P cell neurons at level of facial and abducens nuclei
- activate/inhibit abducens motor neurons |
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What RF group computes the magnitude of rapid eye movements?
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midline group, but a non-5HT kind
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Comparison of modulatory cells (NT releasing) from sensory and motor neurons
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1. non-specific connectivity in mod cells --> projections less topograhically org
2. mod cells fire at decreased rates and broader ap's 3. are fewer mod neurons, but more extensive projections |
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DA vs. NE neurons
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DA - less global and more restricted territories; is 3-4X more DA neurons than NE
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To what tracts do NE neurons project?
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virtually to all parts of brain via.
1. central tegmental bundle 2. dorsal " " (cerebellum) |
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major neuronal groups of DA releasing cells
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1. A9 = SNpc (nigrostriatal DA system)
2. A8 (retrorubral field) and 3. A10 (ventral tegmental area) --> both are sources of mesolimbic and mesocortical DA system |
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Raphe 5HT projecting groups
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1. Rostral group (dorsal and medial raphe) --> to cortex and limbic structures
2. caudal group (obscurus nuc and magnus ) --> into SC and ventral horns |
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what is the mechanism of some nerve agents in regards to modulatory cells?
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irreversible cholinesterase inhibitors
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what modulatory neurons have increased firing during REM sleep?
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ach (is 0 during non-rem)
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what mod neurons have increased firing during non-rem sleep?
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gaba
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what mod neurons have no firing during rem sleep?
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5HT, NE, histamine
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what structure does the vermis overlie?
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4th ventricle
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fn of cerebellar notch
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contains falx cerebelli --> stablizes cerebellar movement (protective)
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what lobe is the tonsil part of?
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posterior --> abuts medulla
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where in the cerebellum is foramen of luschka near?
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posterolateral fissure
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what part of cerebellum overlies superior medullary velum?
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lingula
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what is the vestibulocerebellum made up of?
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flocculonodular lobe and lingula
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deep cerebellar nuclei
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imbedded in internal white matter at its center
1. dentate (most lateral) - generates SCP 2. interpositus (emboliform and globose) 3. fastigial (most medial) |
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What types of fibers do each of the cerebellar peduncles contain?
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1. MCP --> contains exclusively afferents from pontine nuclei
2. ICP (aka restiform body) --> contains mostly afferents from SC (posterior spinocerebellar), but also from inferior olivary complex, RF, and vestibular nuclei 3. SCP --> mostly efferents to red nucleus and thalamus (derived from dentate) - some afferents from colliculi and SC |
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Where do projections from deep cerebellar nuclei go to (vague) and what is the exception?
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go to other parts of brain
exception = vestibular cerebellum --> fibers just exit cerebellum and project directly to vestibular nuclei |
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Spinocerebellar tracts
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way for cerebellum to control spinal movements
1. posterior spinocerebellar - T6 and down --> proprio info from lower limbs via Clarke's column and dentate nucleus 2. cuneatocerebellar tract - T1-T5 - proprio info from upper body via accessory cuneate nucleus 3. anterior spinocerebellar - exteroceptive info, crosses in SC |
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how is the anteior spinocerebllar pathway an ispilateral?
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crosses once in midline, and crosses again as the SCP
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what are the 3 layers of the cerebellar folium and what cells are in it?
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1. outer molecular layer (stellate and basket cells
2. purkinje layer - make up first gray (purkinje cells) 2. Inner granular layer --make up 2nd gray (granule and golgi cells) |
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What cells are inhibitory in the cerebellum folia?
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purkinje cells (not interneurons)
basket, stellate, and golgi - inhibitory interneurons all are gaba-ergic |
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Climbing fibers
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Come from contralateral inferior olive complex to cerebellum
- comes through ICP - innervate deep cerebellar nuclei and purkinje cell - excitatory (glutamine) |
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Mossy fibers
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From SC, pons, medulla, to cerebellum
- have an excitatory effect on deep cerebellar nuclei and granular cells |
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organization of parasagittal zones of cerebellum
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1. vermal/medial zone --> vestibular nuc (via fastigial)
2. intermedate zone --> lateral descending systems (via interpositus nuc) 3. Hemispheric zone --> cerebral cortex for planning and execution (via dentate nucleus) |
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Characteristic symptoms of cerebellar lesions
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hypotonia
ataxia dysmetria dysdiadochokinesis intention tremors |
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Through what pathway does the cognitive cerebellum work?
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Dentate nucleus
- between cerebellum and cerebral cortex |
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what structures do corticospinal UMN's pass through?
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corona radiata --> internal capsule (posterior limb) --> crus cerebri --> pons (many get off and synapse at pontine nuclei) --> medulla pyramids (decussate) --> lateral corticospinal tract (in lateral funiculus)
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where does the ventral corticospinal differentiate from lateral corticospinal tract
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medulla pyramids: ventral stays ipsi and decends in ventral corticospinal tract --> cross SC at anterior commisure
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what part of internal capsule do corticobulbar fibers pass through?
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genu
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What are the destinations of the corticobulbar fibers?
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1. motor nuclei of cranial nerves
2. brainstem sensory nuclei (feedback loop) a. principle sensory nucleus of V (head) b. cuneatus, gracilis (ATL) |
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what portion of the pre-central gyrus to the ATL make up
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dorsal 2/3 of pre-central gyrus
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of the 20 million axons in each crus cerebri, how many synapse at the pons?
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19 million
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what is the topographical organization of the crus cerebri?
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- parietal occipital temporal pontine axons (most lateral/ventral)
- LTA - corticobulbar (most dorsal, almost as medial as FP) - frontopontine (most medial) |
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What is the distribution of corticospinal fibers to the different spinal cord areas?
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55% cervical
25% lumbosacral 20% thoracic |
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where do betz cells mostly terminate?
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cervical cord --> LMN's controlling hand and fingers
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difference in signs of UMN and LMN lesions
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LMN: has atrophy and muscle twitches (fasiculations) (not in UMN)
- hypotonia and irreflexia/hyporeflexia UMN: hyperreflexia and hypertonia |
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what happens in UMN lesion to hypoglossal?
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tongue deviates away from side of lesion
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what happen in LMN lesion to hypoglossal?
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tongue deviates toward side of lesion
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What is the hallmark deficit of cutting pyramidal tract?
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inability to use distal digits independently
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what does the ventral corticospinal tract do?
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involved w/ control of axial musculature, posture, etc.
- can also provide input to reticulospinal brainstem pathways |
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What was found from performing damage on the primary motor cortex?
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Blocks effects of electrical stimulation of motor cortical areas on distal finger musculature
- shows that supplementary and premotor cortex act mainly on distal muscles through their projections to M1 |
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What are the inputs to the motor cortices
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1. peripheral proprioceptive and cutaneous input from ascending spinal inputs via VPL of thalamus
2. Cerebellar to M1 and premotor cortex 3. basal ganglia to mainly supplemental motor cortex |
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From what nuclei in thalamus do the primary, premotor and supplementary motor cortices receive input?
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1. M1 - VL
2. premotor = VL and VA 3. supplementary: VA |
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Babinski reflex
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abnormal plantar reflex --> presence indicates an UMN lesion
the fanning of toes in response to running a sharp stylus from posterior to anterior part of food (normal response is flexion of toes) |
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What would a lesion in the corticobulbar pathway to facial motor nucleus produce?
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"central 7"
- contralateral drooping of lower facial muscles of expression (bilateral input) |
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what would a lesion of the facial nerve itself produce?
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Bell's palsy
- both upper and lower facial drooping on the side of the lesion |
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what is the role of cortex in "encoding" movement
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1. firing of M1 neurons begins before movement onset
2. amount of firing is related to required force 3. different neurons fire in relation to different directions of movement (are "tuned" to a particular direction) |
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What are the properties of M1 neurons that allow them to encode amount of force necessary to be exerted by muscles
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1. firing of M1 neurons begins before movement onset
2. amt of firing is related to the amt of required force (even for the same motion) 3. Neurons are turned, so that neurons fire for movements in a preferred direction, and not for others --> population vector is good predictor of the actual movement direction |
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claustrum
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area of gray matter in between external and extreme capsule
- gets input from sensory areas of cortex |
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what are the different inputs to the caudate and the putamen
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putamen = raw sensory input from cerebral cortex
caudate = more processed info from association areas |
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in what structure does the tail of the caudate nucleus end?
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roof of inferior horn of lateral ventricle
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hemiballismus results from damage to what pathway?
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pallido-subthalamic (contralateral)
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what fibers comprise the thalamic fasiculus?
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1. ansa lenticularis
2. lenticular fasiculus 3. dentothalamic fibers |
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dentothalamic fasiculus
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dentate nucleus generates SCP --> part that continues to thalamus
- joins w/ ansa lenticularis and lenticular fasiculus in field forel H1 to make thalamic fasiculus |
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what are the 2 fiber bundles coming from the medial GP on way to thalamus?
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1. ansa lenticularis
- loops around anterior limb of IC 2. lenticular fasiculus - goes straight through IC both project to VA (on way to supplementary motor cortex) |
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field of forel H2
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lenticular fasiculus
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where does the SN reticulata project to?
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thalamus, superior colliculs, reticular formation
- reciprocal connection? |
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where does the SNpc project to?
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neostriatum
- reciprocal connection |
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what's the major input structure of the basal ganglia?
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caudate/putamen
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what's the major output structure of BG?
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globus pallidus
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what is the only BG structure whose major cell type is excitatory?
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subthalamic nucleus
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what BG structure resembles the medial globus pallidus cytologically and functionally and therefore can be considered as single structure?
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SNpr
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What is the topographical organization of the BG in regards to inputs?
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putamen - mainly involved w/ motor control
caudate - mainly involved w/ eye movements and cognitive functions ventral striatum (nuc accumbens) - related to limbic functions |
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How does the BG acheive its excitatory effects?
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disinhibition
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what are the 2 effects of DA on the striatum?
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1. excites direct pathway neurons to promote movement (via D1 receptors)
2. inhibits indirect pathway neurons to promote movement (via D2 receptors) |
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what would be the results of a lesion to the neostriatum?
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- direct pathway lesion
- produces a loss of inhibitory input to the medial GP - increased inhibition of thalamocortical neurons RESULT = negative symptoms/hypokinetic disturbances (akinesia, bradykinesia) |
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what would be the result of a subthalamic lesion?
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- indirect pathway lesion
- loss excitatory input to medial GP - disinhibition of thalamocortical neurons - leads to hemiballism |
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what are the 3 most common hyperkinetic disturbances?
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1. ballism - uncontrolled flinging of upper and lower extremities
2. chorioform movements - dance-like movements of the limbs; orchestrated and clear, but come at odd times 3. athetoid movements - writhing/snake-like movements of distal extremities |
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Hallmark pathology of parkinson's disease?
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loss of DA synthesizing neurons in SN
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What is the cause of huntington's disease?
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selective degeneration of GABAergic and Cholinergic interneurons in the neostriatum
- slowly lose ability to function and show increasing dementia |
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Possible mechanisms of Degeneration in Huntington's
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1. accumulation of CAG repeats in exon 1 of huntingtin gene
- severirty and onset of disease correlated w/ number of extra CAG repeats 2. excitotoxic processes: release of glutamate stmulates cells to point of dying |
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What pathway does Huntington's disease initially appear to target and why?
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indirect pathway. Have hyperkinetic symptoms, chorioform in particular
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what are the 3 major differences between cerebellum and BG?
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1. BG input from entire cortex
Cerebellum input only from parts of cortex directly related to sensory and motor function 2. Cer output to premotor and M1 no BG output to primary cortex; also projects to prefrontal association cortex 3. Cer receives somatic sensory info directly from SC; has many aff and eff conn w/ brainstem nuclei BG has few brainstem connection and no direct SC connections |
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sharp, prickly pain is transmitted by
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A-delta fibers
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what happens if block A delta fibers?
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lose perception of what the source of the pain is
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What do local anesthetics block?
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C fibers (so now only have sharp pain left)
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allodynia
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decreased threshold for firing
pain to a normally non-painful stimulus -ex = touching back when have a sunburn |
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spontaneous pain
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ectopic firing, sensitiziation
ex. of neuropathic pain, not due to nocieptor itself |
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hyperalgesia
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increased pain to a normally painful stimulus
- increased firing to supratheshold stimuli - extends beyond site of original pain stimulus |
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what occurs during sensitization of nociceptors after injury/inflammation?
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1. release of K+, prostaglandins, 5HT, and bradykinin from damaged tissue
2. release of substance P from nerve endings |
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what is the action of prostaglandins and bradykinin in sensitziation
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activate nerve endings and sensitize free nerve endings
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what is the function of substance P in pain sensitization?
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1. activates mast cells --> release histamine --> increases sensitivity of nerve endings
2. dilates BV's --> causes spread of sensitizing agents over wider area |
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Where in the spinal cord do pain fibers project?
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1. Adelta fibers mostly to lamina I (marginal zone), sometimes to lamina V
2. C fibers to lamina II (substantia gelatinosa) dorsal horn after ascending/descending in lissauer's tract |
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phantom limb
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local pain sensed even when nociceptive pathways have been cut or damaged (like amputation)
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reason for having visceral referred pain
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pain fibers on internal organ and pain fibers on skin (referred area) project to same post-syn cell in SC --> goes up anterolateral column
- brain receives message from spinal neuron but can't tell which input was original source --> misinterprets signal |
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difference between paleo- and neospinothalamic tracts
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1. paleo - C fibers (dull pain); projects to intralaminar nucleus of thalamus
2. neo - mostly Adelta fibers, sharp pain; project mostly to VPL of thalamus |
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Gate theory of pain modulation
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- explains why rubbing on painful area may make it feel better
Have C fiber (only brings pain info), Adelta (only brings in touch info), inhibitory interneuron (inhibits projection neuron), and projection neuron (to activate pain pathway) - C inhibits interneuron, while A excites it - therefore, when only C activated, get a strong pain projection - but when touch/rub area of injury, are activating A fibers too --> activates interneuron and makes a weaker pain projection |
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what do all endogenous opioids have in common?
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Tyr-Gly-Gly-Phe sequence
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Stimulation of what CNS structure is most effective way to alleviate pain?
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periaqueductal gray
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What is the cell mechanism of opioid action in spinal cord?
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acts on receptors both pre- and post-synaptically
1. presyn --> shortens AP --> less Ca in terminal --> less Glu NT released --> decreases EPSP 2. Postsyn: hyperpolarizes projection neuron --> makes membrane potential further from theshold --> harder to generate AP |
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common side effect of morphine or other opioid admin?
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constipation
-are u-opioid receptors in lower bowel too |
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how do peripherally active analgesics work?
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prevent sensitization by blocking prostaglandin sythesis
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Supertasters
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1100 taste buds/cm tongue
25% of population react violently to PROP (bitter) eschew fats sweets are sickening |
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nontasters
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11 TB/cm tongue
large pores do not detect PROP |
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What's the correlation between number of taste buds and number of papillae?
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inverse relationship between number of papillae and number of taste buds/pap
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where are the reeptors for taste located?
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microvilli in the columnar taste cell in the taste bud
- microvilli also contain transduction machinery |
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What are the types of taste cells?
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1. Type 1/Dark --> more like glia
tall microvilli 2. Type 2/Light --> totally responsible for detecting tastants and transducing into special categories; comm w/ type 3 3. Intermediate/Type 3 - single, tall microvillus - acts as intercellular translator --> drops NT (5HT) onto afferent gustatory nerves |
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NCAM and SNAP25
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gustatory sytem: cells that have afferent innervation
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What differentiates umami (amino acid) from sweet tastes?
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- both use same metabotropic PKA-dep mechanism
1. sweet receptors: T1R2 + T1R3 2. umami receptors: T1R1 + T1R3 |
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what receptor family does bitter bind?
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T2R family; many more receptors than other tastants
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gustducin
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taste cell G protein w/ 80% homology to transducin (G protein in vision transduction)
- involved in denatorium (a special bitter substance) tranduction and purinergic signaling |
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purinergic signaling
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way that type 2 and 3 cells communicate; depolarization of type 2 cells results in 5HT release from type III cells onto afferent
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Why can't type II cells release neurotransmitter?
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do not have voltage-activated calcium channels
(but DO have all 2nd messengers to activate TRPM5 and release Ca from intracellular stores) |
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Encoding for gustatory system
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1. spatial = labeled line
2. computational = across-fiber code - nerve fibers are broadly tuned across the 4 tastes - firing rate of a nerve cell higher when exposed to its particular taste that it's tuned for |
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2 parts of NTS
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1. rostral - gustatory/SVA part
does taste for 7, 9, 10 2. caudal - GVA for 9 and 10 - deals w/ respiration, BP, etc. |
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what neurons are resp for detecting taste irritants?
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1. nociceptive neurons (9, 10)
2. Polymodal nociceptive neurons (V3 --> lingual nerve; sensitive to mostly irritants) |
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What is the thalamic taste nucleus?
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VPM
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what part of the cortex does integration of taste and olfation occur?
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orbitofrontal cortex (secondary gustatory cortex)
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what are the 3 cortical areas in which gustatory is represented?
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1. frontal-parietal operculum
2. insular cortex 3. lateral posterior orbitofrontal |
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Aguesia; why is it uncommon?
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total loss of taste
- overlap of 3 taste nerves in NTS |
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AP5
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selective NMDA receptor blocker
- shows that NMDA receptors are required for ocular dominance shift |
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long-term potentiation
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long lasting increase in synaptic strength, due to:
- high frequency activation of synapse, short bursts - activates NMDA receptors - allow Ca influx (lg increase in Ca release --> LTP) |
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long-term depression
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long lasting decrease in synaptic strength due to:
- prolonged, low frequency stimulation - results in a lesser increase in calcium --> LTD - contributes to the pruning out of wrong connections in critical period plasticity |
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what happens when input to a synapse is in phase as opposed to out of phase
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1. inphase --> positive correlation, strengthening of synapse
2. out of phase --> negative correlation; equivalent of not have any input or inapproriate input - synapses that get out of phase input end up retracting and going away |
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strabismus
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eyes not aligned properly (due to VI nerve palsy)
- 1 eye deviates medially - no binocular neurons or capacity for binocular vision - can do surgery to re-align eyes, but connections never fix themselves (cuz no longer in critical period) |
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role of trophic factors in plasticity
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triggers growth (BDNF, NT4/5)
- Ca influx from NMDA receptor opening triggers trophic factor release - trophic factors bind pre-syn terminal and induce growth of more terminals |
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anesthesia dolorosa
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painful lack of sensation (ex. phantom limb)
- classic for people w/ trigeminal neuralgia |
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Neurostimulation
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alternative treatment of chronic pain
- used for neuropathic pain - is a spinal cord stimulator - must place it somewhere between where you sense it in your cortex and where the injury is |
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possible hypotheses of neuropathic pain
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1. sensitization of nerve from excitation
2. loss of descending inhibition 3. de-afferentation --> leads to bursting of neurons (can cause thalamic pain) |
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Intrathecal drug delivery
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-used to treat nociceptive pain
- usually delivers opioids directly into the CSF of lumbar spine |
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ideal candidates for intrathecal drug delivery
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1. continues to have pain after all other options
2. no active infection, no heparin 3. good flow of CSF so meds not blocked 4. already on a high dose of morphine |
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What are the 2 most common types of neuroablation technqiues?
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1. DREZ lesion - lesion dorsal root at entry point of spinal cord
2. cordotomy - lesion the spinothalamic and spinoreticular tracts - great results but only for short time (good for cancer patients |
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from what structure is the cerebellum derived?
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roof plate cells of alar plate
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where do the deep cerebellar nuclei come from?
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cells that stayed near the 4th ventricle (proliferating zone) and did not migrate outward
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3 cerebellar cell layers and how they were derived
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1. outer molecular layer - cells that migrated outwards from the ventricular zone
2. Purkinje cells: cells that migrated outward but got trapped 3. Inner granular layer: cells that reached outer zone and migrated inward |
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at what level do both red nucleus and substantia nigra exist
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superior colliculus
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what plate are superior colliculus cells derived from?
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alar
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red nucleus and substantia nigra derived from:
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alar plate
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the crus cerebri are made up of:
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corticobulbar and corticospinal fibers
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order of development of thalamic nuclei
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1. medial thalalmic
2. lateral thalamic 3. some go out and make part of basal ganglia |
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series of events in cerebral cortex cell layer development
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1. cell division (ventricular zone)
2. S1 S2 phases 3. cell becomes post-mitotic 4. migration to cortical plate (lose processes and become rounded) - sit and wait until all cells that will make cortex have migrated - 1st cell from CP lies on very edge of marginal zone and becomes horizontally oriented 5. cells wait until thalamic input comes in (via internal capsule) |
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what is the order of layer formation in cortex development?
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layer 1 --> layer 6 --> layer 5 --> 4 --> 3 --> 2 --> 1
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Pain and temperature of the head and neck comes in via what 4 nerves, and terminates where?
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comes in via 5, 7, 9 and 10.
- terminates in spinal V nucleus |
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pain from the dura of the posterior fossa is carried by what nerve(s)
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Anterior 2/3 by 5
posterior 1/3 by 10 |
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What are the 2 ganglia associated with vagal afferents
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1. superior/jugular ganglion - carries pain and T to trigeminal nuc (also is a superior ganglion for 9 and 7)
2. inferior/nodose ganglion - carries taste and GVA info to NTS |
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what nucleus for CN IX is for GVE? What does CN IX innervate?
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inferior salivatory nucleus
- parotid gland via otic ganglion to stimulate saliva |
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what nucleus for 7th nerve is for GVE?
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superior salivatory nucleus
- nasal and lacrimal glands via pterygopalatine ganglion - submandibular and lingual glands via submandibular ganglion |
