Neuroanatomy: Block 2 Review:

Front 1

talk about what happens when you damage a specific part of the post-central gyrus:

Back 1

lab showed us the 'hand motor knob' - right behind it is the sensory knob from it. note that messing with the post-central gyrus won't completely screw up sense - just loose discriminitive touch (most ML-transmitted things go directly to the post-central gyrus).

pain/temp can be picked up elsewhere. crude touch elsewhere too. the thalamus might even have something to do with pain perception.

Front 2

if you kill the neurons in the substantia gelatinosa, what happens?

Back 2

ipsilateral loss of pain.

Front 3

what's syringiomelia?

Back 3

in the cervical region, usually end up with widening syrinx. first problem is killing the anterior white commissure, so you early on loose pain/temp.

also loose early hand muscle control.

a syrinx is a cyst in the middle of the cord.

can be caused by an arnold-chariri malformation (where the tonsils and medulla herniate through the foramen magnum and stop the flow of CSF. this can cause hydrocephalis and also stop the pulsatile flow down the cord, which somehow can cause cysts to develop).

Front 4

what's brown-sequard syndrome?

Back 4

loss of half of the cord.

get lower motor neuron signs at the level of the lesion (flacid paralysis, fasiculations) and upper motor neuron signs below (spastic paralysis, babinski sign, etc)

loose dorsal column perception ipsilaterally, and pain/temp contralaterally.

Front 5

anterior medullary syndrome?

Back 5

loose the paramedian branches of the anterior spinal artery.
loose contralateral ML (it's already crossed at this level).

should also use contralateral muscle control (pyramids haven't yet decusated).

Front 6

what's wallenburg syndrome?

Back 6

mess with the PICA, at the level of the inferior olivary nucleus.

so this'll kill contralateral pain/temperature to the body (the tract here is pretty lateral, the ML is protected in the middle).

because you're killing the nucleus and tract of V, loose pain/temp to the IPSILATERAL face.

also likely to produce a horner's syndrome.

think that mark wahlberg is horny, pica, who pulled a guy's eye out with a hook.

Front 7

if you have a pontine lesion at the level of the facial caliculus, what can be expected?

Back 7

loose contralateral motor, contralateral pain/temp/general sensation.

also, likely to loose IPSILATERAL lateral rectus muscle, due to the CN6 nucleus present.

Front 8

if you mess with the motor cortex controlling the face, what happens?

Back 8

contralateral facial muscle weakness, including the tongue. note that there would be upper motor neuron problems, so the patient could still blink both eyes tightly and have forehead tone. but the contralateral rest of the face would be droopy.

Front 9

what disease causes intention tremors?

Back 9

cerebellar fuckups.

Front 10

thalamic review: what happens with lateral geniculate lesions, anteiror nucleus lesions, intralaminar, or multiple nuclei?

Back 10

lateral geniculate lesions cause CONTRALATERAL visual field deficits.

anterior causes memory problems (remember that anterior is getting fed indirectly from the hipocampus, through the mamillary bodies).

multiple nuclei can lead to neglect syndrome.

Front 11

name the blood supply to the thalamus:

what about the internal capsule?

Back 11

thalamoperforating
thalamogeniculates
posterior choroidal.

these are all off the posterior circulation

internal capsule:
lenticulostriate (MCA)
middle striate (ACA)
anterior choroidal (MCA)

Front 12

what's the corpus striatum? lentiform?

Back 12

the putamen, the caudate, and the globis palidis.

lentiform = putamen and GP

Front 13

basal ganglia: what are diseases of the direct and indirect system?

Back 13

diseases of the direct system = diseases of the active system = inactive = hypokinetic = parkinson's

diseases of indirect system = diseases of inhibitory system = hyperkinetic = huntington's and hemibalismus.

Front 14

what leads to parkinsons and why?

Back 14

degredation of the substantia nigra compacta, which normally releases dopamine onto the striatum. usually, this stimulates the direct system. so, screwing with it causes hypokinetic disorders.

Front 15

how about huntington's?

Back 15

comes from screwing with the indirect system - so loosing the caudate nucleus STOPS its ability to inhibit the GPe, which can now stops inhibiting the subthalamus, which goes crazy

Front 16

blood supply to the BG?

Back 16

same as the internal capsule:

lenticulostriates get the body of the caudate, the putamen, globis palidis,

here, the medial striates get the AV system.

the anterior choroidal artery gets the tail of the caudate.

Front 17

Kreisman somatosensory review (17 and 18): what information can the sensory system transmit?

Back 17

midl

modality
intensity
duration
location

Front 18

how are duration and intensity transmitted?

Back 18

duration = how long action potentials fire.

intesnity = action potential frequency. also can be from RECRUITMENT (more receptors activated by pushing harder)

Front 19

what are the 4 primary somatosensory modalities? what can be derived?

what kinds of receptors are there, generally?

Back 19

pressure

temperature

pain

kinesthetic sensation (motion/position).

derived:
vibration
two point discrimination
sterognosis
graphesthesia
judgement of routhness.

generally, receptors include:
mechanoreceptors
thermoreceptors
chemoreceptors
photoreceptors.

Front 20

receptors - which are not laminated?

Back 20

only the rufini! it carries pressure
merciekl is touch
meisner and pactinian corpussles are vibration.

remember that pactinian corpussles and meisner's corpussles are RAPIDLY ADAPTING.

Front 21

position sense - what receptors relay this? how is rate of change and position communicated?

Back 21

"deep receptors"

here, we're talking about those in joints, seem to be modified RUFINI receptors (usually detect pressure).

the burst of ptls at the beginning of movement = rate of change.

steady state potentials = position

Front 22

cold and warm receptors - how do they work? adaptation?

Back 22

cold signals etween 5 to 30 degrees (colder = more firing), warm between 30 and 50?). between 30 and 40, both fire, though cold goes down and hot goes up. above 40, only warm receptors work.

both warm and cold receptors ADAPT QUICKLY (why you get used to a hot shower or a cold pool).

the initial rate of firing signals the rate of change - constant firing = absolute temperature.

Front 23

pactinina, rufini, merckel, meisner's - what tracts do they travel in?

Back 23

all go in ML tract! pain and temp are other receptors, remember.

Front 24

slow vs. fast adapting first order neurons - what kind of neurons are they connected to?

Back 24

up through the thalamus and cortex, fast adapting tend to touch fast adapting in the brain. slow to slow.

so, rapidly adapting pactinian corpussles are wired to fast adapting cortex cells.

note that the thalamus generally projects to 3a and 3b.

3b/1 get somatosensory stuff. 3a is joint stuff.

Front 25

if you want to lesion stereognosis, where's a good place?

Back 25

secondary assocition area for the somatosensory stuff. 5 and 7.

note that in 312, 1 and 2 tend to have the most feature-detecting integrative fancy neurons. some can be direction and movement aligned.

Front 26

which receptors have large and which have small receptive areas?

Back 26

merckel's and meisner's are small.

pactinian are large.

Front 27

what's lateral inhibition, and how does it work? what does this increase?

Back 27

at the relay nuclei for the ML system (the gracile and cuneate nucleus), there is feeed-forward and feed-back inhibition. a signal coming up to the nucleus has two separate mecahnisms to inhibit its neighboring nuclei (remember it's still somatotopically arranged here), so a signal in the center will "stand out" by increasing the signal to noise ratio.

this increases acuity.

Front 28

so the fingers we know have more receptors and smaller receptive fields. do they have lateral inhibition? why or why not, and what does this allow us to detect?

Back 28

yes, they have a lot. without it, it's hard to do two point discrimination.

note that this allows us to detect the edge of objects, which is a huge part of how we identify texture (braille being the most obvious part of this).

Front 29

messing with a homotypic unimodal vs. heteromodal causes what?

Back 29

homotypic unimodal = appreceptive agnosias, problems with a single modality.

homptypic heteromodal = tertiary structures that get all sensory modalities going to it (PTO) = associative agnosias.

Front 30

what's gertsman disease?

Back 30

broadmans' area 39 on the left side. also the angular gyrus, also the inferior parietal lobule.

acalculia
agraphia
finger agnosia
left right confusion

Front 31

when you have a stroke of area 8, what way do you look? what about seizure?

Back 31

think that the right 8 drives the eyes to look the opposite direction - so when you stroke on the right side, eyes can't be pushed left, so they end up right.

seizure = too much actvity, look away from the seizure.

Front 32

talk about general right vs. left cortical prbolems:

Back 32

left has a lot of symptoms like gertsman's - acalculia, agraphia, dyslexia, trouble talking. right left orientation problems

right side - concept problems, emotional blunting, left sided neglect, spacial and contextual problems.

Front 33

what's idemotor apraxia?

Back 33

lack of ability to do something PRACTICED (apraxia) like swing a tool.

poblems with arcuate fibers. premotor areas. corpus calossum.

people have to have intact sensory information.

Front 34

what's conduction aphasia?

Back 34

not wernike's or broca's. problem of higher cortical structure, have intact comprehension and intact speech centers (wernike's and broca's), but can't do REPETITION.

frequent errors. higher cortical functions can't do it. aware of errors, can't correct.

arcucate problems. maybe damage between broca's and wernike's.