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441 Cards in this Set
- Front
- Back
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what system senses the dynamic forces of angular and linear accelerantions as well as the static force of gravity maintain body equilibrium?
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vestibular system
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what are vestibulo spinal reflexes?
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signals from the vestibular apparatus that are essential for postural adjustments and generation of smooth body mvmt that keep the body balanced and prevents falling in gravity environment (standing in subway)
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what are vestibulo ocular reflexes?
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when the vesibular system maintains retinal image stability-keeps retinal image fixed as head is moving (as head turns keeps what you are looking at on the fovea)
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what does the CNS register if both the right and left afferent firing rates are equal?
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that the head is NOT moving-the head and body are stable and NO motor compensatory balance or eye reflexes are needed
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what does the CNS register when the right and left afferent VIII firing rates are NOT equl?
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that the head is moving
lower firing rate = head deflection |
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what problems will you have if you damage the vestibular system?
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problems with eye movements and balance
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waht is vertigo? what is it not?
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illusion of motion (you or the world is spinning)
NOT dizziness: due to low BP |
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what is Nystagmus?
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physiologic reflex consisting of compensatory bilateral slow eye mvmt opposite to a head mvmt with a non compensatory fast saccadic eye mvmt to reset the eye position
*jerky eye mvmts *named for the direction of the fast movment |
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what induces Nystagmus in normal individuals? when does it become pathological?
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rotation, visual or caloric stimulation
*pathological if occurs spontaneously or is sustained? |
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what CNs are associated with the Telencephalon?
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1 and 2
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what CNs are associated with the midbrain?
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3 and 4
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what CNs are associated with pons?
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5, 6, 7, 8
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what CN's are associated with medulla? cervical?
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medulla: 9, 10, 12
cervical: 11 |
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what is the fxnl unit of vestibular system?
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hair cells: neuroepithelial cells
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what do the vestibular hair cells release and how often?
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excitatory transmitter (Glu) tonically so the afferent fiber on which it synpases has a steady, TONIC resting discharge rate
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how are the vestibular hair cells polarized?
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large kinocilium on edge of cell
sterocilia get progressively shorter with distance from the kinocilia |
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where are the cell bodies for CNVIII in vestibular system?
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scarpa's ganglion
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bending sterocilia TOWARDS the kinocilium causes?
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increased # of open tip-link transdxn chanells
depolarization b/c K, Ca current increases at apical membrane from the OUTSIDE of the cell to the INSIDE of the hair cell increasd transmitter release at the BL membrane increased afferent nerve firing |
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when do hair cells have an AP?
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never hve AP
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bending sterocilia away from the kinocilium causes?
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decreased number of open transdxn channels
hyperpol of hair cell b/c K, Ca current decreases decreaed transmitter release decreased afferent nerve firing |
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perilymph consists of what? what is it similar to?
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CSF
extracellular fluid, Low K, high Na surrounds the membranous labyrinth |
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waht makes up endolymph?
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extracellular fluid that is similar to an intracellular fluid with ionic concentrations: high K, low Na
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in the vestibular system, where wuould you find endolymph? perilymph?
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endolymph: w/n membranous labyrinth
perilymph: surrouds the membranous labyrinth |
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overprdxn of endolymph causes?
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Menier's syndrome: high fluid pressure w/n membranous labyrinth
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what do you call the voltage w/n endolymph?
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transepithelial voltage (endocochlear potential = +80mV
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compare the transbasolateral vltage with the transapical voltage?
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transbasolateral mem voltage = -60mv
transapical mem voltage = -140mV |
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the motion of hair cells sterocilia causes K to move along waht type of gradient?
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electrical gradient, NOT a concentration gradient
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what makes up the vestibular labyrinth system?
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2 components: macula and crista ampularries (ampula)
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where are neuroepithelial cells located in the vestibular labyrinth system?
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the ampulla: swellings of semicircular canals
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what are Otolith organs (ear stones)?
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4 areas of neuroepi (sensory epi) in the membranous labyrinth called macula (2 macula/inner ear)
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how many macula are there in the inner ear?
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2 macula/inner ear
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what is the fxn of the macula?
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detect linear forces caused by static displacement (nm) due to gravity
or transient displacment (nm/s2) due to linear acceleration or deceleration |
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what are the 3 planes that linear mvmt can move in?
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X axis: forward and backward
Y axis: left and right Z axis: up and down |
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what are the "bags" of endolymph?
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utricle and saccule
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how many semicircular canals are there per inner ear? names of them?
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3: posterior, anterior, horizontal
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what is the dynamic signal for otolith organs? static signal?
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dynamic: linear acceleration
static: steady tilt of the head/gravity |
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what are otoliths?
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calcium carbonate particles
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waht rests upon gelatinous mass overlying the hair cells and have a higher specific gravity than that of the surrounding endolymph?
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calcium carbonate
therefore they exhibit inertial delay with head motion |
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what does no affect the otolith organs?
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angular acclearations b/c they don't protrude substantially into the lumen of the membranous labyrinth
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how are hair cells oriented in the macula? why?
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back to back with respect to a ridge called the striola
result of this arrangment is that mvmt of the otolithic membrane in any direction will stimulate some hair cells and inhibit others |
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macula in the saccule detects linear changes in what plane?
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vertical plane: upward and downward along Z axis
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macula in utricle detect linear changes in what plane?
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foward and backward along the X axis as well as side to side along the Y axis
riding in a car head tilt |
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what is the fxn of semicircular canals/ampulla?
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detect angular (rotational) accleration or decelerations as small as 0.1 degree/s2 in three planes: horizontal, vertical, and lateral simultaneously
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why is CONSTANT angular velocity not an apporpriate stimulus for the ampulla?
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b/c fluid and crista eventually rotate at the same velocity
brain won't think you are turning when steady..need acceleration |
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how do the 3 planes match the 3 semicircular canals?
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lateral: horizontal
anterior: vertical posterior: vertical |
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what are the 3 degrees of rotational freedom?
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they refer to the body's rotation relative to the x, y, z axes are are commonly referred to as roll, pitch, and yaw
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what is yaw? roll? pitch?
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yaw: rotation around the z axis
pitch: rotation around y axis roll: rotation around x axis |
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what position does flexing the head 30 degrees put the lateral canals in?
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horizontal position (parellel with the horizon)
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how are the kinocilium organized in the horizontal semicircular canals?
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with the kinocilium more medial (closest to utricle)
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yaw is associated with which of the semicircular canals?
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horizontal
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if you are extending the head backward 60 degrees or lifting a supine pts head up 30degrees what direction will the lateral canals be in?
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vertical
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if you turn head L, what direction does the endolymph go in?
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goes in opposite direction of head mvmt(R) closing K channels on R and depolarizing the channels on L b/c of the orientation of the kinocilium (medial)
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which hair cells will repond to acceleration or deceleration forces?
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only hair cells in the ampulla of the semicircular canal which is at right angles to the axis of rotation
ex: hair cells in horizontal canals respond to yaw mvmts |
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in the horizontal ampulla, the cilia are oriented how?
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toward the utricle ( in the other ampulla: oriented away from the utricle)
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if you are moving yaw left, what horizontal canals will you be stimulating?
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afferent firing in L horiontal canal and inhibit firing from R horizontal canal bc they are in same rotational plane
no effect on the 2 paired post and ant canal b/c they are not in the same plane of rotation |
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what is the fxn of VOR?
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causes the eyes to move at a velocity equal to but opp that of rapid head mvmt so the scene on the fovea will not slip off this area or retinal sharp focus during the head mvmt
no nystagmus |
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what is the VOR system insensitive to?
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slow mvmts or perisitant rotaion of the head (if continous rotation, you will see compensatory eye mvmt stop after 30 s of rotation)
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if you move your head to the left, what direction will your eyes go to and how?
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go to the right b/c of endolymph
stimulate L MR and R LR head turns to side of higher AP eyes turn to side of lower AP |
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head goes to side with ____ AP
eyes go to side with ____ AP |
head: higher
eyes : lower |
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how long is the latency from the stimulus till the onset of eye mvmt?
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12 miliseconds
no time for long neuronal mulisyanptic mvmts no afferent info sent to coritcal nuerons for this reflex target pursuit latency: 125ms |
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how long is target pursuit latency?
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125ms
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how fast can your eyes mov/sec? how long to target pursuit velocity?
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300 degrees eye mvmt/sec
target pursuit: 100 degrees/sec to accurately identify (ex eagle) = 30degres/sec |
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what are the results of caloric testing in normal individual?
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warm water induces nystagmus that beats towards the warm ear
cold water induces nystagmus that beats away from cold ear COWS Cold opp the fast mvmt Warm same side |
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in which direction will the eyes go if you place cold water in teh L ear?
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they will go to the opposite side Fast
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in which direction will the eyes go if you put warm water in the L ear?
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they will go fast towards the same side
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in a unilateral lesion in the vestibular pathway, on which side will nystagmus be reduced or absent?
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on the side of the lesion
look away from the lesion |
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what is rotational testing?
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using Barany chair
rotate subject in a swivel chair at a rate of 1 revolution every 2-3 sec for 45sec results in a rotatory nystagmus the nystagmus is in the direction of the chair rotation |
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what happens when you stop spinning someone in the Barany chair?
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the nystagmus wil stop in 30 sec as head semicular canals, and endolymph are all moving at the same velocity
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what happens in rotational testing if the lights are on and the subject can see the environment?
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then optokinetic nystagmus will be seen in the subject and will last as long as the chair turns b/c the eyes are tracking visual cues
ex: I see the blue shirt sensory is CN 2 b/c eyes open and motor is CN 3 and 6 |
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what happens in rotational testing when you stop the chair suddenly?
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postrotary nystagmus in the direction opposite to the direction of the chair movment b/c the sudden stop causes the head and semicircular canals to stop but the endolymph is still moving in the direction the chair was turning causing decreased firing on the side the chair was turning and thus slow eye mvmnts, post pointing and tendency to fall ALL occur to the side the chair WAS turning
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waht is the most common vestibular disorder?
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benign positional vertigo
otoconia displaced from utricle macula becomes lodged in cupula of the post canal (cupulolithiasis) |
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what is the causes of benign positional vertigo?
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otoconia displaced from utricle macula becomes lodged in ampula of the posterior canal
results in brief episodes of vertigo that coincide with changes in body position |
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what is Labyrinthine Disease?
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seasickness, space sickness
pt says world is spinning objective signs: nystagmus, falling or postural deviation, sweating, vomiting, hypotension subjective symptoms: vertigo, nausea, oscillopsia, anxiety |
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what is acute peripheral vestibulopathy?
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spontaneous attack of vertigo of unapparent cause
includes acute laybrinthitis and vestibular neuronitis |
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what is the affect of ototoxic drugs like the aminoglycoside gentamycin?
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cuase ATN and lose hair cells
ex: pt reading and eyes jumped off page with heartbeats |
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what is happening in the resting primary gaze?
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all mm balanced
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if you lesion the MR, where will you look?
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laterally
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what is the primary movment of SO? 2ndary?
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primary: intorsion=uppar pole of eye moves inward
secondary: depression |
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where are the eye mvmt control centers located?
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supranuclear regulation of eye mvmts found in brainstem, cerebellum, and forebrain including BG
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what are the 2 areas controled by the pons in terms of eye mvmts?
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abducens nucleus and paramedian pontine reticular formation (PPRF)
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pons is the ____ eye mvmt control center?
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horizontal
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what does the abducens nucleas control?
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horizontal gaze center as it controls ipsilateral LR and contralateral MR
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what provides the interconnection b/n the occulomotor, trochlear, abducens, and vestibular nuclei?
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medial longitudinal fasciculus (MLF)
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waht is the job of the paramedian pontine reticular formation (PPRF?
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provides output to the abducens from higher cortical eye mvmt control centers
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lesion of the PPRF or abducens nucleus will cause waht?
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ipsilateral horizontal gaze palsy (look to the R , but eyes should look R) this is a problem with moving BOTH eyes in directed gaze
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what is located in the tegmentum (2)?
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1. CN 3 cell bodies
2. reticular formation of CN 5 and 7 |
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if you quickly wipe cotton across the cornea what happens?
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blink bc of sensory 5 and motor 7 *corneal reflex
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if someone is going to poke you in the eyes, what happens, what CN are invovled?
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Blink to Threat
sensory 2 motor 7 |
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demyelination of MLF results in what?
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MS
female presents with complaint the L eye won't go R |
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midbrain is in control of what eye control centers?
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vertical and vergence eye mvmts
controls the SR and IR mm and the IO and SO |
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the dorsal rostral midbrain reticular formation controls waht type of gaze? ventral?
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dorsal: upward gaze
ventral: downward gaze |
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vertical eye mvmts are intitiated where?
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in the rostral midbrain reticular formation and pretectal area
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vergence eye mvmts are initiated where?
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in the midbrain reticular formation controling convergence MR mm and divergence LR mm
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what are the jobs of the frontal eye fields?
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stimulate the contralateral PPRF and generate conjugate eye mvmts (saccades) to the contralateral side
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what are teh 2 forebrain centers that control eye mvmts?
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frontal eye fields
parieto-occipital-temporal cortex |
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lesion of the frontal eye field causes waht?
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both eyes to gaze toward the lesioned side
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waht is the fxn of the PTO: parieto-occipito temporal cortex?
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stimulates smooth pursuit eye mvmts in the ipsilateral direction
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if you stimulate the L frontal eye field where do eyes go?
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to the contralateral side: R unless lesion in which they gaze towards lesion
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in stroke pts what direction do their eyes look?
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eyes deviated to 1 side: lesioned side
away from the paralysis which affects contralateral side |
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fxn of optokinetic eye mvmts?
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to hold the images of the seen world steady on the retina during sustained head rotation or moving environement
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fxn of smooth pursuit?
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to hold the image of a moving target on the fovea
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fxn of nystagmus quick phases?
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to direct the fovea toward the oncoming visual scene during self rotation, to reset the eyes during prolonged rotation
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fxn of saccades?
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to bring images of objects of interest onto the fovea
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fxn of vergence?
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to move the eys in opp directions so that the images of a single object are placed on both foveas
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what are the 2 orbital mechanics needed to overcome the viscous drag and elastic restoring forces of the orbital supporting tissues?
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pulse of innervation: burst of neural activity that is needed to generate a poweful contraction of the extraocular mm to overcome the viscous resistance
step of innervation: tonic steady new baseline level of firing activity that holds the eye as its new eccentric position: must hold the eye activity at the new position |
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what is the fastest of the eye mvts has how fast are tehy?
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saccadic
peak velocity of 700degrees/sec |
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which eye mvmts are ballistic and what does this mean?
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saccades
once started they can't change-can not change course of eye mvmt in response to subsequenct changes in the target during the delay period |
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which eye mvmts allow us to rapidly redirect our line of sigh?
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saccadic: notes to clock (don't register anything you see in b/n the notes and the clock)
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what is the length of time that it takes b/n when you see the target of interst and why you move your eyes?
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200msec delay
a typical saccadic eye mvmt acclerates rapidly reaching its peak velocity b/n 1/3 and 1/2 of the way through the mvmt |
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why do we need smooth pursuit mvts?
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b/c once captured on the fovea by a saccadic mvmt, an image of a moving target would soon slide off the fovea in a short interval b/n saccades
therefore we need smooth pursuit to keep targets on the fovea |
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what isthe catch up saccade?
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the time it takes to track the object of interest with a smooth pursuit
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what happens to smooth pursuit in a pt with cerebellar disease?
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jerky, ataxic
problem with cerebellum velocity is much less than that of the target tehrefore the pt has to make catch up saccades to place the image of the target on the fovea |
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compare visual acuity in saccadic vs smooth pursuit?
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saccadic: poor
smooth: excellent |
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is a target reqd for smooth and saccadic eye mvmts?
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only smooth
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what do vergence eye mvmts do?
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align the fovea of each eye with targets located at different distances from the observer
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waht is the only type of eye mvmts that causes the eye to move in opposite directions?
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vergence: they are disconjugate eye mvmts
line of sight for each eye converges with near object of interest and diverges with far object of interest |
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waht is the near reflex triad?
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convergence
accomadation constriction of pupil |
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what are the 3 types of eye mvmts?
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saccadic
smooth pursuit vergence |
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what 2 systems operate together to hold images stable on the retina?
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vestibular and optokinetic
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what does the VOR compensate for?
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natural head mvmts which are usually rapid and transient by generating an eye mvmt which is equal and opposite of the head mvmt in space
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when is the vestibular system ineffective?
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with steady continuous rotations as the compensatory eye mvmts cease after 30sec
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what is the eye position in space when the head is rapidly turned to the left?
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b/c the mvmts of head and eye in orbit are equal and opposite, the sum eye position in space (gaze) remians zero
if gaze is held steady, then images of the seen world do not slip on the retina and vision remains clear EYE space = Eye orbit + Head space |
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when is the optokinetic system used?
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during sustained or slow head rotation
maintains its effect until the field of vision stops moving acts as a back up to the VOR reflex |
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what is railroad nystagmus?
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person looking out window watching telephone poles go by..this creates nystagmus
composed of pursuit eye mvmt to trach the moving environment and is then reset with a fast saccade |
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how is the optokinetic system a back up to the VOR ?
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VOR by itself can only hold the image on the fovea steady durng the first 30s turning
this stimulates the optokinetic system to stabilize the retinal image |
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in railroad nystagmus or striped drum movment, in which direction are the eyes going as the drum turns?
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during the slow phase the eyes move in the same direction as teh striped drum to keep the drum still on the retina
then you have you the fast saccade |
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how are descending motor pathways divided up?
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lateral and motor based on spinal cord location
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where do lateral motor systems travel?
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in the lateral columns of the spinal cord white matter
axons terminate on lateral groups of ventral horn motor neurons and interneurnes |
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what do the lateral motor systems control?
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mvmts of extremities (distal mm) arms, legs, feet, hands
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what ae the 2 tracts of the lateral motor system?
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lateral corticospinal tract
rubrospinal tract |
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what is clinically the most impt lateral motor system path?
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lateral corticospinal tract
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where is the rubrospinal tract and what does it do?
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red nucleus in the midbrain (mickey eyes)
increases flexor tone in the upper extremities |
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both lateral motor tracts provide for?
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rapid, dexterous mvmts at individual joints or digits
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is it worse to knock out the desc lateral motor system or medial?
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lateral b/c it is only ipsilateral while the medial is bilateral
with desc lateral get weakness in hands and hyperreflexia |
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why do you clinically not need to worry about trunk paralysisi?
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b/c it has bilateral input
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where do the medial motor systems travel in the spinal cord?
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anteromedial columns of the spinal cord
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waht do the medial motor pathways contrl?
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mvmts of the trunk (axial and girdle mm)
they are involved in postural tone, balance, orienting mvmts of the head and neck, automatic gait |
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do the medial motor systems decussate?
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no they descend laterally and terminate on interneurons
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which motor system influences axial musculature bilaterally?
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medial motor systems
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what are the 4 tracts in the medial motor system?
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1. anterior (ventral) cortcospinal tract (doen't cross midline)
2. vestibulospinal tracts (VST's), 2 tracts from vestibular nuclei (lateral VST and medial VST) 3. Reticulospinal tract (2) 4. tectospinal tract: ends in cervical cord |
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what are the vesibulospinal tracts?
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tracts of medial motor system
composed of 2 tracts: lateral VST: runs length of the spinal cord and controls extensor tone medial VST: ends at cervical cord; controls and neck mvmt |
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how many reticulospnal tracts are there and what do they do?
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2: part of medial motor system
one originates in pontine reticular formataion=medial reticulospinal tract other originates in the medullary reticular formation=lateral |
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fxn of tectospinal tract?
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one of the 4 medial motor tracts
provides coordination of head and eye mvmts |
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caudate + putamen =
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striatum
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incoming thalamus goes to waht layer?
outgoing thalamus goes ? |
incoming: layer 4
outgoing: layer 5 |
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waht carries the homunculus descending UMN axons?
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internal capsule: posterior limb
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what perent of the descending lateral corticopsinal pathway decussates?
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90% *make up lateral-hands
10% stay medial to do bilateral innervation of trunk |
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what does paresis mean?
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weakness (partial paralysis)
ex: hemiparaesis clinical symptoms: weakness of one side of the body |
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what does -plegia mean?
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no mvmts
ex: hemiplegia no mmvt on one side of the body |
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what does paralysis mean?
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no mvmt
ex: leg paralysis no mvmt in leg |
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what do Hemi-, Para-, Mono, Di- mean
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Hemi: one side of the body
para: both legs (paraparesis) Mono- one limb Di- both sides of the body eqully affected |
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hemisection of the spinal cord can cause what?
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Brown Sequard Syndrome: ipsilateral UMN signs
ipsi loss of vibration sense, joint position and proprioception contralateral loss of pain and temp, itch and crude touch |
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what happens in an anterior spinal artery occulusion?
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no pain and temp below the lesion bilaterlaly
damage to the anterolateral pathways and ventral horn cells |
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if you have doral spinal artery occulusion, waht do you lose?
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fine touch, proprioception
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what vitamin is reqd for myelin formation?
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B12-causes pernicious anemia
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Vitamin B12 neuropathy?
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Vit B12 is reqd for myelin formation
lack of intrinsic factor cuases tingling and numbness (parathesias) of hands and feet degenration of myelin in the doral columns is greater than degeneration in corticospinal tract |
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poliomyelitis damages what?
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alpha motor neurons in spinal cord due to infectous myelitis like viruses
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MS affects what portions of spinal cord?
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dorsal columns
ALS |
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waht is Guillian Barre syndrome?
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acute inflammatory demyelinating polyneuropathy thatis an immune mediated demylination of peripheral neves
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tectum is composed of?
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superior and inferior colliculi which lie dorsal to the cerebral aquaduct
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tegmentum lies ventral to what?
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ventral to the aquaduct (midbrain) and ventral to the 4th ventricle in the pons and medulla
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the brain stem tegmentum is the location of what?
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the main bulk of the brain stem nuclei and the reticular formation
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where are the main bulk of brain stem nuclei and the reticular formation located
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tegmentum
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what is located in the base of midbrain?
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corticopsinal tract, corticobulbar, corticopontine
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what are the 3 CN that are NOT associated with the brain stem?
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CNI and II (forebrain)
CN XI: cervical spinal cord |
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what are the 2 cn associated with the midbrain?
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III and IV
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what are the 4 CN associated with the pons?
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CN V, VI, VII, VIII
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what are the 3 CN associated with the medulla?
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CN IX, X, XII
9 and 10 think autonomic PNS |
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3 sensory CN:
5 motor CN: 4 mixed CN? |
sensory: 1,2,8
motor: 3,4,6,11,12 mixed: 5,7,9,10 |
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what are the CNs associated with the PNS?
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3,7,9,10 the PNS pregan neuron is cell body is located in specific brain stem nuclei
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nucleus for CN3?
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EW nuclus in midbrain
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nuclues for CN7?
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Superior Salivatory nucleus (ponse)
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Nucleus for CN9?
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Inverior Salivatory nucleus (medulla)
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Nuclus for CN10?
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Dorsal motor nucleus of 10 (medulla)
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the CNs associated with the PNS have postgang neurons that innervate what?
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glands, smooth muscle, cardiac
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where are the postgang PNS neuron cell bodies for CNIII?
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ciliary ganglion-axons project to the eye ciliary muscle and constrictor (sphincor) mm of the iris
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PNS pre and post gang cell bodies for CN III?
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pre: EW nucleus (midbrain)
post: ciliary ganglion |
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PNS Pre and post gang cell bodies for CN7?
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pre: superior salivatory nucleus (pons)
post: sphenopalatine ganglion (lacrimal glands and nasal mucosa)-cries, mucus submandibular ganglion (submaxillary salivary glands)spits |
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PNS pre and post gang cell bodies for CN 9
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pre: inferior salivatory nuclues (medulla)
post: otic ganglion (paratid gland) |
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PNS pre and post gang cell bodies for CN10?
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pre: Dorsal motor nuclues of X (medulla)
post: various terminal ganglia (project to effector organs) |
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does the descending tract from the hypothal that is going to innervate the pregang SNS neurons decussate?
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no
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all the SNS pregang cell bodies are located where?
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in the IML of T1-L3
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the SNS pregan innervating the head are found in the IML of ?
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T1-T2
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the SNS postgang cell bodies lie where?
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superior cervical ganglion
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a lesion of the sympathetic pathway to the head will cause?
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ipsilateral Horner's syndrome b/c desc tract from hypothal does not cross the midline
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what are the classic signs of Horners?
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Miosis: decreased pupil size (dilator not innervated)
Ptosis: drooping eyelid (smooth muscle not innervated) Anhidrosis: lack of sweating onth face and neck |
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mvmt disorders think?
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basal ganglai
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ataxia think?
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cerebellum
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classic slow mvmt disorders? fast?
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slow: Parkinsons
fast: Huntington's |
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what are these symtpoms of: micrographic writing, decrease facial expression, resting tremor, hoarsness, drooling b/c lack automatic mvmts like swallowing
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parkinsons
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are myoclonic mvmts due to basal ganglia what are some examples?
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no, they are cortical problems
hiccup, jerk when falling asleep, startle response |
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HD is a problem with?
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caudate nucleus
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dystonia/wilsons is a problem with?
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putamen
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carbon monoxide is a problem with?
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globus pallidus
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hemiballismus is a problem with?
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subthalamic nucleus
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PD is a problem with
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substantia nigra
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clinically the BG refers to?
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Caudate nucleus
Putamen Globus pallidus Subthalamic nucleus Substantia nigra |
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what lights up in ppl assumed to be in a coma when you tell them to imagine climbing a flight of steps?
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supplementary motor area (SMA)
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what makes up the striatum? what does each do? how are they similar?
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caudate and putamen
putamen: motor control caudate: cognitive/behavioral control, eye mvmts similar histologically |
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what makes up the lentiform nucleus?
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putamen and globus pallidus
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what makes up the corpus striatum?
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caudate, putamen, globus pallidus
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is the putamen medial or lateral?
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lateral
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what will you see in a CAT scan of HD pt?
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caudate nucleus atrophy
entire brain shrinks |
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what is the mxn of wilsons disease?
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chew up putamen bc Cu deposited here 1st
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metabolic lesions cause?
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symmetrical lesions
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what are the components of substantia nigra?
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pars compacta: dorsal
pars reticulata |
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where neurons that die in Parkinson's and therefore lose their black color?
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pars compacta
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what structure is lens shpaed?
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subthalamic nucleus
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lesions in subthalamic nucleus have contr or ipsi problems? cerebellum?
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contralateral: subthalamic
ipsilateral: cerebellum |
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what is the ouput center of the BG?
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Gpi
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what are the 3 excitatory pathways in the motor loop?
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cortex to striatum
subthalamic nucleus to Gpi thalamus to cortex |
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in the motor pathway, what is the inhibititory NT? Excitatory?
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inhibitory: GABA
excitatory: glutamate |
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what is the indirect motor pathway?
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cortex to striatum, stiatrum to Gpe, Gpe to STN, STN to Gpi, Gpi to thalamus, thalamus back to cortex
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are parkinsons, chorea, ballismic mts, dystonia hyperkinetic or hypokinetic?
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hyperkinetic: chorea, ballismus, dystonia
hypokinetic: parkinsonism |
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what is going on in the motor pathway for PD?
|
relative overactivity of Gpi, Gpi normally inihibits thalamus, so more inhibition of thalamus means less info is stimulating the cortex, thus less mvmt
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what is the actvity level of Gpi in hyperkinetic mvmts
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underactivity thus Gpi doesn't inhibit thalamus as much and thus thalamus excites cortex resulting in extra mvms
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substantia nigra projects to where?
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striatum
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dopamine deficiency affects Gpi how?
|
overactivity of Gpi because normally dopaminergic neurons project to striatum via direct and indirect pathways
w/o dopamine the Gpi is overactive and thus over inhibits thalamus via direct and indirect pathways decreasign inhibitory influence of direct increasing excitatory effects of indirect pathway |
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what are the main clincal features of PD?
|
resting tremor
bradykinesia rigidity postrural instability |
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neurochemical abnormality in PD?
|
dopamine deficiency: loss of dopamine produceing cells in substantia nigra
remaining neurons contain lewy bodies (cytoplasmic inclusions) |
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what are lewy bodies?
|
cytoplasmic inclusions that are w/n the remaining neurons in PD pts
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what happens if you give a PD pt too much dopamine?
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get underactive Gpi b/c all the dopamine inhibits the Gpi
thus doesn't brake the thalamus which then overexcites cortex and you get chorea |
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what is the rate limiting step in the prodxn of dopamin? prodxn of what depends on this enzyme?
|
tyrosine hydroxyase
dopamine NE epi |
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what does carbidopa inhibit?
|
aromatic amino acid decarboxylase
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why give carbidopa with levadopa?
|
carbidopa inhibits conversion of L-dopa to dopamine
Levadopa actually enters the brain whereas nromal dopamine does not if you didnt have carbidopa then levadopa would be convereted to dopamine peripherally and wouldn't enter the brain |
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what is sinemet and what do the 2 numbers mean?
|
sinemet is given for PD pts
carbidopa/levadopa |
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what are the 2 ways in which to treat PD?
|
increase dopamine or decrease Ach
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dopamine is brkn down by?
|
MAO-B and COMT into DOPAC and HVA
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COMT causes breakdown of waht?
|
breakdown of dopamine to HVA and DOPAC
also converts L-Dopa to 3-OMD (worthless product) |
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why is COMT bad in PD pts?
|
b/c it will break dopamine down and convert L-dopa to 3-OMD even before it enters the brain therefore need to give COMT inhibitors so more L-dopa can get into the CNS and to keep more dopamine in brain
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what are the classes of drugs that Tx PD?
|
increase dopamine activity
anticholinergic agens surgery anticholinergic agents are cheap but not the best...many side effects |
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as PD progresses, what clinical problems develop?
|
depression 50%
dementia 25% psychosis 25% (visual hallucinations and delusions) chorea(dyskinesia) 70% |
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how is sinemet a 2edged sword?
|
when on: chorea
when off: frozen stiff <40 yrs old on sinemet 100% get dyskinesia therefore don't put young ppl on Sinemet |
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what percent of PD is genetic? what is the inheritance of most?
|
20%
AR |
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why do we see Lewy bodies in PD pts?
|
problems in the Ubiquitin-Protesosome system: the 26S proteosome is inhibited(sporatic PD), parkin deletions and point mutations (juvenile PD) thus Lewy bodies full of proteins that weren't digested
PD is a loss of dopaminergic neurons, with the remaining neurons full of Lewy bodies |
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what is the def of dystonia?
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repetitive, stereotyped involuntary mvmts that can be twisting, writhing, or jerking but can also be fixed abnormal postures
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dystonia is caused by lesions in the what?
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putamen
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when would you have a right hemidystonia?
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left lesion in putamen
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what is a focal dystonia and when do they begin?
|
begin in adulthood
involves only one part of the body cervical dystonia (pulling of head any direction that disappears when rest head on wall) blepharospasm oromandibular dystonia spasmodic dysphonia (whispering, can't project voice) writer's cramp |
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what is a generalized dystonia and when do they begin?
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affects entire body
onset in childhood caused by genetic disorders such as DYT1 gene mutations of the torsin protein |
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what causes generalized dystonia?
|
DYT1 mutations of the torsin protein
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Tx for generalized dystonia?
|
silencing RNA to stop abnormal genes from expressing (DYT1 mtations of the torsin protein)
Anticholinergics Baclofen Benzodiazepines |
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what is hemiballismus?
|
large amplitude throwing, ballistic mmvts on one side of the body (if on R, then lesion on L)
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what causes hemiballismus?
|
lesion in subthalamic nucleus
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what type of mvmt is associated with hunginton's disease?
|
chorea: brief involuntary mvmts that flit from one part of the body to another
Random, unlike dystonia |
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inheritance of HD?
|
AD, 50% for each child of inheriting disease
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what is the chance of suicide in HD pts?
|
10-15% risk of suicide: can't work, can't multitask, irritable, difficulty sleeping, bipolar
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what are the motor disorders associated with HD?
|
chorea
dysphagia (diffculty swallowing) dysarthria (slurred speech) abnormal eye mvmts inability to maintain muscle contraction poor coordination |
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who is HD often transmitted by? what is the repeat expansion?
|
paternal
anticipation with paternal expansion of CAG repeats >40 repeats |
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what are the treatable symptoms of HD?
|
depression
anxiety chorea (with neuroleptics) |
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what are neuroleptics?
|
drugs that block dopamine r's
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how do we treat chorea in HD? what can this lead to?
|
with neuroleptics which can cause tardive dyskinesia syndromes
persistant abnormal involuntary movmts that appear after many years of Tx wth dopamine blocking agents and can be permanent |
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|
what is the cause of tardive dyskinesia
|
iatrogenic: Tx with neuroleptics
possibly caused by striatal dopamine R supersensitvity |
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|
what are tics and kinds can you have?
|
intermittent sterotyped mvmts and sounds: motor (touch things or vocal (golden retriever, retriever, retriever)
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Tics are likely caused by? tx?
|
supersensitive dopamine receptors in the striatum (DO NOT damage the brain!)
Tx: neuroleptics (haldol), clonidine but warn about tardive dyskinesia |
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|
besides the pharmaceutical problems, what can treat tics, PD, dyskineisa?
|
smoking pot b/c THC like and binds to carmabinoid R's
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what are the 5 main neural tracts that can be found coursing through the brain stem and ths can be seen on all transverse sections of the brain stem?
|
1. Medial lemniscus: ascend sensory
2. anterolateral system: ascend sensory 3. corticospinal tract: descend motor 4. descdeding hypothalamic sns fibers 5. medial longitudeinal fasciculus (MLF)-pons and midbrain |
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what is unique about the descending hypothalamic SNS fibers?
|
they descend with the ascending spinothalmic fibers (ALS tract for pain, temp, itch) in the lateral part of the brain stem thus brain stem lesions producing ipsilateral Horner's may also result in contralateral loss of pain and temp sensations from the limbs and body
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brainstem lesions of the MLF produce what? caused by?
|
internuclear opthalmoplegia (INO) and disrupt the VOR
caused by MS plaques, pontine infarcts or neoplasms involving the MLF |
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with INO the eye with the lesioned side cannot what?
|
adduct
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with an INO can you still accomodate?
|
yes because nothing is wrong with endinger westphal nucleus
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what is the tract called that sends UMN fiers that origniate and terminate on motor CN nuclei in pons and medulla?
|
corticobubar fibers=corticonuclear tract
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what CN nuclei are innervated by UMN?
|
all CN nuclei that cause skeletal muscle to contract: CN 5, 7, 10, 11, 12
CN5: mm of mastication CN7: mm of facial expression CN10: palate, pharynx, larynx CN11: sternocleidomastoid and trapezius mm CN12: tongue |
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|
corticobulbar innervation of the LMN in cranial nerves is unilateral or bilateral?
|
bilateral: each LMN of the brain stem receives input from axons arising from both the right and left cerbral motor cortex
except:: CN7 |
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how is CN 7 diffrent in terms of UMN innervation?
|
only receives unilateral innervation unlike 5,10,11,12
facial nerve LMN to the lower face receives only contralatearl UMN innervation therefore if you cut the R CN7 you get Bell's palsy on the SAME SIDE |
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bells palsy facial nerve lesion will cause what? compare this with a corticobulbar lesion
|
ipsilateral total (upper and lower) face paralysis
corticobulbar (UMN) will cause only lower face palsy CONTRALATEAL to the lesion |
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|
what is a central seven?
|
upper motor neuron facial weakness
lower 1/4 face paralyzed can wrinkle forehead and shut eyes b/c there is bilateral innervation of the uppr face, the forehead will be spared |
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|
cranial nerves with motor fxn are found whre?
|
near the midline and their nerve fibers exit the brain stem ventrally near the midline (CN3,4,6,12)--motor medial
|
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cranial nerves with sensory fxn are found where?
|
sensory lateral
found near the lateral border of the brain stem and their nerve fibers exit the brain stem laterally (CN8 |
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|
cranial nervs with mixed fxn are found where in brainstem?
|
near the sulcus limitans which separates motor from sensory areas in the brain stem and their nerve fibers exit the brain stem b/n the motor and sonsory nerve fibers
|
|
|
primary sensory afferent? where does the sensory sensory afferent synapse?
|
1 sensory afferent = nociceptor
2ndary sensory afferent then synpases laterally in brainstem then heads to VPM |
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|
every crosssection of th brainstem will include what cN?
|
CN5: see projectory neuron for CNV
|
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Nucleus solitarious includes what CN? which are rostral/caudal?
|
7,9,10
rostral: 7,9,10 taste caudal: 9,10 ANS sensory |
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|
what is the level of the superior colliculus and CN3?
|
rostral midbrain
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what is the level of genu of CN7
|
caudal pons
|
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what is the level of teh inferior olivary nucleus and CN12
|
rostral medulla
|
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what is the level of the internal arcuate fibers?
|
caudal medulla
|
|
|
what is the level of the pyrimadal tract decussation
|
spinomedullary jxn
|
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|
when the butterfly is down in rostral medualla section are we ventral or dorsal?
|
ventral
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|
what portion of brainstem contains the autonomic centers for respiratory, cardio, and GI control?
|
medulla
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|
where do the nerve fibers for CN12 exit?
|
in rostral medulla b/n inferior olive and the corticospinal tract
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|
lesion of the CN12 LMN causes the tongue to point where?
|
to the side of the lesion hypoglossal nerve or nucleus
get flaccid tongue with weakness, atrophy, fasciculations |
|
|
lesion of the UMN to CN12 causes teh tongue to point wher?
|
way from the lesioned side
get spastic tongue |
|
|
where are cell bodies for CN11 located?
|
in upper 5-6 cervical segments in th spinal accesory nucleus which protrudes b/n the dorsal and ventral horns of spinal cord
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|
lesion of CN11 causes?
|
weakness in turning head to the contralateral side against resistancee and ipsilateral shoulder drop
|
|
|
how many nuclei in the medulla is C10 associated with?
|
4: Dorsal motor neucles of X, Nucelus soltarius, spinal trigeminal, nucleus ambiguus
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what impt landmark will you see in spinomedullary jxn cross-section?
|
pyramidal decussation of corticospinal tract neruon axons
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|
what is the spinal trigeminal tract and what does it provide for?
|
primary sensory axons encoding proprioception, pain, temp itch and crude touch sensation for the face, mouth and ant 2/3 of tongue, nasal sinuses, and supratentorial dura, and pain an temp from the outer eat on craniel nerves 7, 9, 10
|
|
|
what happens after faciculata gracilis synapse with projection neuron cell bodies in teh nucleus?
|
they cross over in the internal arcuate fibrers to become the medial lemniscus
|
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|
pyramids in cuadal medulla contain corticospinal tract motor neuron axons from what side of the cortex?
|
ispsilateral..cross over at spinomedullay jxn
|
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|
which of the neurons from nucleus cuneatus crosses the midline?
|
2ndary projection neuron
|
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|
what symptoms will you have if you damage L pyramid in caudal medulla?
|
contralateral weakness on R b/c they already crossed in spinomedullary jxn
weakness, no atrophy, spasticity |
|
|
damage medial lemniscus where pain?
|
contralateral loss of fine touch, temp, proprioception
|
|
|
if you lesion CN11 on the L, which way will you have weakness in turning your head?
|
to the contralateral side
ipsilateral shoulder drop head deviates towards the lesion |
|
|
which cervical segment is involved with CN11?
|
C2
|
|
|
which of the nuclei that CN10 is associatd with innervates skeletal pharyngeal and laryngeal mm?
|
nucleaus ambiguus
controls mm for swallowing |
|
|
fxn of dorsal motor nucleus of X
|
PNS innervation of smooth and cardiac mm (viscera)
|
|
|
which of the 4 nuclei that CN X are associated with are motor?
|
dorsal motor nuclei of X to viscera
nucleus ambiguus to phayrxn and larynx |
|
|
what is the difference b/n rostral and caudal nucleus soltarius?
|
rostral: "gustatory" special visceral sensory -taste from epiglottis and pharynx
caudal: "cardiorespiratory" general visceral sensory-aortic arch chemo and baro R's monitor BP, PaO2, Pco2, [H] caudal = cardio! |
|
|
if you lesion the spinal trigeminal nucleus what will you experience?
|
loss of pain, temp on ipsi
loss of somatic sensation from external ear and meninges (via C10 superior vagal ganglion) loss of somatic sensation from outer ear and middle ear (via CN9 from superior glossopharyngeal ganglion) |
|
|
what ganglion send primary neurons to synapse in the spinal trigeminal nucleus?
|
superior vagal nucleus for CN10
superior glossopharyngeal for CN9 |
|
|
lesion of the vagus causes what?
|
dysphagia (difficulty swallowing with nasal regurgitation of food) . loss of gag reflex, and cough
dysarthria (diffuculty talking) with hoarseness with fixed vocal cord |
|
|
what is the most common site of stroke in the brainstem?
|
rostral medulla
|
|
|
where are the cell bodies for the climbing fibers?
|
in the contralateral inferior olivary nuclus
|
|
|
where do the climbing fibers project to where?
|
from contra inf olivary nucleus to cortex of cerebellum
|
|
|
what is locatd on the doral surface of ponse?
|
4th ventricle
|
|
|
what do the middle cerebellar peduncles connect?
|
23 million pontine nuclei in the pons base to the cerebellum (bridge pons)
|
|
|
what are the 3 main fiber tracts located in the base of the ponss?
|
corticospinal
corticopontine corticonuclear/bulbar |
|
|
what is going on with the corticopontine tract?
|
the CP tract is located in the base of the pons coming from Frontal, parietal, temporal, and occipatal cerebrum
it enters the pons and synapses right way on the 23 milltion pontine nuclei this is the pontocerebelluar bridge that crosses the midline to head to the contralateral middle peduncles of the cerebellum |
|
|
what area of the pons does the corticospinal tracts pass through on their way down?
|
base of the pons
|
|
|
what is going on with the corticopontine tract?
|
the CP tract is located in the base of the pons coming from Frontal, parietal, temporal, and occipatal cerebrum
it enters the pons and synapses right way on the 23 milltion pontine nuclei this is the pontocerebelluar bridge that crosses the midline to head to the contralateral middle peduncles of the cerebellum |
|
|
what area of the pons does the corticospinal tracts pass through on their way down?
|
base of the pons
|
|
|
what is dysarthria?
|
speech disorder characterized by difficulty speaking properly du to paralysis of the mm of speech**
*no problem understanding speech |
|
|
do ppl with dysartria have a problem understanding speech?
|
no..it is a problem wth paralysis of the mm of speech
|
|
|
#1 area of stroke in brainstem? in what arteries?
|
lateral rostral medulla
vertebral artery PICA |
|
|
where do the vertebral arteries join to form basilar artery?
|
pontomedullary jxn
|
|
|
vertebrobasilar system supplies blood to where?
|
structures in posterior fossa (brain stem and cerebellum)
|
|
|
paired posterior cerebral arteries are located at which jxn
|
pontomesencephalic jxn
|
|
|
paired Posterior communicating arteries connect posteior circulation to wha?
|
anterior circulation
|
|
|
sup cerebellar arteries arise from where? what does it supply?
|
arises from top of basilar artery at level of rostral pons
supplies superior cerebellum an bit of rostral laterodorsal pons |
|
|
aICA arises from what? supplies what?
|
arises from basilar after vertebrals come together at level of caudal pons
supplies lateral caudal pons an a small portion of cerebellum |
|
|
pICA arises from what? supplies waht?
|
vertebral artery at level of medulla
supplies lateral medulla and inf cerebellum |
|
|
midbrain is supplied by waht?
|
PCA and penetrating branches "top of basilar artery"
|
|
|
pons is supplied by?
|
basilar artery
|
|
|
medial medulla is supplied by?
lateral medulla is supplied by? |
medial = basilar artery
lateral= vertebral artery and PICA |
|
|
lateral medulla is supplied by?
|
vertebral artery and PICA
|
|
|
an embolism in brain is often from where
|
cardiac origin
|
|
|
lacunar disease what?
|
small vssl occlusion in the setting of chronic hypertension
|
|
|
what is somnolence and what is it a warning sign of?
|
difficulty keeping pt awake
warning sign of vertebrobailar ischemia |
|
|
how will you know where the lesion is w/n the brain stem?
|
by cranial nerve symptoms
|
|
|
CN 3 and 4 symptoms will tell you the lesion is where?
|
midbrain: see eye down and out with pupil dilated
|
|
|
CN 5, 6, 7,8 symptoms will tell you the lesion is where?
|
pons
w/ 7 see 1/2 face paralyzed |
|
|
lesions in the brain stem to any of the long tracts will result in ipsi or contra BODY deficits?
|
contralateral body deficits
ipsi head deficits except: decd symp hypothalamic fibers except: cerebellar peduncle damage except: damage to CN and nuclei |
|
|
descending sympthathetic Hypothalamic fibers lesion will always result in what syndrome and on what side of body?
|
Horners ipsilateral to the side of the lesion in the brain stem
|
|
|
cerebellar peduncle damage will result in what on what side of body?
|
ipsilateral motor ataxia
|
|
|
damage to cranial nerves and nuclei will result in what on what side of body?
|
ipsilateral head sensory and/or motor devicits
|
|
|
what are the midbran signs of dysfxn?
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impaired consceiousness (can't talk)
flexor posturing (Decorticate) CN 3 palsy unilateral or bilateral pupil dilation ataxia |
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why do you see flexor posturing (decorticate) in midbrain dysfxn if the lesion is above the red nucleus?
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b/c normally the cortex inhibits the rubrospinal tract wich stimulates the flexor mm
therefore if lesion is above the red nucleus get flexor posturing |
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what is decorticate vs decerebrate posturing? which has better prognosis?
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decorticate: flexor
decerebrate: extensor posturing better prognosis with upper midbrain lesion: decorticate |
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if you lesion below the red nucleus how will pt present? what type of damage is this?
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decerebrate posturing: extensor posturing
upper pontine damage: worse prognosis |
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what are the signs of disfxn of ponse?
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impaired consciousness
decerbrate posturing-lesion below red nucleus irregular an apneustic respiration abducens palsy OR **horizontal gaze palsy (look to good side b/c PPRF damaged) bilateral small but reactive pupils b/c CN 3 ok |
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difference in pupis in midbrain damage vs pons damage
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midbrain: NO saccadic mvmt b/c lose MLF therfore also CN 3 palsy, see dilatd pupils
pontine: CN 3 ok so bilateral small but reactive pupils. see abducens palsy or horizontal gaze palsy |
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medulla signs of disfxn?
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resp arrest
vertigo ataxia nausea vomiting |
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#1 most common brain stem lesion? what is the prognosis and what is involved?
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lateral medullary syndrome (wallenburg syndrome)-rostral medulla #1 place of stroke
good prognosis lateral tegmentum involved therfore sensory not too much motor affected |
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if your inf cerebellar peduncle is damaged in lateral medullary syndrome, what features do you see clinically?
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ipsilateral ataxia
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if you vestibular nuclei is damaged in lateral medullary syndrome, what features do you see clinically?
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vertigo, nausea, nystagmus
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if you CN V (spinal trigeminal tract and nuclues) is damaged in lateral medullary syndrome, what features do you see clinically?
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ispi facial loss pain and temp
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if you nucleus ambiguus is damaged in lateral medullary syndrome, what features do you see clinically?
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hoarseness, dysphagia
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if your nuclues solitarius is damaged in lateral medullary syndrome, what features do you see clinically?
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ipsilateral decreased taste
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if you desc spinothalamic fibers is damaged in lateral medullary syndrome, what features do you see clinically?
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ipsilateral Horners
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if your spinothalmic tract (ALS system) is damaged in lateral medullary syndrome, what features do you see clinically?
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contralaeral body decreased pain and temp
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2nd most common brain stem lesion? caused by?
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medial pontine base caused by lacunar diseseas (chronic high BP)
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medial pontine base is also called? on which side is the weakness?
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ataxic hemiparesis
ataxia is same side as weakness |
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paramedian pontine base is supplied by what?
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basilar artery
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if your corticospinal tracts are damaged in a medial pontine base lesion, what clinical features will you see?
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contralateral leg, arm weakness b/c decussates in pyramid
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if your corticobulbar tracts are damaged in a medial pontine base lesion, what clinical features will you see?
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contralateral face weakness "central seven" with dysarthria (b/c CB will eventually synapse on CN7, 9, 10, 12
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if you abducens nerve are damaged in a medial pontine base lesion, what clinical features will you see?
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ipsilateral paralysis of lateral rectus b/c axons run through the lesion
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if your pontine nuclei and pontocerebellar tract are damaged in a medial pontine base lesion, what clinical features will you see?
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contralateral ataxia b/c they cross in base to head to middle cerebellar peduncle
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what is top of the basilar syndrome?
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lesion in midbrain via infarcts of PCA and vssls from the top of basilarartery
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what 3 syndroms are associated with midbrain lesion?
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Moritz Benedikt syndrome
Weber syndrome Occulomotor nerve palsy |
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what is seen in Webersyndrome?
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at level of midbrain
deveiation of eye down and out b/c damage CN 3 tract (can't keep eye open) droopinog of eyelid dilated, non responsive pupil b/c lose EW tracts to ciliary mm contralateral UMN paralysis (CS, CN damaged b/c clip some of cerebral peduncles lose motor that hasn't croseed yet) |
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what is seeen in Occulomotor nerve palsy?
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seen as CN 3 leaves midbrain
deviation of eye down and out drooping of eyelid dilated, nonresponsive pupil **infranuclear below nucleus (which is in tegmentum) |
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major cerebellar input? output?
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input: middle cereballar peduncles via mossy fibers
output: superior cereballar headed towards thalamus |
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waht are the climbing fibers?
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info from inf olivary nucleus through inf cereballar peduncles
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waht is the fxn of cerebellum?
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regulates mvmt and posture INDIRECTLY by ADJUSTING the ouput of the major descending motor systems-compares intention with performance and compensates for errors in mvmt
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what does the cerebellum correct?
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ongoing mvmts when they deviate from intended course and modifies the central program so the next mvmt can fulfill the intended goal
exerts motor control on a moment-by-moment basis** |
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lesions of the cerebellum?
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uncoordinaated and disorganized mvmts = ataxia
disrupt coordination of limb and eye mvmts decrease muscle tone and accuracy of reaching mvmts |
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cerebellum is not reqd for what?
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sensory perception
mvmt of muscles development of muscle strength |
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what happens in a pineal tumor?
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can't look up v/c no vertical or vergence mvmts
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what separates the 2 cerebellum hemispheres?
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midline vermis (worm like)- part of spinocerebellum
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what does the primary fissure divide?
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the cerebellum into an anterior and posterior lobe
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where is cerebellum?
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attached to the dorsal aspect of the pons and rostral medulla by three large peduncles
it is the roof over the 4 ventricle |
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waht makes up the spinocerebellum?
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vermis
paramedium *medial |
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what is the planning area?
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cerebrocerebellum
ex: plan how to hit ball specfically the dentate |
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what divides the posterior lobe from the flocculonodlar lobe?
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posterolateral fissure
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what can increased intracranial pressure, brain swelling, mass lesions of the cerebrum or cerebellum cause?
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cerebellar tonsils to herniate through the foramen magmun
can cause compression of the respiratory centers in the medulla and death |
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complex motor planning occurs where?
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cerebrocerebellum
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paramedian of the spinocerebellum influences waht types of motor tracts?
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lateral motor tracts (lateral corticopsinal and rubrospinal tracts), distal limb coordination (arm and leg mm, walking)
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vermis of the spinocerebellum influences waht types of motor tracts?
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medial motor tracts (V.A.R.T), proximal limb and trunk coordination
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what are the 3 cerebellum fxnl regions?
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cerebrocerebellum
spinocerebellum vestibulocerebellum |
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vestibulocerebellum is also called waht? what is its fxn?
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flocculonodular lobe
balance, posture, and VOR influences the MLF, eye mvmts, gait and posture |
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all of the output of the cerebellar cortex is transmitted by what type of cells? where are the axons of these cells going?
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purkinje cells to the deep cerebellar nuclei
axons from the purkinje cells form inhibitory synapses with the deep cerebellar nulei and vestibular nuclei |
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are deep cerebellar nuclei inhibitory or excitatory to other regions of the CNS (thalamus)?
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excitatory
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are incoming cerebellar inputs via mossy and climbing fibers excitatory or inhibitory to the deep cereballar nuclei?
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excitatory
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where are the climbing fiber cell bodies? where are the mossy fiber cell bodies?
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climbing: inf olivary nucleus (contra)
mossy: pontine nuclei (contra) |
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all OUTPUT from the cerebellum is via waht nuclei?
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Dentate
Emboliform Globose Fastidial |
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waht are the deep cerebellar nuclei from lateral to medial?
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DEGF
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what is dentate nucleus involved in? where does it receive input from?
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motor planning
receives input from cerebrocerebellum |
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when are dentate nuclei active?
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prior to a voluntary nuclei
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what are the 2 interposed nuclei of cerebellar nuclei?
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emboliform and globose
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emboliform and globose receive input form where?
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spinocerebellum (paramedian section) that is involved in the mvmt of appedages
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when are emboliform and globose active? dedate?
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during and in relation to voluntary mvmt
dentate: prior to mvmt b/c involved in planning |
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differece in input to emboliform/globose and fastidial?
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embo/globo: spinocerebellum (paramedian)
fastidial: spinocerebellum (vermis) and vesibulocerebellum |
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waht are the fastidial nuclei involved in?
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trunk coordination and proximal limb mvmt
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what do the vesibbular nuclei fxn as?
what does it receive input from? |
deep cerebellar nuclei
recive innpt from vestibulocerebellum involved in balance and VOR |
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what is known for the double cross? what does this mean?
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cerebellum
lesion L dendate see ataxia on L **ataxia always ipsilateral |
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what is in the paramedial and waht is in the vermis?
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vermis: trunk with bilateral imput from medial motor tracts (4)
paramedian: appendages with unilateral input from lateral motor tracts (2) |
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major input to the cerebellum?
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corticopontine fibers that enter the cerebelum at teh middle cerebellar peduncle and innervate the entire cerebellar cortex as mossy fibers
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what fibers are a major compoennt of the intefior cerebellar peduncle?
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climbing fibers from the inf olive
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waht are the 2 diff fibers taht are component of inf cereellar peduncle receiving input?
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climbing fibers from inf olive
vestibular fibers |
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which vesibular fibers innervate the vermis and vesibulocerebllum?
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primary and secondary
primary that go directly from scarpa's ganglion to cerebellum and secondary after the primary synpase on vestibular nuclei in pons then on cereellum |
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when will you have problems with nystagmus and balance?
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problems with cerebellum
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major output of the cerebullum is ?
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superior cerebellar peduncle
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output from dendate nucleus goes where?
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Va and Vl of thalamus and then to motor and premotor areas for motor planning
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output from ther interposed nuclei is going where?
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bringing info about appendages to lateral descending systems: lateral corticospinal and rubrospinal *unilateral
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output from fastidial nuclei is going were?
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bringing info about trunk to medial motor tracts: V,A,R,T *bilateral
and vestibular nuclei |
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input to fasidial nucleis is from?
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spinocerebellum and vesibulocerebellum
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vestibular nuclei indirect and direct output?
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direct from vestibulocerebellum
indirect from vastidial nuclei |
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what are the 3 layers of the cortex?
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molecular
purkinje granule cell |
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which cerebellar cortex layer is at the surface of the cerebellar cortex? what cell is located tehre?
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molcular layer
purkinje cell dendrites (cell bodies located in purkinje layer) granular cell axons: parallel fibers |
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how many purkinje cell bodies are there? granule cell ?
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7 million purkinje cell bodies
100 billion granule cell **most numerous |
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which neuron is hte only output cell of the cerebellar cortex?
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purkinje neuron
projects to and regulates the actvity of deep cerebellar nuclei and vestibular nuclei inhibitory neuron (GABA) |
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which fiber produces a complex calcium spike and what doest this mean
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climbing fiber from inf olivary nucleus
complex calcium spike forming nuclei in purkinje cell Glu released from climbing fiber opens v-gated Ca channels on Purkinje cell |
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how fast is the comple calcium spike
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1/sec from climbing fiber on purkinje cell
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is spatial or temporal summation seen with climbing fibers? how many synapses occur?
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spatial summation
multisynaptic contact (2-3thousand exciaatory synapses ) of the single climbing fiber (homosynaptic) with its target purkinje cell |
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how many climbing fibers /purkinje cell?
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1:1
one of the most powerful ecitatory synapses in CNs EPSP generated by the climbing fiber always stimulates a comlex AP in the purkinje cell |
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do climbing fibers fire at a high or low freq on purkinje?
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low and produce 1-2 COMPLEX spikes/sec on purkinje cells
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what happens if at the same time on the same purkinje cell a parallel fiber and climbing fire release NT?
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the response of the parallel is weakened b/c the climbing fibers modify th response of purkinje fibers to parallel f iber input
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what type of firing on purkinje cells do parralel fiber have?
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simple spike 50/sec
open Na channels (climbing fibers opened Ca channels) |
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what is the ratio of parrallel fiber synapse to purkinje synapses?
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200,000 parrel: 1 purkinje but not all firing at same time
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do you have temporal or spatial summation with parrel fibers?
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both of smaller EPSPs to produce a single AP in a purkinje cell
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what is the avg number of AP in a purkinje cell?
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51: climbing fibers:1 and parrell:50
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how are climbing fibers involved in memory?
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they can produce long term depression in the efficacy (strenth) of selected parallel fiber synapses-a form of motor memory
but only those parallel fiber synapses firing simultaneoulsy with the climbing fibers will show LTD |
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when when you see LTD?
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with only those parallel fiber synapses firing simultaneously with the climbing fiber firing
parallel fiber synapses will display a deprssed (smaller) epsp for up to one hour following a paired firing of the synapse with a climbing fiber firing |
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what type of channels open when the purkinje cells are depolarizd?
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Ca: the rise in Ca in the purkinge causes an increase in pKC and further release of stored Ca
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when parallel fibers are firing what types of channels are on teh postsynaptic/purkinje cell?
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direct (AMPA-non-NMDA) and indirect metabotropic glutamate R's
AMPA allow Na in to furhter depol cel mGluR allow a rise in intracellular 2nd messengers which release Ca and activate PKC |
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what happens during the learning process to the number of complx and simple spikes?
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nmber of complex spikes increases as teh task is learned the number of complex spikes returns to normal
however, DURING the learning process the number of simple spkes gradually decreases and remains depressed even after the task is learned and the nubmer of comlex spkes has returned to normal |
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what happens to the inhibition of deep cerebellar nuclei with learning?
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before learning: increased AP from purkinje = inhibition of deep cerebellar nuclei
after learning: decreased AP from purkinje therefore less inhibition of deep cerebellar nuclei and more info reaches the Va and Vl of thalamus |
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how are cerebellar circuits modified?
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by expereience=learning
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during learning how does the ratio of complex spikes to simple change?
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increase in complex
decrease in simple |
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ataxia is ipsi or contra to side of the lesion?
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ipsi
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midline lesions of vermis of flocculonodular/vesibular lobes cause what?
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unsteady gait (truncal ataxia)
eye mvmt abnormalities accompanied by intense vertigo and nausea and vomiting which is a medical emergency becae could be due to severe hemorrhage that is pushing down on tonsils |
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how do you determine if someone has a midline vermis lesion?
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Romberg test: have them close their eyes, stand still. if they rock back and forth there is damage
trunk will be reeling from side to side stands on wide base t try to balance |
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lateral lesions of the cerebellum (paramedian) cause?
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unsteeady limb mvmts (appedndicular ataxia)
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how to you test for a paramedian cerebellum lesion?
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b/c lateral lesion test for:
action or intention tremor (try to touch finger than nose)--will see ipsi ataxia asynergia (unsmooth) dysmetria (can't measure distance) dysrhtymia (cant clap followng rythm) dysdiadochokinesia (rapid alternating mvmts) |
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mammary body is impt for?
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memory
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what makes up the diencephalon?
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epithalamus
thalamus hypothalamus |
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waht is the fluid in the thalamus?
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3rd ventricle-CSF
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what iscontained in epithalamus?
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pineal body
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waht is thalamus bounded by?
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relay nuclei
bounded by ant and post commissures |
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what is hypothalamus for
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autonomic, endocrine, homeostasis, limbic system (emotions)
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