Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

441 Cards in this Set

  • Front
  • Back
what system senses the dynamic forces of angular and linear accelerantions as well as the static force of gravity maintain body equilibrium?
vestibular system
what are vestibulo spinal reflexes?
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)
what are vestibulo ocular reflexes?
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)
what does the CNS register if both the right and left afferent firing rates are equal?
that the head is NOT moving-the head and body are stable and NO motor compensatory balance or eye reflexes are needed
what does the CNS register when the right and left afferent VIII firing rates are NOT equl?
that the head is moving
lower firing rate = head deflection
what problems will you have if you damage the vestibular system?
problems with eye movements and balance
waht is vertigo? what is it not?
illusion of motion (you or the world is spinning)
NOT dizziness: due to low BP
what is Nystagmus?
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
what induces Nystagmus in normal individuals? when does it become pathological?
rotation, visual or caloric stimulation
*pathological if occurs spontaneously or is sustained?
what CNs are associated with the Telencephalon?
1 and 2
what CNs are associated with the midbrain?
3 and 4
what CNs are associated with pons?
5, 6, 7, 8
what CN's are associated with medulla? cervical?
medulla: 9, 10, 12
cervical: 11
what is the fxnl unit of vestibular system?
hair cells: neuroepithelial cells
what do the vestibular hair cells release and how often?
excitatory transmitter (Glu) tonically so the afferent fiber on which it synpases has a steady, TONIC resting discharge rate
how are the vestibular hair cells polarized?
large kinocilium on edge of cell
sterocilia get progressively shorter with distance from the kinocilia
where are the cell bodies for CNVIII in vestibular system?
scarpa's ganglion
bending sterocilia TOWARDS the kinocilium causes?
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
when do hair cells have an AP?
never hve AP
bending sterocilia away from the kinocilium causes?
decreased number of open transdxn channels
hyperpol of hair cell b/c K, Ca current decreases
decreaed transmitter release
decreased afferent nerve firing
perilymph consists of what? what is it similar to?
extracellular fluid, Low K, high Na
surrounds the membranous labyrinth
waht makes up endolymph?
extracellular fluid that is similar to an intracellular fluid with ionic concentrations: high K, low Na
in the vestibular system, where wuould you find endolymph? perilymph?
endolymph: w/n membranous labyrinth
perilymph: surrouds the membranous labyrinth
overprdxn of endolymph causes?
Menier's syndrome: high fluid pressure w/n membranous labyrinth
what do you call the voltage w/n endolymph?
transepithelial voltage (endocochlear potential = +80mV
compare the transbasolateral vltage with the transapical voltage?
transbasolateral mem voltage = -60mv
transapical mem voltage = -140mV
the motion of hair cells sterocilia causes K to move along waht type of gradient?
electrical gradient, NOT a concentration gradient
what makes up the vestibular labyrinth system?
2 components: macula and crista ampularries (ampula)
where are neuroepithelial cells located in the vestibular labyrinth system?
the ampulla: swellings of semicircular canals
what are Otolith organs (ear stones)?
4 areas of neuroepi (sensory epi) in the membranous labyrinth called macula (2 macula/inner ear)
how many macula are there in the inner ear?
2 macula/inner ear
what is the fxn of the macula?
detect linear forces caused by static displacement (nm) due to gravity
or transient displacment (nm/s2) due to linear acceleration or deceleration
what are the 3 planes that linear mvmt can move in?
X axis: forward and backward
Y axis: left and right
Z axis: up and down
what are the "bags" of endolymph?
utricle and saccule
how many semicircular canals are there per inner ear? names of them?
3: posterior, anterior, horizontal
what is the dynamic signal for otolith organs? static signal?
dynamic: linear acceleration
static: steady tilt of the head/gravity
what are otoliths?
calcium carbonate particles
waht rests upon gelatinous mass overlying the hair cells and have a higher specific gravity than that of the surrounding endolymph?
calcium carbonate
therefore they exhibit inertial delay with head motion
what does no affect the otolith organs?
angular acclearations b/c they don't protrude substantially into the lumen of the membranous labyrinth
how are hair cells oriented in the macula? why?
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
macula in the saccule detects linear changes in what plane?
vertical plane: upward and downward along Z axis
macula in utricle detect linear changes in what plane?
foward and backward along the X axis as well as side to side along the Y axis
riding in a car
head tilt
what is the fxn of semicircular canals/ampulla?
detect angular (rotational) accleration or decelerations as small as 0.1 degree/s2 in three planes: horizontal, vertical, and lateral simultaneously
why is CONSTANT angular velocity not an apporpriate stimulus for the ampulla?
b/c fluid and crista eventually rotate at the same velocity
brain won't think you are turning when steady..need acceleration
how do the 3 planes match the 3 semicircular canals?
lateral: horizontal
anterior: vertical
posterior: vertical
what are the 3 degrees of rotational freedom?
they refer to the body's rotation relative to the x, y, z axes are are commonly referred to as roll, pitch, and yaw
what is yaw? roll? pitch?
yaw: rotation around the z axis
pitch: rotation around y axis
roll: rotation around x axis
what position does flexing the head 30 degrees put the lateral canals in?
horizontal position (parellel with the horizon)
how are the kinocilium organized in the horizontal semicircular canals?
with the kinocilium more medial (closest to utricle)
yaw is associated with which of the semicircular canals?
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?
if you turn head L, what direction does the endolymph go in?
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)
which hair cells will repond to acceleration or deceleration forces?
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
in the horizontal ampulla, the cilia are oriented how?
toward the utricle ( in the other ampulla: oriented away from the utricle)
if you are moving yaw left, what horizontal canals will you be stimulating?
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
what is the fxn of VOR?
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
what is the VOR system insensitive to?
slow mvmts or perisitant rotaion of the head (if continous rotation, you will see compensatory eye mvmt stop after 30 s of rotation)
if you move your head to the left, what direction will your eyes go to and how?
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
head goes to side with ____ AP
eyes go to side with ____ AP
head: higher
eyes : lower
how long is the latency from the stimulus till the onset of eye mvmt?
12 miliseconds
no time for long neuronal mulisyanptic mvmts
no afferent info sent to coritcal nuerons for this reflex
target pursuit latency: 125ms
how long is target pursuit latency?
how fast can your eyes mov/sec? how long to target pursuit velocity?
300 degrees eye mvmt/sec
target pursuit: 100 degrees/sec
to accurately identify (ex eagle) = 30degres/sec
what are the results of caloric testing in normal individual?
warm water induces nystagmus that beats towards the warm ear
cold water induces nystagmus that beats away from cold ear
Cold opp the fast mvmt
Warm same side
in which direction will the eyes go if you place cold water in teh L ear?
they will go to the opposite side Fast
in which direction will the eyes go if you put warm water in the L ear?
they will go fast towards the same side
in a unilateral lesion in the vestibular pathway, on which side will nystagmus be reduced or absent?
on the side of the lesion
look away from the lesion
what is rotational testing?
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
what happens when you stop spinning someone in the Barany chair?
the nystagmus wil stop in 30 sec as head semicular canals, and endolymph are all moving at the same velocity
what happens in rotational testing if the lights are on and the subject can see the environment?
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
what happens in rotational testing when you stop the chair suddenly?
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
waht is the most common vestibular disorder?
benign positional vertigo
otoconia displaced from utricle macula becomes lodged in cupula of the post canal (cupulolithiasis)
what is the causes of benign positional vertigo?
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
what is Labyrinthine Disease?
seasickness, space sickness
pt says world is spinning
objective signs: nystagmus, falling or postural deviation, sweating, vomiting, hypotension

subjective symptoms: vertigo, nausea, oscillopsia, anxiety
what is acute peripheral vestibulopathy?
spontaneous attack of vertigo of unapparent cause
includes acute laybrinthitis
and vestibular neuronitis
what is the affect of ototoxic drugs like the aminoglycoside gentamycin?
cuase ATN and lose hair cells
ex: pt reading and eyes jumped off page with heartbeats
what is happening in the resting primary gaze?
all mm balanced
if you lesion the MR, where will you look?
what is the primary movment of SO? 2ndary?
primary: intorsion=uppar pole of eye moves inward
secondary: depression
where are the eye mvmt control centers located?
supranuclear regulation of eye mvmts found in brainstem, cerebellum, and forebrain including BG
what are the 2 areas controled by the pons in terms of eye mvmts?
abducens nucleus and paramedian pontine reticular formation (PPRF)
pons is the ____ eye mvmt control center?
what does the abducens nucleas control?
horizontal gaze center as it controls ipsilateral LR and contralateral MR
what provides the interconnection b/n the occulomotor, trochlear, abducens, and vestibular nuclei?
medial longitudinal fasciculus (MLF)
waht is the job of the paramedian pontine reticular formation (PPRF?
provides output to the abducens from higher cortical eye mvmt control centers
lesion of the PPRF or abducens nucleus will cause waht?
ipsilateral horizontal gaze palsy (look to the R , but eyes should look R) this is a problem with moving BOTH eyes in directed gaze
what is located in the tegmentum (2)?
1. CN 3 cell bodies
2. reticular formation of CN 5 and 7
if you quickly wipe cotton across the cornea what happens?
blink bc of sensory 5 and motor 7 *corneal reflex
if someone is going to poke you in the eyes, what happens, what CN are invovled?
Blink to Threat
sensory 2
motor 7
demyelination of MLF results in what?
female presents with complaint the L eye won't go R
midbrain is in control of what eye control centers?
vertical and vergence eye mvmts
controls the SR and IR mm and the IO and SO
the dorsal rostral midbrain reticular formation controls waht type of gaze? ventral?
dorsal: upward gaze
ventral: downward gaze
vertical eye mvmts are intitiated where?
in the rostral midbrain reticular formation and pretectal area
vergence eye mvmts are initiated where?
in the midbrain reticular formation controling convergence MR mm and divergence LR mm
what are the jobs of the frontal eye fields?
stimulate the contralateral PPRF and generate conjugate eye mvmts (saccades) to the contralateral side
what are teh 2 forebrain centers that control eye mvmts?
frontal eye fields
parieto-occipital-temporal cortex
lesion of the frontal eye field causes waht?
both eyes to gaze toward the lesioned side
waht is the fxn of the PTO: parieto-occipito temporal cortex?
stimulates smooth pursuit eye mvmts in the ipsilateral direction
if you stimulate the L frontal eye field where do eyes go?
to the contralateral side: R unless lesion in which they gaze towards lesion
in stroke pts what direction do their eyes look?
eyes deviated to 1 side: lesioned side
away from the paralysis which affects contralateral side
fxn of optokinetic eye mvmts?
to hold the images of the seen world steady on the retina during sustained head rotation or moving environement
fxn of smooth pursuit?
to hold the image of a moving target on the fovea
fxn of nystagmus quick phases?
to direct the fovea toward the oncoming visual scene during self rotation, to reset the eyes during prolonged rotation
fxn of saccades?
to bring images of objects of interest onto the fovea
fxn of vergence?
to move the eys in opp directions so that the images of a single object are placed on both foveas
what are the 2 orbital mechanics needed to overcome the viscous drag and elastic restoring forces of the orbital supporting tissues?
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
what is the fastest of the eye mvts has how fast are tehy?
peak velocity of 700degrees/sec
which eye mvmts are ballistic and what does this mean?
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
which eye mvmts allow us to rapidly redirect our line of sigh?
saccadic: notes to clock (don't register anything you see in b/n the notes and the clock)
what is the length of time that it takes b/n when you see the target of interst and why you move your eyes?
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
why do we need smooth pursuit mvts?
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
what isthe catch up saccade?
the time it takes to track the object of interest with a smooth pursuit
what happens to smooth pursuit in a pt with cerebellar disease?
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
compare visual acuity in saccadic vs smooth pursuit?
saccadic: poor
smooth: excellent
is a target reqd for smooth and saccadic eye mvmts?
only smooth
what do vergence eye mvmts do?
align the fovea of each eye with targets located at different distances from the observer
waht is the only type of eye mvmts that causes the eye to move in opposite directions?
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
waht is the near reflex triad?
constriction of pupil
what are the 3 types of eye mvmts?
smooth pursuit
what 2 systems operate together to hold images stable on the retina?
vestibular and optokinetic
what does the VOR compensate for?
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
when is the vestibular system ineffective?
with steady continuous rotations as the compensatory eye mvmts cease after 30sec
what is the eye position in space when the head is rapidly turned to the left?
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
when is the optokinetic system used?
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
what is railroad nystagmus?
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
how is the optokinetic system a back up to the VOR ?
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
in railroad nystagmus or striped drum movment, in which direction are the eyes going as the drum turns?
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
how are descending motor pathways divided up?
lateral and motor based on spinal cord location
where do lateral motor systems travel?
in the lateral columns of the spinal cord white matter
axons terminate on lateral groups of ventral horn motor neurons and interneurnes
what do the lateral motor systems control?
mvmts of extremities (distal mm) arms, legs, feet, hands
what ae the 2 tracts of the lateral motor system?
lateral corticospinal tract
rubrospinal tract
what is clinically the most impt lateral motor system path?
lateral corticospinal tract
where is the rubrospinal tract and what does it do?
red nucleus in the midbrain (mickey eyes)
increases flexor tone in the upper extremities
both lateral motor tracts provide for?
rapid, dexterous mvmts at individual joints or digits
is it worse to knock out the desc lateral motor system or medial?
lateral b/c it is only ipsilateral while the medial is bilateral
with desc lateral get weakness in hands and hyperreflexia
why do you clinically not need to worry about trunk paralysisi?
b/c it has bilateral input
where do the medial motor systems travel in the spinal cord?
anteromedial columns of the spinal cord
waht do the medial motor pathways contrl?
mvmts of the trunk (axial and girdle mm)
they are involved in postural tone, balance, orienting mvmts of the head and neck, automatic gait
do the medial motor systems decussate?
no they descend laterally and terminate on interneurons
which motor system influences axial musculature bilaterally?
medial motor systems
what are the 4 tracts in the medial motor system?
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
what are the vesibulospinal tracts?
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
how many reticulospnal tracts are there and what do they do?
2: part of medial motor system
one originates in pontine reticular formataion=medial reticulospinal tract
other originates in the medullary reticular formation=lateral
fxn of tectospinal tract?
one of the 4 medial motor tracts
provides coordination of head and eye mvmts
caudate + putamen =
incoming thalamus goes to waht layer?
outgoing thalamus goes ?
incoming: layer 4
outgoing: layer 5
waht carries the homunculus descending UMN axons?
internal capsule: posterior limb
what perent of the descending lateral corticopsinal pathway decussates?
90% *make up lateral-hands
10% stay medial to do bilateral innervation of trunk
what does paresis mean?
weakness (partial paralysis)
ex: hemiparaesis
clinical symptoms: weakness of one side of the body
what does -plegia mean?
no mvmts
ex: hemiplegia
no mmvt on one side of the body
what does paralysis mean?
no mvmt
ex: leg paralysis
no mvmt in leg
what do Hemi-, Para-, Mono, Di- mean
Hemi: one side of the body
para: both legs (paraparesis)
Mono- one limb
Di- both sides of the body eqully affected
hemisection of the spinal cord can cause what?
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
what happens in an anterior spinal artery occulusion?
no pain and temp below the lesion bilaterlaly
damage to the anterolateral pathways and ventral horn cells
if you have doral spinal artery occulusion, waht do you lose?
fine touch, proprioception
what vitamin is reqd for myelin formation?
B12-causes pernicious anemia
Vitamin B12 neuropathy?
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
poliomyelitis damages what?
alpha motor neurons in spinal cord due to infectous myelitis like viruses
MS affects what portions of spinal cord?
dorsal columns
waht is Guillian Barre syndrome?
acute inflammatory demyelinating polyneuropathy thatis an immune mediated demylination of peripheral neves
tectum is composed of?
superior and inferior colliculi which lie dorsal to the cerebral aquaduct
tegmentum lies ventral to what?
ventral to the aquaduct (midbrain) and ventral to the 4th ventricle in the pons and medulla
the brain stem tegmentum is the location of what?
the main bulk of the brain stem nuclei and the reticular formation
where are the main bulk of brain stem nuclei and the reticular formation located
what is located in the base of midbrain?
corticopsinal tract, corticobulbar, corticopontine
what are the 3 CN that are NOT associated with the brain stem?
CNI and II (forebrain)
CN XI: cervical spinal cord
what are the 2 cn associated with the midbrain?
III and IV
what are the 4 CN associated with the pons?
what are the 3 CN associated with the medulla?
9 and 10 think autonomic PNS
3 sensory CN:
5 motor CN:
4 mixed CN?
sensory: 1,2,8
motor: 3,4,6,11,12
mixed: 5,7,9,10
what are the CNs associated with the PNS?
3,7,9,10 the PNS pregan neuron is cell body is located in specific brain stem nuclei
nucleus for CN3?
EW nuclus in midbrain
nuclues for CN7?
Superior Salivatory nucleus (ponse)
Nucleus for CN9?
Inverior Salivatory nucleus (medulla)
Nuclus for CN10?
Dorsal motor nucleus of 10 (medulla)
the CNs associated with the PNS have postgang neurons that innervate what?
glands, smooth muscle, cardiac
where are the postgang PNS neuron cell bodies for CNIII?
ciliary ganglion-axons project to the eye ciliary muscle and constrictor (sphincor) mm of the iris
PNS pre and post gang cell bodies for CN III?
pre: EW nucleus (midbrain)
post: ciliary ganglion
PNS Pre and post gang cell bodies for CN7?
pre: superior salivatory nucleus (pons)
post: sphenopalatine ganglion (lacrimal glands and nasal mucosa)-cries, mucus
submandibular ganglion (submaxillary salivary glands)spits
PNS pre and post gang cell bodies for CN 9
pre: inferior salivatory nuclues (medulla)
post: otic ganglion (paratid gland)
PNS pre and post gang cell bodies for CN10?
pre: Dorsal motor nuclues of X (medulla)
post: various terminal ganglia (project to effector organs)
does the descending tract from the hypothal that is going to innervate the pregang SNS neurons decussate?
all the SNS pregang cell bodies are located where?
in the IML of T1-L3
the SNS pregan innervating the head are found in the IML of ?
the SNS postgang cell bodies lie where?
superior cervical ganglion
a lesion of the sympathetic pathway to the head will cause?
ipsilateral Horner's syndrome b/c desc tract from hypothal does not cross the midline
what are the classic signs of Horners?
Miosis: decreased pupil size (dilator not innervated)
Ptosis: drooping eyelid (smooth muscle not innervated)
Anhidrosis: lack of sweating onth face and neck
mvmt disorders think?
basal ganglai
ataxia think?
classic slow mvmt disorders? fast?
slow: Parkinsons
fast: Huntington's
what are these symtpoms of: micrographic writing, decrease facial expression, resting tremor, hoarsness, drooling b/c lack automatic mvmts like swallowing
are myoclonic mvmts due to basal ganglia what are some examples?
no, they are cortical problems
hiccup, jerk when falling asleep, startle response
HD is a problem with?
caudate nucleus
dystonia/wilsons is a problem with?
carbon monoxide is a problem with?
globus pallidus
hemiballismus is a problem with?
subthalamic nucleus
PD is a problem with
substantia nigra
clinically the BG refers to?
Caudate nucleus
Globus pallidus
Subthalamic nucleus
Substantia nigra
what lights up in ppl assumed to be in a coma when you tell them to imagine climbing a flight of steps?
supplementary motor area (SMA)
what makes up the striatum? what does each do? how are they similar?
caudate and putamen
putamen: motor control
caudate: cognitive/behavioral control, eye mvmts
similar histologically
what makes up the lentiform nucleus?
putamen and globus pallidus
what makes up the corpus striatum?
caudate, putamen, globus pallidus
is the putamen medial or lateral?
what will you see in a CAT scan of HD pt?
caudate nucleus atrophy
entire brain shrinks
what is the mxn of wilsons disease?
chew up putamen bc Cu deposited here 1st
metabolic lesions cause?
symmetrical lesions
what are the components of substantia nigra?
pars compacta: dorsal
pars reticulata
where neurons that die in Parkinson's and therefore lose their black color?
pars compacta
what structure is lens shpaed?
subthalamic nucleus
lesions in subthalamic nucleus have contr or ipsi problems? cerebellum?
contralateral: subthalamic
ipsilateral: cerebellum
what is the ouput center of the BG?
what are the 3 excitatory pathways in the motor loop?
cortex to striatum
subthalamic nucleus to Gpi
thalamus to cortex
in the motor pathway, what is the inhibititory NT? Excitatory?
inhibitory: GABA
excitatory: glutamate
what is the indirect motor pathway?
cortex to striatum, stiatrum to Gpe, Gpe to STN, STN to Gpi, Gpi to thalamus, thalamus back to cortex
are parkinsons, chorea, ballismic mts, dystonia hyperkinetic or hypokinetic?
hyperkinetic: chorea, ballismus, dystonia
hypokinetic: parkinsonism
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
what is the actvity level of Gpi in hyperkinetic mvmts
underactivity thus Gpi doesn't inhibit thalamus as much and thus thalamus excites cortex resulting in extra mvms
substantia nigra projects to where?
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
what are the main clincal features of PD?
resting tremor
postrural instability
neurochemical abnormality in PD?
dopamine deficiency: loss of dopamine produceing cells in substantia nigra
remaining neurons contain lewy bodies (cytoplasmic inclusions)
what are lewy bodies?
cytoplasmic inclusions that are w/n the remaining neurons in PD pts
what happens if you give a PD pt too much dopamine?
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
what is the rate limiting step in the prodxn of dopamin? prodxn of what depends on this enzyme?
tyrosine hydroxyase
what does carbidopa inhibit?
aromatic amino acid decarboxylase
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
what is sinemet and what do the 2 numbers mean?
sinemet is given for PD pts
what are the 2 ways in which to treat PD?
increase dopamine or decrease Ach
dopamine is brkn down by?
MAO-B and COMT into DOPAC and HVA
COMT causes breakdown of waht?
breakdown of dopamine to HVA and DOPAC
also converts L-Dopa to 3-OMD (worthless product)
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
what are the classes of drugs that Tx PD?
increase dopamine activity
anticholinergic agens
anticholinergic agents are cheap but not the best...many side effects
as PD progresses, what clinical problems develop?
depression 50%
dementia 25%
psychosis 25% (visual hallucinations and delusions)
chorea(dyskinesia) 70%
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
what percent of PD is genetic? what is the inheritance of most?
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
what is the def of dystonia?
repetitive, stereotyped involuntary mvmts that can be twisting, writhing, or jerking but can also be fixed abnormal postures
dystonia is caused by lesions in the what?
when would you have a right hemidystonia?
left lesion in putamen
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)
oromandibular dystonia
spasmodic dysphonia (whispering, can't project voice)
writer's cramp
what is a generalized dystonia and when do they begin?
affects entire body
onset in childhood
caused by genetic disorders such as DYT1 gene mutations of the torsin protein
what causes generalized dystonia?
DYT1 mutations of the torsin protein
Tx for generalized dystonia?
silencing RNA to stop abnormal genes from expressing (DYT1 mtations of the torsin protein)
what is hemiballismus?
large amplitude throwing, ballistic mmvts on one side of the body (if on R, then lesion on L)
what causes hemiballismus?
lesion in subthalamic nucleus
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
inheritance of HD?
AD, 50% for each child of inheriting disease
what is the chance of suicide in HD pts?
10-15% risk of suicide: can't work, can't multitask, irritable, difficulty sleeping, bipolar
what are the motor disorders associated with HD?
dysphagia (diffculty swallowing)
dysarthria (slurred speech)
abnormal eye mvmts
inability to maintain muscle contraction
poor coordination
who is HD often transmitted by? what is the repeat expansion?
anticipation with paternal expansion of CAG repeats >40 repeats
what are the treatable symptoms of HD?
chorea (with neuroleptics)
what are neuroleptics?
drugs that block dopamine r's
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
what is the cause of tardive dyskinesia
iatrogenic: Tx with neuroleptics
possibly caused by striatal dopamine R supersensitvity
what are tics and kinds can you have?
intermittent sterotyped mvmts and sounds: motor (touch things or vocal (golden retriever, retriever, retriever)
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
besides the pharmaceutical problems, what can treat tics, PD, dyskineisa?
smoking pot b/c THC like and binds to carmabinoid R's
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
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
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
with INO the eye with the lesioned side cannot what?
with an INO can you still accomodate?
yes because nothing is wrong with endinger westphal nucleus
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
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
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
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
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
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
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
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
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
every crosssection of th brainstem will include what cN?
CN5: see projectory neuron for CNV
Nucleus solitarious includes what CN? which are rostral/caudal?
rostral: 7,9,10 taste
caudal: 9,10 ANS sensory
what is the level of the superior colliculus and CN3?
rostral midbrain
what is the level of genu of CN7
caudal pons
what is the level of teh inferior olivary nucleus and CN12
rostral medulla
what is the level of the internal arcuate fibers?
caudal medulla
what is the level of the pyrimadal tract decussation
spinomedullary jxn
when the butterfly is down in rostral medualla section are we ventral or dorsal?
what portion of brainstem contains the autonomic centers for respiratory, cardio, and GI control?
where do the nerve fibers for CN12 exit?
in rostral medulla b/n inferior olive and the corticospinal tract
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
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
what impt landmark will you see in spinomedullary jxn cross-section?
pyramidal decussation of corticospinal tract neruon axons
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
pyramids in cuadal medulla contain corticospinal tract motor neuron axons from what side of the cortex?
ispsilateral..cross over at spinomedullay jxn
which of the neurons from nucleus cuneatus crosses the midline?
2ndary projection neuron
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?
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?
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? is a problem wth paralysis of the mm of speech
#1 area of stroke in brainstem? in what arteries?
lateral rostral medulla
vertebral artery
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?
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?
impaired consceiousness (can't talk)
flexor posturing (Decorticate)
CN 3 palsy
unilateral or bilateral pupil dilation ataxia
why do you see flexor posturing (decorticate) in midbrain dysfxn if the lesion is above the red nucleus?
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
what is decorticate vs decerebrate posturing? which has better prognosis?
decorticate: flexor
decerebrate: extensor posturing
better prognosis with upper midbrain lesion: decorticate
if you lesion below the red nucleus how will pt present? what type of damage is this?
decerebrate posturing: extensor posturing
upper pontine damage: worse prognosis
what are the signs of disfxn of ponse?
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
difference in pupis in midbrain damage vs pons damage
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
medulla signs of disfxn?
resp arrest
#1 most common brain stem lesion? what is the prognosis and what is involved?
lateral medullary syndrome (wallenburg syndrome)-rostral medulla #1 place of stroke
good prognosis
lateral tegmentum involved therfore sensory
not too much motor affected
if your inf cerebellar peduncle is damaged in lateral medullary syndrome, what features do you see clinically?
ipsilateral ataxia
if you vestibular nuclei is damaged in lateral medullary syndrome, what features do you see clinically?
vertigo, nausea, nystagmus
if you CN V (spinal trigeminal tract and nuclues) is damaged in lateral medullary syndrome, what features do you see clinically?
ispi facial loss pain and temp
if you nucleus ambiguus is damaged in lateral medullary syndrome, what features do you see clinically?
hoarseness, dysphagia
if your nuclues solitarius is damaged in lateral medullary syndrome, what features do you see clinically?
ipsilateral decreased taste
if you desc spinothalamic fibers is damaged in lateral medullary syndrome, what features do you see clinically?
ipsilateral Horners
if your spinothalmic tract (ALS system) is damaged in lateral medullary syndrome, what features do you see clinically?
contralaeral body decreased pain and temp
2nd most common brain stem lesion? caused by?
medial pontine base caused by lacunar diseseas (chronic high BP)
medial pontine base is also called? on which side is the weakness?
ataxic hemiparesis
ataxia is same side as weakness
paramedian pontine base is supplied by what?
basilar artery
if your corticospinal tracts are damaged in a medial pontine base lesion, what clinical features will you see?
contralateral leg, arm weakness b/c decussates in pyramid
if your corticobulbar tracts are damaged in a medial pontine base lesion, what clinical features will you see?
contralateral face weakness "central seven" with dysarthria (b/c CB will eventually synapse on CN7, 9, 10, 12
if you abducens nerve are damaged in a medial pontine base lesion, what clinical features will you see?
ipsilateral paralysis of lateral rectus b/c axons run through the lesion
if your pontine nuclei and pontocerebellar tract are damaged in a medial pontine base lesion, what clinical features will you see?
contralateral ataxia b/c they cross in base to head to middle cerebellar peduncle
what is top of the basilar syndrome?
lesion in midbrain via infarcts of PCA and vssls from the top of basilarartery
what 3 syndroms are associated with midbrain lesion?
Moritz Benedikt syndrome
Weber syndrome
Occulomotor nerve palsy
what is seen in Webersyndrome?
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)
what is seeen in Occulomotor nerve palsy?
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)
major cerebellar input? output?
input: middle cereballar peduncles via mossy fibers
output: superior cereballar headed towards thalamus
waht are the climbing fibers?
info from inf olivary nucleus through inf cereballar peduncles
waht is the fxn of cerebellum?
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
what does the cerebellum correct?
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**
lesions of the cerebellum?
uncoordinaated and disorganized mvmts = ataxia
disrupt coordination of limb and eye mvmts
decrease muscle tone and accuracy of reaching mvmts
cerebellum is not reqd for what?
sensory perception
mvmt of muscles
development of muscle strength
what happens in a pineal tumor?
can't look up v/c no vertical or vergence mvmts
what separates the 2 cerebellum hemispheres?
midline vermis (worm like)- part of spinocerebellum
what does the primary fissure divide?
the cerebellum into an anterior and posterior lobe
where is cerebellum?
attached to the dorsal aspect of the pons and rostral medulla by three large peduncles
it is the roof over the 4 ventricle
waht makes up the spinocerebellum?
what is the planning area?
ex: plan how to hit ball
specfically the dentate
what divides the posterior lobe from the flocculonodlar lobe?
posterolateral fissure
what can increased intracranial pressure, brain swelling, mass lesions of the cerebrum or cerebellum cause?
cerebellar tonsils to herniate through the foramen magmun
can cause compression of the respiratory centers in the medulla and death
complex motor planning occurs where?
paramedian of the spinocerebellum influences waht types of motor tracts?
lateral motor tracts (lateral corticopsinal and rubrospinal tracts), distal limb coordination (arm and leg mm, walking)
vermis of the spinocerebellum influences waht types of motor tracts?
medial motor tracts (V.A.R.T), proximal limb and trunk coordination
what are the 3 cerebellum fxnl regions?
vestibulocerebellum is also called waht? what is its fxn?
flocculonodular lobe
balance, posture, and VOR
influences the MLF, eye mvmts, gait and posture
all of the output of the cerebellar cortex is transmitted by what type of cells? where are the axons of these cells going?
purkinje cells to the deep cerebellar nuclei
axons from the purkinje cells form inhibitory synapses with the deep cerebellar nulei and vestibular nuclei
are deep cerebellar nuclei inhibitory or excitatory to other regions of the CNS (thalamus)?
are incoming cerebellar inputs via mossy and climbing fibers excitatory or inhibitory to the deep cereballar nuclei?
where are the climbing fiber cell bodies? where are the mossy fiber cell bodies?
climbing: inf olivary nucleus (contra)
mossy: pontine nuclei (contra)
all OUTPUT from the cerebellum is via waht nuclei?
waht are the deep cerebellar nuclei from lateral to medial?
what is dentate nucleus involved in? where does it receive input from?
motor planning
receives input from cerebrocerebellum
when are dentate nuclei active?
prior to a voluntary nuclei
what are the 2 interposed nuclei of cerebellar nuclei?
emboliform and globose
emboliform and globose receive input form where?
spinocerebellum (paramedian section) that is involved in the mvmt of appedages
when are emboliform and globose active? dedate?
during and in relation to voluntary mvmt
dentate: prior to mvmt b/c involved in planning
differece in input to emboliform/globose and fastidial?
embo/globo: spinocerebellum (paramedian)
fastidial: spinocerebellum (vermis) and vesibulocerebellum
waht are the fastidial nuclei involved in?
trunk coordination and proximal limb mvmt
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
what is known for the double cross? what does this mean?
lesion L dendate see ataxia on L
**ataxia always ipsilateral
what is in the paramedial and waht is in the vermis?
vermis: trunk with bilateral imput from medial motor tracts (4)
paramedian: appendages with unilateral input from lateral motor tracts (2)
major input to the cerebellum?
corticopontine fibers that enter the cerebelum at teh middle cerebellar peduncle and innervate the entire cerebellar cortex as mossy fibers
what fibers are a major compoennt of the intefior cerebellar peduncle?
climbing fibers from the inf olive
waht are the 2 diff fibers taht are component of inf cereellar peduncle receiving input?
climbing fibers from inf olive
vestibular fibers
which vesibular fibers innervate the vermis and vesibulocerebllum?
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
when will you have problems with nystagmus and balance?
problems with cerebellum
major output of the cerebullum is ?
superior cerebellar peduncle
output from dendate nucleus goes where?
Va and Vl of thalamus and then to motor and premotor areas for motor planning
output from ther interposed nuclei is going where?
bringing info about appendages to lateral descending systems: lateral corticospinal and rubrospinal *unilateral
output from fastidial nuclei is going were?
bringing info about trunk to medial motor tracts: V,A,R,T *bilateral
vestibular nuclei
input to fasidial nucleis is from?
spinocerebellum and vesibulocerebellum
vestibular nuclei indirect and direct output?
direct from vestibulocerebellum
indirect from vastidial nuclei
what are the 3 layers of the cortex?
granule cell
which cerebellar cortex layer is at the surface of the cerebellar cortex? what cell is located tehre?
molcular layer
purkinje cell dendrites (cell bodies located in purkinje layer)
granular cell axons: parallel fibers
how many purkinje cell bodies are there? granule cell ?
7 million purkinje cell bodies
100 billion granule cell **most numerous
which neuron is hte only output cell of the cerebellar cortex?
purkinje neuron
projects to and regulates the actvity of deep cerebellar nuclei and vestibular nuclei
inhibitory neuron (GABA)
which fiber produces a complex calcium spike and what doest this mean
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
how fast is the comple calcium spike
1/sec from climbing fiber on purkinje cell
is spatial or temporal summation seen with climbing fibers? how many synapses occur?
spatial summation
multisynaptic contact (2-3thousand exciaatory synapses ) of the single climbing fiber (homosynaptic) with its target purkinje cell
how many climbing fibers /purkinje cell?
one of the most powerful ecitatory synapses in CNs
EPSP generated by the climbing fiber always stimulates a comlex AP in the purkinje cell
do climbing fibers fire at a high or low freq on purkinje?
low and produce 1-2 COMPLEX spikes/sec on purkinje cells
what happens if at the same time on the same purkinje cell a parallel fiber and climbing fire release NT?
the response of the parallel is weakened b/c the climbing fibers modify th response of purkinje fibers to parallel f iber input
what type of firing on purkinje cells do parralel fiber have?
simple spike 50/sec
open Na channels (climbing fibers opened Ca channels)
what is the ratio of parrallel fiber synapse to purkinje synapses?
200,000 parrel: 1 purkinje but not all firing at same time
do you have temporal or spatial summation with parrel fibers?
both of smaller EPSPs to produce a single AP in a purkinje cell
what is the avg number of AP in a purkinje cell?
51: climbing fibers:1 and parrell:50
how are climbing fibers involved in memory?
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
when when you see LTD?
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
what type of channels open when the purkinje cells are depolarizd?
Ca: the rise in Ca in the purkinge causes an increase in pKC and further release of stored Ca
when parallel fibers are firing what types of channels are on teh postsynaptic/purkinje cell?
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
what happens during the learning process to the number of complx and simple spikes?
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
what happens to the inhibition of deep cerebellar nuclei with learning?
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
how are cerebellar circuits modified?
by expereience=learning
during learning how does the ratio of complex spikes to simple change?
increase in complex
decrease in simple
ataxia is ipsi or contra to side of the lesion?
midline lesions of vermis of flocculonodular/vesibular lobes cause what?
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
how do you determine if someone has a midline vermis lesion?
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
lateral lesions of the cerebellum (paramedian) cause?
unsteeady limb mvmts (appedndicular ataxia)
how to you test for a paramedian cerebellum lesion?
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)
mammary body is impt for?
what makes up the diencephalon?
waht is the fluid in the thalamus?
3rd ventricle-CSF
what iscontained in epithalamus?
pineal body
waht is thalamus bounded by?
relay nuclei
bounded by ant and post commissures
what is hypothalamus for
autonomic, endocrine, homeostasis, limbic system (emotions)