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Q
A
note
What does the superior and inferior colliculus do?
Where are they located?
Dorsal, rostral surface of brainstem
Separated from midbrain by cerebral aqueduct
Function: SC--> eye movements,visual attention; IC--> auditroy processing
081613_FM201_L_Brainstem101
CST travels in what part of the brainstem? What other tract travels with it?
Medulla and pons: Splits at the 2 cerebral peduncles,then comes together at ventral medial surface at pons
Course: From cerebral peduncles --> base of pons --> Medullary pyramids
CBT (corticobulbar tract) travels with the CST from motor cortex --> synapses at the appropriate CN motor nuclei along its course in the brainstem (no oculomotor)
081613_FM201_L_Brainstem101
What are the cerebellar circuitry in the brainstem?
Location of these brainstem nuclei containing cerebellar circuitry?
Medulla: Inferior olive (rostral medulla) --> laterally located, dorsal to CST
Pons: Pontine nuclei/griseum pontis
Midbrain: Red nucleus
* All 3 are located VENTRALLY in brainstem and have connections to cerebellum via cerebellar peduncles
081613_FM201_L_Brainstem101
How does the cerebellar circuitry in the brainstem get to the cerebellum? Location?
CEREBELLAR PEDUNCLES: axons traveling to and from cerebellum
Medulla: Inferior olive --> ICP: dorsal section
Pons: Pontine nuclei --> MCP: dorsal section
Midbrain: Red nuclei --> SCP: dorsal section but double
081613_FM201_L_Brainstem101
Testing cerebellar function
Tandem gait, heel-shin, nose to finger, coordinate rhythm of rapid, alternatingmovements
081613_FM201_L_Brainstem101
What axons/tract forms the inferocerebellar peduncle?
Dorsal spinocerebellar-joint/limb position from lower limb
Cuneocerebellar- joint/limb position of upper limb
081613_FM201_L_Brainstem101
When do you see the cerebral peduncle in a myelin section first? What region?
Midbrain --> split in too
Lots of white matter --> CST, CBT, CPT
081613_FM201_L_Brainstem101
What cranial nerves are attached near midline of brainstem? What CN to what region
3-medial midbrain
4- pons-midbrain jnctn (but dorsal exit)
6-medial pons-medulla jnctn
12- medial medulla
081613_FM201_L_Brainstem101
What CNs are attached to pons? What CN to what region of pons?
5- (lateral) midpons
6 (medial),7-8 (lateral)- ponto-medullary jnctn
081613_FM201_L_Brainstem101
What CNs are attached to medulla? What CN to what region?
9-10-lateral medulla
12-medial medulla
081613_FM201_L_Brainstem101
What is the only CN attached to the dorsal brainstem? What else is special about this?
CN4- trochlear- only CN where motor neurons leaving the brainstem go to CONTRALATERAL side on exit
081613_FM201_L_Brainstem101
Where is the motor and sensory nuclei located in brainstem?
Motor- medial dorsal
Sensory- lateral, even more dorsal
081613_FM201_L_Brainstem101
Sensory nuclei in the brainstem receive info from where?
Cranial nerves
081613_FM201_L_Brainstem101
Difference between somatic and branchial motor nuclei?
FUNCTION/LOCATION in the brainstem
Somatic- 3,4, 6,12 --> move extraocular muscles and tongue; NUCLEI medial
Branchial- 5,7,9,10 --> move muscles of mastication, facial expression, pharynx, larynx; NUCLEI more LATERAL, VENTRAL
081613_FM201_L_Brainstem101
Is there a motor nucleus at every transverse section we cut of the brainstem?
No, the motor nuclei are interrupted
081613_FM201_L_Brainstem101
What is the UMN tract of the brainstem (not corticospinal)?
What tract gives information to the motor nuclei of the cranial nerves?
CorticoBULBAR tract (provide all motor info EXCEPT EXTRAOCULAR--> no CB tract to CN3,4,6)
081613_FM201_L_Brainstem101
What is the blood supply to the BRAINSTEM? Does a stroke take out all regions?
Vertebro-basilar system
VERTEBRAL, Ant spinal, PICA: to CAUDAL and ROSTRAL MEDULLA
BASILAR, AICA: to CAUDAL PONS
BASILAR, pontine, SCA: to MID, ROSTRAL PONS
BASILAR, PCA: to MIDBRAIN (PCA is lateral)
Stroke could take out medial and spare lateral:
MEDIAL- PARAMEDIAN PENETRATING
LATERAL- CIRCUMFERENTIAL PENETRATING
081613_FM201_L_Brainstem101
What is the function of the reticular formation?
Where is it in the brainstem?
What happens if you lesion here?
Reticular formation- central core of brain stem (nuclei and axons)
Function at MIDBRAIN: consciousness --> Lesion= not fatal
Function at MEDULLA: VITALS (respiration, HR control)-->lesion=death
081613_FM201_L_Brainstem101
UMN and LMN saga continues in the brainstem for CN
T or F
tRUE -->same sx
081613_FM201_L_Brainstem101
If the tongue deviates to the left --> is the lesion ipsilateral or contralateral?
Ipsilateral LMN issue
081613_FM201_L_Brainstem101
Why might one have CN3,4,6,12 motor sx (eye/tongue) and bodily motor sx too (neck down)?
Medialy located CN motor nuclei (3,6,12) send axons ventrally and medially -->traveling very close (lateral) to CST
A medial brainstem stroke could take out both of these MOTOR tracts
081613_FM201_L_Brainstem101
CN3 palsy may cause what else other than vision problems?
CN3 controls many extraocular muscles AND LPS (OPENS EYELID) --> full ptosis (not half like Horners)
PSNS fibers travel on CN3 fibers --> PSNS lesion= blown pupil
081613_FM201_L_Brainstem101
Why does pain from middle ear, pharyn, larynx feel sharp and well localized (like somatic pain)
Pain fibers from CN7,9,10 join the spinal5tract and get processed at spinal5 nucleus as if they were somatic sensation
081913_FM201_L_Brainstem2-Trigeminal
What part of the brainstem do you find motor nuclei?
Medial- near the midline
081913_FM201_L_Brainstem2-Trigeminal
When motor neurons leave the brainstem, are they going to the same side or opposite?
All cranial motor neurons leaving the brainstem go to IPSILATERAL skeletal muscle EXCEPT TROCHLEAR (CN4)
What part of the brainstem do you find sensory nuclei?
Lateral, dorsal
Some are more distinct, some run throughout the brainstem (CN5)
081913_FM201_L_Brainstem2-Trigeminal
When sensory info from sensory ganglion cells of cranial nerves enter the brainstem- are they crossed or uncrossed?
UNCROSSED- all the sensory ganglion will also synapse in the IPSILATERAL side of the brainstem
081913_FM201_L_Brainstem2-Trigeminal
What are the 3 sensory nuclei in brainstem and what CNs provide info to each?
. Somatic sensory: CN 5,7,9,10 -->all of face, inside nose, mouth, eye, until middle ear, pharynx,larynx
. Visceral sensory: taste (CN 7, 9,10) inputs from viscera for cardiac, resp, dig fnctns: NUCLEUS SOLITARIUS
. Vestibulocochlear: CN8
081913_FM201_L_Brainstem2-Trigeminal
What is the visceral sensory nuclei in the brainstem?
Visceral sensory: taste (CN 7, 9,10) inputs from viscera for cardiac, resp, dig fnctns: NUCLEUS SOLITARIUS
081913_FM201_L_Brainstem2-Trigeminal
Where are the preganglionic parasympathetic neurons/axons in the brianstem?
No distinct nucleus --> scattered between branchial and somatic motor nuclei
More often located in the RETICULAR FORMATION
081913_FM201_L_Brainstem2-Trigeminal
Why is there only PSNS nuclei in the brainstem- where is the SNS?
Preganglionic sympathetic cell bodies (SNS) are in interomediolateral columns IN THORACIC SC
PSNS output is craniosacral!
081913_FM201_L_Brainstem2-Trigeminal
What is trigeminal neuralgia? Why does it happen?
Trigeminal neuralgia: pain in the V2,V3 region
Etiology: unknown
081913_FM201_L_Brainstem2-Trigeminal
pain and temperature loss on one side of face but opposite side of body?
brainstem lesion is SAME side as the facial sensory loss,
between CAUDAL MEDULLA and mid-pons
STT CROSSES AT ANTERIOR WHITE COMMISSURE IN SC (crossed already)
between MID-PONS and CAUDAL MEDULLA, is the IPSILATERAL SPINAL5TRACT (not crossed yet)
081913_FM201_L_Brainstem2-Trigeminal
PAIN AND temperature loss on one side of face AND SAME side of body?
brainstem lesion is OPPOSITE the side of the facial sensory loss ABOVE MIDBRAIN
STT CROSSES AT ANTERIOR WHITE COMMISSURE IN SC (crossed)
TRIGEMINOTHALAMIC TRACT OF P+T CROSSES AROUND MID-PONS (crossed)
081913_FM201_L_Brainstem2-Trigeminal
When you whack the trigeminothalamic tract carrying MAIN SENSORY NUCLEUS AXONS from mid-pons up, what other sensation might you lose- why?
You may lose 2 point discrimination and limb position from neck down
The trigeminothlamic tract, once crossed travels with the MEDIAL LEMNISCUS (carrying info from POSTERIOR COLUMNS)
081913_FM201_L_Brainstem2-Trigeminal
Why would a high cervical cord injury cause P+T loss in the face?
because you might whack the spinal5 tract and nucleus located in the caudal medulla. These are located at the level of the decussation (junction between spinal cord and brainstem.
081913_FM201_L_Brainstem2-Trigeminal
What tracts carrying similar information (but one from face and one from body) are continuation of each other from cervical cord to brainstem?
. Tract of Lisseur and Substantia Gelatinosa (normally carry pain and temp info from body) -->
Tract of Lisseur turns into spinal 5 tract in the caudal medulla
substantia gelatinosa turns into spinal5 nucleus in the caudal medulla
081913_FM201_L_Brainstem2-Trigeminal
What is the only nucleus in the brainstem where afferent ganglion cell bodies actually live within the nucleus?
Mesencephalic nucleus contains the dorsal root ganglion cell bodies carrying the jaw position sense from CN5
081913_FM201_L_Brainstem2-Trigeminal
What 4 nuclei make an extended column throughout the brainstem?
CN5-sensory; all of midbrain
N. solitarious (7,9,10)- visceral sensory; all of medulla
N. ambiguus (9.10)- motor; rostral medulla
CN12-motor; rostral medulla
082013_FM201_L_Brainstem3-MotorVisc
Why is it that different locations (medial vs. lateral) in the brainstem indicate different vulnarabilities?
Because medial vs. lateral brainsteam are supplied by different arteries (one part can be spared in a lesion)
MEDIAL- Somatic motor, CST
LATERAL- Branchial motor, All sensory, STT
082013_FM201_L_Brainstem3-MotorVisc
What structures will you find in jnctn of spinal cord and brainstem?
Decussation (CST crossing), STT (crossed), NG appearing, spinal5tract and caudal nucleus, solitarious
082013_FM201_L_Brainstem3-MotorVisc
What structures will you find in CAUDAL MEDULLA?
slit like central canal, CN12,NS and dorsal motor nucleus of the vagus, NG, NC, medial lemniscus, spinal 5 tract nucleus and tract, STT, medullary pyramid
082013_FM201_L_Brainstem3-MotorVisc
What structures will you find in ROSTRAL MEDULLA?
CN12motor, NA, solitarious, spinal5tract, dorsal motor nucleus of the vagus
082013_FM201_L_Brainstem3-MotorVisc
What structures will you find in CAUDAL PONS?
CN6,7motor, spinal5tract
082013_FM201_L_Brainstem3-MotorVisc
What structures will you find in MID-PONS?
CN5motor and main sensory nucleus, mesencephalic nucleus
082013_FM201_L_Brainstem3-MotorVisc
What structures will you find in ROSTRAL PONS?
CN4motor axons (nucleus is in CAUDAL MIDBRAIN)
082013_FM201_L_Brainstem3-MotorVisc
What structures will you find in MIDBRAIN?
CN3motor (ROSTRAL MIDBRAIN), CN4motor (CAUDAL MIDBRAIN)
082013_FM201_L_Brainstem3-MotorVisc
What CNs carry PSNS axons? Where are the PSNS nuclei for each one?
CN3- PSNS Nuclei are in the vicinity of the CN3motor nucleus (ROSTRAL MIDBRAIN)- onthe boards, call this edinger-westphal
CN7-PSNS nuclei are in the salivatory nucleus (location unimp)
CN9- PSNS nuclei are in the salivatory nucleus (location unimp)
CN10- Dorsal motor nucleus of the vagus in ROSTRAL MEDULLA
More PSNS scattered around in the reticular formationof ROSTRAL MEDULLA
082013_FM201_L_Brainstem3-MotorVisc
So when CN3 nucleus is busted, the PSNS is often busted too- what are the clinical sx?
UNILAT
. PSNS busted- full mydriasis
. CN3 busted- eye is down and out at rest (SO3LR4 OK), visual issues (diplopia,blurry vision), full ptosis (due to LPS being busted too CN3)
082013_FM201_L_Brainstem3-MotorVisc
Why do unilateral CBT lesion have little effect? What is the effect? How would it be different in an LMN lesion?
. All cranial nerves except CN7 going to lower face gets BILATERAL HEMISPHERIC input EXCEPT FOR CN7 lower face neurons (smile, puff out cheks etc)
. Thus in UMN (CBT) lesions between cortex and LMN, you see weakness of LOWER FACE, forehead is spared
. In an LMN lesion, the weakness would affect the WHOLE SIDE OF FACE, followed by significant ATROPHY
082013_FM201_L_Brainstem3-MotorVisc
What else other than a UMN lesion can take out CN7 commonly? How to distinguish this from a UMN lesion?
Most common CN7 palsy=Bell's palsy (PNS issue) --> recoverable
R/O UMN lesion --> it would be accompanied by loss of sensation or other clues, not just a single sx
082013_FM201_L_Brainstem3-MotorVisc
When a brainstem lesion takes out CN6, why is 7 also gone?
CN7 a branchial motor nerve does a loop around 6 before heading out
082013_FM201_L_Brainstem3-MotorVisc
What is the most important function of the middle ear cavity?
Air-fluid interface from middle to inner ear= 30 DB loss
The bones make up for this loss so the sound is not dampened
082313_FM201_L_EAR_rev
What organs of the vestibular system detect what type of head position?
Utricle macula: horizontal plane- linear acceleration--> stereocilia here are horizontal
Saccule maccula: vertical acceleration --> stereocilia here are lateral
Semicirc canal cristae: angular acceleration
082313_FM201_L_EAR_rev
What happens if the otoconia on top of the gelatinous cupula in the utricle and sacule fall out of place?
BPV- Benign positional vertigo --> need to get them inplace
082313_FM201_L_EAR_rev
What is the tonotopic organization of the basilar membrane of the cochlea?
High freq sounds --> base of cochlea (thick and dense,narrow, stiff)
Low freq sounds --> apex of cochlea (wide, thin and floppy)
082313_FM201_L_EAR_rev
Is there only one stereocilia per hair cell?
No, many stereocilia per hair cell
082313_FM201_L_EAR_rev
How do hair cells work? What happens to the stereocilia to make it send a signal?
Stereocilia on a hair cells are connected by tip-links (proteins)
Moving the tip-links --> short to long will open up the K+ channels (remember these are in endolymph) --> K+ influx= generation of SIGNAL!
082313_FM201_L_EAR_rev
In the reticular lemina of Organ of corti, how many rows of hair cells are there?
What is their output- where is it going?
. 1 row of inner hair cells--> 95% spiral ganglion cells are connected here (Type 1 afferents)
. 3 rows of outer hair cells --> 5% spiral ganglion cells connected here (Type 2 afferents)
082313_FM201_L_EAR_rev
What are the efferents to the hair cells?
. Efferents from brain can go either to IHC or OHCs
082313_FM201_L_EAR_rev
If IHCs send most input to the brain, what is the function of the OHCs?
Receive lots of efferents from the brain -->
Fine tunes the signal--> 306 vs 304 hz?
Resolution of hearing (ie: filtering out background/extra noise=cocktail party syndrome)
082313_FM201_L_EAR_rev
What things can cause sensorineural damage?
1- Noise (includes presbyacusis= cumulative nosi damage seen in the old)
2- Biochemical (Ototoxic drugs= aminoglycosides, cisplatin, loop diuretics- often hit OHCs)
3- Genetic (gap junction (connexin) mutations, cytoskeletal proteins in hari cells)
082313_FM201_L_EAR_rev
Two treatments for hearing loss?
1- Conductive hearing loss- hearing aids
2- Sensorineural hering loss- cochlear implants (if the problems is in cochlea)
082313_FM201_L_EAR_rev
where are the distal and proximal ends of the spiral ganglion cells located?
Distal: Synapse on hair cells
Proximal: Join cochlear nerve --> to brainstem
082613_FM201_L_CentralAuditory
Which compartment of the cochlea are the hair cells located? What are the two compartments above and below it?
Hair cells are in the scala medialis
Above compartment: scala vestibuli
Below compartment: scala tympani
082613_FM201_L_CentralAuditory
What type of fluid fills the scala medialis? Do spiral ganglion cells synapse in this fluid?
ENDOLYMPH fills scala medialis- it's high in K+
The area where spiral ganglion cells synapse is called PERILYMPH-low in K+
082613_FM201_L_CentralAuditory
What is the sensory and motor functions of the hair cells?
. Inner hair cells: SENSORY --> conveys frequency(pitch) and intensity (amplitude) info to CNS (in an economical way)
. Outer hair cells: MOTOR --> shortens/lengthens to provide sensitivity (FINE TUNE) to INNER HAIR CELLS (amplify low-intensity sound ora particular freq)
082613_FM201_L_CentralAuditory
The cochlea transmits what TWO type of sound information?
FREQUENCY (PITCH)
Intensity (AMPLITUDE)
082613_FM201_L_CentralAuditory
How do we localize sound? Which nucleus? Where is it located?
. HORIZONTAL SOUND LOCALIZATION done by TIME OF ARRIVAL @ SUPERIOR OLIVES
. Superior olives= pons (one of pontin nuclei) --> on the path of lateral lemniscus (on the way to inferior colliculus)
. After partially crossing, some axons from the cochlear nucleus will go to superior olives and some will go on to inferior colliculi
082613_FM201_L_CentralAuditory
What are the roles of the efferents in the auditory system?
Where do we find these? (in between what structures?)
. FUNCTION: To fine-tune the system:
ie: efeerents to the OUTER HAIR CELLS --> inhibit too much jiggling at the outer hair cells
. WHERE DO THEY EXIST: brainstem/thalamus; between auditory structures in brainstem; pontine auditory nuclei --> organ of Corti
082613_FM201_L_CentralAuditory
What controls the STAPEDIUS MUSCLES and TENSOR TYMPANI?
What nucleus controls the responseof these muscles?
What are the roles of these muscles?
. Both tensor tympani CN5, stapedius CN7 close in response to CERTAIN SOUNDS
. This reflex is processed at the SUPERIOR OLIVE
. Role : NOT PROTECTION FROM LOUD SOUNDS, possible to filter out low frequency background/extra noise (ie: bells palsy patients complain of hyperacusis)
. Tensor tympani also contracts before we chew/speak --> filters out our own noise or in response to VISUAL STIM
082613_FM201_L_CentralAuditory
What parts of the auditory system have tonotopic organization?
What is the role of this?
.Tonotopic organization: starts at basilar membrane (freq) and continues all the way to cortex
. Role of tonotopy: language? use for cochlear implants!
082613_FM201_L_CentralAuditory
If there is loss of hearing in one ear --> where is the UNILATERAL lesion?
What type of damage is likely to produce that lesion?
. Peripheral to the cochlear nuclei - anything ROSTRAL to this has crossed axons
. Conductive loss: external (ear wax) /middle ear (otitis, sclerosis, perf)
. Sensorineural loss: cochlea (ototoxic drugs), 8th nerve (tumor), cochlear nuclei (lateral brainstem infarct)
082613_FM201_L_CentralAuditory
What is you had a UNILATERAL lesion ROSTRAL to the cochlear nucleus- what would this cause?
. Unilateral lesion ROSTRAL to the COCHLEAR NUCLEUS will produce
1) INABILITY TO LOCALIZE SOUND
2) INABILITY TO FILTER OUT BACKGROUND NOISE
082613_FM201_L_CentralAuditory
Where in the brainstem do you find the vestibular and cochlear nucleus, superior olive?
. Vestibular starts at ROSTRAL MEDULLA---> CAUDAL PONS
. Cochlear around here too --> a little above the ROSTRAL MEDULLA
. Superior olive (localize sound) --> appears between ROSTRAL MEDULLA and CAUDAL PONS --> lateral lemniscus is not visible before the midbrain but it's there
. Can see LATERAL LEMNISCUS in MIDBRAIN as the stem of the wine glass going into the ICP
082613_FM201_L_CentralAuditory
Where is the thalamus in relation to the midbrain?
Anterior and superior to it BUT posterior thalamus hugs the midbrain
082613_FM201_L_CentralAuditory
What is the role of the vestibular system?
What are the long tracts used to accomplish these?
. Detects position of head in space (vestibular nuclei) --> adjusts
1) posture, muscle tone (output via VESTIBULOSPINAL tracts) and
2) eye movements (MEDIAL LONGITUDINAL FASCICULUS=MLF)
082713_FM201_L_EyeMovements
What is the gelatinous cupula?
Membrane that the stereocilia of the vestibular system are attached to --> denser than the endolymph
What structures in the vestibular system are responsible for linear acceleration and head tilt?
What is the name of the sensory patch of epithelium here?
What other important structure is here (that is not in the semicircular canals)?
. Utricle and saccule= LINEAR ACCELARATION, HORIZONTAL HEAD TILT
. Sensory epithelium=maculae
. Stereocilia are attached to a membrane called GELATIONOUS CUPULA
. The calcium carbonate crystals IN MACULAE= OTOCONIA (embedded in gelatinous cupula
082713_FM201_L_EyeMovements
What structures in the vestibular system are responsible for angular acceleration?
. Semicircular canals= ANGULAR ACCELERATION
. Sensory epithelium=cristae ampularis
. Membrane that stereocilia are embedded in= GELATINOUS CUPULA
. No otoconia here
082713_FM201_L_EyeMovements
What is the role of the otoconia in the utricle and saccule?
. When there's a tilt, membrane (gelatinous cupula) flops over
. Otoconia (the crystals)= weight;make sure that the GC stays flopped over
. Ensures that the stereocilia are getting the signal
082713_FM201_L_EyeMovements
What are the inputs to the vestibular nuclei?
1) Vestibular ganglio cells (head movements etc)
2) Cerebellum (vestibular)
3) Cervical spinal cord (about neck muscle activity)
* can't tell where the lesion is just because of a vestibular problem
082713_FM201_L_EyeMovements
What are the outputs from the vestibular nuclei?
1) to thalamus re: head position (not that imp)
2) to vestibular cerebellum
3) To spinal cord --> two tracts (medial and lateral vestibulospinal)
4) to motor nuclei 3,4, and 6 --> medial longitudinal fasciculus (MLF)= eye movements in coordination with head movements (reflex eye movements)
082713_FM201_L_EyeMovements
What are the functions of the two vestibulospinal tracts going from the vestibular nuclei to the spinal cord?
What tract are they part of in the spinal cord?
. Medial vestibulospinal tract-- head position, coordinates head with eye movements--> TO motor neurons of neck muscles
. Lateral vestibulospinal tract-- changes body posture to compensate for tilts or rotation of body/head -->TO motor neurons of antigravity muscles (EXTENSORS)
* These are part of the descending pathways from brainstem in the spinal cord --> the MEDIAL DESCENDING MOTOR TRACTS
082713_FM201_L_EyeMovements
What are the two types of eye movements?
. Vestibular reflex eye movements- AUTOMATIC (just vestibular to motor-visual system not involved)
. Voluntary eye movements- when we want to look at something
082713_FM201_L_EyeMovements
What are the goals of the two type of eye movements (voluntary and automatic)?
. Keep image from moving on the RETINA (so we can see with detail)
. VOR- adjusts optic axis using head movements
. Voluntary (pursuit) system- keeps images on fovea with visual feedback
082713_FM201_L_EyeMovements
What are contributions of the vestibular nuclei to the reflex eye movements (vestibulo-ocular reflex=VOR)?
What structure/tract carries this info?
Which side to which side?
. Medial longitudinal fasciculus (MLF) carries info from vestibular nuclei to motor nuclei 3,4,6 --> adjusts eye movements in response to head movements
. ie: KEEPS EYES LOOKING AT A SINGLE DIRECTION WHEN THE HEAD IS BEING MOVED
. The eyes are always YOKED during VOR
082713_FM201_L_EyeMovements
What if you want to track a moving object with your head and eyes (how to overcome the VOR)?
Cerebellar circuits suppress the VOR when you want to track an object with head AND eyes
082713_FM201_L_EyeMovements
What controls the voluntary eye movements?
Is this related to the vestibular nuclei?
What are the requirements to SEE objects?
. Voluntary eye movements are NOT related to vestibular nuclei
. Controlled by CEREBRAL CORTEX (OCCIPITAL)
. Requirements to see objects:
1) visual image falls on the FOVEA of both eyesfor 0.1 sec
2) image is stabilized during movement
3) object is in focus
082713_FM201_L_EyeMovements
Are voluntary eye movements always yoked?
No- CONJUGATE MOVEMENTS (both eyes same directions) ARE YOKED
VERGENCE MOVEMENT (two eyes different directions) ARE NOT YOKED
082713_FM201_L_EyeMovements
What are the two tests used to test if voluntary movements are intact?
. Saccades- ability to switch focus from one object to next with eyes (nose to finger)
. Pursuit or following movements- slower, smoother movements used to follow a moving target
082713_FM201_L_EyeMovements
What part of the cortex is used to contol VOLUNTARY EYE MOVEMENTS?
Frontal eye fields (frontal cortex) --> SACCADIC MOVEMENT TO OPPOSITE SIDE
. Horizontal saccades - EACH SIDE goes to opposite VIEW FIELD (BUT BOTH EYES MOVE)
. Vertical saccades- BOTH SIDES work together FOR UP AND DOWN MOVEMENTS
082713_FM201_L_EyeMovements
What happens if an acute lesion (ie: stroke) damages the frontal eye field?
. Tendency to gaze at the side TOWARDS THE LESION (but no diplopia- eyes are yoked)
. Cannot look at the OPPOSITE SIDE OF LESION (Saccadic movement impaired)
. UMN paralysis of lower face and body (CBT and CST are often impaired in this lesion due to proximity of FRONTAL EYE FIELDS TO MOTOR CORTEX)
082713_FM201_L_EyeMovements
Pathway for frontal eye centers(voluntary eye movements) to get to motor nuclei in brainstem?
Frontal eye fields (cortex) --< caudate nucleus --< substantia nigra --< SUPERIOR COLLICULUS --< Brainstem Gaze centers --<extraocular motor nuclei
082713_FM201_L_EyeMovements
Does the superior colliculus talk directly to EXTRAOCULAR Motor Neurons?
No
. Sup colliculus --< brainstem gaze centers --< extraocular motor nuclei
082713_FM201_L_EyeMovements
What are brainstem gaze centers?
Where are they located?
Do they project to the same side
. Brainstem Circuits that control horizontal, BUT ALSO vertical (up,down) and vergent movements (no other kind: conjugate or vergent)---< Then talk to 3,4,6 nuclei
. UP, DOWN and CONVERGE centers are near 3 and 4 motor nucleus in MIDBRAIN: UP=dorsal to aqueduct (BILAT), DOWN=ventral to aqueduct (BILAT), CONVERGE=unknown (just one)
. LATERAL centers are near 6 nucleus (LR) in CAUDAL PONS (BILAT)- called PPRF
. The gaze centers project IPSILATERAL
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How do brainstem gaze centers do to establish horizontal eye movements?
Why does lateral movement (LR) require that medial rectus also be activated?
How is this achieved?
. CONJUGATE EYE MOVEMENTS are YOKED: for horizontal movement to one side, LR of one eye must go with MR of the other eye
. Done by connecting CN6 (LR) w/ CN3 (MRandAO) via MLF (medial longitudinal fasciculus that also carries axons from vestibular nuclei)
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What does the CN6 MOTOR NUCLEUS CONTAIN that is involved in the horizontal gaze?
Which side does each axon project?
CN6 contains
1) Extraocular motor neurons to LR -->IPSILATERAL LR
2) Interneurons going to CN3 via MLF --> these CROSS (CONTRALATERAL CN3 nuclei) --> because the MR of CONTRALATERAL EYE must move
082713_FM201_L_EyeMovements
Lesions of the vestibular system - what are they, what do they indicate?
. Vertigo (spinning, less often tilting, leaning)= dysfunction in ANY part of vestibular system: peripheral (CN8, labyrinth) OR central (vest nuclei, cerebellum, other conn)
. Nystagmus (rhythmic uncoorinated eye movements), often accompanies vertigo attacks
. Poor balance
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If horizontal gaze is impaired (involving the medial rectus on one side) --> is convergent gaze (involving the same medial rectus) also impaired?
. Depends on the lesion --> a contralateral CN6 motor lesion could take out LR and MR (OPP SIDES) but convergent gaze for that MR is controlled by the CN3 nucleus (intact)
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What is the syndrome caused by an MLF lesion?
What are the sx?
Cause?
. Internuclear Opthalmoplegia --> MLF lesion UNILATERAL(carrying axons to CN3 nucleus for MR)
. Lose ADDUCTION IPSILATERAL (MR) BUT VERGENCE IS FINE (MR can abduct when STIM by CN3 or CONVERGE CENTER-no MLF involved) --> indicates that the problem is NOT an MR paralysis
. NYSTAGMUS of OPPOSITE EYE (Abducting eye)
. MS plaques/midline pontine infarcts
082713_FM201_L_EyeMovements
The two eye movement systems work together to keep the image from moving on the retina- what if one system is overwhelmed? What clinical sx?
NYSTAGMUS (rhytmic alternating reflex of yoked movesments)
- Slow phase (PURSUE) and fast phase (SACCADE)
- Up, down or torsion
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Can nystagmus be normal- how would a normal condition demonstrate nystagmus?
Yes
1) OPTOKINETIC NYSTAGMUS- watching a landscape out the window = voluntary eye movements do the slow phase
. PURSUE (voluntary) an object until you can't roll the eye any further=SLOW --> SACCADE back to a new focus=FAST
2) POST-ROTATORY NYSTAGMUS- spinning around in chair = VOR responsible for slow phase
. Slow phase LEFT, fast phase RIGHT
3) CALORIC NYSTAGMUS- Pouring water into someone's ear--> moves the endolymph in semicircular canals
. Cold water --> OPPOSITE SIDE NYSTAGMUS (fast phase)
. Warm water --> SAME SIDE NYSTAGMUS (fast phase)
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When you dont see OKN, Post rot or CALORIC NYSTAGMUS, what is this mean?
What are reasons why you must see an ABNORMAL NYSTAGMUS?
. Absence of OKN, Post rot or CALORIC NYSTAGMUS= investigate peripheral and central
. Spontaneous nystagmus: alcohol intox, damage to peripheral or central stuff
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Blood supply of cerebellum and brainstem: what do these supply:
PCA
SCA
AICA
PICA
Vertebral
Basilar
. PCA (post. cerebral) - No CBM, Midbrain w/ BASILAR ARTERY
. SCA (SUP(main) CEREBELLAR ARTERY): Anterior+superior surface of CBM, all DEEP CBM nuclei, SCP; little of rostral pons
. AICA: Little of lateral and inferior CBM, caudal pons w/ BASILAR and PONTINE ARTERIES
. PICA: Little of posterior CBM, rostral medulla w/ VERTEBRAL ARTERY
. Vertebral artery+ Ant spinal arteries: Caudal medulla
* These big branches will send penetrating branches into the BSTEM: PARAMEDIAN (medially) and CIRCUMFERENTIAL (lateral)
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Is one more likely to survive a lateral or medial brainstem stroke?
Lateral brainstem stroke (card/resp centers are not disturbed
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What are descending autonomic tracts?
Where do they run?
. From hypothalamus/thalamus --> carry input to interomediolat columns
. Tracts run LATERALLY IN THE BRAINSTEM near STT
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When you see a Horner's syndrome- is the lesion ipsilateral or contra?
. Horner's syndrome- lesion ALWAYS IPSI
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Medial vs. lateral structures (if vasculature is interrupted?) in medulla
MEDULLA
Medial:12 (rostral), MLF, CST/CBT, medial lemniscus, NG-NF (very caudal)
Lateral: lateral cuneate (very caudal), dorsal nucleus of vagus (caudal-mid), 8 (rostral), 9-10=NA (rostral), NS (cardio/resp=rostral, taste=caudal), Spinal 5 nucleus (p&t=caudal medulla), STT (xed), Spinal 5 tract (P&T), ICP, autonomic control tracts
Both: crossing of olivocerebellar fibers (rostral), reticular formation (card/resp)
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Medial vs. lateral structures (if vasculature is interrupted?) in PONS
PONS
Medial:6 (CAUDAL), MLF, CST/CBT, medial lemniscus(caudal)
Lateral: 5 (mid), 7 (caudal), medial lemniscus (mid-rostral), STT (xed), spinal 5 tract, spinal5nucleus (crude touch,corneal reflex=CAUDAL), main sensory nucleus, mesencephalic nucleus, MCP, autonomic control tracts
Both: crossing of griseum pontis fibers, reticular form (consciousness)
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Medial vs. lateral structures (if vasculature is interrupted?) in MIDBRAIN
MIDBRAIN
Medial: 3,4 (dorsal), MLF, red nucleus, SCP fibers cross, inf/sup colliculus
Lateral: medial lemniscus, STT (xed), TGT (xed), lateral lemniscus, CST/CBT, corticopontine fibers, substantia nigra, autonomic tracts
Both: reticular formation (consciousness)
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Key functions of the caudal reticular formation?
Where are these located?
. RR --> medullary control; lesion= resp arrest/death
. BP, HR --> input from NS (caudal); output to symp neurons
. Posture, muscle tone, locomotion pattern (FLEXOR TONE) --> reticulospinal tracts
. Hiccuping, coughing, sneeze, shiver,gag, vomit, laugh/cry -->weird
. Located in caudal pons/rostral medulla
090313_FM201_C_ReviewBrainstemCerebellum
Key functions of the rostral reticular formation?
Where are these located?
. Alert/conscious state --> connections of consciousness between cortex and RF
. Located in rostral pons/midbrain
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What is coma?
What kind of lesions result in a coma?
Do these have to be bilateral?
. Unarousable/unconscious state in which you cannot elicit meaningful responses from cortical areas
. Lesions that destroy the connections between arousal centers (rostral RF) and cortex (can be thalamic, cortical or RF)
. For full coma --> lesion must be bilateral (unilateral can slightly impair alertness)
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What is the ascending reticular activating system- ARAS?
. System invovled in behavioral alertness and arousal
. Rostral RF --> projects into this system
. Also input from all somatosensory nuclei, emotional/cognitive processes
. Thalamus and hypothalamus involved too
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Who are locked in patients?
. Patients with bilateral damage in the rostral pons/ midbrain that spare the rostral RF and sensory movements
. Fully conscious with no movement (CST/CBT gone)
090313_FM201_C_ReviewBrainstemCerebellum
Pathway of direct and consensual pupillary reflex fully awake and comatose patients?
. Direct and consensual pupillary reflex
. Reticular ganglion cell --> CN2 nucleus --> optic chiasm (BILAT) --> BILAT input to pretectum
. BILAT INPUT to PREGANGLIONIC PSNS NEAR CN3 NUCLEUS --> ciliary ganglion --> BILAT miosis
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How do you distinguish a CN2 from a CN3 lesion with the pupillary reflex?
Shinelight in one eye
. CN2 lesion--> BILAT UNRESPONSIVE (only when light is on the lesioned side)
. CN3 lesion --> UNILAT UNRESPONSIVE (when the light is on either side) --> ANISOCORIA (unequal size of pupils)
090313_FM201_C_ReviewBrainstemCerebellum
What would you see in the eye if there's a full CN3 lesion vs. a partial CN3 lesion?
. Full CN3 lesion --> blown pupil, depressed/out eye, complete ptosis
. Partial CN3 lesion -->
Compression will get the outer PSNS fibers (=blown pupil, can't accommodate)
Small vessel dz gets the inner CN3 axons (= full ptosis, blurry vision)
090313_FM201_C_ReviewBrainstemCerebellum
What is another way to activate pupillary response (constriction) other than direct/consensual response (via CN2)?
What is the wiring here?
. Moving gaze from far to near (accommodation)
. Wiring is through VISUAL CORTEX not CN2 IN, CN3 out
. Visual cortex --> pretectal area -->
1) PSNS near CN3 --> miosis and accommodation (rounder lens for near vision)
2) Convergent gaze centers --> CN3 nuclei of L, R --> medial rectus
090313_FM201_C_ReviewBrainstemCerebellum
What is the wiring for mydriasis?
Sympathetic input:
Hypothalamus --> lateral brainstem (ANS output tract here) --> Interomediolat columns (T1-T2) -->superior cervical ganglion --> carotid plexus (travel up on the internal carotid through the carotid sinus) --> pupil dilator muscle (TARSAL)
. Lesion anywhere along here can mess up the SNS
090313_FM201_C_ReviewBrainstemCerebellum
How could a cortical lesion affect the jaw jerk? bilat/unilat?
BILATERAL CORTICAL/UMN LESION could EXAGGERATE JAW JERK
Because there is BILAT INPUT TO CN5 motor neurons (efferent limb of jaw jerk)
090313_FM201_C_ReviewBrainstemCerebellum
What would the VOR tell you in a comatose patient?
How would you test this?
VOR can tell you what parts of the brainstem are intact (CN8, MLF, 3,4,6)
1) Doll's eye test (open eyes, move head side to side/up-down) --> if eyes remain fixated, most of brainstem is good
. Works without visual input/light
2) Caloric nystagmus (cold water infusion into one ear)
a) Cortex out, brainstem good --> Slow, tonic movement towards infused side with no fast phaseof nystagmus (cortex needed to generate saccades
b) Brainstem damaged --> no movement (BILAT DAMAGE), one eye kinda moves (UNILAT BSTEM DAMAGE)
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What would the corneal reflex tell you in a comatose patient?
Intact corneal reflex=
OK CN5 SENSORY and BILAT CN7 MOTOR NUCLEI
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What would the gag reflex tell you in a comatose patient?
OK 9 and 10
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How could you test a visceral reflex in a comatose patient?
If 9-10 (afferent from carotid sinus) and NS (caudal)-efferent part is intact, BP and HR should both be up in the short term
090313_FM201_C_ReviewBrainstemCerebellum
What are posturing reflexes seen in comatose patients?
Comatose patients with CST/CBT gone --> only have activity from brainstem motor centers projecting to the SC (descending motor pathways from brainstem)
. Only seen in patients with CST/CBT damage
090313_FM201_C_ReviewBrainstemCerebellum
What posturing reflexes would you see in a comatose patient?
Response to pain
. FLEXOR ARM RESPONSE- upper limbs flexes, lower limbs extended --> CAUDAL LESION
. EXTENSOR ARM RESPONSE- all limbs are extended, except wrists are flexed -->MORE ROSTRAL LESION
.Can't localize to a single place
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Patients with which posturing reflexes have better prognosis?
Flexor arm, extensor leg
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What causes a midbrain compression?
What happens in this?
. Epidural hemorrhage, edema, tumor
. Brain is pushed down through the tenctorial notch- compromising the rostral brainstem (thus RF)
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What is the triad of symptoms in a midbrain compression?
. COMA --> Reticular formation BILAT COMPRESSION
. Fixed (no response to light), BLOWN PUPIL (later), IMPAIRED EYE MOVEMENTS--> CN3 nerve/axons
. Hemiplegia, hyperreflexia
. Postural reflexes maybe
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How do you tx a midbrain compression?
Dx early, tx promptly
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