Exam 3 Flashcards
The functions of the vestibular system are to:
(1) Sense & perceive ___
(2) ___ control, which includes orienting to __, stabilizing the __, and controlling the ___
(3) Stabilize ___ to get a stable ___ (via the __ while you’re moving) so you can predict __ requirements.
The functions of the vestibular system are to:
(1) Sense & perceive SELF MOTION
(2) POSTURAL control, which includes orienting to VERTICAL, stabilizing the HEAD, and controlling the COM
(3) Stabilize GAZE to get a stable VISUAL FIELD (via the VOR while you’re moving) so you can predict POSTURAL CONTROL requirements.
The vestibular system consists of:
(1) Peripheral sensory apparatus, namely the __ and __
(2) Central processor, namely __ and __
(3) Generated motor output via the ___ tract for ___ and ____ tract for ___.
The vestibular system consists of:
(1) Peripheral sensory apparatus, namely the SEMICIRCULAR CANALS and OTOLITHS
(2) Central processor, namely VESTIBULAR NUCLEI and CEREBELLUM
(3) Generated motor output via the VESTIBULO-OCULAR tract for EYE MOVEMENT & VOR (via the MLF) and VESTIBULOSPINAL tracts for POSTURAL RESPONSE.
The ____ (for hearing), and the ____ (consists of the __ and __) are imbedded in the ____ portion of the ___ bone [medial/lateral] to the middle ear. The cochlea lies [anterior/posterior/medial/ lateral] and the labyrinth is relatively [anterior/posterior/ medial/ lateral] to the cochlea.
The COCHLEA (for hearing), and the LABYRINTH (SCC & OTOLITH) are imbedded in the PETROUS portion of the TEMPORAL bone MEDIAL to the middle ear. The cochlea lies ANTERIOR and the labyrinth is relatively POSTERIOR & LATERAL to the cochlea.
The bony labyrinth consists of the:
1) ____ (and its ___, __, and ___ sections
(2) ___ (consisting of __ and __)
(3) ___
The bony labyrinth consists of the:
(1) SEMICIRCULAR CANALS (and its POSTERIOR, ANTERIOR, & LATERAL sections)
(2) OTOLITHS (consisting of UTRICLE and SACCULE)
(3) COCHLEA
All 3 semicircular canals are open on [one/both] ends and empty into the ___ which is part of the __. This connects medially to the ___, and the inferior part of that connects with the ___. They’re all interconnected!
All 3 semicircular canals are open on BOTH ends and empty into the UTRICLE which is part of the OTOLITH. This (the utricle) connects medially to the SACCULE, and the inferior part of the saccule connects with the COCLEA. They’re all interconnected!
The semicircular canals are oriented to detect movement in different directions. They work in complementary pairs, meaning the right anterior canal works with the [L/R] [anterior/posterior/lateral] canal. The lateral canals are angled at __* from the [frontal/ transverse/ sagittal] plane. The anterior canal is oriented ___* from the [frontal/ coronal/ sagittal] plane, and the posterior canals are oriented at ___* from the [frontal/ coronal/ sagittal] plane. This is a [redundant/ non-redundant] system.
The semicircular canals are oriented to detect movement in different directions. They work in complementary pairs, meaning the right anterior canal works with the LEFT POSTERIOR canal. The lateral canals are angled at 30* from the TRANSVERSE plane. The anterior canal is oriented 35* from the SAGITTAL plane, and the posterior canals are oriented at 51* from the SAGITTAL plane. (Both anterior & posterior canals are ~45* from sagittal plane). This is a REDUNDANT system.
The __ lines the bony labyrinth, follows its general contours, and is filled with ___. The space between the bone and the membrane is filled with a fluid called ___. These two fluids differ in ___ concentrations. This creates a ___ across the membrane, which is important in the conductance of ___ at the base of the __ where it contacts the ___ nerve.
The MEMBRANOUS LABYRINTH lines the bony labyrinth, follows its general contours, and is filled with ENDOLYMPH. The space between the bone and the membrane is filled with a fluid called PERILYMPH. These two fluids differ in IONIC concentrations. This creates a VOLTAGE POTENTIAL across the membrane, which is important in the conductance of CHARGES at the base of the HAIR CELLS where it contacts the 8TH CRANIAL NERVE.
Perilymph fills the [membranous labyrinth/ bony labyrinth between bone & membrane]. It communicates with the ___. It is [high/low] viscosity, [high/low] sodium, and [high/low] potassium.
The endolymph fills the [membranous labyrinth/ bony labyrinth between bone & membrane]. It [does/ does not] communicate with the perilymph. It is made in the ___. It is [high/low] viscosity, [high/low] sodium, and [high/low] potassium.
Perilymph fills the BONY LABYRINTH BETWEEN BONE & MEMBRANE. It communicates with the SUBARACHNOID SPACE. It is LOW viscosity, HIGH sodium, and LOW potassium.
The endolymph fills the MEMBRANOUS LABYRINTH. It DOES NOT communicate with the perilymph. It is made in the ENDOLYMPHATIC SAC. It is HIGH viscosity, LOW sodium, and HIGH potassium.
All SCCs open at both ends to the __. On [one/both] end(s) of each canal is an expanded portion called the __. This is a specialized __ area of the SCCs. A small bump in the ___ is called the ___ - this is where we find the ___ in the SCC. The crist has protruding ___, the longest of which is called the __. It is covered by a gelatinous ___ which [is/ is not] exposed to endolymph. All cells in a given canal are oriented in [the same/ different] directions. The ___ keeps the ___ standing up straight.
All SCCs open at both ends to the UTRICLE. On ONE end of each canal is an expanded portion called the AMPULLA. This is a specialized RECEPTOR area of the SCCs. A small bump in the AMPULLA is called the CRIST - this is where we find the HAIR CELLS in the SCC. The crist has protruding STEREOCILIA, the longest of which is called the KINOCILIUM. It is covered by a gelatinous CUPULA which IS exposed to endolymph. All cells in a given canal are oriented in THE SAME DIRECTION.
*The GELATINOUS CUPULA keeps the STEREOCILIA standing up straight - the endolymph pushes the cupula which triggers the hair cell receptors!
The semicircular canals detect ___ acceleration (e.g. __ and __). Due to its viscosity, the endolymph [moves simultaneous with/ lags behind] head movement and pushes the __ which causes the ___ on the hair cells to bend and yields an action potential. Moving faster pushes the hair cells further and yields [bigger/more/fewer] APs.
The semicircular canals detect ANGULAR acceleration (e.g. TURNING HEAD and OBLIQUE HEAD MOVEMENTS). Due to its viscosity, the endolymph LAGS BEHIND head movement and pushes the CUPULA which causes the CILIA on the hair cells to bend and yields an action potential. Moving faster pushes the hair cells further and yields MORE APs.
The hair cells (and subsequently CN ___) have a baseline firing rate of __-__ spikes/second. This is caused by __-gated reciprocal opening & closing of __ and __ channels at the base of the cell, AKA electrical __.
Action potentials are generated on the ___ nerve. Bending of the stereocilia [toward/away from] the kinocilium causes an influx of __ ions and local depolarization. These local potentials summate at the base of the cell, causing ___ containing neurotransmitter to be released into the synaptic space –> = [increased/ decreased] firing rate and AP generated in CN VIII.
The hair cells (and subsequently CN VIII) have a baseline firing rate of 80-100 spikes/second. This is caused by VOLTAGE-gated reciprocal opening & closing of Ca++ and K+ channels at the base of the cell, AKA electrical RESONANCE.
Action potentials are generated on the 8th CRANIAL NERVE. Bending of the stereocilia TOWARD the kinocilium causes an influx of K+ ions and local depolarization. These local potentials summate at the base of the cell, causing SYNAPTIC VESICLES containing neurotransmitter to be released into the synaptic space –> = INCREASED firing rate and AP generated in CN VIII. (greater bending = faster firing rate)
How it works: K+ ions that enter through the stereocilia interact with voltage gated Ca++ channels near the base of the cell. Opening these Ca++ channels results in an influx of Ca++ –> depolarization of hair cell. The Ca++ that enters the cell then interacts with K+ channels further down the cell. Opening these K+ channels near the base of the cell causes an efflux of K+ and repolarization of the cell. This reciprocal depolarization/ repolarization is called ELECTRICAL RESONANCE of the hair cells and accounts for the baseline firing rate seen in these cells.
Movement toward kinocilium = [depolarization/ hyperpolarization] = [incr/ decr] CN VIII firing rate
Movement away from kinocilium = [depolarization/ hyperpolarization] = [incr/ decr] CN VIII firing rate
Movement toward kinocilium = DEPOLARIZATION = INCREASED CN VIII firing rate
Movement away from kinocilium = HYPERPOLARIZATION = DECREASED CN VIII firing rate
The SCCs are paired and operate in a push-pull arrangement, generating an [equal/unequal] and [same direction/ opposite] response of complimentary canals. With rotation R, we see [incr/decr] firing on the R and [incr/ decr] firing on the L. The brain detects this movement as the [absolute/ difference in] firing rate between the sides. However, there’s a limit to this! Given the baseline firing rate of 80-100Hz, head velocities of >___*/second drive the inhibited side to __. A healthy brain and vestibular system can still get information from the further increase in firing rate on the intact side. Consider the implication if one side is impaired.
The SCCs are paired and operate in a push-pull arrangement, generating an EQUAL & OPPOSITE response of complimentary canals. With rotation R, we see INCREASED firing on the R and DECREASED firing on the L. The brain detects this movement as the DIFFERENCE IN firing rate between the sides. However, there’s a limit to this! Given the baseline firing rate of 80-100Hz, head velocities of >100/second drive the inhibited side to ZERO. A healthy brain and vestibular system can still get information from the further increase in firing rate on the intact side. Consider the implication if one side is impaired: half of the vestibular system by itself can’t quantify head movement of velocities >100/sec! Many ADLs are >300*/sec.
The __ consist of the saccule and the utricle. The saccule is oriented in the [horizontal/vertical] plane, and the utricle is oriented in the [horizontal/ vertical] plane. This positions them well to detect [angular/ linear] acceleration and head position relative to ___. Their receptor area is called the __. Note that the utricle is [anterior/ post/ med/ lat] to the saccule. The posterior canal opens into the [anterior/ post/ med/ lat/ sup/ inf] aspect of the utricle, which is important in terms of the origin of BPPV.
The OTOLITHS consist of the saccule and the utricle. The saccule is oriented in the VERTICAL plane, and the utricle is oriented in the HORIZONTAL plane. This positions them well to detect LINEAR ACCELERATION and head position relative to GRAVITY. Their receptor area is called the MACULA. Note that the utricle is POSTERIOR to the saccule. The posterior canal opens into the INFERIOR aspect of the utricle, which is important in terms of the origin of BPPV.
Otoliths are sensitive to gravity because of calcium carbonate __ called __. These add mass to the ___ (they lay on top of this gelatinous membrane, analgous to the cupula). Physiologically, this matters because when the head tilts or accelerates, the endolymph causes the gelatinous mass with the __ to deflect, which bends the stereocilia. Beause of the increased mass, the gelatinous mass [moves back to/ stays in] the deflected position until ___ OR until the head regains a __ position. SO, the CN VIII associated with the otoliths have increased firing rates [at initial & end movement/ throughout the duration of movement].
Otoliths are sensitive to gravity because of calcium carbonate CRYSTALS called OTOCONIA. These add mass to the OTOLITHIC MEMBRANE (they lay on top of this gelatinous membrane, analgous to the cupula). Physiologically, this matters because when the head tilts or accelerates, the endolymph causes the gelatinous mass with the OTOCONIA to deflect, which bends the stereocilia. Because of the increased mass, the gelatinous mass STAYS IN the deflected position until MOVEMENT STOPS OR until the head regains an UPRIGHT position. SO, the CN VIII associated with the otoliths have increased firing rates THROUGHOUT THE MOVEMENT - this is a TONIC signal about head position.
Summary of Otolith Function:
- Detect head position relative to __
- [Phasic/ Tonic] Firing due to otoconia
- Head position information is transmitted centrally to the ___ (specifically the __ and __ lobes) and to the ___
- Otoliths also detect [angular/ linear] acceleration
Summary of Otolith Function:
- Detect head position relative to VERTICAL
- TONIC Firing due to otoconia
- Head position information is transmitted centrally to the CEREBRAL CORTEX (specifically the INSULAR and PARIETAL lobes) and to the VESTIBULAR NUCLEI
- Otoliths also detect LINEAR acceleration
The vestibular nerve (CN __) carries impulses away from the peripheral vestibular apparatus; specifically, it conveys information from the __ cells to the ___ in the lateral-dorsal [rostral/caudal] [midbrain/pons/ medulla] and [rostral/caudal] [midbrain/ pons/ medulla]. It consists of special sense ___ neurons.
The vestibular nerve (CN VIII) carries impulses away from the peripheral vestibular apparatus; specifically, it conveys information from the HAIR cells to the VESTIBULAR NUCLEI in the lateral-dorsal ROSTRAL MEDULLA & CAUDAL PONS It consists of special sense BIPOLAR neurons.
The blood supply of the peripheral vestibular apparatus is provided by the ___ artery which is a branch off of either the ___ or the ___ artery. There [is/ is no] collateral or anastomatic circulation to the peripheral vestibular apparatus. This means we expect [no change/ significant damage] in the event of occlusion of these vessels.
The blood supply to central vestibular structures (CNS) is provided by the ___ and the ___
The blood supply of the peripheral vestibular apparatus is provided by the LABYRINTHINE ARTERY which is a branch off of either the ANTERIOR INFERIOR CEREBELLAR ARTERY (AICA) or the BASILAR artery. There IS NO collateral or anastomatic circulation to the peripheral vestibular apparatus. This means we expect SIGNIFICANT DAMAGE in the event of occlusion of these vessels.
The blood supply to central vestibular structures (CNS) is provided by the AICA and the POSTERIOR INFERIOR CEREBELLAR ARTERY (PICA).
There are ___ (#) vestibular nuclei on each side of the brainstem: __, __, __, and __. These are in the [medial/lateral] recesses of the ___ ventricle spanning the [rostral/caudal] [midbrain/pons/ medulla] and [rostral/caudal] [midbrain/pons/ medulla]. Different nuclei have different afferent & efferent connections.
There are 4 (#) vestibular nuclei on each side of the brainstem: SUPERIOR, INFERIOR (DESCENDING), MEDIAL, & LATERAL (DEITER’S). These are in the MEDIAL recesses of the 4TH ventricle spanning the CAUDAL PONS to ROSTRAL MEDULLA. Different nuclei have different afferent & efferent connections.
The vestibular nuclei get input from…(6)
- Semicircular canals
- Otoliths
- Vestibulocerebellum
- Cervical spine (upper C spine is important to detect head position & head speed movements. Proprioceptors on facet jts, muscle spindle input)
- Visual (accessory optic) (If visual field is stable, the vestibular system will know that the VOR it generated was sufficient!)
- Other somatosensory collaterals from RETICULAR formation
The superior vestibular nerve innervates the…
Superior vestibular nerve innervates the:
- Anterior canal
- Lateral canal
- Utricle
The inferior vestibular nerve innervates the…
Inferior vestibular nerve innervates the:
- Posterior canal
- Saccule
The vestibular nuclei project back to the peripheral apparatus (aka the ___ cells) via ___ to modify their firing AND project to the ____.
Descending projections:
- Lateral and medial ___ tracts.
Ascending projections:
- Motor output to ___, __, and __ for control of ___ movements via the ___
- Via the __ to go to the cortex for [motor/sensation] relative to head movement & position.
The vestibular nuclei project back to the peripheral apparatus (aka the HAIR cells) via CN VIII to modify their firing AND project to the VESTIBULOCEREBELLUM.
Descending projections:
- Lateral and medial VESTIBULOSPINAL tracts.
Ascending projections:
- Motor output to CN III, IV, VI for control of EYE movements via the MLF
- Via the THALAMUS to go to the cortex for SENSATION relative to head movement & position.
**A LOT of hte cortex gets vestibular information! Parietal lobe (motor planning) & insular lobe (autonomic function: HR, visceral fxn)
The Medial Longitudinal Fasiculus is a [myelinated/ unmyelinated] tract of axons that connect the vestibular nuclei with the ___, ___, and ___ nuclei from the medulla to the midbrain. This exists [bilaterally/ on one side/ in a single tract centrally].
The Medial Longitudinal Fasiculus is a MYELINATED tract of axons that connect the vestibular nuclei with the ABDUCENS, TROCHLEAR, and OCULOMOTOR nuclei from the medulla to the midbrain. This exists ON EACH SIDE (R & L).
The lateral vestibulospinal tract projects to [only the cervical/ all levels of the] spinal cord and produces [gross equilibrium responses in all extremities & the trunk / head and neck movements].
The medial vestibulospinal tract projects to [only the cervical/ all levels of the] spinal cord and produces [gross equilibrium responses in all extremities & the trunk / head and neck movements].
The lateral vestibulospinal tract projects to ALL LEVELS OF THE spinal cord and produces GROSS EQUILIBRIUM RESPONSES IN ALL 4 EXTREMITIES & TRUNK (big body responses to perturbations & LOB)
The medial vestibulospinal tract projects to ONLY THE CERVICAL spinal cord and produces HEAD & NECK MOVEMENTS (keeps head level)
The vestibulocerebellum consists of the ___ lobe in the Cb. It coordinates all vestibular output & reflexes.
The vestibulocerebellum consists of the FLOCCULONODULAR lobe in the Cb. It coordinates all vestibular output & reflexes.
Reflexes associated with the vestibular system….(3)
Vestibulospinal Reflex (VSR) - Goal is to maintain postural stability in response to head tilt/gravity
Vestibular-Ocular Reflex (VOR)
- Goal is gaze stabilization
Cervico-Ocular Reflex (COR)
- Contributes to gaze stabilization
The goal of the vestibulospinal reflex is to maintain ___ in response to head tilting & gravity. With the head inclined to the right, we see [L/R] extensor response, and [L/R] flexor response. The vestibular system contributes to all postural responses, for example, can trigger ankle & hip strategies with perturbation.
A head tilt is the stimulus for the VS reflex which is sensed by the primary receptor: ___. The signal is then projected through ___ to the ___ nuclei, which activates the motor response via the __ tracts.
The goal of the vestibulospinal reflex is to maintain POSTURAL STABILITY in response to head tilting & gravity. With the head inclined to the right, we see R extensor response, and L flexor response. The vestibular system contributes to all postural responses, for example, can trigger ankle & hip strategies with perturbation.
A head tilt is the stimulus for the VS reflex which is sensed by the primary receptor: OTOLITHS. The signal is then projected through CN VIII to the MEDIAL & LATERAL VESTIBULAR nuclei, which activates the motor response via the MEDIAL (head on neck movement: neck mm) & LATERAL (whole-body response: neck & back mm) VESTIBULOSPINAL tracts.
Why do we need gaze stabilization?
- To keep an image on ___ with head movement for clear vision
- To maintain a ___ target
- To keep image fixed on fovea as a reference point for ___
- Most functional movements are at a velocity that [do/do not] depend on the VOR
Why do we need gaze stabilization?
- To keep an image on FOVEA with head movement for clear vision
- To maintain a VISUAL target
- To keep image fixed on fovea as a reference point for BALANCE
- Most functional movements are at a velocity that DO depend on the VOR
The goal of the vestibulo-ocular reflex (VOR) is to keep the image on the ___ with eye movement - gaze stabilization! This is coordinated by the ___. The vestibular system drives [head/eye] movement in response to [head/eye] movement. An effective VOR depends on:
- Accurate [peripheral/central] input
- Effective vestibular drive of [eye/head] mvmt
- Intact cranial nerves for eye movement: __, __, __
- Coordination by the __
The goal of the vestibulo-ocular reflex (VOR) is to keep the image on the RETINA with eye movement - gaze stabilization! This is coordinated by the CEREBELLUM. The vestibular system drives EYE movement in response to HEAD movement. An effective VOR depends on:
- Accurate PERIPHERAL input
- Effective vestibular drive of EYE mvmt
- Intact cranial nerves for eye movement: III, IV, VI
- Coordination by the CEREBELLUM
VOR pathway:
___ stimulates the VOR which activates a combination of __ and ___ (receptors) depending on the direction of head movement. CN VIII afferents synapse in the ___ which also receive input from the __ system (sensory input) which gives the vestibular system info about __ and if the visual target is held stable on the __ of the __. This area then projects (efferent projection) to the ___ (pathway) to drive [eye/head] movements that are equal and opposite to [head/eye] movements. If the visual target slips on the retina more than __ degrees, vision will be blurred.
VOR pathway:
HEAD MOVEMENT stimulates the VOR which activates a combination of CANALS and OTOLITHS depending on the direction of head movement. CN VIII afferents synapse in the VESTIBULAR NUCLEI which also receive input from the VISUAL system which gives the vestibular system info about GAZE STABILITY and if the visual target is held stable on the FOVEA of the RETINA. This area then projects (efferent projection) to the MLF to drive EYE movements that are equal and opposite to HEAD movements. If the visual target slips on the retina more than 2 degrees, vision will be blurred.
With a R head turn, we see increased vestibular apparatus firing rate on the [R/L] which goes to the [R/L} medial vestibular nuclei in the [midbrain/pons/medulla]. This uses the MLF to grab the [R/L] [oculomotor/ abducens/ trochlear] nucleus & generate equal and opposite [R/L] eye movement to maintain gaze fixation.
With a R head turn, we see increased vestibular apparatus firing rate on the R which goes to the L medial vestibular nuclei in the MEDULLA. This uses the MLF to grab the LEFT ABDUCENS nucleus & generate equal and opposite LEFT eye movement to maintain gaze fixation.
The cervico-ocular reflex contributes to ___ in that it is responsible for __% of compensentory [eye/head] movement in response to [eye/head] movement. Movement of the neck stimulates receptors in the ___ which send signals to the ___. This then uses the MLF to grab the [III/IV/VI] nucleus to generate eye movement.
The cervico-ocular reflex contributes to GAZE STABILIZATION in that it is responsible for 15% of compensentory EYE movement in response to HEAD movement. Movement of the neck stimulates receptors in the CERVICAL FACET JOINTS which send signals to the VESTIBULAR NUCLEI. This then uses the MLF to grab the OCULOMOTOR nucleus to generate eye movement.
The goal of optokinetic nystagmus is to keep a [fixed/moving] image fixed on the retina. The head is [moving/still]. The [fast/slow] phase of the OKR follows the object, and then the [fast/slow] saccadic movements repositions the eyes. Movement on the retina signals the ___ [midbrain/pons/ medulla] which signals the vestibular nuclei –> oculomotor nucleus –> eye movements (like the other reflexes).
The goal of optokinetic nystagmus is to keep a MOVING image fixed on the retina. The head is STILL. The SLOW phase of the OKR follows the object, and then the FAST saccadic movements repositions the eyes. Movement on the retina signals the PRETECTAL MIDBRAIN which signals the vestibular nuclei –> oculomotor nucleus –> eye movements (like the other reflexes).
Dizziness words:
- ____: visual field moving, feels unstable
- ___: Loss of balance
- ____: Sense of movement
Dizziness words:
- OSCILLOPSIA: visual field moving, feels unstable
- DISEQUILIBRIUM: Loss of balance
- VERTIGO: Sense of movement
Peripheral vestibular hypofunction can be [unilateral/ bilateral/ either] and involves decreased function of [receptors/ vestibular nerve/ both/ either]. These are [complete/ incomplete] and [can/cannot] be treated.
Peripheral vestibular hypofunction can be UNILATERAL or BILATERAL and involves decreased function of EITHER RECEPTORS OR VESTIBULAR NERVE. These are COMPLETE and CAN be treated.
With acute unilateral peripheral vestibular loss:
- Vertigo?
- Spontaneous nystagmus?
Acute unilateral loss:
- Vertigo at rest
- Spontaneous nystagmus toward intact side (VOR to impaired side)
At rest both sides are firing symmetrically at ~ __-__ Hz. With unilateral loss, your brain gets data about head movement on the intact side (based on the difference between sides) up until rates of __/sec. At > or = ___/sec, this is the point of ___ cut-off i.e. firing rates on right side have been reduced to 0; faster head turns (>__), the brain cannot detect the difference between this very fast head turn and a fast head turn happening at __ degrees/sec and so cannot make adjustments to the necessary postural response or compensatory eye movements.
At rest both sides are firing symmetrically at ~80-100 Hz. With unilateral loss, your brain gets data about head movement on the intact side (based on the difference between sides) up until rates of 100/sec. At > or = 100/sec, this is the point of INHIBITORY CUT OFF i.e. firing rates on right side have been reduced to 0; faster head turns (>100), the brain cannot detect the difference between this very fast head turn and a fast head turn happening at 100 degrees/sec and so cannot make adjustments to the necessary postural response or compensatory eye movements.
With Bilateral Peripheral Hypofunction:
- Vertigo?
- Spontaneous nystagmus?
What happens with movement?
- NO spontaneous nystagmus and no vertigo b/c no asymmetry in signals (no signals at all!)
With movement, they have a LOT of dysequilibrium (but not vertigo - not spinning).
Post vestibular neuritis is a potential cause of peripheral vestibular hypofunction. It’s the [most common/ 2nd most common/ least common] cause of vertigo and is a result of a [viral/ bacterial] infection of ___. It may be idiopathic, but often follows a ___ infection. It improves within __-__ [hrs/days], and usually resolves within ___ [hrs/days/weeks]. It can be treated with ___ (meds), and recovery can be hastened with vestibular exercises. Recurrent bouts can be cumulative (2/2 loss of hair cells and/or axons of the fibers of the 8th nerve) These patients have:
- Vertigo?
- Nystagmus?
- Imbalance?
- N/V?
Post vestibular neuritis is a potential cause of peripheral vestibular hypofunction. It’s the 2ND MOST COMMON cause of vertigo and is a result of a VIRAL infection of CN VIII. It may be idiopathic, but often follows a RESPIRATORY INFECTION. It improves within 48-72 HRS, and usually resolves within 6 WEEKS. It can be treated with VESTIBULAR SUPPRESSANTS (MECLAZINE, ANTIVERT), and recovery can be hastened with vestibular exercises. Recurrent bouts can be cumulative (2/2 loss of hair cells and/or axons of the fibers of the 8th nerve) These patients have:
- SEVERE ROTATIONAL VERTIGO
- SPONTANEOUS HORIZONTAL Nystagmus
- Imbalance
- NAUSEA
Peripheral hypofunction can also be the result of:
- ___-Related changes (including __ and __)
- ___ 2/2 aminoglycosides
- Traumatic ___ nerve damage
- Post-surgical ____
Peripheral hypofunction can also be the result of:
- AGE-Related changes (including ATHEROSCLEROSIS [slow or fast onset] and NEUROPATHY [slow onset])
- OTOTOXICITY 2/2 aminoglycosides
- Traumatic CN VIII nerve damage
- Post-surgical ACOUSTIC NEUROMA
Acute peripheral hypofunction may include: (5)
Chronic peripheral hypofunction may include: (2)
Acute peripheral hypofunction may include:
- Stroke
- Neuritis
- Ototoxicity
- Trauma
- Post op acoustic neuroma
Chronic peripheral hypofunction may include:
- Age-related
- Cumulative effects of Meniere’s or Recurrent neuritis
Treatment approach to peripheral hypofunction:
Patient may compensate via mechanisms in the [PNS/CNS]. This will increase the __ to remaining vestibular input, as well as __ and __ input. It will challenge the brain to reinterpret asymmetrical input. This all requires an intact ___ to develop compensatory mechanisms.
Treatment approach to peripheral hypofunction:
Patient may compensate via mechanisms in the CNS. This will increase the SENSITIVTY to remaining vestibular input, as well as SS and VISUAL input. It will challenge the brain to reinterpret asymmetrical input. This all requires an intact CNS to develop compensatory mechanisms.
Distorted vestibular function is usually due to ___ malfunctions of the receptor mechanisms: the stimuli are incorrectly transduced. These patients [are/are not] amenable to tx.
Distorted vestibular function is usually due to MECHANICAL malfunctions of the receptor mechanisms: the stimuli are incorrectly transduced. These patients ARE amenable to tx.
___ is the most common cause of vertigo. It is characterized by brief periods of vertigo when pt’s head is in certain positions, usually w/the affected ear [up/down]. It is accompanied by a __ that occurs in the same plane as the affected canal and takes __-__ seconds to come on, and then crescendos/decrescendos over __-__ seconds.
BPPV is the most common cause of vertigo. It is characterized by brief periods of vertigo when pt’s head is in certain positions, usually w/the affected ear DOWN. It is accompanied by a NYSTAGMUS that occurs in the same plane as the affected canal and takes 1-40 seconds to come on, and then crescendos/decrescendos over 10-60 seconds.
There are two primary types of BPPV: __ and __.
In ___, we see immediate onset of sx in the provoking head position. This is because part of the otoconia from the utricle dislodges, floats into the canal, and adheres to the __.
In ___, there is a several second latency until sx onset after assuming the position. This is because the otoconia add mass to the __ and exaggerate the vertigo effect.
There are two primary types of BPPV: CUPULOLITHIASIS and CANALITHIASIS.
In CUPULOLITHIASIS, we see immediate onset of sx in the provoking head position. This is because part of the otoconia from the utricle dislodges, floats into the canal, and adheres to the CUPULA.
In CANALITHIASIS, there is a several second latency until sx onset after assuming the position. This is because the otoconia add mass to the ENDOLYMPH and exaggerate the vertigo effect.
BPPV generally involves the [anterior/ posterior/ lateral] canal. This is 2/2 the anatomy of the peripheral vestibular apparatus: the ___ of the [ant/ post/ lat] canal is located below the ___, so debris from that falls easily into this canal.
What’s the cause?
BPPV generally involves the POSTERIOR canal. This is 2/2 the anatomy of the peripheral vestibular apparatus: the AMPULLA of the POSTERIOR canal is located below the UTRICLE, so debris from the UTRICLE falls easily into the POSTERIOR canal.
It can be IDIOPATHIC, TRAUMATIC, OR ASSOC. W/AGING
Treatment approaches to BPPV (Distorted function) include normalizing the system by ___ OR ___ to abnormal input.
Treatment approaches to BPPV (Distorted function) include normalizing the system by DISLODGING DEBRIS OR HABITUATING to abnormal input.
Fluctuating vestibular function involves [consinstent/ occasional or intermittent] disruption of vestibular input. The input is typically [present/absent] but fluctuates; the diesease is episodic. It is [unilateral/ bilateral/ can be either]. It [is/is not] amenable to PT tx because the __ cannot adapt or compensate. Typical causes of fluctuating function include…(5)
Fluctuating vestibular function involves OCCASIONAL OR INTERMITTENT disruption of vestibular input. The input is typically PRESENT but fluctuates; the disease is episodic. It is UNILATERAL OR BILATERAL. It IS NOT amenable to PT tx because the CNS cannot adapt or compensate. Causes: - Meniere's dz - Perilymph Fistula - Autoimmune dz - Infections - Migranious
In Meniere’s dz, we see abnormal function of the __. The sac expands & puts pressure on the ___ and then suddenly releases built up ___. This affects the __ apparatus or __ and results in episodes of __ loss or vestibular dysfunction. Most acute sx resolve in __-__ hrs with nearly full recovery in [hrs/days/weeks]. This disease results in cumulative loss over time of diminished __ and __ function. Treatment is usually focused on __ and a HEP and preventing secondary impairments.
In Meniere’s dz, we see abnormal function of the ENDOLYMPHATIC SAC. The sac expands & puts pressure on the NERVE and then suddenly releases built up ENDOLYMPH. This affects the VESTIBULAR apparatus or COCHLEA and results in episodes of HEARING loss or vestibular dysfunction. Most acute sx resolve in 24-36 hrs with nearly full recovery in DAYS TO WEEKS. This disease results in cumulative loss over time of diminished HEARING and BALANCE function. Treatment is usually focused on EDUCATION and a HEP and preventing secondary impairments
Perilymph fistula results in a fistula between the __ and __ chamber. Vestibular sx are precipitated by ___ stimulus or change in __ pressure. It can be caused by __ trauma, __, surgery, or a penetrating injury to the ear. It is treated with [ PT / rest or surgery].
Perilymph fistula results in a fistula between the MIDDLE EAR & PERILYMPH chamber. Vestibular sx are precipitated by AUDITORY stimulus or change in AIR pressure. It can be caused by HEAD trauma, BAROTRAUMA (e.g. diving at depth), surgery, or a penetrating injury to the ear. It is treated with REST OR SURGERY
Possible etiologies of central vestibular dysfunction include…(4)
Possible etiologies of central vestibular dysfunction include:
- Vascular (Wallenberg’s syndrome: basilar or PICA artery infarct that takes out the vestibular area)
- Tumor
- Degenerative/ Aging
- Trauma
*Direction changing nystagmus = CENTRAL problem!
Central vestibular problems could involve lesions to a number of locations…Go! (5)
Central vestibular problems could involve lesions to a number of locations.
(1) Vestibular Nuclei
(2) Cerebellum
(3) Other CNS areas (reticular formation)
(4) Visual pathways
(5) Motor output (eye movement or postural mm)
Nystagmus associated with central vestibular lesions may be resting or gaze evoked. A resting nystagmus is the result of impaired ___ mechanisms. A gaze-evoked nystagmus is the result of impaired ___ at the end of a saccade or smooth pursuit. A ___ nystagmus is ALWAYS central.
Nystagmus associated with central vestibular lesions may be resting or gaze evoked. A resting nystagmus is the result of impaired GAZE FIXATION mechanisms. A gaze-evoked nystagmus is the result of impaired NEURAL INTEGRATOR at the end of a saccade or smooth pursuit. A DIRECTION-CHANGING nystagmus is ALWAYS central.
VOR Cancellation involves turning the [eyes/head] and moving the [eyes/head] with it. This is a [use of/ override of] the VOR by the [CNS/PNS]. This involves brainstem mechanisms [above/ below] the vestibular nuclei, so an inability to cancel the VOR indicates [CNS/PNS] involvement.
VOR Cancellation involves turning the HEAD and moving the EYES with it. This is an OVERRIDE of the VOR by the CNS This involves brainstem mechanisms ABOVE the vestibular nuclei, so an inability to cancel the VOR indicates CNS involvement.
There is [good/poor] evidence for the efficacy of vestibular rehab for peripheral disorders, but [good/poor/less] evidence for central disorders. The approach with central disorders is to promote [up/down] regulation of vestibular fxn through vestibular exercises.
There is GOOD evidence for the efficacy of vestibular rehab for peripheral disorders, but LESS evidence for central disorders. The approach with central disorders is to promote UP regulation of vestibular fxn through vestibular exercises.
Differentiate between central & peripheral nystagmus:
Peripheral nystagmus:
- [will/will not] fatigue
- Will eventually be compensated for by the [CNS/PNS]
Central Nystagmus
- [will/will not] fatigue
- Unless there is true recovery of central mechanisms, [will/will not] attenuate over time.
Differentiate between central & peripheral nystagmus:
Peripheral nystagmus:
- WILL Fatigue
- Will eventually be compensated for by the CNS
Central Nystagmus
- WILL NOT fatigue
- Unless there is true recovery of central mechanisms, WILL NOT attenuate over time.
3 types of physiological nystagmus. Are these normal or abnormal?
- End point nystagmus (30% of population)
- Optokinetic nystagmus (tracking element + quick saccadic reset, e.g. Telephone poles in the car)
- Nystagmus with caloric testing (COWS)
3 types of pathological nystgamus. Normal or abnormal?
- Spontaneous (at rest)
- Positional (comes on in a position)
- Gaze evoked (look L, see nystagmus)
Nystagmus stemming from a [central/ peripheral] cause can be suppressed by visual fixation. We can get rid of that visual fixation and prevent the patient from suppressing the nystagmus by using ___.
Nystagmus stemming from a PERIPHERAL cause can be suppressed by visual fixation. We can get rid of that visual fixation and prevent the patient from suppressing the nystagmus by using FRENZEL LENSES.
How do we test the vestibulo-ocular system? 3 main ways…
Vestibulo-ocular system tests:
- Electronystagmography (ENG) (eye movements via oculomotor screen; vestibular function via positional and caloric tests)
- Rotary Chair Test
- Visual-Vestibular Interaction Tests (VVI)
Electronystagmography (ENG) testing consists of tests for ___ movements (aka the ___ screen to look at ___ and ___) and for ___ function (via ___ and ___ tests).
It involves electrodes being placed around the eyes to record ___. This works because the ___ has [negative/positive] potential, so as the __ moves [horizontally/ vertically / both], the charge moves. Electrodes track and record the difference between the location of that potential and the electrode.
Electronystagmography (ENG) testing consists of tests for EYE movements (aka the OCULOMOTOR screen to look at PURSUIT [tracking] and SACCADES [rapid eye movement]) and for VESTIBULAR function (via POSITIONAL and CALORIC tests). It involves electrodes being placed around the eyes to record EYE MOVEMENT. This works because the CORNEA has NEGATIVE potential, so as the EYE moves HORIZONTALLY OR VERTICALLY, the charge moves. Electrodes track and record the difference between the location of that potential and the electrode.
How do we test for the vestibulospinal system? This assesses for both __ and __ strategies.
Test VS system via Posturography - motor and sensory strategies.
E.g.) CTSIB, Balance master, etc.
An ENG test is looking for abnormalities in eye movement at rest and with position changes including:
- Presence of ___ and during eye movement (30*)
- Abnormalities in __ an d__
- Direction and duration of any ___ observed during __ tests
- Presence/absence of __ during ___ testing
An ENG test is looking for abnormalities in eye movement at rest and with position changes including:
- Presence of NYSTAGMUS and during eye movement (30*)
- Abnormalities in PURSUIT and SACCADIC
- Direction and duration of any NYSTAGMUS observed during POSITIONAL tests
- Presence/absence of NYSTAGMUS during CALORIC testing
With caloric stimulation, you [expect/ do not expect] nystagmus in a normal eye. How it works: you irrigate the [internal/external] auditory canal and create a ___ gradient. This stimulates the [ant/ post/ lateral] canals and induces ___. COWS describes the [fast/slow] phase of the nystagmus: C___ = O____, W___ = S____. >__% difference between the 2 sides is significant. The side that has less of a nystagmus is [normal/ hyperfunctioning/ hypofunctioning].
With caloric stimulation, you DO EXPECT nystagmus in a normal eye. How it works: you irrigate the EXTERNAL auditory canal and create a TEMPERATURE gradient. This stimulates the LATERAL canals and induces NYSTAGMUS. COWS describes the FAST phase of the nystagmus: COLD (86F) = OPPOSITE, WARM (111F) = SAME SIDE. >25% difference between the 2 sides is significant. The side that has less of a nystagmus is HYPOFUNCTIONING
In rotational testing, the [head/ body/ head and body] is/are fixed to a rotating chair and ___ movement is recorded. There are two sequences:
(1) Sinusoidal Vertical Axis Rotation (SVAR) in which the head moves with the chair (eyes fixed on target) to test the ___, specifically looking for ___..
(2) Visual-vestibular Interaction Testing (VVI) in which the chair is rotated and your eyes follow a target that rotates with you. This tests ___.
In rotational testing, the HEAD & BODY are fixed to a rotating chair and EYE movement is recorded. There are two sequences:
(1) Sinusoidal Vertical Axis Rotation (SVAR) in which the head moves with the chair (eyes fixed on target) to test the VOR, specifically looking for OPTOKINETIC NYSTAGMUS..
(2) Visual-vestibular Interaction Testing (VVI) in which the chair is rotated and your eyes follow a target that rotates with you. This tests VOR CANCELLATION.
Gaze stabilization can be assessed by looking at gain, phase, or retinal slip.
(1) Gain: ratio of __ to __. Normal = 1. Vestibular patients have a gain of [>/ =/ / =/ __*/second = ____.
Gaze stabilization can be assessed by looking at gain, phase, or retinal slip.
(1) Gain: ratio of EYE MOVEMENT AMPLITUDE to HEAD AMPLITUDE. Normal = 1. Vestibular patients have a gain of LESS THAN 1. Cerebellar patients have a gain of MORE THAN 1 (OVERSHOOT target even w/VORs).
(2) Phase: describes in degrees how much EYE LEAD or HEAD LAG movement is observed.
(3) Retinal slip: calculated as HEAD VELOCITY minus EYE VELOCITY velocity. Normal = ZERO. Retinal slip >2*/second = OSCILLOPSIA.
Recovery terminology after Vestibular Dysfunction:
(1) Compensation = overall process of how __ recovers from vestibular dysfunction. Includes both __ and __.
(2) Adaptation = refers specifically to increasing the ___; true recovery of this means that its accuracy is improving.
(3) Substitution = pt uses other mechanisms to substitute for ___. You [are/ are not] getting adaptation of the VOR.
(4) Habituation = get used to it. This generally is used in patients with [normal/ abnormal] inputs.
Recovery terminology after Vestibular Dysfunction:
(1) Compensation = overall process of how CNS recovers from vestibular dysfunction. Includes both ADAPTATION and SUBSTITUTION.
(2) Adaptation = refers specifically to increasing the VOR GAIN; true recovery of VOR means that VOR accuracy is improving.
(3) Substitution = pt uses other mechanisms to substitute for VOR. You ARE NOT getting adaptation of the VOR.
(4) Habituation = get used to it. This generally is used in patients with ABNORMAL inputs, e.g. BPPV pt who cannot clear
The vestibular system can adapt via either peripheral or central mechanisms. Peripherally, the Cb and vestibular nuclei have direct projections to ___ that can modify the firing rate of the __, so essentially they can slow the baseline firing rate and make the difference between impaired and intact sides [greater/ smaller] leading to [worse/ less bad] vertigo.
The vestibular system can adapt via either peripheral or central mechanisms. Peripherally, the Cb and vestibular nuclei have direct projections to HAIR CELLS that can modify the firing rate of the CN VIII, so essentially they can slow the baseline firing rate and make the difference between impaired and intact sides SMALLER leading to LESS BAD vertigo.
With an acute unilateral peripheral lesion, we see __ and __. Within days, the ___ adapt to make those symptoms at rest subside.
With an acute unilateral peripheral lesion, we see NYSTAGMUS and VERTIGO. Within days, the VESTIBULAR NUCLEI adapt to make those symptoms at rest subside.
