Audiology - balance

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the anterior, lateral Semicircular canals & the utricle are innervated by?: The superior vestibular nerve
The posterior semi circular canal & saccule are innervated by ?: The inferior vestibular nerve
2 pathways from the vestibular nuclei to the spinal cord are?: 1. The lateral vestibulospial tract
2. the medial vestibulospinal tract
The cell bodies of the vestibular nerves are located in?: Scarpa's ganglion
utricular excitation occurs during?: horizontal linear acceleration or static head tilt
Saccular excitation occurs during?: vertical linear acceleration
The ultimate purpose of vestibular otolith organs & semicircular canals is to ?: Transmit mechanical energy, derived from head movement to its hair cells. Each being sensitive to different kinds of movements
Structural & functional organization of 3 semicircular canals?: -2/3 of a circle (by design to give all planes)
-all open to the utricle
-each at rt angle to other two
-named relative to position with head upright
--superior or anterior = vertical
--Inferior or posterior = vertical
--lateral or horizontal - tilts upward 30 deg
-Ampulla - bulbous end houses sensory cells
-5 openings to utricle because 2 ends join to 1
-Crista ampullaris
--ridge of tissue that extends across ampulla at right angles to semicircular ducts
the semi circular canals are filled with?: endolymph
high concentration of K+ low concentration Na+
what is the cupula?: serves as a barrier separating semicircular canals from the vestibule
- has specific gravity equal to endolymph
What is the Crista?: Positioned beneath the cupula, extends across the canal in saddle shape
-contains Hair cells & vestibular afferents
The semicircular canals neuroepithelia are sensitive to what type of motion?: angular acceleration (motion involving rotation)
-under normal conditions the Semicircular canals receptors do not respond to static head position because they are not stimulated by gravitational force
The hair cells of the Crista do what?: -generate action potentials in response to cupular deflection
-deflection of HCs toward kinocillia --> depolarization (excitation)
-deflection away from the kinocillia --> hyperpolarization (inhibition)
In the lateral crista, each hair cell is situated how?: -so that its kinocilium face the utricle
-if the head moves so as to displace the lateral cupula toward the utricle, (utriculopetal deflection)the stereocilia deflect toward the kinocillia get depolarization or excitation
-Cupular deflection away from the utricle (utriculofugal displacement )will hyperpolarize the hair cells -->inhibition
As head turns right, HCs in the right horizontal semi circ canal are? HCs in the left horizontal scc are?: excited

inhibited

push pull dynamics
Hair cells in the verticle SCCs are oriented how?: -so that endolymph motion toward the utricle causes excitation (kinocilia closest to the utricle)
Hair cells of the maculae project into?: -a gelatinous material that is topped with calcium carbonate chyrstals called otoconia
-this gives the otolith organs an inertial mass
The presence of otoconia increases? resulting in?: -the specific gravity above that of endolymph
- as a result the maculae are responsive to linear acceleration, including force of gravity as head is placed in different positions
The kinocilia of the utricle HCs are oriented how? of the Saccule?: - toward their striola

-away from their striola

-utricle excitation occurs during horizontal linear acceleration or static head tilt
- saccular excitation occurs during verticle acceleration
Location of the saccule?: -located in a depression in the wall of the vestibule called the spherical recess
-immediately adjacent to the basal portion of the cochlea and is connected to the cochlear duct by the ductus reuniens
-the endolymphatic compartment of the cochlear duct is in contact with the saccule
In vestibular testing... hierarchy of analysis: 1st - need an ability to deetermine if the test results are normal or abnormal
-next if abnormal, is it peripheral or central
-what is the specific loci of the abnormality
The vestibular system can be damaged in many ways such as:: -toxicity of high doses of antibiotics
-bilateral lesions of the vestibular labyrinths
What tests are conducted in balance testing?: Ocularmotor tests:
Gaze
Saccade
Smooth pursuit
Optokinetics
Dix Hall Pike maneuver (BPPV)
positional testing
calorics
- Tests should be interpretated as a "whole", some are better predictors than others
Abnormalities with occular motor tests are indicative of?: central lesions
Tests that are performed for site of lesion testing are:: 1. ENG/VNG
2. Occular motor evaluation
3. Rotational chair studies
4. VEMP
5. EcochG - electrocochleography
6. Postural control assessment
In looking at VNG/ENG test battery you are looking for ?: -a pattern of results that agree with one another
-VNG/ENG test battery needs to be interpreted as a whole because of the poor specificity of the individual tests
-overall problems in occular motor tests indicate central lesions, however patient factors such as inattention and age can contaminate the results
-large numbers of people will have nystagmus during positional testing. Only abnormal if it has large amplitude, persistant and /or direction changing
What findings are the only ones that localize lesion to the peripheral vestibular ?: dixhall Pike for BPPV-canalithiasis type nystagmus
and
unilateral weakness to caloric stimulus
the primary function of the vestibular system is? what 2 reflex pathways are involved: To maintain balance & gaze stability

1. the vestibulo spinal reflex - produces postural changes to maintain equilibrium
2. VOR (vestibular occular reflex) produces compensatory eye movement to maintain gaze stability
Nystagmus with fixation (eyes open) is always?: abnormal
any persistent nystag for occular displacements of 30deg or less is considered: abnormal
Characteristics of spontaneous nystagmus: -can be peripheral or central in origin
-can be horizontal or vertical
when nystagmus increases with fixation it is called: fixation nystagmus - definitely central
Peripheral vestibular disease results in what kind of nystagmus: -spontanious nystagmus that is horizontal or rotational
-right or left beating
-reduced in amplitude by fixation
-follows Alexanders Law during gaze testing (nystagmus increases when gaze is towards the direction of the fast beat)
-during the acute phase of peripheral vestibular system disease the nystag beats toward the healthy ear
Spontaneous nystagmus, central nervous system disease: -purely horizontal, not attenuated by fixation
-periocdic, alternating nystagmus occurs with a variety of cerebellar conditions
-reverses direction ~ every 2 minutes

There are many drugs that are central acting & can produce spontaneous nystagmus
nystagmus w/o fixation is?: normal unless > 6 deg/sec
Congenital Nystagmus facts: -abnormal eyemovements that are diagnosed shortly after birth
-often increases with fixation
-present in Albanism & chromatopsia
-patients with CN makes interpretation of ENG/VNG difficult
Nystagmus usually beats towards ?: the unaffected ear
(after recovery, the nystagmus decreases and may actually transiently reverse its direction in some patients when central compensation occurs
head thrust test used to assess what?: semicircular canal function
Ascending Axons from the vestibular nuclei form the ...: Medial Longitudinal Fasciculus (MLD)

the MLf has anxons which terminate in the nuclei of cranial nerves III, IV, VI
The vestibular nuclei receive input from sources other than vestibular nerve too. these sources are?: -the visual system
-the cerebellum
-the brainstem reticular formation
-the spinal cord
The eye muscles must be coordinated in complimentary pairs aligned with 3 SCCs ... the pairings are: -Superior rectus & inferior oblique with the Sup SCC
-Inferior rectus and superior oblique with the Inf SCC
-lateral & medial rectus with the horizontal canal
When the eyes move relatively slowly in one direction then quickly return to the midline called?: nystagmus
- The initial slow stage is controlled by the vestibular system
- The quick return to midline is under control of the brainstem reticular formation
nystagmus may occur when?: -spontaneously in various disorders
-when head is placed in certain positions
-may be induced in the clinic by rotational chair or caloric stimulation
Direction of beating in nystagmus is defined by: the fast beating saccadic not the vestibular aspect

whichever direction eyes snap back to the middle is the beating nyst.
Pure vertical nystagmus should be considered of ____ origin until: central origin

proven otherwise
What is version: tandem movement of the eyes, the ability to follow back & forth
What is vergence?: Bringing the eye in close to focus the fovia on a target
VOR ___ & ___ are among the important measures of vestibular function that laboratory tests like ___ ___ use to ____ ____: - gain and phase
-rotational chair
-objectify function
This test stimulates each vestibular system by rotating subjects in the dark.
-nystagmus should be generated for rotations in subjects with normal vestibular function
-the extent of pathology is determined by comparing VOR gain, phase & duration of nystagmus from rotations toward one ear with rotations toward the opposite ear
Describe the VOR: -when the head is rotated to the right, neural discharge is from the right ear, is increased which will be transmitted to the abducens & oculomotor nerves that control the lateral rectus of the left eye & medial rectus of the right eye. These muscles draw the eyes left with the velocity & amplitude of the head movement
What 2 muscles move the eye horizontally?: the medial and lateral recti
what 2 muscles move the eyes vertically: the superior & inferior recti
The superior and Inferior oblique muscles do what?: move the eye tortionally and vertically
what are the cranial nerves III, IV & VI and which muscles do they innervate in the eye?: III = the occulomotor, is the only nerve that innervates multiple muscles
- the sup & inf recti
-the medial recti
-the inferior oblique
IV Trochlear nerve only inervates the Superior oblique
VI - the Abducens only inevates the lateral rectus (horizontal diplopia
In addition to innervating the lateral recti, the abducens sends internuclear neurons where?: to project to the oculomotor nuclei which stimulates the medial rectus (when moving eyes horizontally)
The MLF is a ____ _____ that runs ____ ____ commonly affected by _____ ie ____ resulting in _____: critical pathway
a long distance
diseases like MS
Internuclear opthalomoplegia
Internuclear Opthalmoplegia is?: form of eye muscle weakness
-disorder is caused by injury or dysfunction in the MLF, a heavily myelinated tract that allows conjugate eye movement by connecting the para median pontine reticular formation abducens nucleus complex of one side to the oculomotor nucleus of the opposite side
- MS in young patients almost always the cause.
-In older patients one sided lesions or stroke are possibilities
Semi circular canals measure ____ energy otolith organs measure ____ energy: Kinetic

Static
What causes one & one half syndrome?: If both the abducens & ipsilateral MLF are damaged
What does version require how is it accomplished?: requires that different oculomotor nuclei or subnuclei innervating muscles in each eye are activated together
-accomplished via "yoking" together of the oculomotor nuclei with brain stem tracts so that pairs that activate yoked muscles are adjacent
Disadvantages of EOG: -CRP is affected by light
-retinal degeneration
-diabetic retinopathy
-hypertensive retinopathy
-retinitis pigmentosa
What is CRP?: Corneoretinal potential, a bioelectrical signal that is measured during electro-oculography which is the recording technique used in ENG
The electrical transducer of the visual system is? is also the source of>: retina

corneoretinal potential (CRP)
As metabolic activity in the retina is affected by light CRP values --> How are they affected?: CRP values vary across levels of illumination
-there is a 2 fold increase in measured potentials in light as compared to dark
-Dark room decrease CRP to lowest magnitude
most common contaminant in EOG recordings?: eye blink artifact
-show s in the vertical channel
EOG techniques cannot record what types of eye movements?: -tortional
-BPPV results in eye movements with a strong tortional component, the use of video recording techniques provides a means for identifying visually these movements
The measurement & quantification of VOR enables what? It is these connections that make what? Such as?: -enables clinicians to infer indirectly the functional status of the peripheral and central vestibular systems
-make it possible for clinicians to quantify the dynamics of eye movement subsystems:
-intactness of gaze maintenance
-saccade
-pursuit
-optokinetic subsystems
Fuzzy ENG traces can be due to?: -during automated calibration the computer was increasing the amplification to the max level as the CRP was very small
-Patients with retinal disease could be identified by observing the magnitude of amplification when doing EOG
When can VNG NOT be used?: -patients with ptosis of the eyelids
-children under 5- goggles don't fit
-patients with diseases affecting the shape of the pupil
-patients who are unable to keep their eyes open
-bushy eyebrows/makeup
what is CDP?: Computerized Dynamic Posturography
[patients can have normal results with ENG/VNG but have consistent repeatable abnormalities using CDP]
-helps in establishing basis for a falls/risk assessment & falls prevention program
Facts about posturography testing: -While SOT (sensory organization test) is strictly a functional evaluation with no site of lesion information, the use of MCT(motor control test) & PER progress from functional to site specific info
-full eval of computerized Dynamic Posturograph not needed by all patients. use of history, presenting symptoms with clinical screening tests can be used to identify those who would benefit most.
-use of patient's presenting symptoms together with MCT protocol can help identify which patient needs PER
-PER & MCT protocols are of assistance in evaluating "other than vestibular ocular" pathways
What is SOT?: The Sensory Organization Test (SOT) objectively identifies problems with postural control by assessing the patient's ability to make effective use of (or suppress inappropriate) visual, vestibular, and proprioceptive information.
During the SOT, useful information delivered to the patient's eyes, feet and joints is effectively eliminated through calibrated "sway referencing" of the support surface and/or visual surround. The support surface and/or visual surround tilt to directly follow the patient's anteroposterior body sway, eliminating orientation information. By controlling the usefulness of the sensory (visual and proprioceptive) information through sway referencing and/or eyes open/closed conditions, the SOT protocol systematically eliminates useful visual and/or support surface information and creates sensory conflict situations. These conditions isolate vestibular balance control, as well as stress the adaptive responses of the central nervous system. In short, patients may display either an inability to make effective use of individual sensory systems, or inappropriate adaptive responses, resulting in the use of inaccurate sense(s).
What is MCT?: The Motor Control Test (MCT) assesses the patient's ability to quickly and automatically recover from unexpected external provocations. Sequences of small, medium or large (scaled to the patient's height) platform translations in forward and backward directions elicit automatic postural responses. Measurements include onset timing, strength and lateral symmetry of responses.
The principle output parameter of the MCT test is?: -the latency to onset of active recovery from the unexpected translations
CTSIB test ? (Clinical Test of Sensory Interaction for Balance): The CTSIB test helps determine which sensory system (visual, somatosensory, or vestibular) the person relies on to maintain balance.
The Clinical Test of Sensory Interaction and Balance is a timed test (normal is 30 seconds) that was developed for systematically testing the influence of visual, vestibular, and somatosensory input on standing balance.[2] This test is inexpensive, requires minimal equipment, and is currently in use by some clinicians. Conditions 1, 2, and 3 involve standing on the floor with eyes open, eyes closed, and wearing a visual-conflict dome. The dome provides a sensory conflict by depriving the subject of peripheral vision and introducing a sway-referenced image. Use of the conflict dome results in a discrepancy between vestibular input stimulated by postural sway and visual flow.[1] Thus, conditions 2 and 3 should examine different aspects of sensory organization of visual information that may require different postural adjustments.[3] That is, condition 2 examines how well subjects maintain balance in the absence of any vision, and condition 3 examines how well subjects maintain balance when vision is present but that information conflicts with vestibular information.
Conditions 4, 5, and 6 involve standing on foam and repeating the visual conditions described for conditions 1 through 3. For each condition, the length of time the subject can maintain standing and the amount of body sway that occurs are assessed.
The outcome parameter for the CTSIB is: length of time up to 30 sec that a person could stand w/o taking a step or releasing arms from placement of X on shoulders
The most important aspect of interpretation for the SOT is?: it provides information as to which input system cues, the patient is unable to utilize for performing the task of maintaining postural control

Strictly a test of functional ability
SOT protocol? SOT measures?: Equitest performs this:
-measured is the COP (center of pressure)
-measured from dual force plates
-COP data is used to calculate Center of Mass and gives an "equilibrium score"

SOT measures the ability to perform volitional quiet stance during a series of 6 specific conditions
VEMPS supplement the vestibular test battery by?: Providing diagnostic information about saccular and/or inferior vestibular nerve function
VEMP stands for: Vestibular Evoked Myogenic Potentials
VEMP is mediated by a predominantly ipsilateral anatomic pathway Includes?: -saccular macula
-afferent inferior vestibular nerve
-brainstem vestibular nuclei
-descending medial vestibulospinal tract
-the motorneurons of the sternocleido mastoid muscle
EchoG measures: The relative difference between the scala media & scala vestibuli
-In menieres - Reisners membrane is pushed up --> get pos. eCochg
what eye movement does the saccade represent?: -fast compensatotry movement nothing to do with the vestibular system
-nystagmus - the slow movement component =slow phase
-the nystagmoid beat = slow movement plus saccadic movement
Saccade measurement parameters?: Latency - difference in time between the presentation of a target and the beginning of the saccade intended to acquire the target

Velocity - peak rather than mean speed during movement

Accuracy - prevalence of saccades that are smaller (hypometric) or greater (hypermetric) than appropriate
High level oculomotor control is achieved through? such as?: -systems that rapidly reposition eyes -saccades
-systems that track moving objects -pursuit & optokinetic nystagmus
-fixation circuitry that keeps the lower levels stable
Narrowing of diagnostic possiblities of slow saccades... If saccades slow in all directions? Greater affect in vertical saccades?: Global saccadic paresis - slow in all directions
-drug ingestion, drowsiness, cerebellar degeneration, Huntington's chorea,
-progressive external opthalmoplegia

If greater affect in vertical?
-disorders of midbrain
-ocular muscle involvement typical of thyroid disease
Saccade testing abnormalities do not occur as a result of ____ ____ ____: Peripheral system lesions
What is saccadic latency? Prolongation of saccades is when average is > ___ This is almost always due to? but if not...then ___: latency = the time between when the target moves & the eye moves
when > 400ms
-almost always due to inattention
-if not ... could be due to basal ganglion disorder
Some saccade intrusions & oscillations ... Suggestive of?: -square wave jerks
-macro square wave jerks
-macro saccadic oscillations
-ocular flutter

suggestive of cerebellar and or BS involvement
Saccadic inacuracy is called? In people with normal vision, most common cause?: Dysmetria - most common cause is inabilty to see target
otherwise
due to cerebellar lesions
The speed of saccades is controlled by?: rapidly firing brainstem cells called burst cells
Square wave jerks: inappropriate saccades that take eye off the target, followed by an inter saccadic interval (~200ms) and a corrective saccade to bring the eyes back to the target (can be seen in normal pts)
-may be generated by cerebral hemisphere, cerebellum and superior colliculus
-abnormal in young pts when > 1/sec
-difficult to assess in elderly because it is so common
What makes saccadic control robust?: -the brain stem circuitry is shared by numerous parallel pathways. This central redundancy makes saccadic control very robust
-it is unusual to encounter disorders where saccades cannot be generated
-generally not affected by age
What artifact can look like an overshoot? What else can give false overshoot or undershoot?: Blink artifact
-many pts will blink everytime they complete a saccade

Calibration errors, improper calibration can look like overshoot or undershoot
-actual overshoots & undershoots will have corrective saccades
Describe true overshoot dysmetria: the initial saccade is too large and the corrective saccade occurs in the opposite direction
(transient overshoot dysmetria is not abnormal)
-abnormal if the overshoots do not decrease & disappear as recording progresses
-to be abnormal, overshoot dysmetria needs to occur at least 50% of the time and be larger than 2 deg
-enduring overshoot dysmetria is a classic sign of cerebellar lesions
-can occur in INO
Undershoot dysmetria: -the initial saccade is too small and the corrective saccade continues toward target
-normal subjects will show undershoot of 1-2 deg for 20 deg and larger targets
-constant & significant undershooting can be indicative of basal ganglion disorder,Parkinsons disease
-significant is defined as the 1st saccade achieving less than 50% of the distance to target
-patient can undershoot if he doesn't see the target
Saccadic abnormalities of latency: -both eyes in all directions
--fatigue, meds, drowsy, visual deficits - sever reductions in acuity, amblyopia(lazy eye)
--basal ganglia as in Parkinsons where target location & timing of movement is regular

Abnormally short latency
-highly unusual- most likely pt anticipating target and need reinstruction
Saccade abnormalities of accuracy: Hypometria (undershoot)
-fatigue, meds, drowsy
-unilateral-ipsilateral cerebellar/brainstem
-visual acuity
-myasthenia gravis for large saccades, Burst neurons providing too short a burst
Hypermetria(overshoot
-cerebellar, bilateral cerebellar fastigial nucleus
2 most common causes of abnormal saccades?: CNS disorder
Ocular disorder
Saccadic velocity is ___ ___ across individuals so you need at least ___ saccades varying in size from ___ to ___ to get an accurate estimation of the persons velocity: highly variable
need at least 40 saccades
varying in size between 10deg to 40 deg
must compare to clinics normative values
Saccade considered slow when? appearance of slow saccade 1st consideration should be? 2nd consideration?: -the mean saccadic velocity < lower 5th percentile of normal

1st = drug ingestion 2nd = drowsiness, saccades can be slowed by as much as 50% by drowsiness
Abnormally fast saccades are usually caused by?: an error in calibration or a noise eye movement recording

on rare occasions can be caused by ocular flutter
-ocular disorders that restrict eye movement
The hallmark eyemovement disorder causing disconjugate movement is?: INO -Internuclear opthalmoplegia
-this disorder the adducting eye is abnormally slow
-immediately implies lesion of MLF on side of eye with slow adduction
-indicative of MS
Shortening of saccade latency is always due to?: technical error
Cerebellar damage often manifests as?: -misalignment of the eyes "diplopia"
-commonly impairs neural integraton creating "leaky integrator"
-saccades that miss target due to hyper or hypometria
saccades can (rarely ) be unstable ... called?: ocular flutter (opsoclonus)
-eyes appear to jump widely or flutter
What is Pursuit? Pursuit depends on what three things?: The ability to move one's eyes at the same speed as a target so the target remains stable on the retina
1. visual & other targeting information
2. prediction
3. BS output machinery
What is: Pursuit gain? normal Pursuit? Moderate impairment of pursuit?: pursuit gain = ratio of eye velocity (during non saccadic movement)to target velocity

Normal Pursuit = judged by a lack of "catchup" saccades & pursuit gain of > .8

Moderate Impairment = judged by pursuit with limited "catch up"saccades and pursuit gain of .2-.8
-can be caused by inattention, medication, age or underlying CNS disorder
Pursuit disruptions can be both ___ and ___: unidirectional & bidirectional
In most cases the pursuit abnormality is ___ the ____: toward the lesion side
Cortex lesions (in pursuit) may: be away from the lesion side
The magnitude of the gain disruption is usually greater for lesions in: the lower system pathways versus the cortex
The Pursuit system is not as robust as?: the saccadic system
-it is so easily disturbed that"poor pursuit" is rarely of any clinical significance
symmetrical disturbance of pursuit is: no pursuit -unable to do the task -judged by having a gain of
Asymmetrical Pursuit: -A rare finding but has high clinical utility
-may indicate CNS disorder
-pursuit asymmetry resulting from cortical lesions usually persists for only several weeks
-OPK should also be asymmetrical (do in rotary chair)
When interpreting asymmetrical pursuit, what do you need to be aware of?: presence of spontaneous nystagmus, because it will affect the results
-strong unidirectional spontaneous nystagmus can contaminate the pursuit & look like asymmetrical pursuit
-peripheral spontaneous nystagmus needs to be over 20deg/sec to affect smooth pursuit
-central spontaneous nystagmus may not have to be as intense-these patients will have nystag that is poorly suppressed by fixation & have gaze evoked nystag
summary of possible disorders of smooth pursuit: -advanced age
-BS disorders
-cerebellar disorders
-cerebellar cortical disturbances
-congenital nystagmus
-drug ingestion
-inattention
-visual disorders
What are we looking for with gaze testing abnormal ?findings: looking for the presence of nystagmus or other abnormal eye movements
-gaze evoked nystagmus-congenital, peripheral, integrator, bilateral
-rebound nystagms
-vertical nystagmus
-square wave jerks
a gaze holding system is handled by ?: the neural integrator
-is a network of neurons that computes the correct "holding" torque needed to compensate for the elastic orbital forces & keep the eye from drifting
Gaze evoked nystagmus due to central origin, possible lesion sites will depend on what?: whether the gaze evoked nystagmus is a horizontal or vertical direction
Another name for gaze-evoked nystagmus = which can occur from abnormalities in?: Jerk nystagmus

the central vestibular system or the peripheral vestibular system
Patients with gaze evoked nystagmus are unable to maintain what? therefore... gaze evoked nystagmus is always what?: stable conjugate eye deviation away from the primary position

is always in the direction of the gaze
Gaze stability testing is the only test of the 4 routine tests in which: lesions of either the peripheral or centralvestibular & oculomotor systems can produce abnormalities
The principle abnormality noted in gaze stability testing?: development of nystagmus or other repetitive eye movement in place of steady gaze
the most common form of gaze nystagmus is?: bilateral nystagmus
-beats right on rightward gaze & left on leftward gaze
-may be accompanied by vertical nystagmes
-velocity "usually" increases by fixation
-indicates BS, cerebellar lesion
What is Alexanders Law: As pertainging to peripheral characteristics...
-horizontal nystagmus increases in its intensity as the patient gazes further in the direction of the fast component of the nystagmus
When gaze evoked nystagmus is direction fixed in character, follows Alexanders law & enhanced with fixation removed ... site of lesion =: peripheral
What is rebound nystagmus?: a response to prolonged eccentric gaze holding (10 sec)
-when the eyes are brought back to center they drift for several seconds in the direction of the previous holding
this is reported mainly in patient with cerebellar disease
Nystagmus that is not present in eccentric gaze but appears (or is stonger) when eyes return to primary gaze is called?: rebound nystagmus

abnormal if 3 or more beats of clear nystagmus with slow velocity toward the previous position of gaze
Gaze evoked nystagus w/o rebound is a ___ finding Gaze evoked nystagmus with __ is a ___ finding: weak finding

rebound is highly significant
Rebound nystagmus is always pathologic, indicates BS or cerebellar lesion
End gaze nystagmus is considered...?: normal when symmetrical and transient
Vertical nystagmus occurs in gaze testing when? Vertical nystagmus is a ____ finding for?: Occurs when gazing upward, downward or in primary position

Strong finding for an acquired central lesion
-central lesion
-cerebellum or medulla
The main characteristics of jerk nystagmus caused by central vestibular systems?: direction changing nystagmus
-pure vertical or pure torsional nystag
the main characteristics of jerk nystagmus caused by peripheral systems: -enhancement of nystagmus with fixation removed
-enhancement of nystagmus post head shake testing
Bruns nystagmus looks like?: -asymmetrical - eye drifts... then corrects
Bruns nystagmus (integrator nystagmus): see little or no spontaneous nystagmus but gaze nystagmus is assymmetric. Can occur with cerebellar lesions
-Gaze evoked nystagmus that is a drift of the eye toward the center of the orbit with corrective outward saccades
-nystag will likely occur on the lateral or upward gaze not on downward
-slow phase will decrease in velocity as the eye moves
-once other causes ruled out... indicates BS or cerebellar lesion
OPK: optokinetic nystagmus
-has minor diagnostic ability due to poor sensitivity
-often not recorded in a full field so not a true OKN
-not as influenced by inattention and medication as other oculomotor tests
-you are really measuring smooth pursuit so it can at least be a check on smooth pursuit testing
what is the purpose of doing the Dix Hall Pike maneuver?: looking for torsional nystagmus due to BPPV
-may have torsional or vertical nystag
-not there when you first reach the position
A positive Dix Hall Pike for ____: BPPV
-is sensitive & specific test that can be interpreted in isolation
-head tiltes toward affected ear -canalithiasis of the posterior canal of that ear
-head center -canalithiasis of the anterior canals
A positive Dix Hall Pike NOT BPPV =: you will see linear nystagmus w/o characteristic latency, duration and fatigability
-nystagmus will last as long as the head position is held
-this tye of "positional" nystagmus indicates CNS lesion
Positional nystagmus: Remember:nystag abnormal if...
-presence of any nystagmus with fixation is abnormal
-the slow component velocity exceeds 6 deg/sec in a single head or body position
-if nystag is present > 3deg/sec in a number of positions
-if the directon of the nystag changes within a body position -abnormal 100% of the time
Direction changing nystagmus in a single head positon also called: periodic alternating nystagmus
-IS ALWAYS ABNORMAL
-very rare
indicative of cerebellr lesion
Direction changing positonal nystagmus w/o fixation...: -can be central or peripheral in origin
Geotropic nystgmus - beats towards ground in lateral head turn positions
-usually peripheral but not always
Ageotropic nystag -beats toward ceiling in lateral head turned positions
-less common thatn geotropic
-usually indicated central lesion but not always
need to rule out PAN
Positional nystagmus with fixation is abnormal when?: ALWAYS
-if accompanied by a sense of dizziness, and if it is enhanced with no fixation then peripheral
-if it is accompanied by little or no vertigo, is increased with fixation & persists as long as the head is in that positon it is CNS
Purpose of caloric testing?: -used to validate a tentative diagnosis of asymmetirc function of the peripheral vestibular system
5 possible findings for caloric testing?: 1. Unilateral weakness (>25%)
2. Directional preponderance (>30%)
3. fixation suppression - difference between eyes open should drop 60% suppression w/fixaton
4. Hyperactive response
5. Normal response

Technical difficulty - patient not allerted properly
A unilateral weakness in caloric testin is typically what type of lesion?: typically peripheral but not always
Most common cause of unilateral weakness is?: end organ disease
-most common = Meniere's
-other end organ dieseases include, syphilis, bacterial meningitis, vascular disruption from migrane or cerebrovascular disease
Most common neural origin = acoustic neuroma, others are MS,benign intercranial hypertension, vestibular neuronitis
central causes- MS and BS disease
Directional preponderance: clinical significance has been debated
-most often seen in pts with strong spontaneous nystagmus
-some software programs will allow a correction of caloric test on basis of spontaneous nystag.this frequently eliminates most directional preponderance
-associated with lesions in
-labyrinth
-cranial nerve VIII
-BS & cortex
abnormal preponderance exists when?: nystagmus responses in one directon are significantly stronger than nystagmus responses in the opposite direction
-indicates an asymmetry in the VOR
Hyper active response in calorics: -very uncommon finding
-non organic sources
-enhancement of transfer qualitites due to mastoidectomy, tymp perf, and excessive nervousness of pt.
-otherwise bilateral hyperactive responses may indicate a cerebellar system disease
Impaired fixation suppression: -record ongoing nystagmus then record nystagmus when person fixates on a clearly visible object to determine the fixation index
-peripheral vestibular nystagmus is usually well supressed by fixation
-congenital nystag & central nystag are unaffected or increased by fixation
Impaired fixation suppression is a strong...: central sign
calorics also affect the ____ canals, not as much but if the ___ canals not working, may see______: vertical canals(to a lesser degree)
if lateral canals not working
may see stimulation of vertical canals
if bilateral weakness is confirmed: -most common etiology = ototoxic drugs
-other peripheral causes are infection, menieres, aied
-central causes include head trauma, congenital malformation & tumors
-bilateral weakness always needs to be confirmed with ice calorics or rotary chair
Acronym COWS =: Cold opposite warm same (for direction of nystagmus in caloric testing)

Warm will increase the temperature of a porton of the endolymph in the lateral duct, causing it to rise and deflect the cupula toward the utrical. The resulting increase in discharge from the right will produce right beating nystagmus

a Cool stimulus produces a response in the opposite direction . In that case endoymph in the lateral SCC is cooled, becomes more dense and sinks so that the cupula will be deflected away from the utricle. Reduced discharge right makes left ear dominant get left beating nystagmus
Temperature for water warm vs cool: Warm =44deg C
cool = 30 deg c
Caloric inversion: The entire caloric response beats in the wrong direction
-extrememly rare finding check electrodes
-determine if there is very strong positional spontaneous or congental nystag that is overcoming the caloric
-in large type perfs, warm air stimulation can cause evaporation of mositure in the middle ear cavity creating cooling instead of warming. Accordingly warm air irrigation in rt ear might yield left beating nystag
if not these..
BS disease
premature caloric reversal: -in some normal individuals the slow phase component of the caloric nystag disappears after 200 sec and the a secondary nystag that beats in the opposite direction appears
-if this reversal occurs within the 1st 140 sec of recording & opposite beating > 6 deg /sec then premature caloric reversal has occurred
-very rare finding - can occur with Friedrichs Ataxia or in patients with extensive degeneration of vestibular nuclei
influence of spontaneous nystagmus must be ruled out

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Number of cards 158

Created By josyg