Vestibular Anatomy, Physiology, and Testing Principles Flashcards

Question

List the indications for ENG/VNG 7

Answer 1

1. Confirm diagnosis of unilateral vestibular loss (e.g. post vestibular neuritis) 2. Confirm and measure bilateral vestibular hypofunction (BVH) 3. Document or Measure nystagmus (e.g. in Central lesions) 4. Meniere's disease 5. Preoperative: e.g. prior to cochlear implantation or for candidacy for labyrinthectomy or translabyrinthine surgery 6. Difficult BPPV/CPN (Central positional nystagmus) 7. Malingering "U Beat Beat Nystagmus Me Me Plop"

Answer 2

1. Does not necessarily “rule out vestibular hypofunction” - Normal VNG can be found in: BPPV, MD, Vestibular schwanomma 2. Does not often localize lesion (just cuz you test one side is weak doesn’t mean that’s the problem) 3. Does not make a diagnosis or identify underlying disease process causing the weakness VNG does not replace a good clinical assessment

Answer 3

1. Long test 2. Expensive equipment 3. Large space needs 4. Patient discomfort/tolerance 5. Laden with artifact - Test - Technical - Patient performance - Interpretation 6. Spurious results require experienced interpretation

Answer 4

Patients with fluctuating vestibular conditions: 1. Meniere's Disease 2. Vestibular migraines 3. Autoimmune inner ear disease 4. BPPV Other: Vestibular Schwannoma "Vestibular BAM Vestibular"

Answer 5

1. Stop all CNS-active 2. Medications/vestibular suppressants 24-48 hrs prior 3. No alcohol 48 hrs prior 4. No facial creams/lotions (affect mask) 5. No eating 2-3 hours before (nausea and vomit) 6. Cardiac issues 7. Seizure disorder 8. Visual/eye issues 9. Cooperation level 10. Motion/vision sensitivity

Answer 6

TEST FACTORS: 1. Can only measure horizontal eye movements, not vertical or torsional 2. Ambient light level can disturb recording 3. Recording based on comeoretinal potential PATIENT FACTORS: 1. Changes in skin resistance (sweating) 2. Age 3. Fatigue 4. Congenital nystagmus 5. Level of attentiveness 6. Presence of sedating medications 7. Interference from eye blinking BALL SACS Blinking Attentiveness Light level (ambient) Laziness (fatigue) Sweating/Skin Age Congenital nystagmus Sedating medication

Answer 7

CENTRAL PATTERN (Gaze evoked nystagmus, abnormal tracking, failure of fixation suppression, downbeat nystagmus, abnormal saccades): 1. Antivertigo or Antinausea medications (e.g. Meclizine, Drmamine, Phenergan) 2. Anticonvulsants (e.g. Dilantin, Tegretol) 3. Tranquilizers, Benzos (e.g. Valium, Xanax) 4. Antidepressants/Anti-anxiety (e.g. Paxil, Prozac, Lithium, SSRI/TCAs) 5. Sedatives, Barbituates (e.g. Phenobarbital, Demerol, Codeine, Sleeping pills) 6. Nicotine, Street drugs SEDATION PATTERN (Suppression of calorics/spontaneous nystagmus/positional nystagmus/reduced saccades and OPK velocity): 1. Tranquilizers, Benzos (e.g. Valium, Xanax) 2. Antidepressants/Anti-anxiety (e.g. Paxil, Prozac, Lithium, SSRI/TCAs) 3. Sedatives, Barbituates (e.g. Phenobarbital, Demerol, Codeine, Sleeping pills) 4. Antihistamines, Cold medications (e.g. Benadryl, Actifed, Aspirin) VESTIBULAR PATTERN (e.g. inducing positional nystagmus) 1. Antivertigo or Antinausea medications (e.g. Meclizine, Dramamine, Phenergan) 2. Sedatives, Barbituates (e.g. Phenobarbital, Demerol, Codeine, Sleeping pills) 3. Nicotine, Street drugs 4. Antihistamines, Cold medications (e.g. Benadryl, Actifed, Aspirin - TRANSIENT 5. Aminoglycosides, Chemotherapeutic agents (e.g. Gentamicin, Cisplatin) - PERMANENT 6. Diuretics (e.g. Lasix) - TRANSIENT 7. Alcohol

Answer 8

Alexander's Law = Intensity of nystagmus will increase when looking in the direction of the nystagmus (ie. the fast phase) - And decreased during gaze in the direction of the slow phase Mechanism of action: The natural tendency for the eye to recoil to midline is additive to the slow phase movement of the eye when looking in the direction of the nystagmus Example: Left peripheral vestibulopathy - Increased right sided stimulation (compared to left) - Body feels that it is turning right - Slow phase drift will move left - Fast phase will move right (like an airplane with a broken will trying to re-adjust itself) - When looking right: Eyes will want to drift left due to recoil, which is additive to the slow phase draft --> therefore need to "pull eye back more/faster" because there is "more pressure on the slow phase to go slow" - When looking left: Eyes will want to drift right due to recoil, which is subtractive to the slow phase drift --> therefore don't need to "pull as hard" onto the fast phase cuz the slow phase is not as intense

Answer 9

A. GAZE TESTING (with and without fixation) - examine ability to maintain steady gaze with and without fixation. 1. Spontaneous nystagmus - Peripheral lesion: Will be consistent with Alexander's law. Should be suppressed with visual fixation - Central lesion: Vertical or direction changing nystagmus 2. Static positional testing (e.g. look left/right) - stability of eccentric gaze/"gaze test" Notes on gaze testing: - Nystagmus measures slow-phase velocity and direction - Any nystagmus in gaze testing will be present in other parts of VNG - so this should match your clinical findings B. OCULOMOTOR TESTING (with fixation) - *abnormal oculomotor testing typically seen with central lesions* 1. Smooth Pursuit (the first test that I tried, looking at a red dot and just following it) - Tracking movements of eyes used to follow an object moving across the field of view, caused by either motion of the object or motion of the viewer, are mediated by the smooth-pursuit system. - Tested by having patient follow targets moving no faster than 20degrees/second. - Abnormal = Asymmetry in horizontal tracking, presence of more corrective saccades - Measures: Tracking Gain (Ratio of peak eye velocity to peak target velocity, at different frequencies - age dependent) 2. Saccades - Rapid changes in gaze from one target to another is achieved by saccades; test examines patient's ability to make voluntary fast eye movements for gaze adjustments - Tested by asking patient to alternately fixate with head still (look at nose, then finger, nose, finger - 15 degrees away). - Abnormal = dysmetria (over or under shooting of saccades) - Measuring effects of a neural pulse ("step") and a match between pulse and step - Need to tell patient not to anticipiate (can affect the results) and do NOT move head (eyes only) 3. Optokinetics (the second test that I tried with my eyes with all the lines) - Optokinetic system drives the eyes to follow visual surround during low-frequency (sustained) head movements - Optokinetic nystagmus is a response to motion of the entire visual field rather than to motion of a particular target (which smooth pursuit is used for) - E.g. automatic visual tracking of a picket fence seen from a moving car - Tested using optokinetic tape - Smooth-pursuit tracking contributes to the generation of optokinetic responses; so defects in smooth-pursuit also lead to impaired OKN C. VESTIBULAR RESPONSE TESTING 1. Calorics (low velocity vestibular response) - 8-80 degrees/second is normal - < 8 degrees/sec may suggest hypofunction on that side - See separate caloric testing card for deatils D. POSITIONAL TESTING 1. Dix-Hallpike testing NOT PART OF THE STANDARD BATTERY: 1. Rotary chair (mid velocity vestibular response) - not classically part of VNG battery per Vancouver notes 2. Video Head Impulse Testing (high velocity vestibular response) - not classically part of battery per Vancouver notes ## Footnote Saccades graph: Figure 166.6 Cummings

Answer 10

MEASUREMENTS: 1. Accuracy - how accurate is the eye movement - Lesions: Cerebellar lesions (dorsal vermis), Brainstem (PPRF and MLF) 2. Velocity - how quickly does the eye move (peak velocity ~700 degrees/second) - Lesions: Ocular issues, INO 3. Latency - how long before the eye starts to move - Lesions: Neurodegenerative disorders NEURAL PATHWAYS: 1. Pulse-Step Generator: Paramedian Pontine Reticular formation 2. Pulse amplitude set by: Cerebellar vermis and Cerebellar Flocculus SACCADE PATHOPHYSIOLOGY (Slide 48): 1. Short pulse duration (hypometric saccade) 2. Reduced pulse amplitude (slow saccade) 3. Inappropriate step size (Gaze-Evoked Saccade) 4. Disconjugate gaze (Pulse-Step Mismatch) 5. Saccadic slowing (decreased velocity) 6. Delayed saccades (increased latency) NORMAL LATENCY: - 200ms latency is normal time it takes eyes to match target SACCADIC SLOWING (Decreased Velocity - more slope-y than vertical): 1. Localization: Basal Ganglia, Brainstem, Cerebellum, Peripheral oculomotor nuclei/muscles 2. Etiology: - Drugs or intoxicatioin - Neurodegenerative disease (Spinocerebellar degeneration, Parkinson's, Huntington's, Supranuclear palsy) - Metabolic problems - INO - Inattention DELAYED SACCADES (Increased latency - horizontal goes past the target) 1. Localization: Frontal or Frontoparietal cortex, or basal ganglia 2. Etiology same as saccadic slowing (especially Parkinson, Huntington, Alzheimer) 3. Artifact may be due to: Inattention, poor visual acuity, malingering, drugs (e.g. sedatives, EtOH, etc.) FAST SACCADES: - Myasthenia gravis - Orbital tumors DYSMETRIA: 1. VNG tracing: - Hypermetric -- vertical portion pasts the normal target line and then comes back to the target (Slide 60 VNG talk) - Hypometric -- opposite 2. Localization/Etiology: - Hypometria: Cerebellar flocculus (short pulse duration); although 10% is acceptable - Hypermetria: Cerebellar Vermis (long pulse duration) or brainstem lesion - Etiology: The Big 5 - Cerebrovascular - Tumour - Inflammatory/MS - Degenerative/atrophy - paraneoplastic ## Footnote Pathway: Slide 47-65 Darren VNG talk Draw the PPRF pathway from Darren's talk

Answer 11

1. Bilateral defects: Diffuse cortical, basal ganglia, cerebellar disease 2. Unilateral: Focal lesion involving ipsilateral cerebellar hemisphere, brain stem, parieto-occipital region 3. Vertical pursuits: Not that useful clinically, as rarely positive without abnormal horizontal pursuits as well PERFORMANCE FREQUENCY: - 0.2-0.8 Hz BILATERAL IMPAIRED SMOOTH PURSUIT: 1. Medication side effects (e.g. anticonvulsants, sedatives) 2. Neurologic conditions (e.g. Parkinson's Progressive Supranuclear Palsy, Alzheimer's, Schizophrenia)

Answer 12

PURPOSE: - Test of tracking - True optokinetic tests represent reflexive response to moving full-field visual stimuli (like a truck moving in your peripheral vision makes you hit the brake) - Normal = 20-40 degrees per second TIPS: - No head movements, eyes only - Can use the "LOOK" method (follow the targets all the way) or "STARE" method (follow the target at the centre) - basically ask them to "count the number of lines that show up" as the line tape moves MEASURE: - Slow phase velocity (SPV) of nsytagmus should match the velocity of targets - Everyone can do 20deg/sec - test of malingering DISADVANTAGES: 1. Very costly/difficult to make proper full-field visual stimulus (light bar and rotating drum is not true full field) 2. Any testing using light bars or dots is probably just a test of tracking 3. Probably of limited diagnostic value as a test 4. Testing both tracking and OPK with the same test; so utility is limited ARTIFACT: - Technical - Cooperation/poor tolerance - Superimposed nystagmus ABNORMAL RESULT: 1. Malingering 2. Cerebellum 3. Brainstem 4. Absence or asymmetry of OPK suggests peripheral vestibular lesions

Answer 13

Localization: - Non-localizing Clinical utility: - Normal people can have different types of mild slow positional nystagmus - Apogeotropic and Geotropic variations of positional nystagmus are common and not necessarily pathologic - Migraine and VM patients often have positional nystagmus

Answer 14

POSITIVE is RIGHT (horizontal) / UP (vertical) and NEGATIVE is LEFT / DOWN - Slope is the velocity - Shallow slope = slow fase - Steep slope = fast correction phase Slow phase Velocity: Distance that the eye travels over time - For one nystagmus beat, need to determine the distance the eye travels during the slow phase, and divides that by the amount of time is takes - SPV = change in theta (degrees) divided by change in time - Easier way would be to draw a line of best fit of the slow phase, and measure the slow of this line (y2-y1/x2-x1). - Slope of the line calculated can then be described as "eye movement per 1 second" and be calculated over a preset amount of time (SPV = change in theta prime, divided by 1) Looks like a saw tooth pattern (See Kevan Otology page 25) ABNORMAL RESULTS: 1. Horizontal: > 4 degree/sec 2. Vertical: > 7 degree/sec What does "degrees per second" mean? - 4 degrees per second = turning a full circle in 90 seconds - 360 degrees per circle / 4 degrees per second = 90 seconds per circle ## Footnote Darren VNG Lecture 2023 https://www.audiologyonline.com/ask-the-experts/calculating-slow-phase-velocity-nystagmus-555

Answer 15

OVERVIEW OF CALORIC TESTING: - Allows one labyrinth to be studied independently of the other - compares responses to hot (excitatory) and cold (inhibitory) stimulation between right and left sides - Stimulates (warm) or inhibits (cold) the vestibular system using water in the EAC of different temperature (air used if TM perf) - Horizontal canal is affected by temperature change - located closest to EAC and oriented in the same plane as the temperature gradient generated by temporal bone - Caloric nystagmus can be suppressed with visual fixation in healthy people (failure of fixation - can be seen in central/cerebellar disorders) TWO WAYS CALORIC TESTING CAUSES RESPONSE: 1. Convective component: Temperature gradient across horizontal canal causes density difference within endolymph of canal; effect is dependent on head position (as it relies on gravity). Accounts for 75% of response. - HOB 90 degrees from supine (or 60 degrees backwards from upright) - causes horizontal canal to be vertical to earth. Here, denser fluid sinks in the lower position in canal and less dense fluid rises to upper part of canal - With gravity, flow of endolymph occurs from cooler denser region to warmer less dense region. Ampulla is closest to canal (therefore cold away from ampulla, warm toward ampulla) - Movement of fluid within canal defects the cupula and leads to change in discharge rate of vestibular nerve afferents - Warm irrigation = endolymph flows toward ampulla, increase in discharge (stimulatory) - Cold irrigation = endolymph flows away from ampulla, decreased in afferent discharge (inhibitory) 2. Non-convective component: Excitation of canal when ear is warmed, inhibition of canal when ear is cooled. This component does not vary with head position - Accounts for 25% of response HOW CALORIC TESTING IS DONE - Patient eyes open in darkness, mental arithmetic is used to maintain alertness, Frenzel lenses used - Wax should be debrided to reduce false-positives - Alternate binaural, bithermal caloric testing is most common protocol - Using water, 250mL over 30 seconds - Cool water 30 degrees, warm water 33 degrees - Can also use air (8L over 1 minute, 50 degrees hot and 24 degrees cold) - Administered for 60-90 seconds in each ear in a set order (e.g. Right warm, left warm, right cold, left cold). 10 minutes required in between irrigations due to heating effect - Eye movements are recorded for several seconds before and during irrigation, and after nystagmus has ended - Slow phase velocity is plotted vs time - Data is interpreted in terms of unilateral weakness (UW) and directional preponderance (DP) PHASES: 1. Phase 1 (Onset): 10-15 seconds after onset of irrigation (any nystagmus during this time is spontaneous and should match other testing) 2. Phase 2 (Peak caloric response): 60-90 seconds after onset of irrigation is the peak caloric response 3. Phase 3 (Fixation Response): Fixation response - turning it on and off again, occurs right before and after fixation ARTIFACT: - Temperature variations (water or air) - Reliability of irrigation – narrow canals, wax, etc. - Habituation of vestibular response - Requires alert patient and cooperative - TM anomalies/mastoidectomy etc make calorics unusable/uninterpretable - Medications - Head position - Eye blinks JONGKEE'S FORMULA OF UNILATERAL WEAKNESS: Total response from the right vs. total response from left, divided by total response - Comparing each vestibular organ's responsiveness to stiulation - Maximum slow component is determined on the basis of 3-5 slow components with highest velocity as the value - Use ABSOLUTE VALUES (Forget about the +/-) - Smaller numbers = weaker side - ((RW+RC) - (LW+LC)) / (RW+RC+LW+LC) - > 20% difference between sides is abnormal (reported as "xx% weakness on the xx side) DIRECTIONAL PREPONDERANCE - Looks at the difference in total eye speeds between right going nystagmus and left going nystagmus - Might be more useful to see what the degree of compensation is (e.g. “how much less are they beating now”) - Right going response = RW + LC (Cold opposite, warm same) - Left going response = LW + RC - DP = ( (RW+LC) - (LW+RC) ) / (RW+RC+LW+LC) - Normal is ≤ 25% (or means that it's "compensated", therefore higher means not compensated) Significance of positive DP: - Underlying spontaneous nystagmus (e.g. right-beating spontaneous nystagmus will lead to a DP for right-beating responses on caloric test) - Without spontaneous nystagmus, DP may also be a central sign that indicates asymmetric sensitivites of central vestibular neurons to inhibitory-excitatory stimuli - Increased warm and decreased cold response can also result in DP - seen in Meniere's Can also reverse the equations to look at differences the other way around (compare the right ear to the left ear): E.g. Jongkee ((LW+LC) - (RW+RC)) DP (LW+RC) - (RW+LC) FIXATION INDEX: - Measure of nystagmus intensity during fixation as a ratio of nystagmus before fixation - Not a very useful test clinically, some people don't fixate well and vision problems/nausea can affect result - One FI for each side, but no normalized values and range is large, generally > 60% is abnormal - FI % = SPV (fixation) / SPV (no fixation) x 100 ## Footnote Cummings Chapter 166

Answer 16

1. UNILATERAL WEAKNESS + DIRECTIONAL PREPONDERANCE = UNCOMPENSATED WEAKNESS - Directional preponderance is due to the presence of spontaneous nystagmus --> may be bias in testing (e.g. at baseline, prior to putting water in, eyes are already moving thus introducing bias) 2. UNILATERAL WEAKNESS + NO DP = COMPENSATED WEAKNESS - Spontaneous nystagmus has disappeared 3. NO UNILATERAL WEAKNESS + DP = CENTRAL PATHOLOGY (OR OTHER) - Many scenarios possible, therefore not localizing

Answer 17

1. Meniere's disease 2. Ototoxic medications 3. Meningitis 4. Autoimmune (Cogan's) 5. Neurodegenerative disorders (e.g. ALS) 6. NF2 7. Bilateral Temporal Bone Trauma 8. Sepsis "MOM ANTS"

Answer 18

1. Spontaneous nystagmus with normal calorics 2. Gaze-evoked nystagmus 3. Direction changing nystagmus independent of stimulus change 4. Vertical, down-beat (although can be any direction) 5. No fixation suppression 6. Abnormal oculomotor testing/tracking (e.g. smooth pursuit, saccades, optokinetics), especially with normal calorics 7. Bilateral reduced or absent caloric responses without a history of labyrinthine or middle ear disease 8. Hyperactive caloric responses: loss of cerebellum-generated inhibition Other characteristics of central nystagmus: 1. No latency 2. Non-fatiguing 3. Less associated with nausea/emesis

Answer 19

1. Fatiguing positional nystagmus 2. Direction-fixed nystagmus (no direction changing) 3. Unilateral caloric weakness 4. Bilateral caloric weakneess with a hiistory of labryinthine disease or administration of ototoxic drugs 5. Intact fixation suppression response 6. Follow's Alexander's laws 7. Not purely vertical 8. Jerk nystagmus 9. Fixation suppression (therefore wear goggles to elimninate fixation)

Answer 20

UP-BEATING NYSTAGMUS: 1. Paramedian medulla 2. Ponto-medullary junction 3. Fourth ventricle - Note: Less localizing than down-beating nystagmus overall DOWN-BEATING NYSTAGMUS: - Worse in lateral gaze (sometimes only present on lateral gaze) Localization: 1. Vestibular-cerebellum 2. Posterior midline cerebellum 3. Cranio-Cervical Junction ETIOLOGY: - Most common = Chiari malformation (compression of the cerebellum) - If positional, may be part of central positional nystagmus - Other etiology: "The Big 5" 1. Cerebrovascular 2. Tumor 3. Inflammatory/MS 4. Degenerative/Atrophy 5. Paraneoplastic

Answer 21

- Triggered nystagmus - Vertical nystagmus (usually DBN) occurring after horizontal canal stimulation (like head shake, or a vHIT) - Assuming there is no spontaneous DBN

Answer 22

"Everything Suppressed" - Think of all the VNG tests, then suppress all the responses: gaze, oculomotor, calorics, positional, alerting 1. Suppression of caloric response 2. Suppression of spontaneous nystagmus 3. Suppression of positional nystagmus 4. Reduced saccades and OPK velocity (ie. slowing) 5. Difficulty with alerting

Answer 23

Similar to "BALL SACS" FACTORS THAT AFFECT MEASUREMENT ACCURACY: 1. Mascara 2. Poor ambient light 3. Poor eye opening or blinking 4. Sweat (Affects electrode pickup) FACTORS THAT AFFECT PATIENT PERFORMANCE: 1. Age 2. Fatigue 3. Medications (depressants) - 1st generation antihistamines - Antiemetics like Gravol - Benzodiazepines - Sedatives - SSRIs, SNRIs - Alcohol - Narcotics 4. Medications (stimulants) - Caffeine - Amphetamines

Answer 24

How to stimulate the superior SCC: 1. Turn lateral (to align the superior/anterior SCC in plane with gravity) (*this stimulates the lateral canals and they are the ones involved with moving the lateral/medial rectus*) 2. Stimulation = leaning forward (ampullofugal) *Stimulated response will move the eyes in the opposite direction* SRIO = SR ipsi, IO contra STIMULATED: 1. Ipsilateral superior rectus (no angle change to eyeball when looking up) 2. Contralateral inferior oblique (has some angle change and rotation) INHIBITED: 1. Ipsilateral inferior rectus 2. Contralateral superior oblique ## Footnote See photos of me that Camilla used to demonstrate the angle part Vancouver 236 Eye diagrams / movement

Answer 25

STIMULATORY: 1. Contralateral Lateral rectus 2. Ipsilateral Medial rectus INHIBITED: 1. Ipsilateral lateral rectus 2. Contralateral medial rectus

Answer 26

How to stimulate the posterior SCC: 1. Turn lateral (to align the posterior SCC in plane with gravity) (*this stimulates the lateral canals and they are the ones involved with moving the lateral/medial rectus*) 2. Stimulation = head backwards (ampullofugal) - like Dix-Hallpike Test *Stimulated response will move the eyes in the opposite direction* SOIR = SO ipsi, IR contra STIMULATED: 1. Ipsilateral superior oblique 2. Contralateral inferior rectus INHIBITED: 1. Ipsilateral inferior oblique 2. Contralateral superior rectus

Answer 27

- 0.1-10 Hz angular acclerations

Answer 28

OVERVIEW OF ROTATIONAL CHAIR TESTING: - Analyzes the responses of both semicircular canals together (rather than calorics assessing one at a time) - Tests vestibular function at lower frequencies than impulse testing - Not as good at side localization as calorics (since testing them altogether) Advantage over Calorics: - Less calibration error, the stimulus is always the same whereas there is variation in caloric stimulation (ie. depends on patients middle ear anatomy, etc.) - Better tolerated than calorics INDICATIONS: 1. Suspected bilateral vestibular hypofunction 2. Patients receiving vestibulotoxic medications (ototoxicity) 3. Children or anyone who do not tolerate caloric testing well (e.g. impaction, perforation) 4. Determine presence/absence of vestibular function in patients undergoing genetic evaluation for hearing loss 5. Evaluate vestibular function after meningitis, especially if there is hearing loss 6. Monitor compensation after acute injury 7. Monitor changes in vestibular system over time 8. Cerebellar abnormalities 9. Identify residual labyrinthing function in patients with no caloric response HOW IT WORKS: - Head aligned with chin pitched 30 degrees nose down (horizontal SCC in plane of rotation) - Chair spins 10 cycles of sinusoidal head-velocity stimulus are delivered for each of several test frequencies with patient in darkness - head is strapped to chair - Several test frequencies are performed, over range of 0.01-0.7 Hz - Eye-movement tracings are measured and recorded with a camera - Results are averaged over successive cycles - Velocity and direction of eye movements are compared to that of the chair RESULTS INTERPRETATION (Sinusoidal Harmonic Acceleration/SHA testing = produces Gain, Phase, Symmetry) 1. GAIN - = Ratio of the amplitude of the maximum slow-phase eye velocity, divided by amplitude of the maximum stimulus (chair = head) velocity - = Normal result should be equal but opposite, where head goes one way and eyes go the other way and the same speed, indicating perfect VOR (ie. Gain = 1, test is never PERFECT so need to compare it based on other normal tests based on the system you use to calculate it) - In peripheral disorders, gain < 1 - but you cannot say which canal is affected based on this test alone - VOR gain is frequently used as physiologic measure of vestibular function - the amount of eye rotation relative to the amount of head rotation - VOR velocity should parallel rotatory chair angular velocity. If not, this suggests hypofunction or suppression - Vestibular hypofunction typically has decreased gain - May be normal if brain has compensated for loss 2. PHASE - = Temporal shift in eye velocity relative to head velocity - Aka. the Delay between head motion and eye movement onset - Eyes should move in phase/time with the chair (or even lead chair movement). When they move exactly same velocity but opposite directions, they are said to be "exactly out of phase" or "Phase Zero" or 180 degrees. It is more difficult and poorer to be Phase Zero as Stimulus Frequency DECREASES (ie. this is physiologically expected for low frequency usually < 0.04Hz). This is because the stimulus is so small that it is not as efficient in displacing the cupula, therefore not generating as good of a VOR response. - Because of this above physiologic finding, the VOR must be assisted by other central neural pathways to give the full response - this is called the "Velocity Storage System". - So, when there is a hit in the central vestibular system, or a unilateral vestibular lesion, the phase will not be normal. However, if a peripheral lesion has been compensated, then you might get normal VOR gain, normal symmetry, but the VOR velocity storage system never really repairs itself so if that is hit then the phase will still be abnormal. - If the reflex eye movement leads the head movement, a "phase lead" is present (velocity of eyes is reached first before the head). In peripheral vestibulopathy, the eyes will take longer to react to head movement, and will "lead" the head - "phase lead". This is the MOST reproducible finding - Doesn't really make sense - how can you have the eyes move before the head? It's mostly because velocity is plotted against velocity rather than movement, therefore it looks like a phase "lead" because the velocity is faster. - May be normal if brain has compensated for loss 3. ASYMMETRY - VOR responses should be equal turning towards the left and to the right. - If not symmetric, this suggests a unilateral peripheral vestibular lesion - HOWEVER it is still NOT LOCALIZING to left and right - Similar to Directional Preponderance - asymmetry just represents how well the system BEATS to the right vs. BEATS to the left. - Often asymmetry, like DP, is usually due to results of underlying spontaneous nystagmus (which usually means unilateral lesion) - perhaps this nystagmus is now being "brought out" and identified during rotational testing 4. BIAS VELOCITY (Not a result, but helps explain cause of asymmetry) - Similar to directional preponderance - Spontaneous nystagmus may cause a bias velocity. If a patient has spontaneous nystagmus, their slow phase response will be additive to their rotational response and shift the response towards the direction of the slow phase - Bias may be seen even after spontaneous nystagmus has resolved - The direction of bias alone does not identify the affected ear, because both irritative lesions (as with Meniere's, Serous labyrinthitis, labyrinthine fistulas, and acoustic neuromas) as well as ablative lesions can also cause bias but in opposite directions Changes in phase and gain with vestibular hypofunction: 1. Decreased gain 2. Increased phase lead POSSIBLE CHAIR RESULTS: 1. LOW GAIN = Vestibular dysfunction 2. HIGH GAIN = Central vestibular dysfunction 3. Phase lead = Central or peripheral dysfunction, old age 4. Bias = Central dysfunction ## Footnote Cummings Chapter 166 Kevan Otology page 27 https://www.youtube.com/watch?v=odU78mE87lU

Answer 29

1. Vestibulospinal 2. Vestibulo-ocular (oVEMP) 3. Vestibulocolic (cVEMP) 4. Vestibuloautonomic

Answer 30

1. Vestibuloocular reflex (VOR) regulates the six extrinsic eye muscles to maintain gaze during head movements - Stabilizes eye position in space with respect to movements - Angular VOR is mediated by the SCCs, and compensates for translation - Linear VOR is mediated by the otolithic organs, and compensates for translation - Occurs through the medial longitudinal fasciculus (MLF) 2. Vestibulocollic reflex (VCR) controls the neck muscles to support the head during movements - Stabilizes the head position via cervical spinelower motor neurons - The reflex head movement produced counters the movement sensed by the otolithic or semicircular canal organs - VCR can be measured with a cVEMP - Occurs through the Medial Vestibulospinal tract 3. Vestibulospinal reflex (VSR) controls the muscles of the body and limbs to maintain posture and position in space - Controlled by otolithic organs - utricle and saccule - Stabilizes the body via the spinal Lower motor neurons - Occurs through the lateral vestibulospinal tract - Symptoms of otolithic organ dysfunction: feeling the ground falling out from underneath, being pushed against the wall, and nausea - Posturography can test the VSR but not side specific

Answer 31

VEMP = Vestibular evoked myogenic potentials - Tests the function of the vestibulospinal reflexes and function of the otolithic organs - Can help differentiate between SVN and IVN dysfunction (SVN innervates utricle, IVN innervates saccule) TYPES: 1. cVEMP (Cervical VEMPs) 2. oVEMP (Ocular VEMPs) CLINICAL USE OF VEMPS: 1. DIAGNOSING SCCD (or any third window condition): VEMPs will show decreased threshold to trigger a response, and increased amplitude of the response 2. MENIERE'S DISEASE: Not very accurate, sensitive, or specific. May have higher thresholds for responses to cVEMPs; not recommended by AAOHNS CPG for diagnosis but can be used to confirm efficacy of ablative treatment 3. ENLARGED VESTIBULAR AQUEDUCT: Acts like a pseudo 3rd window, and would behave similarly to SCCD 4. VESTIIBULAR LOSS: Will have absent reflexes ## Footnote Kevan Otology Page 28 Example of cVEMP

Answer 32

A. CERVICAL VEMP (cVEMP): - Sound stimulation results in the relaxation of the ipsilateral SCM muscle (inhibitory response - therefore muscle needs to be contracted first) - Tests the vestibulocolic reflex 1. Method of measurement: - EMG is used to monitor ipsilateral SCM during sound stimulation - Patient must be actively contracting muscle (e.g. lifting head off of the bed ± turn head away from the tested ear ± look down, asked to tense muscles during stimulation otherwise no VEMP is produced) - Relaxing the ipsilateral SCM allows you to turn towards the direction of the sound - Electrode placement: Ground on forehead, active on middle third of SCM, reference on sternum/clavicle 2. Testing conditions: - Clicks or tone bursts at 80-100dB applied (usually inserts, but can use bone conduction for patients with CHL - although doesn't localize to sides as good) - Tested at 500Hz or 1000Hz for older patients 3. Pathway: - Loud sound to ear --> footplate --> SACCULE --> IVN --> Vestibular nucleus --> Medial vestibulospinal tract (MVST) --> Ipsilateral XI nucleus --> Ipsilateral SCM - Normal threshold for reflex = 80dB 4. Parameters/Outcomes: - Amplitude, peak, asymmetry ratio, threshold (quietest sound to elicit VEMP) and trough latencies (latency however is the poorest parameter of vestibular function) - "EMG Scaling": Need to normalize the EMG to account for differences in initial muscle contraction (Calculated by Averaged VEMP response amplitude divided by root mean square of pre-stimulation EMG activity) - Biphasic tracing: Initial positivity = p1 (previously called p13 using a click stimulus), followed by negativity = n1 (n23 click stimulus) - Latency: Time to p1 or time to N1 (not much clinical use for latency) - Amplitude: Measured from 0 on the y axis (microvolts) to each point, then amplitude = P1-N1 - Amplitude asymmetry (best measure clinically) = (Largest amplitude - Smallest amplitude) / (R + L amplitudes);; provides % of whether they're significantly different from each other (abnormal > 30-35%) - Threshold: Quietest level you can record a VEMP; clinically looking for threshold asymmetries, and for thresholds under 80dB nHL - Frequency: As frequency increases the VEMP decreases; expecting that 500Hz has the largest amplitude (might shift in older individuals) 5. RESULTS/ABNORMALITIES: - Thresholds higher than normal OR Low amplitudes (suggests dysfunction on pathway): saccular disorders or CHL - Low amplitudes: IVN disturbance (therefore usually normal in vestibular neuritis because it tends to affect SVN) - Lower than normal threshold: Tulio's phenomenon (e.g. SCD) - Asymmetrical amplitude (or one ear has higher amplitude - suggests more sound entering that ear than given): Tulio's phenomenon (e.g. SCD) - Prolonged latency of p1: Suggests central pathology - CHL can obliterate cVMP (blocks access to footplate), whereas SNHL does little or nothing to cVEMP response ## Footnote https://www.youtube.com/watch?v=phJvGaQnhCE

Answer 33

B. OCULAR VEMP (oVEMP): - Tests the vestibuloocular reflex 1. Method of Measurement: - EMG to contralateral inferior oblique/rectus in response to sound stimulus - Patient must be actively looking up to better record response 2. Testing conditions: - Start with the patient looking up - 500Hz frequency - Crossed vestibulo-ocular response - Tend to use Bone conduction stimulus more, because air conduction sounds will require large intensities; BC delivered to the junction of the midline of forehead and hairline, either by a tendon hammer or a mini-shaker - Active electrode is on contralateral inferior orbit 3. Pathway: - Loud sound to ear --> footplate --> UTRICLE --> SVN --> Vestibular nucleus --> MLF --> CONTRAlateral oculomotor nucleus --> Contralateral inferior oblique/rectus 4. Parameters: - First wave is "negative" (because contralateral) - so N1 (sometimes called N10 based on timing) first, followed by a positive P1 (sometimes called P15 based on timing) - N1 is driven by contraction of the inferior oblique muscle (excitatory response) 5. Conditions of Abnormal oVEMP - Loss of superior vestibular nerve function reduces or abolishes contralateral oVEMP N1 (ie. Right loss gives absent Left oVEMP) - In SSCD, oVEMP N1 on unaffected side would have the greater amplitude (opposite of cVEMP) - because of the contralateral crossing effect - In Meniere's attack, contralateral oVEMP is enhanced (ie. ipsilateral side of the Meniere's attack - cuz the vestibular response will be relatively higher on the good non-Meniere's side) ## Footnote https://www.youtube.com/watch?v=wFjZxrVUqYE

Answer 34

1. Conductive Hearing loss - Increased threshold - Decreased amplitude 2. Saccule disorders - Increased threshold - Decreased amplitude 3. Meniere's disease - Increased threshold - Decreased amplitude 4. Enlarged vestibular aqueduct - Decreased threshold - Increased amplitude - Short latency - cVEMP usually more sensitive 5. SSCD - Decreased threshold - Increased amplitude - Short latency 6. Vestibular neuritis - Usually spares IVN, but if it involves IVN then absent or reduced amplitude, and delayed latency 7. Vestibular Schwannoma - Increased / Delayed latency - Reduced or absent amplitude

Answer 35

1. Healthy patient - Lateral HIT: WNL - Vertical HIT: WNL - cVEMP: WNL - oVEMP: WNL 2. Lateral canal - Lateral HIT: Abnormal for impulses toward the side of the lesion - Vertical HIT: WNL - cVEMP: WNL - oVEMP: WNL 3. Anterior canal - Lateral HIT: WNL - Vertical HIT: Abnormal for downward impulses when head is turned away from side of the lesion (ie. when the Canal is brought anteriorly) - cVEMP: WNL - oVEMP: WNL 4. Posterior canal - Lateral HIT: WNL - Vertical HIT: Abnormal for upward impulses head is turned towards the lesion (canal brought posteriorly) - cVEMP: WNL - oVEMP: WNL 5. Utricle - Lateral HIT: WNL - Vertical HIT: WNL - cVEMP: WNL - oVEMP: Abnormal for the eye muscle contralateral to the lesion 6. Saccule - Lateral HIT: WNL - Vertical HIT: WNL - cVEMP: Abnormal for the side ipsilateral to the lesion - oVEMP: WNL 7. Superior vestibular nerve (Utricle, Lateral, Anterior/Superior canal) - Lateral HIT: Abnormal for impulses to side of the lesion - Vertical HIT: Abnormal for impulses when head turned down and away from lesion - cVEMP: WNL - oVEMP: Abnormal for eye muscle contralateral to lesion 8. Inferior vestibular nerve (Posterior canal, Saccule) - Lateral HIT: WNL - Vertical HIT: Abnormal for impulses when head turned up and toward lesion - cVEMP: Abnormal on ipsilateral side - oVEMP: WNL 9. Total unilateral vestibular loss - Lateral HIT: Abnormal for when head turned towards side of lesion - Vertical HIT: Abnormal for impulses when head turned up and toward lesion; and down and away the lesion - cVEMP: Abnormal on ipsilateral side - oVEMP: Abnormal on contralateral eye

Answer 36

DYNAMIC POSTUROGRAPHY: - Global functioning testing of balance including vision, vestibular function, and proprioception - Tests the vestibulospinal reflex - Involves 6 different test conditions of increasing difficulty COMPONENTS: 1. Sensory organization: Integration of vestibular, visual, and proprioceptive balance input 2. Movement coordination: Automatic neuromuscular responses triggered by proprioceptive changes; measures latency, amplitude, and symmetry TEST CONDITIONS: Conditions 1-3 = Ground is Fixed (Support Fixed) 1. Ground fixed, eyes open, background/surround fixed 2. Ground fixed, eyes closed, background/surround fixed 3. Ground fixed, eyes open, background/surround sway Conditions 4-6 = Ground is swaying (Support Sway) 1. Ground sway, eyes open, background/surround fixed 2. Ground sway, eyes closed, background/surround fixed 3. Ground sway, eyes open, background/surround swaying ## Footnote Kevan Otology Page 29

Answer 37

1. Baseline prior to treatment 2. Selecting rehabilitation strategy 3. Chronic disequilibrium 4. Other tests are normal 5. Monitor results of ablation 6. Persistent vertigo despite treatment B-SCOMP

Answer 38

1. Inconsistent measurements (1, 2) 2. Better on 5, 6 compared to 1, 2 (actively trying not to fall, and can do so, but when the ground is still they pretend to fall over) 3. Circular sway without falling 4. Exaggerated motor responses 5. Inconsistent motor responses to different motions 6. Poor test-retest reliability BICEPS

Answer 39

1. Condition 5: Eyes closed, Ground movement, surround fixed 2. Condition 6: Eyes open, Ground movement, surround movement In these conditions, you are taking away proprioceptive and visual outputs, leading patient to rely solely on vestibular input

Answer 40

VHIT = Video Head Impulse Test How it's performed: - Head impulse test is performed in a direction of all six semicircular canals independently - Patient wears video-goggles and any catch-up saccade is noted (positive test) Contraindications: - Neck trauma or inability to mobilize the neck Abnormal gain ≤ 0.8 Testing Horizontal Canals: - Head down 30 degrees (align the plane of rotation with horizontal SCC) - Jerk head to right: Testing R HSCC - Jerk head to left: Testing L HSCC LARP Plane (Left anterior, Right posterior): - Head turned to the RIGHT (30-45 deg) to be in line with the plane of the left anterior and right posterior SCC - Jerk head down = testing left anterior - Jerk head up = testing right posterior RALP Plane (Right anterior, Left posterior): - Head turned LEFT 30-45 degrees to be in line with plane of right anterior and left posterior SCC - Jerk head down = testing right anterior - Jerk head up = testing left anterior VHIT GRAPH: - Y axis = Velocity (degrees per second) - X axis = Time - Head moves in one direction, eye moves in another direction - Overt saccade = Saccade beginning AFTER the end of a head movement. Pathologic that can be seen with the naked eye, when the eyes clearly move after the head turn has been made - Covert saccade = Saccade begining BEFORE the end of a head movement. Pathologic, but may not be as clearly noticed with the naked eye (sometimes occurs when the eyes know they need to look, so they are delayed in looking but start looking as the head turns away) ## Footnote Vancouver 242 image lining

Answer 41

1. Romberg or Tandem Romberg (stand with eyes closed for 30 seconds, tandem is having one foot in front of other) 2. Tandem gait (close eyes and walk one foot in front of other) 3. Fukuda step test (march in place - will turn towards lesion) 4. Past-pointing

Answer 42

1. End-gaze nystagmus - Gaze-evoked nystagmus in the absence of pathology, attributed to normal variation in gaze-holding ability (in the cerebellar neural integrator) - > 40 degrees 2. Post-rotatory nystagmus (endolymph still moving after rotation as stopped) 3. Induced nystagmus (e.g. calorics) 4. Optokinetic nystagmus: Constant reflex - Holds images of seen world steady on retina during no head rotations induced by a moving full-field visual stimulus either during sustained self-rotation in the light or by the visual stimulus rotating around the subject. - Tracking objects in motion when your head is not in motion. Example - being observing individual telephone poles on the side of the road as one travels by them in a car - Complements the vestibulo-ocular reflex by responding best to very slow, very long, or constant velocity (zero acceleration) head movements - Slow phases are in the direction of visual motion and can be horizontal, vertical, or torsional depending on the stimulu

Answer 43

1. Jerk nystagmus (VOR, OKN): Constant slow phase velocity interrupted by quick phase saccades, horizontal or vertical 2. Torsional 3. Gaze-paretic / Gaze-evoked nystagmus (cerebellar) - decreasing slow phase velocity 4. Congenital nystagmus: increasing slow phase velocity 5. Pendular nystagmus: Equal to and from velocities/ossilations (e.g. demyelinating diseases - MS, inferior olivary hypertrophy in palatal myoclonus) 6. See-saw nystagmus: Disconjugate eye movements, usually due to parasellar mass, brainstem stroke, post-traumatic

Answer 44

1. Vestibular (motion - VOR) - Reflex - Holds image of seen world steady on retina during brief head rotations 2. Fixation - Voluntary, holds image of stationary object on fovea 3. Smooth pursuit - Voluntary, holds image of a moving target steady on fovea - Like fixation, it involves the frontal and occipital eye fields, corticobulbar fibers, brainstem nuclei, cerebellum 4. Saccades - Voluntary - Rapid eye movements that shift the line of sight between successive points of fixation - Brings images of objects onto fovea 5. Vergence - Voluntary - Moves eyes in opposite directions to track target moving closer or farther away so that images of a single object are placed simultaneously on both fovea - Linked to the accommodation reflex **(activation of ciliary body and pupillary sphincter)** - Modifies VOR depending on target distance

Answer 45

SUPPRESSION: 1. Fixation (peripheral cause) ENHANCEMENT: 1. Gaze (Alexander's law) 2. Position (Otolithic) 3. Fixation (unable to fixate = central cause)

Answer 46

1. Present at extremes of gaze (> 30-40 degrees) 2. Usually weak, symmetric, and poorly sustained 3. Due to variations in gaze holding capability

Answer 47

- Sudden deceleration is akin to acceleration in the opposite direction - Hence, post-rotatory nystagmus has fast phase in the opposite direction of the original rotation

Answer 48

1. Visual Fixation: Holds the image of a stationary object on the fovea 2. Vestibular: Holds images of the seen world steady on the retina during brief head rotations 3. Optokinetic: Holds images of the seen world steady on the retina during sustained head rotations 4. Smooth pursuit: Holds the image of a moving target on the fovea 5. Nystagmus: The repetition of a compensatory slow-phase and quick-phase resetting movement of the eyes 6. Saccade: Brings images of objects of interest onto the fovea 7. Vergence: Dysjunctive movement of the eyes in opposite directions so the image of a single object can be placed simultaneously on both foveae

Answer 49

1. Supraversion (UP) 2. Infraversion (DOWN) 3. Dextroversion (RIGHT) 4. Levoversion (LEFT)

Answer 50

1. Grade I (First Degree): Nystagmus only when looking in the direction of the fast phase (weakest) 2. Grade II (Second Degree): Nystagmus when looking in neutral (forward) position 3. Grade III (Third degree): Nystagmus when looking in all directions (strongest) - but still maximal in the direction of the fast phase

Answer 51

Classically seen with a lesion at the medial longitudinal fasciculus on the side of the slowly adducting side - Issues with crossing fibers via the MLF (paired, highly myelinated tract in dorsal pons/midbrain) - Causes a reflexive palsy of CNIII due to failure of signal transcution from the ipsilateral abducens nucleus to the contralateral III nucleus and medial rectus - Convergence is preserved (not a medial rectus problem, but a VOR problem with respect to the MLF. So you can still do normal adduction because there are different pathways from the ocular/visual cortex that go to the oculomotor nucleus for it to function, but only when you're testing the VOR does the MLF/adduciton not work). - Unless lesion extends to midbrain Most common in Multiple Sclerosis - Can also be seen with lyme disease, syphillis, trauma, brainstem lesions or fourth ventricle lesion, strokes, chiari malformations, or drug intoxication (phenothiazines & TCAs) (or the Big 5) - Myesthenia Gravis can mimic INO Findings in INO during eye movements: - Eye that is adducting will have a slow slide towards midline (due to medial rectus palsy or paresis) - decreased velocity - Eye that is abducting will be hypermetric and will show nystagmus (because brain thinks its looking middle, so keeps trying to pull that eye back to the middle) Can be unilateral or bilateral (depends on area of the lesion): - Unilateral: Findings of adduction and abduction would just apply to the affected eye (which is contralateral to the site of lesion) - Bilateral: Midline hit - Therefore, must record eyes separately Which eye is it? Example: Right INO - Right INO - by definition means a hit on the right side going to the right oculomotor nucleus, so the right (ipsilateral) medial rectus isn't working well - Therefore adduction is slowed on the right side (when looking to the left) - When further looking to the left, the right eye cannot go past midline, so it stays centered and brain thinks its moving centered - The left eye continues to look left but the brain thinks its looking center, so the medial rectus function pulls the left eye back to stay centered, giving nystagmus when abducting in the left eye ## Footnote Darren VNG lecture slide 51 Vancouver 238 https://www.youtube.com/watch?v=MWJz75R01s4

Answer 52

1. Scanning or staccato speech 2. Nystagmus 3. Intention Tremor

Answer 53

GAZE-EVOKED NYSTAGMUS: - Jerk Nystagmus that is triggered by eccentric (not centered) gaze - Slow phase decreases as gaze approaches neutral gaze - No nystagmus at neutral gaze - No suppression with visual fixation - Opsoclonus: Spontaneous nystagmus/oculomotor dyskinesia, often due to brainstem lesions LOCALIZATION: - Neuro-integrator gaze holding mechanisms in cerebellum/brainstem (ie. Cerebellar FLocculus) ETIOLOGY: "The Big 5" 1. Cerebrovascular 2. Tumor 3. Inflammatory/MS 4. Degenerative/Atrophy 5. Paraneoplastic End-point nystagmus: Physiologic, just present at extremes of gaze (>30-40 degrees) ## Footnote Darren VNG talk Slide 33

Answer 54

GAZE PARETIC NYSTAGMUS: - Subtype of Gaze Evoked nystagmus (which is nystagmus provoked by moving eyes to eccentric (ie. not neutral) gaze position and not present at neutral) - This nystagmus occurs from weakness of EOMs - Typically occurs during the recovery period after a central gaze palsy, e.g. from MG or GBS - Barany Classification: The term should only be applied in cases of gaze-evoked nystagmus associated with paresis of gaze (e.g. from brainstem or hemispheric lesions or EOM weakness such as MG) PRESENTATION: - Initially during eccentric gaze, there is little to no nystagmus - As eccentric gaze is held and the EOMs fatigue, nystagmus will develop - Nystagmus is in the direction of eccentric gaze (e.g. looking right = nystagmus to the right) - When it is unilateral, its direction is towards the side of the causative lesion CAUSES: 1. CPA tumor 2. Brainstem infarct 3. Myasthenia Gravis 4. Guillain Barre Syndrome

Answer 55

REBOUND NYSTAGMUS: - Nystagmus appearing transiently upon return to the straight-ahead gaze position after sustained eccentric gaze - Typically assocaited with gaze-holding nystagmus (a type of gaze evoked nystagmus caused by lesions in the brainstem and cerebellar networks that control eye movements) PRESENTATION: - Slow phase draft will draft back towards the direction of the previously held gaze - Fast phase will beat away from the direction of the previously held eccentric gaze CAUSES: 1. Brainstem lesions 2. Cerebellar lesions

Answer 56

BRUN'S NYSTAGMUS: - Type of asymmetric nystagmus seen with large cerebellopontine angle lesions - A special type of nystagmus terminology that is a combination of a peripheral vestibulopathy (e.g. with a vestibular schwannoma) as well as a central vestibulopathy due to mass effect on the cerebellum - Basically, your tumor is so big that it is compressing the ipsilateral vestibular nerve (giving you contralateral peripheral type jerk nystagmus); as well as compressing the ipsilateral cerebellum (which gives you ipsilateral gaze-evoked nystagmus) FINDINGS: (e.g. left CPA mass) 1. Peripheral Vestibulopathy (left) - Increased right sided firing vs. left results brain to think head is moving to the right - Corrective slow phase will be towards the left - Fast phase nystagmus towards the right - Because of Alexander's law, this will be more promiennt when looking towards direction of nystagmus (ie. to right) 2. Central Vestibulopathy - Results in ipsilateral gaze-evoked nystagmus (from cerebellar flocculus compression) - May have torsional component as well - Coarse, slow nystagmus with off-center gaze - Caused by EOMs being unable to maintain eccentric gaze due to cerebellar compression. This results in a slow drift back to midline with corrective nystagmus to regain eccentric focus - Hence, when looking left, there will be a coarse slow left beating nystagmus (slow coarse, large amplitude) NET RESULT: 1. Fast nystagmus when looking away from side of lesion 2. Slow/coarse nystagmus when looking toward side of lesion ## Footnote https://youtube.com/watch?v=pFRvyQGXn9g

Answer 57

INFANTILE NYSTAGMUS: - Not congenital truly as you're not born with it, usually develops after birth - Form of central nystagmus 1. Nystagmus without oscillopsia (sensation that the surrounding environment is constantly in motion) 2. Worsens with fixation and improves when fixation removed (and decreased by eyelid closure) 3. Will have a null point (a gaze position where nystagmus is minimal; hence patients will compensate by looking to the side) 4. Can often be pendular (slower back and forth nystagmus) 5. Can be direction changing 6. Usually horizontal nystagmus CONGENITAL Mnemonic C - Convergence decreases nystagmus (near vision usually better than distant vision as nystagmus is dampened) O - Oscillopsia absent N - Null point (often in primary) G - Gaze uniplanar (ie. still horizontal nystagmus despite looking up or down) E - Equal amplitude and frequency usually (ie. pendular) N - Near acuity is good I - Inverted optikinetic nystagmus; ie. the eye beats in the opposite direction when tracking moving objects T - Turned head to achieve null point A - Abolished in sleep (ask partner) L - Latent (worse when covering 1 eye)

Answer 58

1. Spontaneous nystagmus is worse when looking towards direction of the fast phase (Alexander's law) 2. Nystagmus worse with fixation removed 3. Corrective saccade on HIT 4. Gait disturbance 5. Ocular tilt reaction (loss of utricular nerve activity)

Answer 59

OCULAR TILT REACTION 3 FEATURES: 1. Head tilt (towards the hypofunctioning side) 2. Skew deviation (pupil on the intact side is elevated, pupil on the affected side is depressed "falls down") - disconjugated deviation 3. Static conjugate ocular roll (Superior pole of each eye rolls towards affected utricle) Normal occular counter roll - eyes are kept straight, rotating to the opposite ear ETIOLOGY: - Damage to the vestibular pathways that mediate head-eye posture in the roll plane - Acute unilateral vestibular loss of utrivular nerve or midbrain activity - Majority of ocular tilt reactions are transient with spontaneous recovery in many cases LOCALIZATION: - Utricle/labyrinth - Vestibular nerve - Brainstem - Cerebellum CAUSATIVE LESIONS: Variable, but commonly - Stroke - Demyelination - Trauma - Iatrogenic/post-surgical - hemorrhage - Tumor

Answer 60

HINTS exam: 1. Head impulse test 2. Nystagmus 3. Test of skew - Think stroke if all of the following are met: HIT negative, direction changing or vertical nystagmus, and a positive test of skew - 95% sensitivity and specificity HINTS + hearing - hearing loss would be even more suspicious Head impulse is the most discriminatory because there is only one type of stroke that will cause it and it’s an AICA stroke (ie. which one test will you pick)

Answer 61

PERIODIC ALTERNATING NYSTAGMUS (PAN): - Congenital or acquired spontaneous central nystagmus NYSTAGMUS: - Conjugate binocular Nystagmus that reverses direction periodically (typically every 90-120 seconds) - Usually horizontal - Presents with or without fixation LOCALIZATION: - Cerebellar Nodulus/uvula - Dorsal Medulla ETIOLOGY: Big 5, and alcohol intoxiaction and Medications 1. Cerebrovascular 2. Tumor 3. Inflammatory/MS 4. Degenerative/Atrophy 5. Paraneoplastic 6. Alcohol Intoxication 7. Medications (e.g. anti-convulsants) 8. Bilateral vision loss

Answer 62

OCULOPALATAL TREMOR: - Form of spontaneous central nystagmus - aka. Oculopalatal myoclonus NYSTAGMUS: - Multi-vectored large amplitude low frequency pendular nystagmus CLINICAL FEATURES: - Associated with soft palate synchronized tremors LOCALIZATION: Degeneration of the inferior olivary nucleus in the Guillain-Mollaret triangle (Dentato-Rubro-Olivary tract): 1. Red nucleus 2. Inferior olivary nucleus 3. Contralateral dentate nucleus ## Footnote Darren VNG 2024 lecture Slide 42

Answer 63

- Square wave jerks - Nystagmus-like movements but not true nystagmus - Small 2Hz movements off gaze target then back - Singular or multiple - Fairly normal and common, worse in elderly

Answer 64

1. Spontaneous nystagmus - fast phase towards contralateral ear 2. Decreased VOR Gain - corrective saccade on head thrust test on pathologic side 3. Increased VOR Phase Lead at low frequency - loss of velocity storage 4. Ocular Tilt reaction - Vertical skew deviation, head rotated towards weak labyrinth, ocular counter roll with superior polls rotated towards weak labyrinth 5. Disturbance of gait - fall towards hypoactive labyrinth

Answer 65

- Present when head is still, dampened by visual fixation, increase or becomes apparent when fixation is eliminated Horizontal component: Fast phase towards intact ear Torsional component: Superior poles beat toward intact ear ("stronger ear pulls") - The vertical contributions to the slow phases of nystagmus from anterior and posterio canals of the intact side cancel one another - Leaving unopposed horizontal and torsional vestibular slow phases toward the lesioned side

Answer 66

WHAT IS IT: - Seen most often in superior vestibular neuritis - Dysfunction in the horizontal canal contributes to the horizontal component - Dysfunction in the anterior canal contributes to the torsional and small upbeat components - A similar nystagmus trajectory can occur in central disorders such as lateral medullary syndrome (Wallenberg)

Answer 67

1. INFECTIOUS - Labyrinthitis (Viral or Bacterial) - Vestibular Neuronitis - Ramsay-Hunt - Otosyphillis 2. DEGENERATIVE - Fistula - Cholesteatoma 3. IATROGENIC - Labyrinthectomy - Vestibular nerve section 4. OTOTOXICITY - Gentamicin - Streptomicin 5. TRAUMA - Blunt - Barotrauma - Labyrinthine concussion 6. VASCULAR - Labyrinthine Apoplexy (form of CV sudden occlusion of labyrinthine artery) 7. IDIOPATHIC - Meniere's 8. OTHER - BPPV - SCCD

Answer 68

1. CPA tumor 2. Ototoxicity (acute or gradual) 3. Presbystasis (dysequilibrium from aging) 4. Autoimmune 5. Otosyphillis 6. Neurodegenerative "ON A COP" Otosyphillis Neurodegenerative Autoimmune CPA tumor Ototoxicity Presbystasis

Answer 69

1. Ototoxicity 2. Meningitis 3. Trauma 4. Meniere's

Answer 70

1. Antiepileptics (e.g. Dilantin, Tegretol) - Cerebellar Toxicity 2. Antihypertensives - Causes Hypotension and decreased Cerebral Blood Flow 3. Anticoagulants - Hemorrhage in inner ear/brain 4. Ototoxic drugs (e.g. Aminoglycosides, Cisplatin) 5. CNS Depressants (e.g. Benzodiazepines, Barbiturates, TCA, Alcohol)

Vestibular Anatomy, Physiology, and Testing Principles Flashcards

(95 cards)