Vestibular Disorders Diagnosis and Treatment PDF

Table of Contents The Basics 2 ENG/VNG 4 VNG Test Protocol 5 VEMPs 9 Bedside Tests 11 vHIT 12 Computerized Dynamic Posturography 13 Rotary Chair 15 Diagnostic Key 18 **Peripheral Vestibular Pathologies** **19** BPPV 19 Meniere's Disease 19 Vestibular Neuritis 21 Vestibular...

Table of Contents The Basics 2 ENG/VNG 4 VNG Test Protocol 5 VEMPs 9 Bedside Tests 11 vHIT 12 Computerized Dynamic Posturography 13 Rotary Chair 15 Diagnostic Key 18 **Peripheral Vestibular Pathologies** **19** BPPV 19 Meniere's Disease 19 Vestibular Neuritis 21 Vestibular Labyrinthitis 22 Bilateral Vestibulopathy 22 Vestibular Schwannoma 22 Vestibular Paroxysmia 23 SCCD 23 Perilymphatic Fistula 24 **Central Vestibular Pathologies** **25** Vestibular Migraine 25 3PD 25 Vestibular Compensation and Rehabilitation 26 The Basics Vestibulo-ocular Reflex (VOR) - Purpose: hold images steady on the retina by producing compensatory eye movements during brief head rotations or translations - Created by the three-neuron arc: - Primary sensory afferent neuron ⇒vestibular nucleus neuron ⇒oculomotor neuron Saccades - Mediated centrally (cerebellum) - Purpose: rapid, brief, conjugate eye movements that shift the line of sight to bring target images onto the fovea---visual scene exploration - Types: - Volitional - Reflexive (ex. Looking towards action/loud sounds) - Predictive (ex. Watching a target too fast for smooth pursuit) - Memory guided (habitual) Smooth Pursuit - Purpose: maintain the image of a small, slowly moving target on the fovea while the head is still - Voluntary, driven by visual objects and modulated by attention and motivation - Can also suppress vestibular and optokinetic responses during head and eye tracking (cortically motivated) Optokinetic Response - Purpose: stabilize retinal images during head movements (like VOR) but uses visual inputs to infer the direction and speed of head motion rather than responding directly to head velocity signals - Necessary during prolonged head movement - Slow phase like VOR or smooth pursuit, fast phase like saccade Nystagmus - Two Phases - Slow phase: peripherally generated - Fast phase: cortically generated - Purpose: reset the eyes during prolonged rotation and direct gaze toward the oncoming visual scene - Form of saccade - Naming Nystagmus - Nystagmus is named after the fast phase - Degree and severity are based on the slow phase - Degrees: - 1^st^ degree: only present when gazing towards the fast phase direction - 2^nd^ degree: present when gazing toward fast phase and ahead - 3^rd^ degree: present when looking in all directions (usually acute) - Can be linear or torsional (torsion is named clockwise or counterclockwise) - 6° is significant - Peripheral gaze evoked nystagmus - Suppresses with fixation (unless is very acute phase) - Follows Alexander's law - Fast phase toward the healthy ear - Greatest velocity when looking toward the healthy ear, decreases at midline, further decreases when looking at the impaired ear - Direction fixed - Only for gaze-evoked nystagmus - Must have a horizontal component (may have some vertical via a torsional component, but will not have a purely vertical component) - Linear slow phase - Central gaze evoked nystagmus - Pure vertical involvement - Direction fixed or direction changing - Can persist well beyond the acute stage - Enhances/unaffected by fixation - Nonlinear (decreasing) slow phase velocity - Other (non-pathological) nystagmus - Rebound: a few beats of nystagmus (opposite fast phase) following eccentric gaze for an extended period - Endpoint: at extremes of gaze - Congenital: may appear as a direction-changing gaze-evoked nystagmus that is not affected by fixation. Distinguishing characteristics: - Present since childhood - Typically, horizontal - Has a null point where it will settle if a patient holds eyes or head in a certain way - Non-linear, increasing slow-phase velocity - Uses the corneorentinal potential of the eye - Front of eye (cornea) is + - Back of eye (retina) is -- - Sensitive to changes in light (so, don't change light during the testing) - Eyes move right: (+5mV) + (-2mV)= +3mV - Eyes move left: (+2mV) + (-5mV)= -3mV - Pros: - Less expensive in short-term - Useful in situations where goggles can't be uses - Cons: - Can't record torsional eye movement - Eye blink artifact - Set-up time VNG - Uses dichroic glass to reflect the image from eyes to camera - Pros: - Video recording - Torsional views - Cons: - Upfront investment - Glasses don't fit everyone - Ptosis (droopy eyelids) VNG Test Protocol Gaze Testing - Evaluate ability to maintain stable gaze and look for nystagmus - Tests in primary gaze (spontaneous nystagmus) and eccentric gaze (gaze evoked nystagmus) Saccades - "A red light will pop up in different locations---move your eyes to it quickly and accurately. Avoid predicting locations." - Measures: - Accuracy: how far over/under target (%) - Hypometric: undershoot target before correcting---creates shoulders - Rule out visual impairments, alertness, fatigue, medications, and blinking - Hypermetric: eyes overshoot and correct to target - Rule out visual impairments, blinking, improper calibration - Generally, abnormal saccade accuracy is a central (cerebellar) issue - Velocity: how fast eyes move to the target in degrees/second - Internuclear ophthalmoplegia: normal abduction (out), slowed adduction (in) due to median longitudinal fasciculus lesion - Latency: time between presentation of the target and start of eye movement (ms) - Abnormal latency can be due to Parkinson's or other central pathology or fatigue Smooth Pursuit - Maintain the image (dot) on fovea during continuous movement - Influenced by motivation - Measure: - Gain: how closely eyes follow target - Abnormal: central pathology - Rule out medication, inattention, fatigue, and head movement - Bilaterally impaired smooth pursuit= saccadic overlay to smooth pursuit aka cogwheeling Optokinetic (OPK) - Stabilizes objects while head/full field is moving (at least 90% of the visual field must be filled with stimuli to stimulate) - Combines smooth pursuit and saccade systems - Test at 20°/s and 40°/s velocity for 20 seconds - Measure: - Velocity gain: how closely eye movement matches stimulus - Bilateral reduction: disorder in smooth pursuit of saccadic systems (central issue). Rule out: attention, visual impairment, and medication - Asymmetry: \>25% is significant, often caused by overlaying spontaneous nystagmus Positional Nystagmus - Placement of head/body into static positions to look for "static positional" nystagmus - Test vision denied---if there is nystagmus, test with vision to assess visual suppression - Ask alerting questions - Measures: - Strength, duration, direction, and visual suppression of the nystagmus Positioning Nystagmus - Before testing: vertebral artery screen - Have patient look left or right with head looking upward for about 30 seconds. Identifies problems with blood flow from the vertebral arteries to the brain. - Ask about dizziness, lightheadedness, nausea, blurred vision, double vision - If screen is positive: don't do the Dix-Hallpike - Head Shake Test - Vision denied with head 30° downward (so it is in line with the HSCC) - Examiner shakes head for 20 seconds at 2 Hz with a 30° left/right displacement - Analysis - In normal or bilateral loss= no nystagmus - Dynamic imbalance= nystagmus beating toward the better ear, which should decay in about 30 seconds - Dix-Hallpike - For posterior or anterior BPPV - Rotate head 45° left or right, have patient quickly lay back, have 30° cervical extension, watch for nystagmus - Interpretation: - Beats toward the affected ear - PSCC: up beating, torsional - ASCC: down beating, torsional - Roll Test - For horizontal BPPV - Supine with head lifted 30°, turn head quickly to one side looking for nystagmus, then to the other side - Interpretation: - Geotropic (toward the ground) nystagmus: Canalithiasis - The more intense response is the affected ear - Caused by free-floating otoconia - Should fatigue in 15-30 seconds - Slightly delayed nystagmus onset - Ageotropic (away from the ground) nystagmus: Cupulolithiasis - Side with less intense response is affected ear - Caused by displaced otoconia that adhered to the cupula - Persistent nystagmus when in the position - Immediate nystagmus onset - Canal jam: otoconia become stuck in the narrow point of the canal - Constant nystagmus - Positional Alcohol Nystagmus - Direction-changing peripheral nystagmus - PAN I: move into position (supine with right or left head turn) - Alcohol reaches cupula before endolymph and cupula floats= geotropic nystagmus - PAN II: move out of position - Alcohol leaves cupula earlier than endolymph and cupula sinks= ageotropic nystagmus Caloric Test - Assess responsiveness and symmetry of HSCC and superior vestibular nerve - Caloric heat/cold changes endolymph density, therefore changing the balance of force across the cupula (note: there are some direct temperature effects) - Test at 30° supine - Air: - Warm (50°C), cool (24°C), flow rate (800 mL) - Water: - Warm (44°C), cool (30°C), flow rate (250 mL) - Excitation patterns: - Warm: ampullopetal deflection= excitatory= fast phase toward the irrigated ear - Cool: ampullofugal deflection= inhibitory= fast phase away from the irrigated ear - COWS: cool opposite, warm same - Limitations: - Only tests HSCC and SVN - Must ensure equal stimulation, bilaterally - Not always well tolerated - Keep in mind middle ear status - Low frequency stimulation relative to optimal frequency of stimulation of the vestibular system - Analysis: - PODS/butterfly - First, calculate total response - TRE= PeakRC-PeakRW (add absolute values) - TLE= PeakLW-PeakLC - Next, calculate for unilateral weakness - UW%= (TRE-TLE)/(TRE+TLE) - If positive: left weakness - If negative: right weakness - Bilateral hypofunction: TRE \140° - Rule out calibration or technology error - Could be loss of VOR inhibitory function at the level of the vestibular nuclei - Possible cerebellar lesions - Fixation suppression: FI% \>0.6 - Bilateral: cerebellar degeneration - Unilateral: CPA tumor - Additional measures: Directional preponderance - Nystagmus response is greater in one direction compared to another - Atypical if \>30% Ice Water Caloric - Test when you don't get a response from standard caloric (TRE or TLE \40: mean+2SD= 47.86% - Latency: generally, does not hold much diagnostic value but individuals with MS show shifts - Threshold: thresholds below 75 dB are indicative of semicircular canal dehiscence\  oVEMP - Test of utricle and SVN - Recorded from contralateral inferior oblique - Biphasic wave form: n11, p15 - Pathway: - Utricle ⇒ SVN ⇒ Brainstem vestibular nuclei⇒ oculomotor and trochlear nerve motor neurons ⇒ipsilateral inferior oblique and contralateral superior rectus - Parameters: - Low frequency tone burst - Measurement variables: - Affected by gaze (should be 30 degrees upward) - Age plays a big effect, uncommon to have a response at age 60 and variable above age 40 - Affected by CHL - Analysis: - All or nothing response (above 95 dB) - Interpretation is amplitude symmetry between ears - Large high intensity tone burst amplitude at 500 HZ + a present waveform AT 4000 Hz is indicative of semicircular canal dehiscence Bedside Tests Ocular stability test---test of skew - Evaluating for vertical ocular drift (central test) - Protocol: - have patient fixate on a small visual target (ex. Tip of pen) while the examiner is alternating covering one eye after the other. - Examiner looks for compensatory vertical eye movements of the eye that was just uncovered---typically, in a positive test, one eye will drift up and the other will drift down Head-impulse test - Tests the VOR---allowing for side-specific and canal specific VOR analysis - Protocol: - Examiner asks the patient to fixate on their nose and quickly moves the patients head in an unpredictable fashion - Examiner looks for an incomplete VOR necessitating catch-up saccades Head-shake Nystagmus - Evaluates for a unilateral peripheral vestibulopathy - Protocol: - Have patient tip their head 30 degrees forward, examiner shakes the patient's head for about 15 seconds at a 2 Hz frequency - Examiner looks for a contralesional nystagmus following the shake Postural tests: - Romberg test: - Protocol: - Have patient stand with arms next to their body or crossed in front of them with their eyes closed. - Scored based off seconds that they can maintain balance - Tandem gait test: - Protocol: - Walk in a straight line heel-to-toe with arms at side - Rate their walk as ataxic or normal - Fukuda step test: - Protocol: - "Frankenstein's monster" walk with eyes closed for 50-100 steps - Assess degree of bodily rotation and overall balance maintenance - Timed-up-and-go (TUG) test: - Protocol: - Have patient start seated, stand up, walk 3 meters, turn around, and return to their seat and sit. - Assess time to complete task. \>= 13.5 seconds is predictive of fall risk vHIT Basics - Measure of eye movement in response to fast, passive, unpredictable head turns with abrupt starts and stops - Allows for the evaluation of all six SCC Analysis - 1\. Look at tracings for overt and catch-up saccades - 2\. Assess VOR gain: eye movement compared to head movement - Norms: 0.79-1.20 - 3\. Assess gain symmetry Catch-up Saccades - Catch-up saccades are the result of incomplete VOR (excitation toward lesioned side) - There is a natural asymmetry in the dynamic range of excitation and inhibition - Excitation: baseline is 90-100 spikes/sec with a max of 400 spikes/sec - Inhibition: baseline is 90-100 spikes/sec with a min of 0 spikes/sec - So, you will get abnormal responses with the impulse toward the lesioned side because you can't drive a response based off of inhibition alone---requiring centrally-processed catch-up saccades - Why are there catch-up saccades when excitation is toward the healthy side? - Excitation, alone, is also not enough to match head velocity - The inhibited ear, when functioning, sends an inhibitory signal up its vestibular nucleus. The VN, then decreases its inhibition of the opposite VN. This basically raises the ceiling of firing. - Without the central disinhibition from the inhibited side due to a lesion, the VOR will be incomplete vHIT vs Caloric - Average head movement is 2 Hz horizontally and 5.8 Hz vertically - Caloric is 0.003 Hz and vHIT is 5 Hz - Often caloric and vHIT are in agreement, but lack of agreement can point toward some pathologies: - Normal caloric + abnormal vHIT= can be due to site of lesion or partial damage - Abnormal caloric + normal vHIT= can be documentation of recovery/compensation or evidence of structural changes Computerized Dynamic Posturography Overall benefits of CDP: - Provides objective assessment of major sensory and motor components of balance - Can provide insight into patient's functional balance capacity outside of clinic - Can aid in determining non-physiologic causes of unsteadiness - Repeatable and reliable Terminology - Center of gravity: center of weight distribution - Base of support: perimeter of the area of contact between the environment and the feet - Postural stability: ability to keep center of gravity of the base of support - Limits of stability: the farthest in any direction that a person can lean away from midline without altering the base of support by stepping, reaching, or falling Sensory organization test (SOT) - 6 subtests: - 1\. Eyes open, fixed visual and surface - 2\. Eye closed, fixed surface - 3\. Eyes open with sway visual, fixed surface (assess visual preference) - 4\. Eyes open with fixed visual, sway surface - 5\. Eyes closed with sway surface (test vestibular system) - 6\. Eyes open with sway surface and visual (test vestibular system) - Patterns of results: - Abnormal 5 and/or 6: vestibular dysfunction - Abnormal 4, 5, and 6: visual and vestibular dysfunction - Abnormal 2, 3, 5, and 6: somatosensory and vestibular dysfunction - Abnormal 3 and 6: visual preference - Abnormal 3, 5, and 6: vestibular dysfunction with a visual preference Motor control test (MCT) - Assess patient's ability to generate effective motor responses to sudden surface translations - Produces sudden back/forth surface translations assessing the latency of postural adjustment relative to platform movement - Assesses VSR---measure of long loop neural pathways and the biomechanics of the lower limbs - Used for rehabilitation planning and prognosis, medical/legal performance documentation, and disability/return to work - Measures: symmetry (R/L), latency (ms), and strength of motor response Adaptation test - Measures a patient's ability to minimize sway upon sudden change in surface inclination - Measures: force produced by patient to minimize postural sway - Good for assessing fall risk Rotary Chair When to do RC - Bilateral hypofunction---is it central or peripheral - SHA+VVOR - Monitor compensation - Remember---SHA phase is more reliable, symmetry and gain improve with compensation - Patients who refuse VNG - Normal VNG but vestibular symptoms - Is it central? SHA+ VST - Utricle assessment - oVEMP+SVV Pros of RC - Allows for evaluation of peripheral system beyond the low frequencies (caloric= 0.003 Hz), comparable to more natural movement. - Better tolerated by patients than caloric - Important for assessing bilateral peripheral losses - Can test compensation and smaller VOR changes due to controlled rotational stimulus Cons of RC - Stimulates both labyrinths simultaneously, so side of lesion can be hard to determine - Costly - Tine-intensive - Uncomfortable for claustrophobic patients RC Basics - Rotary chair names nystagmus based on slow phase, disregarding fast phase - Patient sits in a rotational chair in a dark room with their head tilted 30 degrees forward, wearing video goggles to monitor eye movement  Sinusoidal Harmonic Acceleration (SHA) test - Patient is spun at different frequencies (note: faster frequencies require more cycles to acquire adequate data) - Recommended frequency order: 0.08, 0.04, 0.01, 0.16, 0.32, 0.64 - Parameters: - Gain: how much eyes move relative to chair movement (slow phase velocity versus chair velocity) - Related to alertness - Changes based on compensation - Phase and symmetry are calculated based on gain, so it must be above 0.15 to find reliable phase/symmetry values - Phase: timing difference between head/chair movement and eye (slow phase) response to that movement - Key diagnostic feature because it is the most stable and repeatable - Phase lead= eyes lead - Phase lag= eyes lag - Eye velocity naturally leads at lower test frequencies as they are unnatural velocities of movement and VOR is incomplete - Symmetry: peak slow-phase velocity on a right turn versus a left turn - Not a definite indication of laterality of lesion---more similar to directional preponderance on caloric - Changes with compensation - Analysis: - Abnormal gain (must be at least two consecutive frequencies): - Mild gain reduction for low frequencies (\2.5 degrees off from true vertical - Right lean= right utricle dysfunction - Left lean= left utricle dysfunction - If oVEMP is normal and there are signs of central pathology, analysis is different: - Vestibular nucleus lesion will have an ipsilateral tilt - Upper brainstem lesion will have a contralateral tilt Dynamic Unilateral Centrifugation - Patient is rotated at 300-400°/s with a left or right chair translation to make the left or right utricle the axis of rotation - Symmetry of response is measured - This is not used clinically Diagnostic Key Prolonged Spontaneous Vertigo - From sudden, permanent impairment of the function of one peripheral labyrinth or its central connections - Improvement occurs via compensation not restoration - Symptoms last several days - Central causes: CVA (stroke) in the brainstem, labyrinthine, or cerebellum, Multiple Sclerosis, concussion syndrome - Peripheral causes: vestibular neuritis/labyrinthitis, labyrinthine concussion Recurrent Spontaneous Vertigo - Not generally responsive to therapy unless periods of remission are becoming symptomatic (onset of permanent damage)---mostly manage symptoms - Central causes: vestibular migraine - Peripheral causes: Meniere's disease, perilymphatic fistula, vestibular paroxysmia Positionally Provoked Vertigo - Results from sudden inappropriate excitation of the vestibular system, usually triggered by a change in position relative to gravity - Central causes: spinocerebellar atrophy, MS, Chiari malformations, brainstem/cerebellar tumors - Peripheral cause: BPPV Peripheral gaze evoked nystagmus - Suppresses with fixation (unless is very acute phase) - Follows Alexander's law - Fast phase toward the healthy ear - Greatest velocity when looking toward the healthy ear, decreases at midline, further decreases when looking at the impaired ear - Direction fixed - Only for gaze-evoked nystagmus - Must have a horizontal component (may have some vertical via a torsional component, but will not have a purely vertical component) - Linear slow phase Central gaze evoked nystagmus - Pure vertical involvement - Direction fixed or direction changing - Can persist well beyond the acute stage - Enhances/unaffected by fixation - Nonlinear (decreasing) slow phase velocity Peripheral Vestibular Pathologies Benign paroxysmal positional vertigo (BPPV) - Pathophysiology: - In your utricle, the otoconia may become loose due to injury, infection or age. As your head position changes, the otoconia roll around and push on tiny hair-like structures (cilia) within your semicircular canals. Those cilia help transmit information about balance to your brain. Vertigo develops when the cilia are stimulated by the rolling otoconia. - Test Results: - Dix-Hallpike - For posterior or anterior BPPV - Rotate head 45° left or right, have patient quickly lay back, have 30° cervical extension, watch for nystagmus - Interpretation: - Beats toward the affected ear - PSCC: up beating, torsional - ASCC: down beating, torsional - Roll Test - For horizontal BPPV - Supine with head lifted 30°, turn head quickly to one side looking for nystagmus, then to the other side - Interpretation: - Geotropic (toward the ground) nystagmus: Canalithiasis - The more intense response is the affected ear - Caused by free-floating otoconia - Should fatigue in 15-30 seconds - Slightly delayed nystagmus onset - Ageotropic (away from the ground) nystagmus: Cupulolithiasis - Side with less intense response is affected ear - Caused by displaced otoconia that adhered to the cupula - Persistent nystagmus when in the position - Immediate nystagmus onset - Canal jam: otoconia become stuck in the narrow point of the canal - Constant nystagmus - Treatment: - Dislodging the otoconia through a Epley maneuver or the Lempert maneuver Meniere's Disease - Pathophysiology: - Buildup of endolymph in membranous labyrinth (hydrops) - Theories: genetics, constrictions in blood vessels, consequence of viral infections, allergy, or immune reactions - Histopathological consequences: - 1\. Hair cell death due to repeated attacks causing stress or electrochemical damage - 2\. Mechanical changes---dilation of cochlear/saccular ducts that can lead to membrane rupture - Reisner's membrane in the cochlea - 3\. Cochleovestibular nerve damage through neurotoxicity - Diagnostic Criteria: - Possible: - Episodic vertigo without hearing loss OR - SNHL with fixed disequilibrium - Probable: - One definitive episode of vertigo - Documented hearing loss on at least one occasion - Tinnitus or aural fullness - Definite: - 2+ episodes of vertigo lasting 20 minutes to 12 hours - Low to mid frequency SNHL - Fluctuating tinnitus and/or aural fullness - No better diagnosis - Additional Information: - Slowly progressive - Usually unilateral, but it can progress to bilateral - Commonly presents around age 50-60 - Is more prevalent in women than man (3:2) - Clinical Presentation: - Vertigo - 20 minutes to 24 hours, but usually 2-4 hours - Drop attacks - Hearing Loss - Progressive low frequency (below 2kHz) SNHL - Progresses to a flat or peaked pattern - Stages (based on average of.5, 1, 2, and 3 kHz): - 1: \70 dB - Note: fitting hearing aids on this population can be difficult because it is fluctuating hearing loss with a low frequency pattern. So, undershoot low frequency targets and/or add a low frequency roll-off to avoid the upward spread of masking. Also, add several programs for different hearing days. - Tinnitus and/or aural fullness - Roaring/rushing tinnitus - Usually episodic, preceding an attack - Test Results: - VNG or RC with Caloric - Unilateral weakness (48-73% of time)---usually post-attack or further in disease progression - Spontaneous or positional nystagmus that may be direction changing during an attack - It is an irritative nystagmus, so it will beat toward the bad side - vHIT - Usually normal - Normal vHIT + abnormal caloric = indicative of Meniere's - VEMPS - Variable, more for ruling out other pathologies - ECochG - If abnormal, can be strong diagnostic indicator - If normal, does not rule out Meniere's - Clinical Phases: - Early: fluctuating hearing loss, good discrimination, fluctuating tinnitus/fullness, infrequent vertigo, no unsteadiness or positional vertigo - Middle: fixed flat hearing loss, decreased discrimination, constant tinnitus/fullness, severe vertigo, occasional unsteadiness/positional vertigo - Late (burnout): fixed flat hearing loss, poor discrimination, constant tinnitus/fullness, no vertigo, frequent unsteadiness and positional vertigo - Treatment: - Non-surgical - Manage symptoms: hearing aids, attack management strategies, post-burnout vestibular rehabilitation - Diet changes: low sodium, avoid caffeine and alcohol - Surgical - IT steroid injection - Endolymphatic shunt - Meniett device - Worst case, accelerate burnout: gentamicin injection, labyrinthectomy, vestibular nerve section Vestibular Neuritis/Neuronitis/Neuropathy - Overview: - Inflammation of vestibular portion of the VIIIth nerve, believed to be associated with, preceding, or accompanying a viral infection - Presents with vertigo, nausea, gait imbalance - Clinical Presentation: - Sudden vertigo onset lasting hours to days - Worsened but not really caused by head movement - Possible nausea and vomiting - Vertigo period fatigued and was followed by disequilibrium - May have had a recent upper respiratory virus - Can occur in the SVN, IVN, or both - SVN is the most common - Severity of symptoms: both\>SVN\>IVN - Test Results: - VNG: spontaneous nystagmus (depending on stage of compensation), unilateral weakness - vHIT: unilateral weakness - VEMP: depending on site of lesion, but likely absent or reduced - Treatment: vestibular rehabilitation Vestibular Labyrinthitis - Inflammation/infection affecting the vestibular nerve and labyrinth - Symptoms of vestibular neuritis with a permanent SNHL Bilateral Vestibulopathy - Diagnostic criteria: - At least two of the following: - Gait instability - Motion-induced blurred vision (oscillopsia) while walking or on rapid head movement - Worsening of instability in dark room or on uneven ground - No symptoms under static conditions - No vertigo - No better diagnosis - Test results: - vHIT: bilaterally reduced gain (gain\