LP [10]47
Evaluation and Management of Vestibular Disorders Texas Academy of Audiology
Samuel N. Bittel, Au.D. Slide 1
LP [10]47 Option 1 Cover (I think this is my preference) Lindsay Peters, 3/27/2017 Course Outline
• Anatomy and physiology review • Vestibular reflex pathways • Vestibular disorders and case studies o Peripheral
o Central • Case Hx, Sx, and potential Dx • Brief introduction to VRT and BRT Laws That Govern Vestibular Science
o Ewald’s 1st Law endolymph moves in opposite direction of head, causing eyes to move in same direction as endolymph; eyes move in same plane as stimulated canal
o Ewald’s 2nd Law excitation stronger than inhibition; will address more in VOR section Importance of Ewald’s Laws
• Ewald’s 1st Law o Premise of VOR
o Slow phase of nystagmus driven by ear • Ewald’s 2nd Law o With movement, unequal contribution at level of vestibular nucleus
o Excited ear drives reflex
o What happens right vs. left rotary chair or head impulse? Basic Vestibular A&P
• Equilibrium is most basic sense • Vestibular system evolves earlier • Hearing arises from vestibular system • Not just ear and peripheral system: o Cerebellum (ascending/descending)
o Eyes (ascending/descending)
o Muscles of postural stability
o Ascending sensory tracts
o Descending motor tract Basic Vestibular A&P
• Vestibular system consists of a number of complex anatomical structures and reflex pathways • Structures code a change in acceleration of the head and/or body • They also interpret the pull of gravity • NOT sensitive to a consistent speed/motion Basic Vestibular A&P
• Important definitions: o With hearing
o Peripheral = cochlea, ME
o Central = VIIIth nerve and up
o With vestibular
o Peripheral = end organ (ear), VIIIth nerve
o Central = cerebellum, brainstem, brain
• Question: o Is a vestibular schwannoma a central or peripheral lesion? Peripheral A&P Anatomy Semi-Circular Canals • Sensitive to angular change in acceleration = yaw, pitch, and roll • Oriented at right angles to one another • Horizontal canal sits at 30-degrees • Ampulated ends contain crista ampullaris Semi-Circular Canals
The semicircular canals lie perpendicular to each other
Superior/Anterior
A n te r io r
The canals are actually
Posterior/ tilted at about 30 degrees I n fe rio r L a t er a l/
H o r izo n a l
Semi-Circular Canals Semi-Circular Canals Semi-Circular Canals
• Cupula has mass o Lags behind endolymph w/ initial movement o Will eventually catch up to endolymph o After movement stops, endo will stop and cupula will continue to move Semi-Circular Canals
• Oriented in matched pairs o Ears work in tandem = push-pull system
o One stimulatory response, other inhibitory
o Neural homeostasis achieved (when not moving) if equal response from both ears (clinical correlate: vn) Semi-Circular Canals
• Thoughts o Ears have a spontaneous firing rate
o Vestibular nucleus (central) is comparing/contrasting firing rate from both sides
o Difference between sides = perception of movement Utricle and Saccule
• Sensitive to linear acceleration • Gravity detector • Utricle oriented in horizontal plane • Saccule oriented in vertical plane • Each structure has slight curvature, which allows different sections to be stimulated by slightly different motions Utricle and Saccule
• Each contain a sensory structure- macula o Hair cells imbedded in a gelatinous layer
o This layer contains otoconia, which add weight and create drag Utricle and Saccule
•Macula of the utricle is oriented in a horizontal plane •Macula of the saccule is oriented in a vertical plane Otoliths Otoliths Utricle & Saccule Biomechanics
• Otoliths are made from calcium carbonate (Latin for “ear stones”) • The endolymph in the utricle and saccule are calcium deficient • The otoliths have a life span and are being constantly recycled – they dislodge from macula and float in endolymph Utricle & Saccule Biomechanics
• As we age: o Our calcium absorption slows (vitamin D)
o Protein matrix around otoliths break down and become less “sticky”
• This may cause a higher concentration of free-floating otoliths
• More free-floating otoliths = higher calcium concentration = poorer absorption of newly dislodged otoliths Cranial Nerve VIII and Blood Supply Vestibular Branch of VIII
•Superior branch innervates HC, AC, and utricle •Inferior branch innervates PC and saccule Cranial Nerve VIII • Differentiating which branches are involved helps with diagnosis • We have tests that look at each branch individually o Calorics, oVEMP, RC, etc. = superior branch
o cVEMPs = inferior branch
o ABR, hearing, etc. = cochlear branch • If you see deficits in all 3 branches unilaterally, a mass lesion should be r/o Cranial Nerve VIII
• Bony canal of superior nerve is longer and has less space (with nerve and blood supply) • Superior nerve more susceptible to “entrapment” and damage due to inflammation • VN more often causes superior nerve damage
• Goebel, JA (2001), et al. Anatomic considerations in vestibular neuritis, Otol Neurotol, 22(4), 512-518. Blood Supply
•Inner ear fed by posterior circulation = vertebral arteries join to form basilar artery •Common blood supply between cochlea and vestibular system at level of basilar artery (and outward) •Differentiate after AICA Blood Supply
• Food for thought o A lot of talk about identifying damage in specific canals, otolithic organs, etc.
o vHIT, oVEMP, cVEMP
o Although possible, how common?
o Is vestibular damage typically localized to the end organ or VIIIth nerve? Blood Supply
• Food for thought: o If peripheral vestibular system is fed by posterior circulation, can a pathology effecting cortical blood flow (migraine) damage the ear????
o We will talk more about migraines during the pathologies section Central A&P Central Vestibular System
• Vestibular system multisensory o Vestibular input
o Visual input
o Somatosensory input
o Motor input • Information from each system is integrated in the vestibular nuclei • Equilibrium and postural control information sent to other brain structures Central Vestibular System
• Balance information sent from midbrain to multiple regions of the cortex • Connections to a multitude of brain areas • Diffuse pathways are difficult to study • However, it is generally agreed upon that there are 4 major brain regions for balance Central Vestibular System • Four major areas of the brain for balance: o Voluntary motor movement = frontal lobe, specifically precentral cortex and connections to pyramidal system
o Visual information = occipital lobe w/ connections to frontal cortex
o Deep brain basal ganglia = help coordinate muscle movement
o Cerebellum = control of posture, coordinate sensory and motor information Central Vestibular System • Efferent and afferent connections between systems o Information from each sensory system is received and integrated in the vestibular nuclei
o Corrective postural and visual control information is sent to the muscles of the neck, trunk, legs, arms, and eyes • Also connections with reticular formation (autonomic nervous system) Reflex Pathways • Three primary pathways measured clinically: o Vestibulo-Ocular Reflex (VOR)
o VNG, VAT, CD-VAT
o Vestibulospinal Reflex (VSR)
o SOT
o Vestibulocollic Reflex (VCR)
o cVEMP Vestibulo-Ocular Reflex Vestibulo-Ocular Reflex (VOR) • VOR o Helps with gaze stabilization during head/body movement
o Allows desired object to stay on fovea, even when walking/running or moving head
o Deficit = oscillopsia Semi-Circular Canals
• Each SCC is connected to extra-ocular muscles • Excitation: o Horizontal canal:
o Ipsilateral medial rectus
o Contralateral lateral rectus
o Anterior canal:
o Ipsilateral superior rectus
o Contralateral inferior oblique
o Posterior Canal:
o Ipsilateral superior oblique
o Contralateral inferior rectus • Inhibition in corresponding antagonist muscles Eye Muscle Anatomy
Vestibulo-Ocular Reflex (VOR)
• Limited range of eye deflection o Eyes can only move so far
o If body continues to rotate, eyes will eventually reach limit
o CNS will cause eyes to rapidly move back to center to establish new focal point = saccade Vestibulo-Ocular Reflex (VOR) • If body continues to rotate after eyes have moved to center: o Repeat of slow movement in direction opposite of head/body movement
o Eyes will again reach their limit, and have saccadic rapid movement back to center
o This alternating slow and rapid eye movement is called nystagmus
o Note: slow movement of eyes occurs at same speed as head/body movement (equal and opposite) Nystagmus
• We describe nystagmus in reference to the fast phase (direction “beating”) • Remember: o Slow phase is driven by the ears
o Fast phase is driven by the CNS
o Nystagmus beats towards a stimulated ear
o Nystagmus beats away from an inhibited ear Back to Ewald’s 2nd Law
• Excitation is stronger than inhibition • Let’s measure a patient’s nystagmus o Patient has a deficit in the right vestibular system
o Spin the patient right
o Spin the patient left
o How would the nystagmus compare between directions? Why? Nystagmus
• How does nystagmus look with a deficit on one side? • The vestibular nucleus does not understand that one side is lesioned when integrating sides • Nystagmus beats away from the side with a deficit-causing lesion • Nystagmus beats towards the side with an irritative lesion. Example???? Clinical Correlate
• If we know our ear anatomy and the specifics of the VOR, we can identify the side of lesion by watching a patient’s eyes for nystagmus
• We have clinical tests (calorics) that can stimulate/inhibit an ear individually, and we can measure nystagmus Nystagmus
• A few thoughts/questions: o What would nystagmus look like with a bilateral and equal vestibular deficit?
o Does nystagmus persist indefinitely after a permanent lesion?
o Can spontaneous nystagmus be caused by problems in places other than the ear? Nystagmus - Peripheral
• Typically only observed w/ vision denied (unless acute) • Direction fixed • Alexander’s law (law???) • Suppresses with vision • Enhances dynamically • Linear slow component • Horizontal nystagmus (right/left beating) Nystagmus - Central
• With vision enabled (fixation) nystagmus persists • Does not lessen over time (no central compensation) • Direction fixed or changing • Rarely in primary • Vertical/rotary • Enhanced with vision enabled • Vertical nystagmus post HFHS • Does not enhance dynamically Nystagmus - Central
• If vertical and/or rotary during gaze testing, lesion should be considered central until proven otherwise • Only known peripheral condition to cause pure vertical down- beating nystagmus = bilateral SCDS Nystagmus - Central
• Rebound nystagmus: o Nystagmus beats in direction of most recent eye movement after eyes returned to center
o For example, after completing right gaze and eyes returned to center (moving left), a left-beating nystagmus is observed
o If eyes held eccentrically for an extended period (~ 20+ sec.), normals may have a few (2-3) beats Nystagmus - Central
• Vertical: o Down-beating nystagmus:
o Craniocervical junction pathology
o Arnold-Chiari malformation
o Low posterior fossa
o Vestibulocerebellum
o Up-beating nystagmus:
o Lower brainstem
o Medullary regions Nystagmus - Central
• Vertical: o Important points-
o Lesions in posterior fossa that produce purely down-beat nystagmus may not cause abnormal oculomotor tests (saccades and smooth pursuit)
o If only persistent vertical nystagmus is noted, posterior fossa lesion should be ruled out Nystagmus - Central
• Can peripheral nystagmus be direction changing? o Horizontal canal BPPV
o Geotropic: canalithiasis
o Side with more intense nystagmus = involved
o Ageotropic: cupulolithiasis
o Side with less intense nystagmus = involved • Pearls: o With positioning not position
o Associated vertigo Nystagmus – Let’s Pull This Together
• If you spin a patient to the right o Describe the slow and fast phase of their nystagmus
o Which ear is being stimulated? Inhibited? • If a patient has a left ear lesion (reduced output; uncompensated) o Which way will their nystagmus beat?
o Why? • How are calorics related? o Warm = stim; similar to spinning patient to right
o Cool = inhibited; similar to spinning patient to right nd o Why are warm calorics often larger? (hint- Ewalds 2 law) ABA Tier 1 Question
1)Peripheral vestibular nystagmus in a static position is: A. Horizontal B. Vertical C. Rotary ABA Tier 1 Question
2)Nystagmus is composed of both a slow and fast phase. Which phase is driven by the peripheral vestibular system? A. Fast B. Slow ABA Tier 1 Question
3)The canalithiasis variant of horizontal canal BPPV is characterized by: A. Geotropic nystagmus B. Ageotropic nystagmus C. Geotropic or ageotropic nystagmus, depending on which ear is down Vestibulospinal Reflex Vestibulospinal Reflex (VSR)
• Connection between vestibular system and stability muscles of the torso and lower extremities (below the neck) • Vestibular system detects movement and postural sway and corrective signal sent to muscles to maintain balance and coordinate movement • Can be volitional or reflexive Vestibulospinal Reflex (VSR)
• Volitional o Conscious shifting of weight from center of gravity to move
o Modified over time through learning • Reflexive o Short-latency response to perturbation
o Ankle strategy = small/slow perturbation
o Hip strategy = weight shifts
o Suspensory strategy = lowering COG
o Stepping strategy = new COG Vestibulospinal Reflex (VSR) Vestibulocollic Reflex Vestibulocollic Reflex (VCR)
• Vestibular system’s connection to stabilization muscles of cervical spine • Righting reflex • Helps maintain upright head position • Independent of trunk movement • Mediated through otolithic organs and medial vestibulospinal tract Vestibulocollic Reflex (VCR)
• Tested through cVEMP • Auditory stimulus saccule and creates neural impulse o Impulse sent through inferior vestibular nerve to vestibular nucleus
o Vestibular nucleus sends signal to SCM through descending medial vestibulospinal tract ABA Tier 1 Question
4)The originating organ for the cVEMP is: A. Utricle B. Saccule C. Horizontal semicircular canal Pathologies Pathologies
• I made a conscious effort to leave out BPPV, vestibular neuritis, and labyrinthitis • Instead, I will focus on: o Peripheral- SCDS and Meniere’s disease
o Central- Migraine and psychogenic dizziness Superior Canal Dehiscence SCDS SCDS
• Possible symptoms: o Tullio’s phenomenon
o Hennebert’s sign
o Autophony
o Hyperacusis
o Dizziness/disequilibrium
o Aural distortion
o Pulsatile tinnitus SCDS
• Clinical findings: o Multifactorial disequilibrium
o Nystagmus with vocalization
o Positive perilymphatic fistula test
o Pseudo conductive hearing loss
o BC at 250 Hz too good
o Conductive HL w/ present reflexes
o Abnormally low VEMP threshold
o Air-bone gap w/ present VEMP
o Abnormally large VEMP response SCDS
• Should always consider SCDS if: o Air-bone gaps with present stapedial reflexes
o Air-bone gaps with present VEMP • Cause o Can occur after head trauma
o Often idiopathic
o Increased intracranial pressure? SCDS – Normal Cochlea
From: www.dbi.udel.edu/MichaelTeixidoMD/DownloadableTeachingMovies.html SCDS – Normal Cochlea
From: www.dbi.udel.edu/MichaelTeixidoMD/DownloadableTeachingMovies.html SCDS – Tullio’s Phenomenon
From: www.dbi.udel.edu/MichaelTeixidoMD/DownloadableTeachingMovies.html SCDS – Tullio’s Phenomenon
From: www.dbi.udel.edu/MichaelTeixidoMD/DownloadableTeachingMovies.html SCDS – Hennebert’s Sign
From: www.dbi.udel.edu/MichaelTeixidoMD/DownloadableTeachingMovies.html SCDS – Hennebert’s Sign
From: www.dbi.udel.edu/MichaelTeixidoMD/DownloadableTeachingMovies.html SCDS – Autophony
From: www.dbi.udel.edu/MichaelTeixidoMD/DownloadableTeachingMovies.html SCDS – Autophony
From: www.dbi.udel.edu/MichaelTeixidoMD/DownloadableTeachingMovies.html SCDS – Conductive HL
From: www.dbi.udel.edu/MichaelTeixidoMD/DownloadableTeachingMovies.html SCDS – Conductive HL
From: www.dbi.udel.edu/MichaelTeixidoMD/DownloadableTeachingMovies.html SCDS Repair
• Typically surgical • Symptoms have to warrant intervention • Most of my patients live w/ it BREAK – 30 minutes Patient J.F. Patient J.F.
• 50 y/o female • Self-referred: o J.F. president of local self-help group for individuals w/ vestibular disorders
o Met J.F. at vestibular workshop
o She had been extensively evaluated, so was very reluctant to see me Chief Complaints
• 37-year Hx of episodic vertigo o Several hour attacks (1-2 hrs.) multiple times/year
o Right aural fullness and fluctuating hearing (may not occur when vertiginous)
o Previous right middle ear involvement w/ PE tube implantation
o Symptoms resolved after tubes
o No long-duration vertigo since 2005
o No tinnitus Chief Complaints
• Seasonally since onset: o Short-duration (seconds) transient vertiginous events
o Provoked with positioning: lying supine, rolling in either direction, rising from supine, and with head pitch
o Has not experienced for several months Chief Complaints
• Current Symptoms: o General disequilibrium
o Veering when walking
o Increased lightheadedness w/ complex visual stimuli
o Bilateral sound sensitivity
o Issues ambulating in dark Medical Hx
• Medical Diagnoses o IBS
o Seasonal allergies
o Migraine (when younger w/ oral contraceptive) • Medications o Allegra & Flonase for allergies
o Valium as needed for dizziness
o Furosemide Vestibular Hx
• Consultations o Neurology
o Otology (x2)
o Otolaryngology
• Previous testing o VNG
o ECoG
o Rotary chair
o Brain and IAC MRI
o Serial audiograms Test Findings
• VNG: o Left caloric weakness (74%)
o No spontaneous/provokable nystagmus
o Oculomotors WNL • ECoG: o No raw data
o Report said abnormal left Test Findings
• Rotary chair: WNL • MRI: negative • Serial audiograms: o BC never conducted at 250 Hz
o AC asymmetry at 250 Hz and 500 Hz
o BC at 500 Hz relatively symmetrical (within 5-10 dBHL)
o No immittance Audiogram 6/06 Audiogram 9/07 Audiogram 9/09 Previous Vestibular Dx
• Meniere’s disease left o Poorer left hearing
o Left abnormal ECoG
o Left caloric weakness
o Description of fluctuating hearing and aural fullness (right???) • BPPV o Transient vertiginous events
o Positive Hallpike (side not reported) Previous Vestibular Tx
• Vestibular Rehabilitation Therapy o 6-month course
o “Great help” • Canalith repositioning o “No real improvement” • Furosemide and valium o Unsure of diuretic’s benefit
o Valium helps Current Evaluation
• My thoughts prior to evaluation: o Etiology of hearing asymmetry has not been well established
o Pt. describes right-ear fluctuating hearing and aural fullness, while test results indicate left ear involvement (M.E. ???)
o Pt. has not experienced tinnitus
o Unsure if vestibulopathy was uncompensated during previous evaluation Current Evaluation
• My thoughts prior to evaluation: o We need to investigate each clinically evaluated reflex pathway
o We must establish current level of central compensation
o Etiology of HL critical for making diagnosis
o Although patient reports “vertigo,” she was very unclear on actual sense of rotation, might be closer to disorientation Current Evaluation • My thoughts prior to testing: o I have evaluated several pts from this vestibular self-help group
o Pre-occupation with dizziness
o Sxs often much broader than diagnosis
o Certain amount of somatization
o Pt. has “been through the mill” a number of times and is desperate for an answer
o Pt.’s symptoms sound like uncompensated vestibulopathy – worse than expected… Current Evaluation
• Pertinent history-related details o No concomitant or subsequent headache
o No photophobia/phonophobia
o No oscillopsia
o No Tullio’s phenom. or Hennebert’s sign
o No current positional provocation
o Patient did describe bilateral sound sensitivity Current Evaluation • Sensory Organization Performance Test:
• CD-VAT: o No significant degradation in visual acuity with volitional head movements in vertical and horizontal planes
• Vertebral Artery Screening: Negative Current Evaluation
• VEMP: o Abnormally large response at 100 dBnHL for the left (500 µV) o Abnormally low threshold left (75 dBnHL) o Right WNL
• Binocular Video-oculography o Gaze: no clinically significant nystagmus o HFHS: no provokable nystagmus o Hallpike: negative o Positionals: no clinically sign. nystagmus o Gaze w/ vocalization: no nystagmus Current Evaluation
Left VEMP Current Evaluation Clinical Thoughts • With true conductive HL on left, should not have VEMP and/or reflexes
• Left VEMP and BC findings may be consistent with inner ear third window
• Pt’s equilibrium poorer than expected given time since vertigo and course of VRT
• Did not see deficit in VOR Recommendations • High-contrast temporal bone CT-Scan to r/o abnormal inner ear third window
• Consultation with otologist for possible dehiscence
• Do not recommend current course of VRT/BRT (yet…) Left CT-Scan Right CT-Scan Diagnosis and Management
• Bilateral SCDS, larger on left
• Patient elected for surgery on left o Post auricular approach
o No complications
o Otologist concerned about surgery w/ Meniere’s disease…
• Recently spoke w/ patient: “I have not felt better in 30 years.” Discussion
• Does this patient have Meniere’s disease? o Hearing asymmetry not SNHL
o No tinnitus
o Fluctuating hearing and aural fullness on contralateral side
o What about positive left ECoG??? ABA Tier 1 Question
5)What hearing loss pattern is characteristic of superior canal dehiscence syndrome? A. Mixed B. Low frequency sensorineural C. Low frequency conductive Meniere’s Disease Meniere’s Disease
• This is something you all know about • However, this condition is often considered a “waist-basket” diagnosis • It is often over diagnosed and misdiagnosed • Let’s review incidence, symptoms, diagnosis, etc. Meniere’s Disease Diagnosis
• Diagnosis is based on symptoms (NOT A TEST) • AAO released position statement due to over Dx • MUST have triad of symptoms for definitive Dx o Episodic vertigo lasting 30 min to 1 day
o Tinnitus in effected ear
o Fluctuating hearing in effected ear • May also have aural fullness in effected ear Meniere’s Disease Diagnosis
• Although clinical testing may aid in Dx, its clinical definition requires a diagnosis to be made on Sxs and not testing • Hearing loss is sensorineural (bone scores should be considered) and typically low frequency • If you have any asymmetry at 250 Hz and you have not completed masked bone, you will misdiagnose your patients!!! Migraine Migraine
• Pathophysiology: o Neuronal process (spreading wave of depression), causes:
o Dilation of cerebrovascular beds
o Activation of pain fibers located on these blood vessels
o Transmission of painful impulses to the brain • Incidence: o 6% of Western men
o 18% of Western women
o Most often Caucasian females Migraine • Migraine: o Episodes of head pain, worse with movement
o Associated with nausea, photophobia, and/or phonophobia
o Unilateral head pain in ~60%
o Throbbing pain in many (not all)
o 1/3 experience aura
o Visual or sensory
o Expanding with time
o 15 minutes to 1 hour Migraine
• Migrainous vertigo is a recent addition to IHS classification • Suggested diagnostic criteria: o Recurrent vestibular vertigo
o Migraine according to IHS
o Migrainous symptoms during at least 2 vertiginous episodes (photophobia, phonophobia, aura)
o Vertigo not attributed to another disorder Migraine
• Dizziness with migraine: o Common- dizziness with some or all headaches
o Less common- known migraine headaches, but dizziness occurs in isolation
o Least common- no history of headache, but have migraine- associated dizziness Migraine
• Other related details: o If genetic predisposition, can be provoked with exogenous factors (stress, foods, etc.) or endogenous factors (change in level of estrogen)
o Can also experience benign recurrent positional vertigo (migrainous positional vertigo) Migraine • Vestibulopathy in 44% of migraineurs • Meniere’s disease is 2x more common • BPPV is 3x more prevalent • Can look like Meniere’s disease o Fluctuating HL (permanent)- less common
o Episodic vertigo
o Episodic tinnitus
o Often unilateral • Although the above is published in the audiology literature, there is a BIG problem Migraine
• Migraine: 11,350 / 100,000 people • Meniere’s: 210 / 100,000 people
• In other words, migraine is 54 times more common than Meniere’s disease
• Further reading: o Cutrer FM, Baloh RW. Migraine-associated dizziness. Headache. Jun 1992;32(6):300-4. Migraine
• Common migraines are a cortical event o Depolarization of neurons on cortex
o Change in blood flow on cortex • This is problematic when we think about pathophysiology o The inner ear is fed by what blood supply?
o How do we have a cortical pathology effecting and causing damage to ear? Psychiatric Disorders 20th Century Syndromes
• Phobic Postural Vertigo (PPV) o Dizziness, subjective imbalance
o Sense of body movement
o With anxiety & autonomic arousal
o Provocative stimuli- crowds, street, etc.
o Onset after stress, vestibular insult, etc.
-Brandt (1996); Brandt & Dieterich (1986) 20th Century Syndromes
• Space and Motion Discomfort (SMD) o “Uneasiness” about balance
o Issues with spatial orientation
o Swaying/rocking sensation
o Heightened awareness of movement
o Worse in environments with conflicting stimuli
-Jacob et al., (1993) 20th Century Syndromes
• Visual Vertigo (VV) o Dizziness when in environments of complex visual stimuli
o Sensitivity to erroneous visual stimuli
-Bronstein (1995) 20th Century Syndromes
• Issues with these definitions: o Complex visual stimuli provocative with uncompensated vestibulopathy
o Uneasiness about balance expected with vestibular issues
o Heightened arousal can enhance sense of underlying vestibular problem in the absence of pathological psych. issue
o Rocking/swaying occurs with MDDS 21st Century Syndrome
• Chronic Subjective Dizziness (CSD) o Attempts to further define and incorporate many of the older definitions
o Defined by Jeffrey Staab, M.D.
• Persistent Postural-Perceptual Dizziness (PPPD) o Consensus document – International Classification of Vestibular Disorders Chronic Subjective Dizziness
• Core Features o Persistent, non-vertiginous dizziness/disequilibrium for 3 mos.
o Chronic hypersensitivity to motion
o Exacerbated by complex visual stimuli
o Absence of active physical illness or med
o Normal brain imaging
o Normal (or nonspecific) vestibular testing
-Staab (2006) Chronic Subjective Dizziness
• Associated Features o Neurotic or phobic-anxious temperament
o Precipitated by med or psychiatric event
o Panic attacks • Pathophysiology o Operant conditioning
o Sensitization of vestibular pathways through interaction of threat systems
-Staab (2006) Persistent Postural-Perceptual Dizziness (PPPD)
• Dizziness, unsteadiness= present most days for at least 3 mos. • Sxs persistent, but wax/wane; progress over day • Momentary flares w/ sudden movement • Sxs worse with o Upright posture
o Active or passive motion
o Exposure to complex visual stimuli • Precipitating vestibular or stressful event • Not attributable to other disorder • Cause significant distress or functional impairment Psych as Primary Cause
• Pre-existing anxiety = predisposed for chronic dizziness after vestibular incident • Dizziness/lightheadedness common with panic attacks • Conversion disorders = abnormal gait, postural sway, etc.
-Jacobson, et al. (2008) Vestibular as Primary Cause
• Vestibular disorders = higher rate of depression and anxiety (BPPV, Meniere’s disease, etc.) • Ultimate improvement poorer if comorbid anxiety/depression o Severity of anxiety is best predictor of functional impact
o Prognosis might be dependent on psych factors
Eagger at al., (1992); Best et al., (2006); Staab, (2006) Considerations
• Is psych path primary cause? • Is underlying ear issue cause? • Is psych path response to ear issue? • Are Sxs from both factors? • Which/what to treat? Treatment
• Psychological o Cognitive-behavioral therapy
o Desensitization • Psychiatric o SSRIs • Vestibular rehabilitation therapy o Has shown good efficacy in literature
o Habituation??? Patient N.S. Patient NS
• 28 year old male • Referred by his PCP • Chief complaint: o 20 yr. internal sensation of spinning
o At heights
o In dark rooms
o Riding elevator
o Large open spaces
o In confined spaces Patient NS
• Pertinent history: o Never has experienced vertigo
o Symptoms more pronounced with heightened anxiety
o Right aural fullness
o Bilateral sound sensitivity Patient NS
• Medical history: o Began Paxil 8 years ago
o Feels Paxil not managing anxiety
o Not under care of psychiatrist
o Well-controlled hypertension and hypothyroidism
o Had vestibular and neuro testing as a child, which were unremarkable
o Denies migraine (age of onset…) Patient NS
• Clinical findings: o Hearing and middle ear status WNL
o Balance WNL
o Normal VIIIth nerve function
o No vestibular deficits
o CNS findings WNL Patient NS
• Overall impression: o Not vestibular
o Environmental and situational aspects of symptoms suggest psych cause
o Referred for VRT w/ emphasis on habituation
o Suggest psychiatric consult
o Referred to Dr. Briggs for consult Case History Pearls Subjective Experience
• Vertigo o Illusion of spinning
o Internal vs. room
o Hallmark of vestibular dysfunction
o However, not specific central vs. peripheral
o Product of nystagmus Subjective Experience • Syncope and pre-syncope o Losing consciousness or feeling faint
o Typically cardiovascular
o Orthostasis
o Decreased cardiac output
o Dehydration
o Also vasovagal
o Parasympathetic activity in limbic system
o Decreased b.p. and pulse
o Fight or flight response
o Not vestibular!!! Subjective Experience
• Lightheadedness o Fairly non-specific
o Usually means disorientation
o Can be reported w/ uncompensated vestibulopathy
o If no vertigo at any point, probably not vestibular Duration of Attack (Vertigo)
• Brief o Instantaneous (less than 1 second)
o Indicative of unequal vestibular input
o Seconds to minutes
o BPPV
o SCDS
o Perilymphatic fistula
o Arnold-Chiari malformation
o MS
o Cerebellar lesion Duration of Attack (Vertigo)
• Intermediate o 20 minutes to 24 hours
o Meniere’s disease
o Migraine
o TIA
o Acute intoxication
o Panic attacks
o MS Duration of Attack (Vertigo)
• Long o Days
o Vestibular neuritis
o Labyrinthitis
o MS
o Infarct- brainstem, cerebellum
o Labyrinthine concussion
o Labyrinthine ischemia Symptom Specifics
• Frequency of episodes (vertigo) o Single vs. recurrent
o Typically inversely proportional to duration
o Single = longer duration
o Recurrent = shorter duration
o If recurrent, how often??? Frequency of Episodes (Vertigo)
• Single o Vestibular neuritis (unless recurrent)
o Labyrinthitis
o Stroke/TIA
o Labyrinthine concussion/ischemia Frequency of Episodes (Vertigo)
• Recurrent o BPPV
o Meniere’s disease
o Migraine
o Panic Attack
o SCDS
o MS Provoking Factors
• Can your symptoms be provoked? o Positioning
o Complex visual stimuli
o Motion
o Open spaces, crowds, situational
o Loud sound, increased intracranial pressure
o Environmental
o Foods, smells, sleep deprivation, hormonal Provoking Factors
• Positioning o BPPV = lying supine, rolling, head pitch, rising from supine, bending at waist
o Orthostatic hypotension = rising from supine or seated; NOT lying supine
o Head pitch = neck hyperextension?
o Vertebrobasilar insufficiency
o Cervicogenic Provoking Factors
• Complex visual stimuli – Optic flow o Driving down road w/ trees
o Walking down grocery isle
o Video games
o Can be seen w/ vestibular lesions
o Psychogenic?
o Migraine? Provoking Factors
• Motion o Self vs. environment
o Self = vestibular system activated
o Environment = optic flow, motion intolerance
• Open spaces, crowds, situational o Psychogenic
o Agoraphobia Provoking Factors
• Environmental o Ambulating in dark environments or uneven surfaces
o Dark environments = visual preference
o Uneven surfaces = surface preference
o Falls = inside vs. outside
o Weather change = migraine Provoking Factors
• Migraine o Smells = perfume, cleaning solutions, smoke (do not wear perfume in clinic)
o Sleep deprivation
o Foods = tannins, chocolate, aspartame, MSG, hard cured meet & cheese
o Hormonal (females) = menses cycle • Meniere’s disease o Alcohol, caffeine, salt (is this supported in the literature?) Concomitant Symptoms
• Concomitant symptoms o Nausea and emesis common w/ vertigo
o Otologic symptoms = ear
o Neurological symptoms = central
o Psychogenic symptoms = positive review of systems Otologic Symptoms
• Aural fullness o Meniere’s disease
o Vestibular schwannoma • Otalgia or Otorrhea o Middle ear disease
o Temporal bone disease • Tinnitus o Meniere’s disease
o Labyrinthitis
o Vestibular schwannoma Otologic Symptoms
• Hearing loss o Meniere’s disease
o Vestibular schwannoma
o Labyrinthitis
o Perilymphatic fistula
o Vestibular ischemia Otologic Symptoms
• Aural distortion o Vestibular schwannoma
o SCDS • Autophony, misophonia, hyperacusis o SCDS
o Perilymphatic fistula
o Psychogenic Neurological Symptoms
• Facial symptoms o Weakness = tumor, MS
o Asymmetry = vestibular schwannoma, stroke, Bell’s palsy, MS, migraine
o Numbness/tingling = MS, stroke, migraine • Ataxia o Poor control over lower extremities
o Never vestibular • Headache Psychological Symptoms
• Positive review of systems o Every symptom
o Precipitating stressful event
o Phobic or anxious temperament
o Avoidance
o Overly emotional during Hx Introduction to VRT/BRT Test Protocol • Permanent lesion: o Calorics
o VEMPs • Uncompensated lesion: o VSR: SOT and posturography
o VOR: gaze, positionals, HFHS, VAT, CD-VAT • Clinical correlate: o You can have permanent vestibular lesion, which is already compensated
o Calorics and VEMP will not improve w/ VRT Background
• Vestibular rehabilitation therapy (VRT) is the most effective treatment for UVD and BVD • Identification of the specific underlying pathology is crucial for long-term outcomes • Only indicated for stabilized conditions Background
• Symptoms from uncompensated vestibulopathy can cause primary Sxs • Can also cause secondary symptoms: o Adoption of sedentary lifestyle
o Decrease in general physical condition
o Maladaptive/avoidant strategies Background
• VRT based on 3 strategies: o Adaptation
o Substitution
o Habituation • The specific therapy-type (strategy) can be diagnosis and condition specific Background
• Vestibular adaptation: o Facilitate neuronal change in central vestibular system
o Encourages and speeds up natural compensation process
o Inducing retinal slip encourages compensation Background
• Vestibular adaptation: o Requires both visual inputs and movement of body and head
o Best stimuli incorporates movement of the head and a visual input
o Exercises will typically progress from fairly static to more dynamic Background
• Vestibular substitution: o For severe, bilateral loss of function
o Cannot entirely compensate for full loss of bilateral function
o Helps utilize other sensory systems and environmental cues to help patient ambulate safely • Vestibular habituation: o Patient exposed to provocative stimulation repeatedly until desensitized Goals of VRT/BRT
• Improve patient’s functional balance and decrease disequilibrium • Decrease oscillopsia (VOR dysfunction) • Increase patient’s overall general physical condition and activity level • Reduce social isolation Recovery Expectations
• Recovery may be delayed if patient restricts head movements or if visual input minimized • Long-term use of vestibular suppressant medication o Delay compensation
o Increase disequilibrium Recovery Expectations
• Compensation influenced by presence of other peripheral/central disorders • Rate and final level of recovery can be affected by age-related changes in the vestibular, visual, and somatosensory systems • Remember, anxiety is the biggest predictor of ultimate VRT outcome Treatment Considerations
• Customized, supervised exercises are more effective than self- directed • Treatment should begin early, as delayed therapy prolongs Sxs • Exercise can be for brief periods of time multiple times/day • Head movement and reintroduction of daily activities should be encouraged Treatment Considerations
• VRT can increase a patient’s symptoms, so counseling is crucial • Improved function should be expected within 6 wks with UVD • BVD can take greater than 6 months for recovery • Recovery can be slowed by other factors- illness, stressor, etc. Treatment Considerations
• After compensation has occurred, patients can undergo decompensation o Recurrence of symptoms w/ no change in function
o Occurs w/ stressor, illness, etc.
o Test findings indicate uncompensated lesion
o Treated through updated VRT Treatment Considerations
• A number of factors can result in poorer outcomes: o Migraine
o Neurological dysfunction
o Diabetes
o Reduced vision
o Peripheral neuropathy
o Anxiety
o Involvement of contralateral ear (BVD) Treatment Considerations
• Overall outcome not influenced by: o Older age
o Gender
o Length of symptoms Treatment Considerations
• VRT gold standard treatment for stabilized peripheral conditions • However, there is significantly less research supporting efficacy with central disorders • Sparse research has shown better outcomes in those w/ central vestibular lesions and long-term outcomes Treatment Considerations
• A patient should be challenged throughout the program • If the patient finds the activities easy or not provocative, they may not work • Reaching a plateau is a real concern • Progress and level-of-challenge should be monitored throughout the program Treatment Considerations
• Typical therapy program progresses from more static to more dynamic activities • VRT is not intended to be continued indefinitely • However, conditioning (BRT) should be completed long term Treatment Considerations • BRT can be completed even if a vestibular deficit is not suspected • Concentration unique: o Fall prevention
o Lower extremity strengthening
o ADLs
o Fall prevention
o Assistive device evaluation/use
o Strengthening/conditioning
o Etc. Treatment Considerations
• Clinician vs. self directed o Clinician directed typically more effective
o Compliance is an issue, so ongoing clinician contact helps
o A clinician can modify program as it progresses
o Some patients do not have time to meet weekly with a therapist
o Both types are within an audiologist’s scope of practice… Treatment Considerations
• I am of the opinion that VRT is indicated for uncompensated lesion • If a vestibular lesion is compensated, should a patient receive VRT??? o Is the patient dizzy from the ear problem
o Are you over-referring or “chicken souping”
o If compensated, what are you treating
o If a patient is still dizzy, are you clinician/test centered or patient centered Treatment Considerations • The underlying cause to a patient’s symptoms should be identified prior to beginning VRT • A solid diagnosis should drive therapy • Calling a lesion “vestibular” without identifying what the lesion is caused by is dangerous and unethical • I have seen patients with large tumors whose treatment was delayed because a proper diagnosis was not achieved prior to completing a course of VRT Treatment Considerations • VRT will not fix structural conditions o SCDS
o Perilymphatic fistula
o Vestibular Schwannoma
o Brainstem/brain mass
o Enlarged VAS
o Etc. Questions/Comments