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University of Kansas
Department of Otolaryngology
Division of Otology
Roles vary with frequency of action
Vision - active at low frequency
Shake hand
Inner ear - active at high frequency
Shake head
Somatosensory - active at very low frequency
Inner ear motion sensors
Rotational
Semicircular canals
Inner ear motion sensors
Linear - forward / back, up / down
Otoliths
116 pt > 70 y/o seen in Otology and Neurology clinic
85% cause of dizziness diagnosed
BPPV
Cerebrovasular disease
Parkinsons
Medication
Postural Hypotension
Cardiac
History and Physical
History is 90% of the diagnosis
Vertigo - illusory sensation of movement
Rotational, translational, tilting of self or surround
Patient vs. surround - not important
Spells
Character and duration
First episode - compensation factors
Imbalance possibly
Associated with nausea and vomiting
Precipitating factors
Associated symptoms
Otologic examination
Pars flaccida
Fistula test
Hearing test - formal audiogram or tuning fork - 512 Hz
Weber - inner ear
Rinne - middle ear
AC > BC is + or normal
Schwabach
Nystagmus with frenzel lenses
Vestibulo-ocular reflex (VOR)
Bedside VOR - dynamic visual acuity, fundoscopy with high freq, small head movements
Positional and positioning maneuvers
Direction fixed - peripheral
Direction changing - peripheral or central
Fukada stepping test - vestibulospinal system
Past pointing
Dix - Hallpike
Cranial nerves - nystagmus
Other
Sensory
Cerebellar
Gait - tandem walking
Romberg
Electronystagmogram (ENG)
Peripheral and central test
Nystagmus
Present at rest
Suppression with gaze
Positional
Caloric response - which ear is producing symptoms
Central test
Cerebellar
Brainstem
Basal ganglia
Rotary Chair
Peripheral test mainly
Better stimulus to inner ear
More realistic frequency
State of compensation
Platform posturography
Tests vision, somatosensory and vestibular systems independently
Test overall balance function quantitatively
Useful in vestibular retraining exercises
Vision or somatosensory dependent
Malingerer
Benign Paroxysmal Positional Vertigo (BPPV)
Vestibular Neurolabyrinthitis (Vestibular Neuronitis)
Labyrinthitis
Endolymphatic hydrops (Ménière’s Disease)
Chronic ear disease - Cholesteatoma
Most common cause of dizziness
True vertigo - less than 30 seconds - with position changes
Top - shelf vertigo
Mean age at onset - 54 (11 - 84 yrs)
Can range from one bout to recurrent bouts over many years
30% have episodes over more than a year
Etiology (Baloh)
Idiopathic 50%
Post - traumatic 15%
Viral neurolabyrinthitis 15%
miscellaneous 15%
Secondary to other IE disease
Pathophysiology
Otoliths from the utricular macular lodge in the canal and on the cupula
Abnormal posterior semicircular canal function
Becomes a linear gravity sensor
Diagnosis
History
Positional
Previous otologic history
Characteristic nystagmus
Torsional (upper pole toward dependent ear) and vertical (up)
Fatigue
Latency
Duration - less than one minute
Beware some posterior fossa lesions can present like BPPV
Sudden hearing loss ± vertigo or vestibular symptoms only
Preceded by systemic viral illness which may be subclinical
Epidemic
Virus can selectively infect the inner ear neurosensory structures
All common viruses implicated
Symptoms
Sudden deafness - typically unilateral
Acute vertigo
Gradual resolution over few days
Generally complete recovery within 3 months
Not always - particularly elderly may have exacerbations
Usually less severe, may be recurrent
Diagnosis
Absence of other neurologic symptoms
Hearing testing
ENG - RVR
R/O retrocochlear disease
ABR - cochlear pathology vs MRI
Treatment
Symptomatic treatment for vertigo
Steroids - 1 mg/kg for 7 days and taper
Vasodilators - no benefit
Inflammatory process of the inner ear - typically vestibular and auditory symptoms
Types
Bacterial
Viral
Bacterial - otic capsule into membranous
Suppurative labyrinthitis
Direct extension from middle ear or CSF
Profound combined auditory and vestibular destruction
Serous or toxic labyrinthitis
Diffusion via the round window
Subtle symptoms with minimal damage
High frequency hearing loss
Fluctuating hearing loss and tinnitus, episodic vertigo, and fullness and pressure.
Incomplete presentation initially is frequent
Symptoms
Attacks
Fullness and pressure
Increasing tinnitus (roaring)
Distortion and fluctuating in hearing
Culminates in vertigo lasting several hours
Feel ill all day
Variations are possible - cochlear symptoms only
Drops attacks - Crisis of Tumarkin
Ménière’s is idiopathic endolymphatic hydrops
Non-Ménière’s hydrops - unusual
Prior ear injury - delayed endolymphatic hydrops
Other sources - syphilis, head trauma, labyrinthitis, tumors.
Pathophysiology of endolymphatic hydrops (ELH)
Fluid overload in the endolymphatic space
Membrane breaks - perilymph and endolymph mix
Cytotoxic leading to cell death
Hearing loss and vestibulopathy
Treatment - medical vs surgical
Medical management - prophylaxis - 90% successful
Control fluid in EL space
Sodium restriction - 1500 mg/day
Caffeine and alcohol restriction
Symptomatic treatment
Vestibular suppressants
Meclizine
Lorazepam
Valium
Compazine
Scopolamine
Surgery
Bilateral disease - ablative vs supportive
Endolymphatic sac enhancement or shunting
Vestibular nerve section or labyrinthectomy
Pathophysiology
Eustachian tube dysfunction - retraction pocket - choleasteatoma
Invasion of the inner ear - typically the lateral SCC
Vertigo and hearing loss, particularly when applying external canal pressure at otoscopy
Diagnosis
History
ETD, chronic ear infections
PE: Tympanic membrane retraction - pars flaccida, + fistula test
Treatment
Surgery vs observation
CT scan
Vertigo - initial symptoms in 48%
Abrupt in onset, last several minutes, assoc. with N&V
Other symptoms nearly always present
Visual hallucinations
Drop attacks or weakness
Visceral sensations
Visual field defects
Diplopia
Associated with risk factors for ASVD - MI or peripheral disease
Between episodes the exam is normal
ENG - 25% have unilateral weakness
Therapy of vestibular problems
Formerly: medical suppression of symptoms or surgery
Now have alternative
In an acute vestibular lesion:
3 - 4 days acute vertigo, nystagmus which rapidly lessens in severity.
Symptoms occur only with rapid movements
At 3 - 4 months - full recovery
Compensation via CNS processes
Suppression (drugs) and visual deprivation (eyes closed) inhibit compensation
Compensation process mechanisms
Adaptation
Habituation
Failure of compensation
Alternative strategies
Adaptation
Stimulus for inducing adaptation is motion across the retina and head movements
Exercises involve a variety of head motions and head movements across a range of frequencies
Fixate on an imaginary target while moving the head.
Alternative strategies
Bilateral vestibular paralysis - substitution of visual and somatosensory information to stabilize the visual world and maintain postural stability
Exercises to improve input of cervical-ocular reflex - Combined eye-head movements and body-on-neck rotation
Vestibular rehabilitation - encouraging natural compensation mechanisms
Education on alternative strategies
Treatment controversies
Application of vestibular rehabilitation
Treatment
Repositioning maneuvers
Semont
Epley
Vestibular Rehabilitation - Habituation exercises
Premedication - Valium
Vertigo
Sleep upright - 48 hrs
Neck considerations
Habituation exercises
PT based
Customized routine
Home based treatment
Follow-up 1-2 weeks (? via phone)
Further refinement if needed
Vestibular dysfunction is a prominent part of balance disorders particularly in the elderly and a significant source of morbidity.
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