7 Vestibular Rehabilitation Flashcards
Sensory components of balance
Vision- to cortex, BG, ventrolateral thalamus, back to cortex
Vestibular- to brainstem/cerebellum, BG, ventrolateral thalamus, cortex
Somatosensory- to SC through DCML, to brainstem/cerebellum, etc.
Sensory processing occurs…
At vestibular nuclear complex and cerebellum
Two otolith organs
Respond to gravity and linear acceleration, send afferent information to vestibular ganglion
Utricle- horizontal
Saccule- vertical
Structure of semi-circular canals
Ampulla houses sensory hair cells, hair cells project into gelatinous mass (cupula), movement in plane of canal causes endolymph to push against cupula
Superior vestibular nerve innervates…
Anterior SCC, horizontal SCC, utricle
Inferior vestibular nerve innervates…
Posterior SCC, saccule
Vestibular nuclear complex projections
Spinal cord, cerebellum, nuclei of CN III, IV, VI for control of eye, head, and body movements
Vestibular nuclear complex components
Superior and medial nuclei- control gaze
Lateral (Deiter’s) nucleus- postural reflexed
Inferior nucleus- integration of vestibular and motor signals
Roles of vestibulocerebellum
Adaptation
Compensation for motor deficits
Motor learning
Regulation of balance and eye movements
Vestibular nuclear complex pathways
To thalamus and cortex- sensation and perception of head movement
Vestibulospinal pathways- motor commands to muscles of neck, upper torso, lower limbs to maintain balance and posture
Vestibulo-ocular pathways- to CN III, IV, VI for VOR
VOR
Maintains steady image on retina for high frequency head movements
VOR gain should be 1
Cervico-ocular reflex
Like VOR but slower speeds
Cervical proprioception drives eye movement
Used in presence of vestibular dysfunction
Other sources of dizziness (not central or peripheral vestibular)
Diabetes, hypoglycemia, infection, meds, emotional/psychological, hypotension, arrhythmias, multi-factorial fallers
Etiology and epidemiology of BPPV
Idiopathic in 50-70%, recurrence rate 27-41%, incidence increases with each decade of life
Clinical presentation of BPPV
Brief vertigo with position changes/head movements
<60 seconds for canalithiasis, >60 for cupulo
Latency of seconds
Nystagmus
Symptoms fatigue with repetition
Nystagmus quick beat towards involved side with Dix-Hallpike
Horizontal canal BPPV
Geotropic- canal affecting most symptomatic side
Ageotropic- if more than one minute, cupulo affecting least symptomatic; if less than one minute, canal affecting least symptomatic
Treating BPPV
Epley maneuver- posterior or anterior canalithiasis
Liberatory (Semont)- anterior or posterior cupulo
BBQ roll- horizontal canalithiasis
Modified Liberatory (Semont)- horizontal cupulo
Vestibular neuritis/labrynthitis presentation
Secondary to viral infection, neuritis = CN VIII, labrynth- endolymph fluids
Acute- severe vertigo and nausea lasting days, horizontal gaze-evoked nystagmus, abnormal VOR, impaired DVA
Sub-acute- prolonged disequilibrium without true vertigo, inadequate VOR, postural instability, gait, falls, deconditioning, CN VIII dysfunction
Vestibular neuritis/labyrnthitis treatment
Vesibular depressants in acute phase only
Vestibular rehab improves 80% of patients
Meniere’s disease presntation
Over-accumulation of endolymph in inner ear causes abnormal firing of hair cells
Episodic exacerbations (vertigo) minutes to hours with full recovery, but over time get permanent damage and unilateral hypofunction
Rotary vertigo, low-tone sensorineuronal hearing loss, tinnitus, aural fullness, nausea and vomiting
Chronic- imbalance, dizziness with head turns
Meniere’s disease treatment
Vestibular sedatives, anti-emetics (diazepam), intra-tympanic gentamycin
Endolymphatic sac surgery or ablative surgery for intractable symptoms
Low salt diet, avoidance of caffeine
Vestibular schwannoma/ acoustic neuroma
Variable presentation
Dizziness, disequilibrium, unilateral hearing loss, tinnitus, +CN signs (V, VII, VIII)
Trauma/skull fracture
Temporal bone fractures result in variable symptoms
Perilymphatic fistula
Tear or deficit in small and/or round windows separating middle and inner ears allowing fluid to leak to air-filled middle ear
Changes in pressure (altitude, increased CSF pressure from lifting, bending, cough/sneeze) stimulate balance and/or hearing strucures
Aural fullness, fluctuating hearing, dizziness w/o true vertigo, motion sensitivity
Treatment- repair if symptoms don’t resolve
Superior canal dehiscence
Opening in temporal bone overlying superior SCC from developmental abnormality (1-2%)
Vertigo and oscillopsia from loud noises and/or maneuvers that change middle ear of intracranial pressure (coughing/sneezing, straining)
Autophony, hypersensitivity to bone-conducted sounds, apparent conductive hearing loss
Avoid stimuli if possible, surgery for severe cases
Bilateral hypofunction diagnoses
Otoxic meds Idiopathic vestibular loss Bilateral Meniere's Trauma Autoimmune disease (RA, psoriasis) Meningitis Neurofibromatosis type 2
Ototoxic meds
Gentamicin affects hair cells- irreversible damage
Symptoms of bilateral hypofunction
Oscillopsia during head movement
Instability of gait
Disequilibrium
No vertigo!
Central dysfunction signs
Constant symptoms Nystagmus not suppressed by visual fixation Pure vertical nystagmus Impairments in smooth pursuits/saccades Impaired VOR cancellation
Vertiginous migraine
Vascular origin, about 25% of those with migraine have vertigo
Can occur with or without headache
Symptoms seconds to days
Treatment- trigger avoidance, migraine preventative meds, vestibular rehab
PT- VOR exercises, COR reflex, depth perception, sensory integration for balance, gait, aerobic exercise
Concussion
Anxiety, cognitive problems, depression, fatigue, HA, irritability, photo/phono-sensitive, sleep disturbances
Dizziness, imbalance, visual disturbances
23-81% of people have dizziness in first few days
PT- VOR exercises, static standing balance, gait exercises, cervical spine interventions
Multiple sclerosis
Plaques in brainstem, visual pathways, cerebellum can cause vestibular symptoms
34.7-50.9% of those with MS have brainstem and cerebellum lesions
Peripheral vestibulopathy in up to 85% of those with MS
PT- can improve fatigue, balance, disability by DHI
Cervicogenic dizziness
Non-specific sensation of altered orientation in space and disequilibrium from abnormal afferent activity from neck
Mis-match of proprioceptive and vestibular input
Symptoms- unsteadiness, imbalance, light-headed, disorientation minutes to hours; neck pain, HA, jaw pain, tinnitus
Electronystagmography/ videonystagmography
Caloric test- gold standard
Irrigate external canal with cold or warm water/air and watch nystagmus
Cold = away from irrigated ear
Warm = toward irrigated ear
Sinusoidal harmonic acceleration test
Rotary chair test
VOR measured during rotation of body in dark
Assesses horizontal canal and/or superior vestibular nerve
Identifies central impairment, bilateral vestibular dysfunction, and central compensation
Vestibular evoked myogenic potential (VEMP)
Tones in ears while evoking responses from specific muscles
Cervical VEMP- saccule and inferior nerve
Ocular VEMP- utricle and superior nerve
Oculomotor exam components
Alignment- tropia, phoria, exo-, eso- ROM Convergence Nystagmus (spontaneous, gaze-holding)- unable to suppress with visual fixation in central dysfunction Smooth pursuit, saccadic movement Head impulse test VOR cancellation DVA (>2 line drop can indicate deficit)
Dizziness handicap inventory
0-100 (higher number is greater handicap)
0-30 mild
31-60 moderate
61-100 severe handicap
Sensory organization test
1- fixed support and surround/ EO
2- fixed support and surround/ EC
3- fixed support, responsive surround/ EO
4- responsive support, fixed surround/ EO
5- responsive support, fixed surround/ EC
6- responsive support and surround/ EO
Clinical test of sensory interaction and balance
1- firm EO 2- firm EC 3- firm visual conflict 4- foam EO 5- foam EC 6- foam visual conflict
Modified CTSIB
1- firm EO
2- firm EC
3- foam EO
4- foam EC
Motion sensitivity quotient
16 changes of head or body position 0 (no dizziness) to 5 (severe) Duration- 1 (5-10 sec), 2 (11-30 sec), 3 (>30 sec) 0-10%- mild 11-30%- moderate 31-100%- severe motion sensitivity
Adaptation
Induce CNS plasticity by creating error signal (retinal slip) to change VOR gain
VORx1, VORx2
For unilateral hypofunction, bilateral if residual function, central if appropriate
Can add visual stimulation, duration/rate up to 2 Hz for 2 minutes
Substitution
Use alternative strategies- saccadic movements dissociated from head movement
Pts may need AD for somatosensory input
For bilateral hypofunction, central
Habituation
Desensitization to provocative stimuli via repetitive exposure
Visual vertigo- exposure to optokinetic stimulation can help in cases where over-reliance on visual input creates symptoms in visual/vestibular conflict
For unilateral hypofunction and central vestibular dysfunction
Rehab effects for bilateral hypofunction
Adaptation, gait, and balance activities
Significantly improves DVA similar to unilateral hypofunction
Age not a factor in recovery
Recovery in approximately 5 weeks of exercise
