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Vestibular Rehabilitation
Vestibular Rehabilitation
Vestibular Rehabilitation - Amy (Dizzy Day Clinics)
Introduction
Amy is a physiotherapist at Dizzy Day Clinics in Melbourne, with a background in neurophysiotherapy.
Thanks to Laura Power and Doctor Kate Murray for their contribution.
Lecture is divided into four sections:
Review of the vestibular system and symptoms of dysfunction.
Assessment of the vestibular system.
Common vestibular disorders (BPPV, vestibular neuronitis/neuritis, Meniere's disease, acoustic neuroma, vestibular migraine).
Vestibular rehabilitation.
Prevalence & Importance
Dizziness is common, affecting ~20% of working-age adults visiting GPs.
80% of dizzy individuals seek medical help due to ADL disruption or work absence.
Vestibular dysfunction increases fall risk by eightfold.
Understanding vestibular anatomy is key to rehab.
Anatomy of the Vestibular System
Peripheral Vestibular Apparatus
Inner ear system: semicircular canals, saccule, and utricle.
Central Processor
Brain areas receiving input from the inner ear.
Motor Output
How the vestibular system impacts movement.
Five parts to each inner ear system.
Semicircular Canals
Oriented at roughly 45-degree angles (anterior, posterior, and horizontal).
Filled with endolymph: fluid movement stimulates the cupula.
Cupula: dome-shaped structure with hair cells at the canal's base.
Fluid movement deflects the cupula, stimulating hair cells.
This signals head motion to sensory nerve fibers.
Canal Pairs
Right anterior & left posterior: detect diagonal movement on one plane.
Left anterior & right posterior: detect diagonal movement on another plane.
Horizontal canals: detect side-to-side movement.
Otolith Organs (Utricle & Saccule)
Contain otoconia: calcium carbonate crystals on a gel.
Detect linear acceleration and gravity.
Head moves forward -> crystals fall backward -> stimulate hair cells.
Going up in a lift -> gravity pushes crystals down -> compress hair cells.
BPPV Relevance
Benign Paroxysmal Positional Vertigo.
Crystals displace from utricle into semicircular canals.
Causes spinning sensation due to inappropriate crystal location.
Vestibulo-Ocular Reflex (VOR)
VOR enables eyes to remain fixed on a target during head movement.
Semicircular canals detect head movement.
Vestibular nerve transmits info to vestibular nuclei in the brainstem.
Information relayed to medial and lateral rectus muscles to stabilize gaze.
Reflexive eye movement stabilizes the target; gaze stability.
VOR Gain
Ratio of eye movement to head movement velocity.
Ideally, eye velocity = opposite head velocity (VOR Gain = 1).
Head moves 100°/s right; eyes move 100°/s left.
If eye movement is slower than head movement, VOR Gain < 1, causing blurring or 'catching up' sensation.
Central Processor (Brain)
Vestibular nuclear complex (superior, medial, lateral, descending nuclei) in pons and medulla.
Clinical relevance in assessing dizziness to rule out stroke in the pontine or medullary area of the brain.
Relays information for the VOR and vestibulospinal reflex.
The brain helps coordinate eye stability during head turns and maintains upright posture.
Cerebellum
Receives inner ear input; adapts VOR gain and coordinates vestibulospinal reflex.
Clinical cerebellar testing via limb coordination assesses potential cerebellar pathology in vestibular clients.
Motor Output
Ocular muscles & motion nuclei via the medial longitudinal fasciculus mediate reflexive eye movements during head motion (VOR).
Vestibulospinal reflex activates spinal muscles for protective extension during head turns, preventing falls.
Vestibular colic reflex stabilizes the head via neck muscle activation during head turns.
Symptoms of Vestibular Dysfunction
Complex system: motion sensor, eye stabilizer, balance maintenance.
Primary Symptoms
Dizziness: impaired motion sensing.
Vertigo: spinning sensation (e.g., Meniere's, BPPV).
Imbalance and unsteadiness: peripheral or central issues.
Gaze instability: blurred vision during head movement.
Nausea and vomiting.
Secondary Symptoms
Fatigue: system's role in posture, eye stability, and head position.
Concentration issues: "foggy head".
Anxiety: concern about serious conditions.
Depression and frustration: prolonged recovery.
Loss of confidence: in walking and balance is affected.
Functional Restrictions
Impact on activities of daily living (ADLs): difficulties with putting on shoes).
Driving limitations: head checks are difficult.
Return to sports is challenging (especially post-concussion).
Gardening difficulties: head down.
Balance-dependent activities: roller skating is affected.
Increased fall risk: reduces independence.
Social isolation: fear of dizziness in crowds.
Movement avoidance: stiff necks from guarding.
Neck and shoulder issues: guarding posture.
Reduced fitness and endurance: overall decline.
Clinical Examination of the Dizzy Patient
Subjective Examination
Detailed history: differentiate spinning vs. dizziness vs. imbalance.
Objective Examination
Visual testing.
Dix-Hallpike test: crystal assessment.
Balance and gait assessment.
Possible vestibular function tests or MRI brain.
Subjective Examination Details
Type of sensations (true vertigo vs. vague dizziness).
Imbalance or disequilibrium.
Falls.
Lightheadedness.
Note:
Vestibular dysfunction should not cause fainting.
Onset (acute vs. gradual) suggests different etiologies.
Sudden onset suggests crystal problem.
Gradual onset suggests acoustic neuroma.
Duration of attacks is important.
Short spins (seconds, e.g., BPPV).
Minutes to hours (e.g., Meniere's, vestibular migraine).
Hours to days (vestibular neuronitis, stroke red flag).
Associated symptoms:
Hearing loss (unilateral: acoustic neuroma, labyrinthitis; bilateral: age/work-related).
Tinnitus: ringing in ears (high or low pitched).
Aural fullness: Meniere's disease.
Headaches, photophobia, phonophobia: vestibular migraine.
Exacerbating factors:
Movements (rolling in bed exacerbates crystals in wrong spot).
Upright posture and head turns: vestibular neuronitis.
Dietary factors (chocolate, coffee, red wine): vestibular migraine.
Oculomotor Examination
Eyes provide info about the inner ear and brain.
Nystagmus
Involuntary eye movement from peripheral or central nervous system dysfunction.
Defined by the direction of the fast phase.
Upbeat, downbeat, horizontal, or torsional (BPPV).
Spontaneous nystagmus: observe eye movement with patient looking straight ahead.
Gaze-evoked nystagmus: observe eye movement when patient looks left and right.
Downbeating nystagmus in all planes is a central sign.
Smooth Pursuit
Eyes smoothly follow a moving target.
Peripheral pathology: smooth movement is expected.
Saccadic smooth pursuit: jerky eye movements suggesting cerebellar pathology.
Saccadic Eye Movements
Quick and accurate movement between two points.
Normal saccades: quick and accurate.
Slow saccades: slowness and inaccuracy suggest central pathology.
Head Impulse Test
Tests peripheral vestibular function.
Patient fixates on clinician’s nose during quick head rotations.
Normal: eyes remain fixed on target.
Abnormal: eyes fail to stay fixed on the target; corrective saccade is observed.
Positive head impulse test suggests VOR impairment.
Dynamic Visual Acuity Test
Active VOR testing.
Patient reads a chart (Snellen) or looks at a target while head rotates.
Note any blurring or dizziness.
Compare visual acuity during head movement to acuity at rest.
More than three lines difference implies vestibular deficit.
Dix-Hallpike Examination
Assesses for crystals in the wrong part of the inner ear system; BPPV.
Contraindications: vulnerable necks (recent surgery/trauma), rheumatoid arthritis, neck instability, myelopathy etc.
Technique: Turn the head 45 degrees and lie the patient down with 20-30 degrees of head extension.
Positive test: Patient experiences severe vertigo and torsional nystagmus.
Balance Examination
Tests vestibulo spinal reflex.
Romberg test (feet together, one foot in front of the other).
Standing on soft surfaces with eyes closed.
Assesses vestibular contribution by noting postural sway with eyes closed and head turns.
Gait Assessment
Walking with head turns assess vestibulospinal reflex.
Assess comfortable pace, tandem walking, eyes closed.
Common Vestibular Problems
Benign Paroxysmal Positional Vertigo (BPPV)
Crystals (otoconia) from the utricle enter the semicircular canals.
Canalithiasis: Crystals floating in the canals.
Cupulolithiasis: Crystals stuck to the cupula.
Most common cause of dizziness.
Peak onset: 50-70 years old (but also seen in younger people after head trauma).
Posterior canal BPPV: most common type (85%).
Symptoms: brief episodic positional vertigo.
Diagnosis: positive Dix-Hallpike test.
Treatment: Epley maneuver, Semont maneuver, Brandt-Daroff exercises.
Epley Maneuver
Sit patient long sitting, turn head to the side of the problem, and bring into Dix hallpike position
If the test is positive (vertical and upwards rotary nystagmus during vertigo), proceed.
Keeping the tilt, rotate the head 90 degrees towards the other shoulder.
Chin tuck, nose points down. Wait a minute.
Lift the patient to a sitting position, keeping their head turned.
Used to re-position crystals back in the utricle.
Vestibular Neuritis or Labyrinthitis
Inflammation of the vestibular nerve (superior and/or inferior).
Suspected viral cause (shingles, respiratory virus).
Labyrinthitis involves hearing organ: hearing loss occurs as well.
Accounts for ~7% of presentations to dizzy clinics.
Occurs in younger people (30-60 years old).
Males are slightly more affected.
Low recurrence rate.
Symptoms: acute onset severe vertigo lasting hours to days.
Nausea/Vomiting.
Hearing loss (labyrinthitis).
Impaired balance and dizziness.
Clinical examination:
Spontaneous horizontal nystagmus (beating to the side that is working well).
Positive head impulse test on affected side.
Balance impairments.
HINTS Examination
Head Impulse, Nystagmus, Test of Skew.
Performed in acute setting on patients with continuous vertigo/nystagmus.
Differentiates vestibular neuronitis from stroke.
Reassuring HINTS: unidirectional nystagmus, positive head impulse, no vertical skew.
Worrisome HINTS: direction-changing nystagmus, abnormal skew, normal head impulse.
HINTS Helpful only in acute settings
Treatment
Bed rest.
Prednisolone or corticosteroids (within 72 hours ).
Stematil for nausea.
Vestibular rehab (gaze stability, walking).
Meniere's Disease
Endolymphatic hydrops: fluid buildup in the inner ear due to endolymphatic sac dysfunction (volume/pressure regulation) leading to swelling/pressure.
May have genetic component.
Can be bilateral.
Symptoms: Vertigo longer than BPPV 20 minutes to 24 hours.
Nausea/vomiting.
Hearing loss (fluctuates with vertigo).
Low roaring tinnitus.
Aural fullness.
Bouts of vertigo that go for longer.
Oculomotor examination is normal between episodes. head impulse and dix hallpike test are negative.
Treatment
Medical treatment.
Medications: diuretics, circ (ineffective).
Stematil for nausea (short-term only).
Low-salt diet.
Surgical intervention: Gentamicin ablation, steroids.
Physiotherapy: for chronic imbalance between bouts (not for acute vertigo).
Acoustic Neuroma (Vestibular Schwannoma)
Benign tumor of the vestibular nerve.
Peak incidence 40-60 years old.
Slow-growing -> may not cause dizziness, but may see them post-surgically.
Must be medically diagnosed by neurosurgeon or ENT specialist.
Diagnosis: MRI with contrast is gold standard.
Unilateral hearing loss requires assessment by ENT specialist.
Other symptoms: tinnitus, imbalance, headaches, mandibular aching, facial numbness, rare vertigo.
Clinical examination: eye signs are normal, head impulse test usually negative, Dix-Hallpike test negative.
Treatment: observation, microsurgical removal, stereotactic radiosurgery; pre/post-surgical vestibular rehab.
Vestibular Migraine
Migraine causing vertiginous symptoms.
Second most common cause of dizziness.
7-11% of specialized dizzy clinics, 1% of general population.
Women affected more.
Mean age onset 50.3 years old
Symptoms: episodic vertigo (short spins or longer spells as in Meniere's disease/vestibular neuritis).
Headache, photophobia, nausea/vomiting, tinnitus, aural fullness sound sensitivity present.
Eye sign results are usually normal.
Can be tricky to diagnose.
BPPV can be a trigger.
Treatment spends long time talking about prevention. dietary changes can also help with triggers.
Medical referral to neuroautologists.
Migraine preventer medications may be helpful such as Sandomigraine, Propranolol or Topamax act on the brain (6 weeks at least).
Vestibular rehab is important for vestibular system strengthening.
Vestibular Rehabilitation
Detailed assessment: history, oculomotor exam, head impulse/Dix-Hallpike, active VOR, balance/gait, neuro exam.
Treatment is then customized to the patient's needs.
Goals of Vestibular Rehabilitation
Enhance gaze stability (VOR).
Enhance postural & gait stability.
Improve dizziness with ADLs.
Cardiovascular fitness.
Specific Exercises
Gaze Stability Exercises
:
Retrain VOR (improve gain).
Focus on a small target with head movements.
Horizontal, vertical.
Small but frequent, three times a day.
Habituation (Desensitizing) Exercises
:
Repeated graded exposures to provocative movements.
Spinning, head shaking, bending over.
3 times a day.
Balance and Gait Training
:
Exercises with head turning (vestibulospinal reflex).
Standing on foam with eyes closed (reduce visual input).
Standing on one leg doing gaze stability.
Ball throwing.
Emphasis on returning to normal activity e.g. Trampolining, swimming, sports.
General Principles
Patients generally need to get moving again.
Maintain an active lifestyle (walking, running, exercise, bike, Tai Chi, yoga).
Strong evidence for treating BPPV.
Who to Refer
Stable vestibular lesion (vs. fluctuating).
Meniere's patients also help with balance for stable vestibular lesion vs fluctuating.
Movement-provoked symptoms.
Impaired balance and gait.
Limited lifestyle.
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