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Rehabilitation of Peripheral Vestibular Disorders

Kelly S. Beaudoin, Kathleen D. Coale, and Judith A. White

Impairments Resulting from Peripheral Vestibular Disorders

Physical and occupational therapists who treat vestibular disorders often have extensive knowledge about treating patients with balance/gait dysfunction and deficits in gaze stability. Common impairments accompanying vestibular dysfunction include decreased gaze stability secondary to abnormal vestibulo-ocular reflex, abnormal motion perception caused by mismatch of sensory inputs affecting sensory integration necessary for balance, abnormal postural control (distorted labyrinthine and otolithic inputs causing impaired equilibrium and body alignment), decreased static and dynamic balance/gait secondary to vestibulospinal outputs responding incorrectly to mismatched sensory inputs, decreased sensory integration for balance (the balance system requires robust inputs from visual, vestibular, and sensory systems to make proper balance reactions), and anxiety. Movement increases instability in a vestibulopathic patient and yet is the absolute requirement for recovery. Physical deconditioning may develop when patients become fearful of movement and severely limit all mobility.

Patients with peripheral vestibular dysfunction present to rehabilitation with the following problems¹: decreased vestibulo-ocular reflex (VOR) gain,² abnormal sensory integration for balance,³ abnormal vestibulospinal reflex (VSR)/ balance/gait,⁴ vertigo provoked by position change,⁵ limited community mobility,⁶ and lack of knowledge regarding their diagnosis and prognosis.

Diagnoses seen by vestibular therapists commonly include both unilateral and bilateral disorders such as labyrinthitis/neuronitis, temporal bone fracture with concussion or benign paroxysmal positional vertigo (BPPV), Meniere’s syndrome (acute and chronic), acoustic neuroma (both resected and unresected), herpes zoster oticus/Ramsay Hunt syndrome, labyrinthine infarct, anterior-inferior or posterior-inferior cerebellar stroke, cervicogenic vertigo, BPPV, phobic postural vertigo, aminoglycoside ototoxicity, and hereditary insidious vestibular loss. Central vestibular disorders are not addressed in this chapter.

Evaluation of Peripheral Vestibular Disorders

Clinical evaluation performed by the vestibular therapist consists of tests of gaze stability (Table 32–1), static balance/sensory integration for balance (Table 32–2), gait, postural control, and positional and positioning testing (see Benign Paroxysmal Positional Vertigo, later in chapter).

Findings from the initial vestibular assessment, along with vestibular laboratory testing results when available, assist the therapist with determining if the deficit is central or peripheral, unilateral or bilateral, or acute or chronic. Once impairments are identified, treatment planning and outcome prediction begin.

The static and dynamic balance tests are intertwined with the sensory integration examination, and information is gleaned about strategies used (ankle, hip, stepping) as well as ability to regain the center of mass over the base of support.¹ Determining which strategies the patient has available for balance recovery aids the therapist in treatment planning to facilitate safe community mobility and prevent falls. Computerized dynamic platform posturography (CDP) is used in tertiary care centers to evaluate sensory integration for balance, center of mass, and sway information. These machines can also measure motor latencies for translational platform movements. Clinical gait examinations commonly employ the Dynamic Gait Index,² the Berg Balance Scale,³ the Timed Up and Go test,⁴ and more recently the Functional Gait Assessment.⁵ Many of these tests have been shown to be specific for predicting fall risk and assessing outcomes in this patient population.^6–8

Positional and positioning testing is performed using infrared video-oculography or Frenzel goggles to eliminate visual fixation and allow the examiner to directly visualize torsional nystagmus. The examiner must be knowledgeable in recognizing which nystagmus patterns indicate BPPV (Table 32–3) and which patterns indicate other pathophysiology within or outside the peripheral vestibular system.

Other components of the clinical examination include strength, flexibility, and sensory testing of the lower extremities and careful consideration of cervical contributions. Manual segmental testing of the cervical spine can provide insight into the patient’s problem when peripheral vestibular testing is nonlocalizing.⁹ Careful attention to the patient’s comorbidities must be given for both treatment planning and outcome prediction. Knowledge of normal age-related changes in visual, sensory, and vestibular function should be employed when treating this population.

Self-perception of dizziness and resultant handicap is commonly measured with the Dizziness Handicap Inventory,10 the Activities Specific Balance Control Questionnaire,¹¹ or the Vestibular Activities of Daily Living scale.¹² These questionnaires can be used pre-, mid-, and posttreatment to evaluate results of rehabilitation intervention.

Treatment of Peripheral Vestibular Disorders

Once impairments and functional limitations are identified, research indicates that treatment should begin promptly for optimal outcomes.¹³ Recovery of function after vestibular loss involves three different mechanisms¹: spontaneous recovery,² vestibular adaptation/plasticity,³ and substitution of other strategies.¹⁴

Much of the static imbalance of vestibular dysfunction resolves spontaneously prior to the initiation of vestibular therapy. Vestibular rehabilitation usually takes place in the subacute stage and utilizes both adaptation and substitution to regain gaze and gait stability as well as community mobility recovery. An error signal is needed to stimulate compensation.¹³ Therapists strive to elicit the error signal while treating patients by utilizing active head motion to present the brain with a reduced gain situation causing retinal slip of the foveal visual image. Developing strategies for varied environments found in the community adds context specificity and improves outcome.¹³ Utilizing a variety of inputs—visual, vestibular, and somatosensory—enables the patient to develop new strategies for balance control and gaze stability in varying environments. Unilateral vestibular deficits recover gaze and gait stability quite well. Bilateral vestibular loss patients do not return to premorbid activity levels. Bilateral vestibular loss requires more substitution strategies, such as preprogrammed saccades, to facilitate gaze stability while the patient is in motion. Assistive devices, such as canes and walkers, are not often required longterm for the unilateral peripheral vestibular patients. Bilateral vestibular patients have greater loss of vestibular input for balance, and therefore commonly require an assistive device for safe mobility. Recent research in the area of virtual reality is promising to promote treatment in multimodal sensory situations to facilitate better sensory integration for balance.¹⁵

Based on identified impairments and goals, treatments are provided one or two times per week for 4 to 6 weeks as outlined in Tables 32–4 to 32–8.

Benign Paroxysmal Positional Vertigo

Etiology and Presentation

BPPV is the most common peripheral vestibular disorder resulting in complaints of vertigo.^18–20 A study performed in which the patients were considered to have BPPV only if they presented with nystagmus during a Dix-Hallpike test, established an incidence of 10.7 per 100,000 population per year.¹⁸ A study performed by Oghalai et al²¹ found that 9% of community-dwelling elderly randomly tested were found to have undiagnosed BPPV, suggesting that BPPV may be more common than estimated. In approximately one third of individuals, BPPV will spontaneously resolve. Many individuals may experience chronic or recurrent BPPV lasting for weeks, sometimes years. New research developments, as well as an increased understanding of vestibular physiology and the pathophysiology of BPPV, have directed new treatment protocols and maneuvers for the specific semicircular canals involved.

BPPV is usually idiopathic and occurs spontaneously; however, it may occur following head trauma or in conjunction with vestibular neuritis or labyrinthitis.^22–24

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