|
|
Vestibular rehabilitation therapy
Byung In Han, M.D.
Do Neurology Clinic, Daegu
1, Introduction
Identifying dizziness due to vestibular pathology is not always easy, because standard vestibular tests are restricted to the examination of the horizontal canal, and does not test vertical canal, otolith and vestibulospinal reflex functions. Dizziness is also a common complaints of people with normal vestibular function, which may result from deficits of the motor system or the musculoskeletal system.
Treatments of patients with vestibular problems are also difficult, because there are gaps between the knowledge of vestibular pathophysiology and treatment options. Medical management may not be appropriate in all patients and prolonged use of vestibular suppressant delay recovery. In the past several years, there have been tremendous changes in the treatment of BPPV and vestibular hypofunction with specific exercises. Although, vestibular rehabilitation therapy now accepted as an appropriate and valuable treatment, it is relatively unfamiliar to physicians. This paper provides the concepts of exercise treatment and systemic approach to rehabilitation of vestibular disorders.
2, History of rehabilitation therapy
Cawthorne, a physiotherapist, developed a generalized physical therapy in conjunction with Dr. Cooksey in 1945. Cawthorne-Cooksey exercises include movements of the head, tasks requiring coordination of eyes with the head, total body movements, and balance tasks[1, 2]. The advantage is that they are very low cost and often effective. In those days therapists treated all dizzy patients with the same protocol (e.g.. the Cawthorne-Cooksey). Cawthorne-Cooksey exercise(1944) was developed to treat patients with vestibular deficits and were not customized for the individual patients. Details are described below.
Cawthorne-Cooksey exercise
A. In bed .....(omitted)
B. Sitting .....(omitted)
C. Standing (in class)
1-1. Eye movements
a. up and down
b. from side to side
c. focusing on finger moving from 3 ft to 1 ft away from face
1-2. Head movements at first slow, then quick; later with eyes closed
a, bending forward and backward
b, turning from side to side
1-3. Bending forward and picking up objects from the ground
2. Changing from sitting to standing position with eyes open and shut.
3, Throwing a small ball from hand to hand (above eye level).
4, Throwing ball from hand to hand under knee.
5. Changing from sitting to standing and turning round in between.
D. Moving about (in class) ....(omitted)
Igarashi et al (1975) found squirrel monkey given exercise had less nystagmus[3]. Horak et al(1992) started individualized individualized physical therapy to customize individual diagnoses or at least functional patterns[4]. Therapists performed an evaluation to adjust their treatment program. The disadvantage of individualized physical therapy is the higher cost compared to the Cawthorne-Cooksey exercise. Horak found that the group receiving medications such as meclizine and diazepam did not show improvement. Shepard and Telian(1995) showed a significant reduction in dizziness by using customized vestibular exercise[5]. Herdman et al (1995) compared the vestibular adaptation exercise with exercises designed to be vestibular neutral (smooth pursuit eye movements performed with the head still)[6]. They found that patients performing the vestibular adaptation exercise had less disequilibrium than did patients in the control group performing exercises designed to be vestibular neutral.
3, Mechanisms of recovery after vestibular lesion
Several mechanisms are involved in the recovery of function following unilateral vestibular loss. These mechanisms include spontaneous recovery, adaptation, substitution, and habituation.
(1) Spontaneous recovery is that the recovery of the resting firing rate of the vestibular nucleus neurons. Spontaneous recovery is probably due to the development of denervation supersensitivity and to axonal sprouting [7].
(2) Adaptation is that the vestibular system makes long-term changes in the neuronal response to input. Recovery of the dynamic disturbance of vestibular function requires both visual inputs and movements of the body and head. Recovery of vestibulo-ocular gain begins when the animals are returned to a lighted environment [8].
(3) Substitution is that vision and somatosensory information substitute partially for missing vestibular information for the purpose of static and dynamic orientation. Substitution is not desirable because this does not adequately substitute for the lost vestibular function[9].
(4) Habituation is a decrease in response magnitude to repetitive sensory stimulation. Habituation occurs through repetitive exposure to movement [9].
4, Predictors of outcome
Patients with less initial disability and those seen earlier after onset have a better recovery[10]. Patients with head injury associated with a vestibular deficit show less improvement with treatment [11]. Patients with central vestibular deficit showed the same improvement as those with peripheral vestibular lesions [12]. Shepard NT found that age was not a factor based on the length of recovery period and the final level of recovery[13]. In contrast, Norre and Beckers found that the patients age 60 year and older recovered more slowly than younger subjects[14]. Vestibular suppressant prolong the recovery period but do not prevent recovery[13].
5, Goals of rehabilitation therapy
The goals of vestibular rehabilitation are to (1) improve the functional balance during ambulation; (2) decrease complaints of dizziness; (3) improve the ability to see clearly during head movement; and (4) improve the general activity level [9, 15].
6, Rehabilitation therapy assessment
(1) Subjective history
Knowing what positons, movements. or situations aggravating the patient's symptoms is the first step in treatment planning. In BPPV, attacks of vertigo frequently occur in the morning and are most pronounced during the first change in position after sleep. This occurs because during sleep, the free-floating otolithic particles settle in the most dependent portion of the canal and form a heavy conglomerate. Subsequently, when the patient gets up, changing head position causes these particles to move[16].
Vertigo of vestibular neuritis is not much provoked by head positioning. Vertigo is precipitated while standing, rather than lying down, so that the patient feels better while lying in bed. It is helpful to inquire about the direction of rotation of the body when the eyes are closed, as it is typically away from the side of the lesion. Usually, patients with VN lie on one side, with the affected ear uppermost to reduce the vertigo[17].
Several methods have been made to define the subjective symptoms of dizziness in an objective manner. The Dizziness Handicap Inventory (DHI) and the Disability Scale are useful clinical tools[18, 19].
(2) Clinical examination
Clinical examination of a patient with vertigo and disequilibrium includes oculomotor and vestibulo-ocular examination, motion sensitivity tests. static balance (e.g., Romberg test, performed with eyes open and closed, and on the foam), dynamic balance (e.g., Fukuda's stepping test), and gait assessment(e.g., tandem walk, walk while turning head)[20].
(1) oculomotor and vestibulo-ocular examination
The first step is observing for the presence of spontaneous or induced nystagmus. Video Frenzel goggles are a powerful tool for examining eye movements including spontaneous and gaze-evoked nystagmus, head-shaking nystagmus, tragal-pressure nystagmus, hyperventilation nystagmus, and positional nystagmys. Then head thrust test is performed to see corrective saccade with rapid head movements.
Electronystagmography(ENG) provides an objective assessment of the oculomotor and vestibular systems. A newer method called Video Nystagmography(VNG) is the use of infrared video systems which allow for a more detailed observation and analysis of these eye movements.
ENG or VNG can be used to record nystagmus during oculomotor tests such as saccades, pursuit and gaze testing, optokinetics and also calorics. Abnormal oculomotor test results may indicate either systemic or central pathology as opposed to peripheral (vestibular) pathology. However, many ENG abnormalities are nonlocalizing; therefore, the clinical history and otologic examination are vital in formulating a diagnosis[21].
(2) Motion sensitivity tests
Motion sensitivity tests are to assess the positions and movements that provoke symptoms. Frenzel glasses may be used. Motion sensitivity tests are associated with consecutive maneuvers including sitting to supine, supine with head rotate to both sides, supine to sitting, both Dix-Hallpike maneuvers, sitting with head tipped to both knees, sitting with head turning horizontally 5 times, sitting with head moving vertically 5 times, and standing with turning 180 degree to either sides. BPPV can be revealed with these motion sensitivity tests and easily treated by canalith repositiong therapy. Although rare, vertebral artery compression should be distinguished by having the patient sitting and leaning forward slightly. In this position, the head is extended and turned 45 degree to one side, in which the head ends up in an upright position), the posterior canal on that side would not be affected by the pull of gravity.
Other movements such as rolling, supine to sit, reaching in sitting toward the floor, and sit to stand can be tested[20]
Fig. 1. Motion sensitivity tests. These tests are associated with consecutive maneuvers including sitting to supine, supine with head rotate to both sides, supine to sitting, both Dix-Hallpike maneuvers, sitting with head tipped to both knees, sitting with head turning horizontally 5 times, sitting with head moving vertically 5 times, and standing with turning 180 degree to either sides.
(3) Static balance tests
Static balance requires the organization of vision, somatosensory and vestibular inputs. Static balance tests include single leg stance(SLS), Romberg, and the sharpened or tandem Romberg performed with eyes open and closed. The patients with balance disorders other than from vestibular dysfunction may have difficulty with these tests. Standing sway is measured using a sway grid or force flatforms(posturography). The way of stand should be standardized to the most stable way like that subjects stand in double limb stance in the 25 degree, toe-out position[20].
The Clinical Test for Sensory Interaction in Balance (CTSIB) designed by Shumway-Cook and Horak (1986) is an extension of the Romberg test. The protocol of CTSIB is that body sway is measured while the subject stands quietly for 20 seconds under six different conditions which alter the availability and accuracy of visual and somatosensory inputs for postural orientation. Somatosensory information is altered by having the patients stand on foam. Vision is eliminated with eye closure or blindfolds. Vision is altered by having patients view the inside of dome (a modified Japanese lantern with vertical stripes inside) attached to their heads[22].
Fig. 2. The Clinical Test for Sensory Interaction in Balance (CTSIB). CTSIB is a static balance test evaluating the ability to maintain balance under altered sensory conditions.
Fig. 3. Vestibular hypofunction. Histograms for fore-aft and lateral postural sway during upright stance with eyes open and eyes closed obtained with force-measuring platform. Preferred direction of postural instability and body sway in unilateral vestibular hypofunction is in the lateral direction.
Fig. 4. Posterior type BPPV. Preferred direction of postural instability and body sway is in a diagonal fore-aft direction in posterior type BPPV.
(4) Dynamic balance tests
Fukuda's stepping test assesses balance while the subject marches in place first with eye open and then with eye closed. The forward progression of the subject less than 50 cm as well as the degree of turning less than 30 degree at the end of 50 steps are regarded as normal [23].
Fig. 5. Fukuda's stepping test. This test is a dynamic balance test, in which the forward progression of the subject less than 50 cm as well as the degree of turning less than 30 degree at the end of 50 steps are regarded as normal.
(5) Gait assessment
First, the patient is asked to walk while turning the head either to the left and right or up and down. The next tasks include tandem walking, sidestepping, backward walking, and walking in a figure of eight. Another task requires the patients to walk quickly and then to stop immediately on the therapist's command. To enhance task difficulty, the patient may be asked to perform the same task with eyes closed.
The Singleton test requires the patient to walk quickly and pivot to the right or left immediately on the therapist's command. The patient should perform the Singleton test at a faster speed.
The patient's ability to monitor postural control while manipulating an object can be tested in a variety of ways. The patient can be asked to walk, pick up one or more objects, and continue walking. Many patients with vestibular loss will bend at the knees and avoid flexing the head or bending at the hips[20].
Fig. 6. Gait assessment. Examples of gait assessment are tandem walking(left), or walking while turning the head either to the left and right or up and down(right).
7, General consideration in rehabilitation therapy
* The vestibular system functions at higher frequencies than do the visual or somatosensory systems, which would accounts for why neither visual nor somatosensory cues can substitute completely for loss of vestibular cues[24].
* Therapists should determine whether the patient will be able to recover previously used strategies or will need to develop compensatory strategies. Recovering of normal balance strategies is needed in the patients of temporary deficits, while compensatory strategies, for example relying on alternative somatosensory cues, is needed in the case of permanent vestibular deficit[15].
* Treatment should begin early. Recovery is delayed if visuomotor experence is prevented during early stage after unilateral vestibular loss[25]
*Even brief periods of stimulation can produce VOR gain changes that is useful for acute recovery[26].
* Chronic use of vestibular suppresants actually prolongs the recovery period[27].
* Compensatory strategies developed by patients are not always optimal, an important goal in treatment is to improve the efficiency of compensatory strategies used to perform functional tasks. Therefore, solving the stability problems related to tasks should be achieved rather than repetitively practicing normal patterns of movements[15].
* Fluctuating vestibular deficit (e.g. Meniere's disease), incomplete damage, positional phenomenon (BPPV), and slowly progressive tumors are difficult for the central nervous system to compensate[15].
* Good visual inputs (bright room lights, curtains open) should be encouraged.
* Head movements must be encouraged both to induce vestibular adaptation and to habituate the symptoms provoked by movement.
9, Rehabilitation therapy for BPPV
Exercise treatments described here are mostly for the patients with vestibular hypofunction. Similar concepts can be applied to BPPV. Exercise treatments for BPPV include canalith repositioning therapy (e.g. Epley maneuver for posterior cancal BPPV), liberatory therapy (Brandt-Daroff exercise for cupulolithiasis type BPPV), and habituation exercise (Brandt-Daroff exercise). Variations of exercise have beep developed. Brandt-Daroff exercises are usually performed with the eyes closed to minimize the visual-vestibular conflict contributing to the nausea. The positional changes used in the Brandt-Daroff habituation exercise may be modified to enable the patient to perform them. Medications are not indicated in the treatment of BPPV other than to relieve the nausea that can accompany the episodic vertigo[28]
BPPV patients often have decreased postural stability and rely on excessively on visual or somatosensory cues to maintain balance. For most patients, improved postural stability occurs with remission of vertigo following canalith repositioning therapy. The positional instability of patients with BPPV may not be related to debris in the canal itself. Either previous head injury or horizontal canal hypofunction could result in postural instability[29, 30]. Exercise to improve postural stability in the patients with BPPV should be considered[28].
Fig. 7. Brandt-Daroff exercise. The patient sits and then moves rapidly to the side, and remains in the position for 30 seconds, and then sits up for 30 seconds before assuming the opposite head-down position for 30 seconds. This exercise plays the role of liberatory and habituation exercise.
10, Treatment of unlocalized dizziness
At all ages, about one-third of patients with dizziness will go undiagnosed. These patients usually need to be followed more closely than patients in whom a clear diagnosis is available. Empirical trials of medication, psychiatric consultation, and vestibular physical therapy may be helpful options[31]. Recognition of patients for whom the symptoms are not the direct result of a vestibular lesion does not prevent use of a vestibular rehabilitation as an adjunct treatment. Habituation exercise is particular appear to be a promising approach[32]. When a diagnosis is not available, the problems can be identified by patient history or by the presence of other deficits that localize the problem. It is reasonable to use balance and habituation exercise in an attempt to decrease symptoms and improve functions[32].
11, Individualized rehabilitation therapy for vestibular hypofunction
(1) Exercise to improve gaze stability
In the acute stage after unilateral vestibular loss. decreased VOR gain results in visual blurring. Adaptation exercise can be used to improve VOR gain and therefore improve gaze stabilization. Horak started individualized exercise to customize individual diagnoses or at least functional patterns in 1992 [33]. Exercises to improve gaze stability for acute stage or chronic uncompensated patients are as followings[9];
1. A fixed target is designated. The patient moves his head horizontally for one minute
2. This is repeated moving the head vertically.
3. A large pattern such as a bookshelf or a curtain is designated. The patient moves his head horizontally for one minute.
4. This is repeated moving the head vertically.
Each exercise should be repeated at least three times a day.
Fig. 8. Exercise to improve gaze stability. The patient moves the head horizontally and then vertically while looking at a target.
Fig 9. Exercise to improve gaze stability. This exercise can be performed while looking a calendar on the wall
Fig. 10. Exercise to improve gaze stability. This exercise can also be performed while walking.
(2) Otolith rehabilitation exercise
Bouncing up a beach ball may be advocated to build up the otolith-ocular reflex as well as otolith-postural reflexes[33].
Fig. 11. Otolith rehabilitation exercise. Bouncing up a beach ball builds up the otolith-ocular reflex and otolith-postural reflex.
(3) Exercise to improve postural stabillity
The goal when retraining postural stability is to help the patient learn to effectively coordinate sensory information to meet the demands of postural control[15]. A well cordinated adult uses the ankle strategy in response to a small anterior/posterior perturbation, and the hip abduction/adduction strategy to lateral perturbation. A larger perturbation causes greater amounts of hip strategy. The hip strategy occurs in situations where the ankle is unable to exert the appropriate torque necessary to restore balance, such as when an individual stands on a small, narrow support surface. A large enough to move the center of mass outside the base of support, a stepping strategy is used[15]
To improve postural stability, three movement strategies must be improved. Exercise should be included well-reounded program and synthesize the use of visual and somatosensory cues. For example, balance exercise should "stress" the system by having the patient work with and without visual cues or while alert!ing somatosensory cues by having the patient stand on foam. Standing on foam with eyes closed fosters the use of vestibular cues[9].
Fig. 12. Three movement trategies for balance. An ankle(1), hip(2), and stepping(3) strategy for anterior/posterior direction. An ankle(4), hip(5), and stepping(6) strage for the lateral direction.
<a> Developing an ankle strategy
Patients are asked to practice swaying back and forth, and side to side, within small ranges, keeping the body straight and not bending at the hips or knees.
Unsteady patients should practice close to a wall behind or a table in front of them. Pertubation by a therapist can be applied at the hips or shoulders to develop strategies for recovery of balance[15].
Fig. 13. Developing an ankle strategy. This exercise includes swaying back and forth, and side to side, within small ranges, keeping the body straight and not bending at the hips or knees.
<b> Developing a hip strategy
Patients are ask to maintain balance without taking a step, and using displacement in larger ranges than those used for an ankle strategy. Possible examples include standing on a narrow beam, standing heel/toe or single limb stance[15].
Fig. 14. Developing a hip strategy. Hip strategy can be improved by exercise swaying back and forth bending at the hips.
<c> Developing a step strategy
Stepping can be facilitated by the therapist by passively shifting the patient's weight to one side and quickly bringing the center of mass towards the unweighted leg and manually assisting the patient to lift the foot for a step. To ensure a patient's safety, stepping should be performed near a wall[15]
Fig. 15, Developing a step strategy. Therapist shifts the patient's weight to one side and manually assists the patient to lift the foot for a step.
(4) Improving vestibular information
<a> Visual dependence exercises
Patients who show increased reliance on vision for orientation are asked to perform a variety of balance tasks when visual cues are absent or reduced. Alternatively visual cues can be made inaccurate for orientation through the use of glasses smeared with petroleum jelly, prism glasses, vision reversing plastic mirrors, or viewing a complex moving visual scene.
Decreasing a patient's sensitivity to visual motion cues can be done by asking the patient to maintain balance during exposure to optokinetic stimuli, such as moving curtains with stripes, or moving large cardboad posters with vertical lines. Author usually ask patients to rotate the head without gaze fixation in front of a bookshelf. When oscillopsia is a problem, voluntary head oscillation at progressively increasing frequency while maintaining visual fixation on texture objects or reading material, can also promote habituation[15].
Fig. 16, Decreasing sensitivity to visual motion cues. Rotating the head without gaze fixation in front of a bookshelf induces optokinetic stimuli.
<b> Somatosensory dependence exercises
Patients who show increased reliance on somatosensory input for balance are ask to perform tasks when somatosensory input is distorted using tilt-boards, slabs of foam, or just by walking on the bed[33].
Fig. 17. Somatosensory dependence exercises. An example is walking on a tilt-board or slant.
<c> Combined visual and somatosensory dependence exercise
In order to enhance the patient's ability to use remaining vestibular information for postural stability, exercise are given that ask the patient to balance while both visual and somatosensory inputs for balance are simultaneously reduced, such as standing on complaint foam or an inclined surface with eye closed or with complex visual motion cues[15].
Fig. 18. Exercise that improves use of vestibular information. The patient stands on one leg with eyes closed.
Fig. 19. Exercise that improves use of vestibular information. Standing on a cushion with eye closed.
Fig. 20. Exercise that improves use of vestibular information. Marching in place on a cushion with eyes open or closed.
(5) Habituation of vertigo
Motion- and visually-provoked symptoms are treated with habituation exercise. Many patients with visual sensitivity are also instructed to walk in visually challenging environments[32]. The repeated exposure to a provocative stimulus will result in a reduction in the pathological response to that treatment. The motion sensitivity test, developed by Shepard and Telian, uses a series of movements and positions as the basis for establishing an individualized exercise program for patient with chronic unilateral vestibular hypofunction[34]. Exercise to habituate vertigo includes repetition of the Dix-Hallpike position, walking while turning the head to the left and right, and large, circular motion of the head and trunk while maintaining visual fixation on an hand-held ball[15].
Fig. 21. Habituation exercise with repetition of the Dix-Hallpike position. This is an example to reduce positional vertigo.
Fig. 22. Habituation exercise with bending over and head turning. This exercise habituates the provoking position for a patient who experiences vertigo only when bending over and turning the head.
11, Rehabilitation therapy for complete vestibular loss
Substitution should be involved in recovery of complete vestibular loss[9]. Although patient with bilateral vestibular loss initially are more dependent on visual cues than on somatosensory cues[35], the exercise must be directed at the substitution of both visual and somatosensory cues to improve gaze and postural stability[24].
<a> Exercise to improve gaze stability for complete vestibular loss
Central preprogramming is probably the primary mechanism by which gaze stability is improved in patients with BVL. However, it is not effective in situation in which head movements are unpredictable, such as while walking[36].
Modification in saccadic and pursuit eye movement is also a mechanism to improve gaze stability[37]. Patients with complete BVL make hypometric saccade toward a visual target. They make saccadic eye movements during combined eye and head movements toward a target, and then make corrective saccades back to the target as the head movement pulls the eyes off the target. Pursuit eye movement work at frequencies of up to 1 Hz and at velocities of up to 30 degree per second[37].
To foster the use of saccadic or pursuit eye movement and central preprogramming, the following exercises should be encouraged. Look directly at one target. Look at the other target with the eyes and then turn the head to the target. Saccades should precede head movement. Repeat in the opposite direction. To foster central programming the following exercises should be performed. Look at a target directly in front of you. Close your eyes and turn your head slightly, imagining that you are still looking directly at the target. Open your eyes and check to see of you have been able to keep your eyes on the target[24].
Fig. 23. Exercise to improve gaze stability for complete vestibular loss. (1) Look directly at one target. (2) Look at the other target with the eyes. (3) Then turn the head to the target.
Fig. 24. Exercise to improve central programming for gaze. (1) Look directly at one target. (2) Close your eyes, (3) and turn your head slightly, imagining that you are still looking directly at the target. (4) Open your eyes and check to see of you have been able to keep your eyes on the target.
<b> Exercise to improve postural stability for complete vestibular loss
Exercise to improve postural stability helps that patients develop confidence and establish functional limits. The following exercises are performed.
Stand with the feet close together with both hands helping you maintain your balance by touching a wall. Take your hand or hands off the wall for longer and longer periods of time while maintaining your balance. The next exercises improve ability of substitution with visual cues. Stand with your feet shoulder width apart with eyes open, looking straight ahead at a target on the wall. Progressively narrow your base of support from feet apart to, feet together to, a semi-heel-to-toe position to, heel almost directly in front of the toes. Do the exercise first with arms outstretched, and then with arms close to your body, and then with arms folded across your chest. Varieties of exercise can be developed upon the patients[24].
Fig. 25, Exercise to improve postural stability for complete vestibular loss. Stand with the feet close together with both hands touching on the wall. Then, take hands off the wall.
Fig. 26. Exercises to improve ability of substitution with visual cues. Stand with the feet shoulder width apart with eyes open, looking straight ahead at a target on the wall. Progressively the base of support is narrowed from feet apart, feet together, and a semi-heel-to-toe position, to heel almost directly in front of the toes.
12, Conclusion
Vestibular rehabilitation therapy is effective if the best type of exercise is properly selected. Restricting movement, preventing visual inputs, and the use of vestibular suppressant medications delay the onset of recovery and limit the final level of recovery. Therefore, vestibular rehabilitation therapy should be recommended as early as possibel to all patients with vestibular hypofunction.
References
1, Cawthorne T. The physiological basis for head exercise. J of the chatered society of physiotherapy1944;30:106
2, Cooksey FS. Rehabilitation in vestibular injuries. Proc R Soc Med 1946;39:273-275.
3, Igarashi M, Alford BR, Kato Y, Levy JK. Effect of physical exercise upon nystagmus and locomotor dysequilibrium after labyrinthectomy in experimental primates. Acta Otolaryngol. 1975 Mar-Apr;79(3-4):214-20.
4, Horak FB, Jones-Rycewicz C, Black FO, Shumway-Cook A. Effects of vestibular rehabilitation on dizziness and imbalance. Otolaryngol Head Neck Surg. 1992 Feb;106(2):175-80.
5, Shepard NT, Telian SA. Programmatic vestibular rehabilitation. Otolaryngol Head Neck Surg. 1995 Jan;112(1):173-82.
6, Herdman SJ, et al. Vestibular adaptation exercises and recovery: acute stage after acoustic neuroma resection. Otolaryngol Head Neck Surg. 1995 Jul;113(1):77-87.
7, Precht W. Recovery of some vestibuloocular and vestibulospinal functions following unilateral labyrinthectomy.Prog Brain Res. 1986;64:381-9.
8, Fetter M, Zee DS, Proctor LR.Effect of lack of vision and of occipital lobectomy upon recovery from unilateral labyrinthectomy in rhesus monkey.J Neurophysiol. 1988 Feb;59(2):394-407.
9, Herdman SJ, Whitney SL. Treatment of vestibular hypofunction. In: Herdman SJ. Vestibular rehabilitation. 2nd ed. F.A. Davis Company.
10, Shepard NT, Telian SA. Programmatic vestibular rehabilitation. Otolaryngol Head Neck Surg. 1995 Jan;112(1):173-82.
11, Telian SA, Shepard NT, Smith-Wheelock M, Kemink JL. Habituation therapy for chronic vestibular dysfunction: preliminary results. Otolaryngol Head Neck Surg. 1990 Jul;103(1):89-95.
12, Keim RJ, Cook M, Martini D. Balance rehabilitation therapy. Laryngoscope. 1992 Nov;102(11):1302-7.
13, Shepard NT, Telian SA, Smith-Wheelock M, Raj A.Vestibular and balance rehabilitation therapy.Ann Otol Rhinol Laryngol. 1993 Mar;102(3 Pt 1):198-205.
14, Norre ME, Beckers A. Benign paroxysmal positional vertigo in the elderly. Treatment by habituation exercises. J Am Geriatr Soc. 1988 May;36(5):425-9.
15, Shumway-Cook A, Horak FB, Bronstein AM. Rehabilitation of balance disoders in the patient with vestibular pathology. In:Bronstein AM, Brandt T, Woollacott M, ed. Clinical Disorders of Balance Posture and Gait.
16, Han BI. Vertigo in the elderly.The Korean geriatric medical association 2007;3: processing.
17, Leigh RJ, Zee DS. Clinical features of acute peripheral vestibulopathy. In:Leigh RJ, Zee DS. The neurology of eye movements. 4th ed.
18, Jacobson GP, Newman CW. The development of the Dizziness Handicap Inventory. Arch Otolaryngol Head Neck Surg. 1990 Apr;116(4):424-7.
19, Shepard NT, Telian SA, Smith-Wheelock M. Habituation and balance retraining therapy. A retrospective review. Neurol Clin. 1990 May;8(2):459-75.
20. Whitney SL, Herdman SJ. Physical therapy assessment of vestibular hypofunction. In: Herdman SJ. Vestibular rehabilitation. 2nd ed. F.A. Davis Company.
21, Electronystagmography. Available URL from:http://en.wikipedia.org/wiki/Electronystagmography.
22, Shumway-Cook A, Horak FB. Assessing the influence of sensory interaction of balance. Suggestion from the field. Phys Ther. 1986 Oct;66(10):1548-50.
23, Fukuda T. The stepping test: Two phase of the labyrinthine reflex. Acta Otolaryngol 1959;50:95-108
24, Herdman SJ, Clendaniel RA. Assessment and treatment of complete vestibular loss. In: Herdman SJ. Vestibular rehabilitation. 2nd ed. F.A. Davis Company.
25, Fetter M, Zee DS.Recovery from unilateral labyrinthectomy in rhesus monkey.J Neurophysiol. 1988 Feb;59(2):370-93.
26, Pfaltz CR.Vestibular compensation. Physiological and clinical aspects.Acta Otolaryngol. 1983 May-Jun;95(5-6):402-6.
27, Shepard NT, Telian SA, Smith-Wheelock M, Raj A.Vestibular and balance rehabilitation therapy.Ann Otol Rhinol Laryngol. 1993 Mar;102(3 Pt 1):198-205.
28, Herdman SJ. Tusa RJ. Assessment and treatment of patients with BPPV. In: Herdman SJ. Vestibular rehabilitation. 2nd ed. F.A. Davis Company.
29, Black FO, Nashner LM.Postural disturbance in patients with benign paroxysmal positional nystagmus.Ann Otol Rhinol Laryngol. 1984 Nov-Dec;93(6 Pt 1):595-9.
30, Blatt PJ, Georgakakis GA, Herdman SJ, Clendaniel RA, Tusa RJ.The effect of the canalith repositioning maneuver on resolving postural instability in patients with benign paroxysmal positional vertigo.Am J Otol. 2000 May;21(3):356-63.
31,Hain TC, Ramaswamy T. Dizziness in the Elderly. Availabler from URL:http://www.galter.northwestern.edu/geriatrics/chapters/dizziness.cfm
32, Shepard N, Asher A. Treatment of patients with nonvestibular dizzienss and diswquilibrium. In: Herdman SJ. Vestibular rehabilitation. 2nd ed. F.A. Davis Company.
33, Hain TC. Balance and Vestibular Rehabilitation Therapy. Available from URL:http://www.tchain.com/otoneurology/treatment/rehab.html
34, Shepard NT, Telian SA, Smith-Wheelock M. Habituation and balance retraining therapy. A retrospective review. Neurol Clin. 1990 May;8(2):459-75.
35, Bles W, Vianney de Jong JM, de Wit G.Compensation for labyrinthine defects examined by use of a tilting room.Acta Otolaryngol. 1983 May-Jun;95(5-6):576-9.
36, Barnes GR. Visual-vestibular interaction in the control of head and eye movement: the role of visual feedback and predictive mechanisms. Prog Neurobiol. 1993 Oct;41(4):435-72.
37, Kasai T, Zee DS.Eye-head coordination in labyrinthine-defective human beings.Brain Res. 1978 Apr 7;144(1):123-41.
