8 Vestibular and Balance Rehabilitation Vestibular and balance rehabilitation has become an integral part of the management of patients with vestibular disorders. The concept of vestibular and balance rehabilitation hinges on the fundamental properties of vestibulo-ocular reflex (VOR) and vestibulospinal reflex (VSR) central plasticity and compensation for acute and chronic vestibular deficits. These compensatory mechanisms have been observed clinically and verified in animal experiments that showed predicted behavioral changes in the vestibular and posture systems after vestibular diseases and experimentally created vestibular deficits. Some of these compensatory mechanisms, especially in humans, are “intuitive” but counterproductive. Clinical experience has shown the tendency of dizzy patients to consciously avoid natural head movements and to alter their movement and balance strategy, which results in delay in vestibular compensation and subsequent prolongation of vestibular and balance symptoms. Vestibular rehabilitation is probably the only modality that can reverse these conscious changes in balance strategy and initiate and maintain the compensatory mechanisms. Currently there are no standards of practice, and most centers have developed their own protocols, mostly based on the Cawthorne1 and Cooksey2 traditional exercises. Our approach is aimed at establishing a comprehensive, cost-effective, home-based vestibular rehabilitation program that is easy to implement and administer. A team approach that incorporates physical and occupational therapy (when needed), psychology, and psychiatry is invaluable in the care of the vestibular patient. This chapter reflects the authors’ experience with vestibular and balance rehabilitation since 1985. Some of the concepts are new and may contradict traditional approaches, but they open the doors for further research into vestibular rehabilitation. We emphasize that these concepts are based on existing medical and physiologic knowledge of the vestibular system, and they incorporate aspects of general medicine that should augment the process of vestibular rehabilitation. This chapter addresses the scientific foundation of vestibular rehabilitation, and the indications for and methods of vestibular and balance rehabilitation. When appropriate, medical interventions that are necessary to promote compensatory processes are discussed. Knowledge of the anatomy and physiology of the vestibular system and the mechanisms of balance compensation is essential to understanding and implementing a successful vestibular rehabilitation program. The knowledge base of neural plasticity, neurochemistry, and pharmacology of the vestibular system are also critical. The anatomy and physiology of the vestibular system are addressed in Chapter 1. The physiology of balance, neurochemistry, and pharmacology are summarized here. Readers are encouraged to review additional key historical reports on the anatomy and physiology of the vestibular system.3–11 Maintaining balance requires the continuous interaction of the vestibular, visual, and proprioceptive systems at a subconscious level. The most important function of this interaction is to maintain visual acuity (gaze stabilization) and controlled posture during active head and body movements. The vestibular system is most important. It is the least redundant (i.e., most stable) and has the shortest response time of the three systems. Without it, we cannot see clearly during motion. The vestibular responses are much faster than the oculomotor and posture responses. Therefore, vestibular signals have to be “stored” for the other system to use at a later time, a process commonly referred to as the velocity storage of the VOR. For clinical and rehabilitation purposes, it is helpful to visualize the vestibular system as a “centering” system of the eyes and the body to maintain balance (static balance). The centering is achieved by each labyrinth “pushing” the eyes (VOR) and the body (VSR) to the center. This new concept of viewing the vestibular function helps in teaching and in explaining the clinical signs and symptoms of vestibular diseases to patients and professionals. If, for example, one labyrinth fails to provide its centering function, the eyes and the body deviate, slowly, to the diseased side that can no longer oppose the signals of the healthy side. This slow deviation results in nystagmus (an abnormal VOR) and body shift (an abnormal VSR) toward the affected hypoactive labyrinth. It is also helpful to think of the vestibular system, during active motion, as a “push-pull” system that controls dynamic balance. During angular acceleration, the canal, or canals, in the direction of motion become excitatory (a “push”) and the canal in the opposite direction of motion becomes inhibitory (a “pull”). This push-pull action ensures that the eyes and body are “dynamically stable” with a minimum expenditure of energy, and prevents falling in the case of excessive motion. The same line of thinking can be applied to the otolith organ; however, the stimulus is linear motion in multiple directions. The VOR dynamic range extends from 0.01 to 10 Hz, and peak head acceleration during natural head movements can reach 3000 deg/sec2. The VOR frequency response gain and phase are relatively linear in the 0.01-to 0.32-Hz range and close to unity in the 1- to 5-Hz range. The VOR function beyond the 5-Hz range is difficult to test. This VOR frequency response has specific implications as far as evaluation and rehabilitation of the vestibular system. Permanent vestibular pathology is usually evident as a low-frequency phase shift with normal gain and phase in the high frequency, typically after labyrinthectomy. Bilateral vestibular loss can be in the low or the high frequency range. Loss of high frequency VOR is usually associated with subjective inability to focus (oscillopsia) during active head movements. The VSR dynamics are limited by the timing of the long loop reflexes needed to adjust postural stability in response to peripheral vestibular perturbations. Vestibular rehabilitation is based on the well-established concept of vestibular plasticity and compensation.12–18 Vestibular compensation is defined as the short-term recovery (static compensation) from symptoms and the long-term recovery (dynamic compensation) of “normal” balance function following unilateral or bilateral vestibular deficits. Vestibular plasticity is the neuronal process underlying vestibular compensation. The vestibular system provides an excellent model to study neural and behavioral plasticity in humans and animals because peripheral vestibular lesions can be made and reproduced independent of the central vestibular system. Furthermore, the time course of recovery can be quantitatively measured functionally (vestibular tests are discussed in Chapter 5) and electrophysiologically with single-unit recordings19 after unilateral labyrinthectomy. The ipsilateral lesion makes the vestibular nuclei neurons become silent due to loss of afferent signal from the labyrinth and simultaneous inhibitory influence from the contralateral vestibular nuclei via the commissural fibers.20 However, shortly after the acute event, the ipsilateral neurons increase their intrinsic excitability.21 This process is mediated by changes in their own membrane properties,22 interactive regulation between glutamenergic and GABAergic receptors, and by the activation of nuclear glucocorticoid receptors23,24 presumably in the cerebellum.25 Several studies showed that the vestibulocerebellum (flocculus, nodulus, and uvula) plays a critical role in vestibular compensation. Ablation of the vestibulocerebellum, or disruption of climbing fibers inputs to the flocculus, severely impedes compensation.26 Studies also showed that intrafloccular microinjection of dexamethasone enables a compensatory increase in intrinsic excitability of medial vestibular nucleus ipsilateral to the lesion side. Intrafloccular microinjection of the glucocorticoid receptor antagonist prevents the increase in intrinsic excitability in animals given systemic dexamethasone.27 These findings support behavioral and cellular studies of the role of stress hormones, corticosteroids, and glucocorticoid receptors in the process of vestibular compensation.24,25 During the acute phase of vestibular compensation, there is a rapid downregulation of the inhibitory neurotransmitters γ-aminobutyric acid (GABA)21 and glycine receptors in ipsilateral neurons to counteract acute inhibition from the contralateral side.26 During the first week after the acute lesion, the recovery of a normal resting discharge in ipsilateral vestibular nuclei plays a key role in the resolution of the static deficit by restoring the balance between the activities of neurons in both vestibular nuclei.27 Some studies showed that vestibular compensation is also dependent on age, glutamic acid, and benzodiazepine receptor distribution. The time course and behavioral recovery of vestibular compensation in adult (3 months) and old (24 months) rats were correlated with modifications of glutamic acid decarboxylase (GAD) messenger RNA (mRNA) expression and benzodiazepine receptor density in different brain areas.28 Compensation in adult rats was complete 28 days after hemilabyrinthectomy, whereas old rats still showed significant behavioral impairment.29 Other studies showed that vestibular suppressants, sensory deprivation, restricted mobility, and blindfolded animals did not achieve adequate vestibular compensation.30–32 It was also found that lack of cognitive insight into dizziness outcome retarded compensation.33 From a clinical point of view, several relevant concepts of vestibular compensation are established. First, vestibular compensation takes place in both the short term and the long term. Short-term compensation requires adequate residual vestibular function and is evident by the disappearance of vestibular symptoms of nausea, ataxia, and nystagmus that classically follow unilateral labyrinthectomy. Long-term compensation is indicated by behavioral modification of head and body movements in response to vestibular dysfunction. Second, the vestibular nuclei, commissural fibers, vestibulocerebellum (flocculus and nodulus), vision, and higher cognitive function must be intact for successful long-term vestibular compensation. Third, evidence exists that stress hormones and glucocorticoids augment vestibular compensation. Fourth, older age, restricted mobility, and vestibular suppressants delay and possibly prevent adequate vestibular compensation. Fifth, vestibular rehabilitation and modulating physical and emotional factors influencing central nervous system (CNS) plasticity help augment the process of vestibular compensation.
Scientific Foundation of Vestibular and Balance Rehabilitation
Vestibular and Balance Physiology
Vestibular Plasticity and Compensation
Indications and Contraindications for Vestibular Rehabilitation
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
