Vestibular compensation involves multiple, parallel plastic processes at various sites in the brain. Experimental evidence suggests that adaptive changes in the sensitivity of ipsilesional vestibular neurons to the inhibitory neurotransmitters GABA and glycine, changes in the electrophysiological excitability of vestibular neurons, changes in the inhibitory control of the brainstem vestibular networks by the cerebellum, gliosis and neurogenesis in the ipsilesional vestibular nuclei and activity-dependent reorganization of the synaptic connectivity of the vestibular pathways are mechanisms involved in compensation [5].

Rehabilitation specifically acts activating one or more of the neurophysiological phenomena of vestibular compensation. They are as follows [6, 7]:

Restitution can be defined as a complete reparation after a temporarily limited lesion.

Adaptation means that the human equilibrium system can adapt itself to physiologically, as well as pathologically, altered conditions. The central regulatory system can alter the sensitivity of the vestibular, retinal and other receptors used to regulate equilibrium. It comprises all phenomena which ensure that a patient with a persisting peripheral dysfunctional state attains a normal – or near-normal – behaviour in relation to his/her space orientation and balance in rest as well as when executing movements. He/She again maintains his/her erect standing position and has no more “odd” feeling categorized as vertigo or dizziness. Hereto a number of mechanisms contribute, acting at different levels of the central nervous system. The first definition can be applied to adaptation in the strict physiological sense: a change of response during application of a stimulus, as, e.g. a prolonged acceleration which brings about a response decline. Fatigue is characterized by a response decline which develops slowly. It increases with stimulus intensity and progresses indefinitely with time. Such adaptation is characterized by a response decline which develops rapidly at first and thereafter slowly, finally reaching a constant or fully adapted level. Adaptation phenomena in the same time sense are also attributed to a mechanism at the level of the cupola, which is also direction specific. The second definition fits the broader concept of adaptation. The messages sent by the sense organs into the brainstem are more and more suppressed and prevented from reaching the higher centres the longer the steady state in the surrounding world persists. The subject has adapted itself to conditions imposed by the outer world. Yet the slightest change in stimulatory conditions not pertaining to the steady state will alarm.

Habituation is defined by the reduction of the intensity and duration of the subjective vestibular reactions, for example, vertigo and nausea in the case of seasickness. Habituation is a term used in the sense that repeated exposure to a “mismatched” sensory situation (e.g. during caloric testing, postural vertigo, motion sickness conditions) induces such changes in the central processing as to annihilate the undesirable effects and to do so with a prolonged effect. It has been based upon the development of conditioned compensatory reactions to oppose inappropriate responses associated with visuo-vestibular conflicts and exposure to unusual motion environments. The basic characteristics of vestibular habituation, regarding oculomotor aspects, are:

Habituation is a specific phenomenon. The possibility of obtaining unilateral habituation by unidirectional vestibular stimulations suggests that habituation is due to selective mechanisms that modify not only the gain but also the dynamic characteristics of the VOR. Unilateral habituation to step stimulation has been shown in the cat. VOR habituation is direction specific. It proves that right and left VOR pathways can be controlled separately in order to obtain a greater system adaptability. Habituation is a central mechanism for which vestibular stimulation is not a necessary condition, since exposure to purely non-vestibular input led to vestibular habituation. The production of nystagmus by the habituating stimulus seems unrelated to the efficacy. The habituating stimulus must produce the same subjective sensation of motion as that produced by true body motion in order to habituate vestibular nystagmus. Habituation represents the simplest type of negative learning: stimuli that have lost their significance for the individual are eliminated

Compensation describes another type of central nervous counter-regulation as a result of functional deterioration due to a vestibular or other equilibrium lesion. It utilizes supplementary functions which are added so that an overlay of additionally activated functions covers the underlying equilibrium lesions by means of its neuronal plasticity. However primary lesion continues to exist and can, in the case of a special conflict, manifest itself in the clinical phenomenology. Compensation is a term used in the context of phenomena which are described after unilateral failure of vestibular function. Restricted to the vestibular sphere, it includes those phenomena which cause the imbalance of vestibulo-ocular and vestibulospinal responses seen immediately after an acute unilateral failure of the vestibular system disappear. This compensation at the vestibular level consists in the disappearance of all asymmetries (static and dynamic) in the ocular and vestibulospinal responses. In many cases substitutive interactions by visual and proprioceptive systems are required as well as some more central processes of reorganization of the reflexes in order to reach a sufficient adaptation level. Compensation is a learning process. The phenomenon resembles a sensorimotor relearning process implicating the activity of many integrative CNS structures. Active sensorimotor exploration provides the information to detect the errors and to correct them. Repetition of trials promotes the restructure of the motor programmes. Compensation implies reorganization of the remaining structures. Changes induced by the lesion as such would not necessarily lead to functional appropriate adaptation, but rather to randomly formed synapses which may or may not be mismatched to functional needs. This “rewiring” does not result in functionally meaningless outcome, but rather leads to a new and complex circuitry, the activity of which is appropriate for the restoration of normal function. It is a goal-directed process induced by some recognized “error” in the system and directed to its elimination. Thus compensation may be defined as an error-controlled and goal-directed learning process.

These phenomena lead to different levels of recovery. Recovery is essentially due to the integration of different levels of substitution:

Knowledge of the recovery phenomena following human balance control disturbance (VDU) is fundamental for planning a correct treatment.

Acute vestibular lesion is a good model to explain the main neurophysiological processes involved in the recovery of equilibrium function. Its evolution has been broadly studied in animals and it can be schematically subdivided into different stages:

The duration of each period is species dependent as is the level of recovery achieved.

Generally speaking, the evolution of a lesion can be interpreted into three stages of damage:

Treatment had to be pointed to limit primary damage (usually by means of pharmacotherapy), to reduce secondary damage and to avoid tertiary damage.

According to the MCS model, we can simplify the course of the disease hypothesizing that each phenomenon acts separately and consequently from each other.

The first mechanism following a vestibular injury is adaptation, acting by activation of the internuclear inhibition [8] that is aimed to reduce the activity of the healthy vestibular nuclei. In compensation considered at vestibular level, the commissural fibres play an important role, especially for dynamic compensation. The influence of the remaining labyrinth upon the deafferented nucleus can take place via the commissural fibres, which are the natural means of reciprocal influencing. Another early mechanism is the inhibitory influence of the cerebellum. It has been called the “first line of defence”. It is considered a reset to zero as a preliminary requirement to the subsequent recalibration process. This can be considered a mechanic phase of compensation. This phase is activated by feedback signals.

Vestibular inhibition is supported by the first compensation phenomenon: sensorial substitution. In particular, vision experience is critical for the acquisition and maintenance of recovery for the abnormally reduced VOR gain created by unilateral vestibular lesion. There has been evidence for the effect of darkness upon the evolution of the lateral head tilt, in the cat, after hemilabyrinthectomy [7, 9]. When put back in the dark at a late postoperative stage, already-compensated animals lose their symmetrical head position. Static visual input is a necessary condition for compensation of both ocular and postural deficits. Vision provides a sensory supply in place of the deficient vestibular supply. This supposes an increased sensitivity of the neurons of the vestibular nuclei for fast changes in the environment. Sensorial substitution is rapidly followed by and it is based on the law of “redundancy.” Human balance control is multisensorial based. In this way a vestibular sensorial input deficit may be compensated by reducing inhibition of cervical or other proprioceptive information or increasing visual inputs to the vestibular nuclei. The choice of which sensorial input will substitute the loss input is based on individual preference.

The second phase is recalibration that requires modification of the calibration of the subsystems. It is often accompanied by habituation phenomena. This can be considered the cybernetic phase of compensation [10].

The last phase of compensation is radical reorganization of balance control. The law is the equifinality that is behavioural substitution. Sensorial inputs, activity of vestibular nuclei, motor outputs and in general sensorimotor patterns are reorganized to allow the same function: equilibrium. Structural reorganization leads to a total or partial recovery of function and involves plastic structural changes and/or more global functional rearrangements of the neuronal networks, which are generally considered as the main processes underlying behavioural adaptations. This is the synergetic phase. This is the ultimate goal of the treatment.

Vestibular rehabilitation is a special rehabilitation of motion intolerance and imbalance problems. Vestibular rehabilitation (VR) is an exercise-based treatment programme designed to promote vestibular adaptation and substitution. The goals of VR are (1) to enhance gaze stability, (2) to enhance postural stability, (3) to avoid vertigo and (4) to improve activities of daily living. VR facilitates vestibular recovery mechanisms: vestibular adaptation, substitution by the other eye-movement systems, substitution by vision, somatosensory cues, other postural strategies and habituation. The key exercises for VR are head–eye movements with various body postures and activities and maintaining balance with a reduced support base with various orientations of the head and trunk while performing various upper-extremity tasks, repeating the movements provoking vertigo and exposing patients gradually to various sensory and motor environments. VR is indicated for any stable but poorly compensated vestibular lesion, regardless of the patient’s age, the cause and symptom duration and intensity.

The concept of head, body and coordinated eye exercises as a treatment for vestibular disorders is actually over 70 years. As far back as the mid-1940s, an English otolaryngologist, Sir Terence Cawthorne [11], observed that some patients who experienced dizziness did better or recovered sooner when performing rapid head movements. In cooperation with a physiotherapist, Cooksey [12], they developed a regimen of exercises which, with some modifications, are frequently still used today. The earliest vestibular rehabilitation, thus based on the so-called Cawthorne–Cooksey exercises, was developed to treat patients with labyrinth injury resulting from surgery or head injury. Their value in managing all forms of peripheral vestibular disorders rapidly became apparent, and they now form the mainstay of treatment for this group of patients. Cawthorne–Cooksey [13] protocol is shown in Table 4.1.

Generally speaking, the exercises for vestibular rehabilitation can be categorized [14, 15] into two types: (1) physical therapy for vestibular hypofunction and (2) canalith repositioning therapy for benign paroxysmal positional vertigo (BPPV).

This point of view, on one hand, is reductive and, on the other, is wrong.

The eye–head and head–body exercises of Cawthorne–Cooksey protocol, combined with proprioceptive exercises (so-called balance rehabilitation therapy, balance retraining therapy), may be used to improve static and dynamic balance control in the major part of the diseases and disturbances that provoke vertigo, dizziness and/or unsteadiness (VDU).

Furthermore, under the point of view of rehabilitative medicine, physical therapy that promotes functional restoration despite the persistence of the lesion is considered rehabilitation, exercises or manoeuvres that solve both the impairment and the “lesion”, as in the case of BPPV, in which one has to consider re–education. Even if the two terms are used synonymously, they regard two completely different approaches and have completely different goals and outcome expectations. In other words, the aim of re–education is restitutio ad integrum, while the aim of rehabilitation is restitutio ad functionem.

Rehabilitation is mainly a teaching process that begins in the brainstem and the cerebellum and leads to a radical reorganization of both subcortical and cortical sensorimotor pattern by which the patient learns how to manage her/his disease, to cope her/his symptoms, to recover her/his impairment and to avoid disability. Thus, as far as our experience is concerned, the keyword of balance control rehab is learning. The other two keywords of rehabilitative medicine, in general, are efficacy and efficiency Thus, the scope of our approach is to rehab the major part of patients complaining VDU, despite the disease, as effectively and efficiently as possible.

Each pathological condition induces VDU through specific key mechanisms and thus rehab recognizes specific key points for specific treatments. Furthermore, rehab has to be as more customized as possible.

We named our rehab approach Vertigo School because, combining Cawthorne–Cooksey protocol and MCS model, we can prepare disease-specific programmes that can be customized on the basis of the diagnosis of treatment (see Chap. 2). The term vertigo is used in this context as generally used by population and thus as generic synonymous of VDU.

Vertigo School approach is inspired by Back School and Neck School principles.

The Back School method was developed in 1969 by Mariane Zachrisson Forssell, with the goal of preventing and avoiding recurrent episodes of low back pain. The programme is composed of 4 sessions lasting approximately 45 min, each session being organized by theoretical components, which include anatomy and spinal biomechanics, epidemiology, physiopathology of the most frequent back disorders, posture, ergonomics, common treatment modalities and a practical component (exercises for the maintenance of a “healthy back”) [16].

The Neck School [17, 18] is based on multimodal treatment emphasizing proprioceptive exercises with both neck lecture and activated home exercise and neck lecture with a recommendation of exercise in patients with chronic nonspecific neck pain.

Our VDU rehab protocols are based on the same mix of educational and training approach. Vertigo School is organized into three phases: