Vestibular Therapy

Abstract

Vestibular therapy is a common topic in physicians’ search for updated clinical practice. Early and appropriate vestibular rehabilitation makes a difference in a patient’s outcome. Peripheral vestibular impairments are often unilateral and heterogeneous. For this reason, treatment differs depending on the etiology, the moment from the onset, and the age of the patient. Following issues will be addressed in this chapter: medical treatment in the acute phase and subacute/chronic phase of unilateral vestibular loss; repositioning maneuvers for different types of BPPV; vestibular rehabilitation individualized programs, for vestibular neuritis, otolith dysfunction, visual vertigo, bilateral vestibular loss; virtual reality in vestibular rehabilitation programs; evaluation of vestibular rehabilitation programs; and new research treatment options—vibrotactile Balance Bely and vestibular implant.

1. Introduction

Vestibular lesions have a noticeable impact on patient’s quality of life. Depending on the disease itself, but also on the patient’s psychological status, vestibular impairment has severe long-term functional consequences in many cases. After headache, vertigo is one of the most frequent presenting symptoms to physicians in many disciplines, with a lifetime prevalence of almost 30% [1].

Dizziness is a pathologic condition that includes disorders of spatial orientation and motion perception and disturbances in gaze stability, posture, and gait. About 5% of the general population has dizziness, vertigo, or disequilibrium and their prevalence, frequency, and severity increases, in general, with age [2]. It is considered that half of the patients with dizziness have a vestibular dysfunction and in those in whom vestibular lesion is symptomatic, the odds of falling are 12-fold greater [3].

Four out of five patients report severe impairment of daily activities. This is an important issue to address when we talk about vestibular therapy and its benefit for the patient, but also is a parameter which expresses the economic burden of vestibular diseases: absenteeism, high use of health care, and increased risk of fall with its consequences (e.g., hip fracture in elderly).

Dizziness is the main reason for physician appointments in patients over 75 years of age and represents a significant risk factor for falls. Falls are considered the leading cause of serious injury and death in elderly—10% of hospitalization and 50% of accidental deaths.

For all medical, psychological, and economical reasons, vestibular therapy should have appropriate time-course customization, based on the phase of the disease (acute or chronic) and type of the peripheral vestibular pathology (single episode, recurrent episodes), and etiology, if possible (BPPV, vestibular neuritis, endolymphatic hydrops, labyrinthitis, vestibular paroxysmia, third window syndrome, or bilateral vestibular loss). Once the diagnosis is established, a correct drug with appropriate dosage and sufficient duration should be considered. Too low or too high initial dose might be ineffective or not well tolerated. Also, duration is important for better recovery—prolonged antivertiginous agents delay vestibular compensation phenomenon, and diseases such as Menière disease and vestibular migraine require long-term treatment [4].

Treatment management must take into account the natural recovery of a unilateral peripheral vestibular deficit (UVL), through the central vestibular compensation process. This represents a neuroplasticity model of recovery after a UVL, with the highest intensity in the first week after vestibular injury and continues slowly over a long period of time (1 year) [5]. It is an imperfect and incomplete (high acceleration or velocity head movements are not always compensated) phenomenon. Central vestibular compensation must be enhanced and accelerated for the best outcome for the patient, in the shortest possible period of time. This can be obtained with prolonged treatment (at least 3 months) with betahistine associated with vestibular rehabilitation physical programs, bimodal management widely accepted [6, 7, 8, 9].

Vestibular rehabilitation (VR) program is based on physical exercises specially designed to overcome imbalance issues and minimize the negative consequences of vestibular impairment, by creating new cortical models of reaction to daily balance challenges.

VR exercises target a reset of the brain through habituation (reduces avoidance of certain positions), adaptation (teaching the unaffected balance receptors to undertake the function of destroyed ones), and substitution (teaching other sensory systems to compensate for the vestibular impairment) strategies. The treatment is focused on improving clear vision when moving the head, reducing the intolerance to movement by use of repetitive eye, head, and body movement, and relearning of balance.

Central compensation of dynamic symptoms involves multiple processes:

• Restoration of peripheral function.

• Compensatory readjustments of brainstem vestibular processing.

• Sensorial substitution of the impaired vestibular function by other sensorial systems (visual and somatosensorial)—use of smooth pursuit instead of the nonfunctional vestibulocular reflex (VOR), for example.

• Functional substitution—use of alternative strategies, with different effectors than the damaged vestibular ones: prediction, saccades instead of VOR, or extensive use of cervical inputs.

• Behavioral changes in order to minimize vestibular challenges and demands.

All above-mentioned processes except the first one (restoration of peripheral function) act competitively: all start simultaneously and act redundantly but using one of them may eliminate the need for others. This selection of the main central compensation process is one of the explanations for variable outcomes of the same process in different patients—dependence on visual substitution impedes upon somatosensorial substitution mechanisms and vice versa.

Customized vestibular rehabilitation programs might diminish this limit of the natural recovery phenomena [10, 11, 12, 13, 14, 15], as well as specific drug therapy [16]. The overall outcome of the central compensation process is also influenced by its delay in action. There is a critical period when neuroplasticity of the vestibular central structures is highest (first month after the acute injury) and patients must take advantage of this time-window opportunity in order to trigger early recovery mechanisms [17, 18].

Vestibular rehabilitation exercises may include specific movements which will trigger the symptoms, in order to “desensitize” the vestibular system (habituation) for positional or motion-provoked symptoms and progressively improve the gain of the vestibular reflexes (adaptation). Substitution phenomenon also occurs in order to replace the vestibular lost function through other senses involved in stabilizing gaze, stance, and equilibrium. Besides alternation of the sensory inputs, prediction and anticipation strategies can be implemented. For example, when vestibulo-ocular reflex is impaired, visual stability is obtained through cervical-ocular reflex.

Coordinating learning strategies in order to maximize adaptation and motor learning and avoid overstimulation is very important as well [19].

2. Treatment management of peripheral vestibular dysfunction

Management of a peripheral vestibular syndrome includes often combined vestibular therapies—medication, repositioning maneuvers, vestibular rehabilitation, psychotherapeutic measures or, rarely, surgery and should be customized to the individual particularities of each patient.

This will be the issue to address in the following pages.

2.1 Medical treatment

Anatomical connections between vestibular nuclei and autonomous system explain symptoms associated with a peripheral vestibular lesion:

• Nausea and vomiting

• Pale

• Cold sweating

• Respiratory and circulatory disturbances

All these symptoms appear due to the functional asymmetry of the vestibular nuclei, which receive different information from the inner ear vestibular receptors and the treatment target is to restore the balance between the vestibular nuclei. To achieve this goal, the acute stage treatment implies:

• Sedation of the vestibular system in order to “silence” the difference in activity.

• Reduction and elimination of the autonomous symptoms.

2.1.1 Symptomatic pharmacotherapy: for the first 1: 3 days

Prolonged use impedes central vestibular compensation, a vital process for a good recovery of the vestibular deficit.

1. Targeting the vestibular neurotransmitters:

   1. Cholinergic: anticholinergic drugs = scopolamine, meclizine. They inhibit stimulation (excessive impulses) from the peripheral organs and vestibular nerve and inhibit transmission in the lateral vestibular nucleus. Are contraindicated in high blood pressure and closed angle glaucoma and have important adverse reactions—dry mouth, dilated pupils, urinary retention, sedation, constipation, and confusion.

   2. Histaminergic: antihistaminergic drugs = dimenhydrinate. Its mechanism is uncertain, but it has a central effect by blocking H1 receptors and inhibiting synaptic transmission on medial vestibular nucleus.

   3. GABA neurotransmitters: GABA-ergic drugs = lorazepam, valium. They provoke a central suppression of the vestibular response, reduce anxiety, and also have a sedative and hypnotic effect. They impair central vestibular compensation, and this is the reason they should be administered for at most 3 days. As side effects, impaired memory and addiction should be known.

2. Targeting the vomiting center transmitters:

   1. Dopaminergic (selective dopamine D2 antagonist) = droperidol, has a low incidence of extrapyramidal effects, antiemetic action, improved blood flow, mucosal secretion in GI, antivertigo, anti-migraine headache, and antidepressant activity (in low doses).

   2. Histaminergic (H1).

   3. Serotoninergic (5-HT3 antagonist/5 hydroxytryptamine subtype 3 receptor)—Ondensetron/granisetron, less effective for vestibular emesis and has a high cost.

Other drugs might also be used in the acute phase, such as:

• Calcium channel blockers = Flurnarazine/Cinnarazine

  • vestibular suppression on Ca channel in hair cells

  • antihistamines and anticholinergic activity

  • side effects: sedation, weight gain, Parkinsonism

• Sodium channel blockers = Phenytoin/nerontin/tegretol

  • affect GABA neurotransmitters; glutamate antagonist

  • induce central nystagmus

  • uncertain mechanism

• Histamine agonists (H1/H3—receptors agonist) = Betahistine

  • increase circulation to the inner ear

  • suppress vestibular function on the healthy side

  • facilitate central vestibular compensation

  • side effects: nausea, headache

  • caution: peptic ulcer, pheochromocytoma

• Acetyl-leucine

  • vestibular suppressant

  • rapid antivertigo effect (IV)

2.1.2 Etiologic-based treatment

General medical treatment mentioned above is associated with an etiological therapy when etiology of the peripheral vestibular deficit is known.

• Steroids—for vestibular neuritis and Menière disease; reduce the duration of vertigo episodes.

  • methylprednisolone 100 mg/day, doses tapered by 20 mg every fourth day within 3 days of symptom onset has a significant effect in improving the recovery of peripheral vestibular function [5].

  • intratympanic corticosteroids—repeated series of weekly injections of 10 mg/ml dexamethasone for 1 month reduce vertigo spells in 48% of patients, without deterioration of auditory hair cells (preserved transient otoacoustic emissions) [20].

• Dietary salt restriction—for Menière disease.

• Diuretics—Menière disease:

  • thiazide diuretics

  • potassium-sparing agents = spironolactone, thiazide + amiloride; at least 3 months of diuretic therapy recommended before discontinuing

    1. sulfa allergies—can try loop diuretics or alternate therapies

  • carbon anhydrase inhibitors (acetazolamide)

    1. “inner ear glaucoma”

    2. decreased Na-H exchange in tubule

    3. decreased CSF production

    4. diuretic effects not as long-lasting

    5. dide effects—nephrocalcinosis, mild metabolic acidosis, GI disturbances

• Betahistine (H1-agonist and H3-antagonist)

  • for Menière disease—at least 48 mg tid for at least 6–12 months

  • for unilateral vestibular loss (UVL), to facilitate and enhance vestibular central compensation—48 mg tid for 3 months

  • for bilateral vestibular loss (in the first 3 months)—48 mg tid for 3 months

  • it improves the labyrinthine microcirculation by acting on the precapillary sphincters of the stria vascularis [21] and it reduces the production and increases the absorption of endolymph

• transtympanically gentamicin—20–40 mg/injection at intervals of 4–8 weeks, depending on the efficacy or single-shot injection with follow-up, to avoid ototoxicity for disabling vertigo, after trial of adequate medical therapy [22]. Gentamicin is primarily vestibulotoxic—may impair vestibular dark cells (endolymph), but has an inherent hearing loss risk (30%).

  • gentamicin is injected over round window, with patient supine, ear up for 30 min

  • patients is instructed not to swallow

• low dose of carbamazepine (200–600 mg/day) or oxcarbazepine (300–900 mg/day) for vestibular paroxysmia [23]

  • if these are not tolerated, we can try phenytoin, valproic acid or acetazolamide

• antibiotics, in labyrinthitis and otosyphilis; otosyphilis is treated with the same protocol as neurosyphilis, with Penicillin, if no allergy is present.

  • Intravenous Crystallin Penicillin G 18–24,000,000 UI at 4 h intervals for 10–21 days, continued with intramuscular benzathine Penicillin 2,400,000 UI three times in 1 week.

2.2 Repositioning maneuvers

For benign paroxysmal positional vertigo (BPPV), the most common cause of peripheral vestibular syndrome, treatment is based on physical maneuvers of repositioning the otoconial fragments from the semicircular canal into the utricle.

Canal repositioning procedures differ for each semicircular canal and also for different pathophysiological mechanisms—canalithiasis or cupulolithiasis. For this reason, a precise diagnosis is mandatory, to establish which ear and which semicircular canal is affected, which semicircular canal/ear is affected more in cases of multicanal BPPV and if the otoconial fragments float free or are attached to the cupula.

For diagnostic and treatment as well, there are some contraindications:

• absolute contraindications: cervical spine trauma or recent surgery

• relative contraindications: glaucoma, morbid overweight

For patients with cupulolithiasis, we first try to dislocate the otoconial fragments from the cupula by vibrations applied on the affected mastoid or head-shaking maneuver and transform the cupulolithiasis into a canalithiasis, which has much higher success rate by repositioning treatment.

For patients in whom an appropriate canal repositioning procedure (CRP) is not possible, Brandt–Daroff vestibular habituation exercises are recommended. Otherwise, several CRP is used.

1. canalithiasis of the posterior semicircular canal (pc)—the most frequent affected:

   • Semont liberatory maneuver (Figure 1): From a sitting position, patient is swiftly placed laterally on the affected ear, with nose facing upwards (i.e., for left posterior semicircular canal canalithiasis, head is turned 45° to the healthy right ear and patient is placed laterally on the left side of the trunk). After nystagmus ceases, the patient is moved quickly through 180° while maintaining the original head position to lie face down on the opposite side. This may trigger further nystagmus and symptoms. Return the patient to the seated position when nystagmus and symptoms stop.

   • recently, a variant (Semont plus), is recommended, with better results [24, 25]. The difference from the original Semont maneuver is that in the first position, head is extended off the examination coach.

   • Epley canal repositioning procedure (Figure 2), with very high rates of success: The patient is seated upright. Turn his head 30–45° to the affected ear. Supporting his head, lie him backward quickly, with the neck slightly hyperextended off the bed. After the nystagmus ceases, turn the patient’s head 90° toward the healthy ear. After 2 min in this position, the patient should rotate his body on the healthy side, facilitating further head rotation to 90° (nose towards the ground). This may trigger further nystagmus and symptoms. When the nystagmus and symptoms stop, return the patient to the seated position and bent the head forward for another 2 min.

2. canalithiasis of the horizontal semicircular canal (hc)—several methods of treatment are used, with variable success rates

   • forced prolonged positioning on the healthy side (head and whole body), for 12 h [26]

   • “barbecue” maneuver [27] (Figure 3). From supine position, patient is turned in steps of 90° toward the healthy ear until laying on the affected ear lateral decubitus and then returned to the sitting position. Each position must be maintained for 1 min.

   • Gufoni maneuver (Figure 4) removes detritus from the horizontal semicircular canal. From the sitting position, patient is brought to the side position on the healthy. After 20 s, the head is rotated in the yaw plane 45° down. After 1–2 min in this position, the patient is brought back to the sitting position, in which the head may rotate back to the neutral position.

3. cupulolithiasis oh the horizontal semicircular canal (hc)—the aim of the liberatory maneuvres is to transform the cupulolithiasis into a canalithiasis, either by modifying the canalithiasis maneuvers, either by applying a vibrator on the affected mastoid during the repositioning maneuver

   • Gufoni maneuver (Figure 5)—from the sitting position, patient goes to the side position on the affected ear and after 20 s, head is turned for 45° with nose up. After 1–2 min in this position, the patient is brought back to the sitting position, in which the head may rotate back to the neutral position.

   • Kim maneuver [28]. From the supine position, patient turns on the affected side and head is turned another 45° towards the lesion side. Vibration is applied on the affected mastoid and then head is turned back 45° towards the healthy ear. In complete lateral decubitus on the affected ear of the patient. Next position of the patient is supine again, followed by lateral decubitus on the healthy side, when vibration is again applied on the healthy ear (for the variant of cupulolithiasis when fragments are on the short arm of the horizontal semicircular canal). Then patient reaches the prone position and slowly the patient is brought back to sitting position without neck extension.

   • Zuma maneuver [29]. From the sitting position, patient is swiftly placed on the affected side (upper trunk). After 3 min, head turned upwards 90° and maintained in this position for another 3 min. Next, patient turns into the supine position with the whole body and head is turned 90° towards the healthy ear. After another 3 min, head is tilted forward, and patient returns to the initial position (sitting)

4. anterior semicircular canal (ac) canalithiasis—the rarest form of BPPV, probably because repositioning is taking place spontaneous during night, raised many controverses regarding treatment.

   • One of the first treatment options was to perform an Epley maneuver for the healthy ear, taken into consideration the co-planarity of the two vertical semicircular canals—the anterior from one ear and the posterior from the opposite ear, but it proves a low efficiency [30, 31, 32].

   • The Yacovino maneuver was seen to be an effective treatment option for ac-BPPV without having to determine the side involved. However, simulations showed that the classical Yacovino maneuver carried a risk of canal switch to the posterior canal. The Yacovino maneuver consists of four steps each performed at an interval of 30 s: from the sitting position, patient lies down with head in head-hanging position, 30° below the horizontal plane. After 30 s, head is elevated so that the chin touches the chest and then patient returns to the sitting position [33, 34].

   • To overcome this risk, a modified Yacovino maneuver is suggested [35]. In this variation, the subject is brought directly from the head-hanging position to the sitting position. After an interval of 30 s, the neck of the subject is flexed forward at an angle of 45°.

Figure 1.

Semont liberatory maneuver.

Figure 2.

Epley canalar repositioning maneuver.

Figure 3.

Barbeque maneuver.

Figure 4.

Gufoni maneuver for right-hc canalithiasis.

Figure 5.

Gufoni maneuver for left-hc cupulolithiasis.

2.3 Vestibular rehabilitation

For stable, definite unilateral vestibula loss (UVL), treatment is more complex because recovery of the long-term deficits induced by UVL should start as soon as possible. As mentioned before, there is a critical period in which the neuroplasticity mechanisms (central vestibular compensation) should start and act at their maximal potential in order to give patients the best opportunities to recover their balance functionality, to return to their daily activities, job, and physical hobbies.

In order to achieve these,

• Symptomatic medical treatment of the acute phase should not exceed 3 days.

• Central compensation process should be facilitated and enhanced by long-term (3 months) treatment with Betahistine and vestibular rehabilitation (VR) customized program [36, 37].

VR promotes vestibular compensation by:

• Habituation mechanisms

• Enhancing adaptation of VOR & VSR

• Substitution strategy of balance (pursuit, saccades)

Physical exercises based treatment, which gradually and progressively stimulates the vestibular system and facilitates vestibular compensation. Starting point is the minimal skill level the patient if able to perform and, as compensation and habituation occurs, speed and complexity of the exercises are increased. Vestibular rehabilitation uses neuroplasticity central mechanisms (adaptation, habituation, sensorial, and functional substitution) to increase static and dynamic postural stability and to improve visual-vestibular interactions [36, 38, 39].

Before vestibular rehabilitation program is designed, a detailed evaluation of equilibrium abilities must be performed, in terms of functionality (gait with head movement, static and dynamic balance in fixed and altered inputs—Timed Up and Go Test, posturography), alternative sensorial systems capabilities (visual and somatosensorial) and fall risk (Unipedal Stance Test).

Also, specific activities and head or body positions that provoke symptoms should be determined.

Today vestibular rehabilitation programs are still based on Cawthorne–Cooksey exercises developed [40] and modified by Susan Herdman [41], due to their excellent results in building up the tolerance. These exercises include eye and head movements, coordination of eyes and head movements (visual-vestibular interaction), postural control exercises, balance tasks with gradually increased difficulty (eyes opened, eyes closed, large base support, uneven base support, while walking, in heavy visual or noisy environments). Exercises are recommended to be performed twice a day, for 30 min, with 10 repetitions of each exercise.

2.3.1 Cawthorne-Cooksey exercises

1. In bed

   1. Eye movements: at first slow, then quick

      • up and down

      • from side to side

      • focus on finger while moving from 1 m to 30 cm away from face

   2. Head movements: at first slow, then quick. Later with eyes closed.

      

      • turn from side to side, shoulder to shoulder

      • bend backward and forward

2. Sitting

   1 and 2 as above

   
   

   1. Shoulder shrugging and circling

   2. Bend forward and pick objects from the ground

   3. Rotate on a chair from one side to another, while fixation an image

3. Standing and walking

   
   

1. As A1, A2 and B3

2. Change from sitting to standing with eyes open, then eyes closed

3. Throw a small ball from hand to hand (above eye level)

4. Throw a ball from hand to hand under the knee

5. Change from sitting to standing and turn around in between

6. Walk 5–7 m distance while moving head side to side, backwards to forwards and from one shoulder to another

2.3.2 Vestibular rehabilitation exercises

At-home exercises are associated, when possible, with weekly sessions of vestibular rehabilitation exercises based on visual feedback (Figure 6) on specific equipment, very expensive, unfortunately—Equitest, Bertec, Virtualis, CAREN, etc.

Figure 6.

Visual feedback-based vestibular rehabilitation. (a) Equitest-Neurcom. (b) Bertec system. (c) CAREN system.

When patients have multifactorial causes of balance difficulty (e.g., elderly with vision disturbances—cataract, peripheral neuropathy, osteoarthritic pathology), balance recovery is more difficult and good outcome comes with longer time, but with a positive impact on possible complications of falls. Positive effects on walking, postural control, balance, and mobility in the elderly have been reported with exercises in the form of interactive games where virtual reality technologies are used [42, 43, 44, 45, 46].

Vestibular rehabilitation programs must take into consideration some very important factors:

• age (mobility decreases with age)

• patient’s daily activity and physical condition—non-sports people versus sportive people

• other comorbidities involve the other sensorial systems involved in balance, vision, proprioception, superficial somatosensorial inputs—tactile receptors (touch, foot pressure) and proprioceptive or deep somatosensory inputs—muscle and tendon stretch receptors. For these patients’ safety has to be enforced for at-home exercises, in order to prevent falls.

• for patients with bilateral vestibular loss, VR is the only efficient method in diminishing the severity of gait disturbances. Results come later (after at least 6 months) and treatment lasts for at least 1 year, but usually, some daily exercises are recommended “forever”.

• during the COVID-19 pandemic, vestibular rehabilitation was based mainly on telemedicine, with periodic follow-up via internet-based audio and video connection (WhatsApp was affordable for the majority of patients). Hand out and links to instruction films for at-home use were created, available on different websites or especially designed apps. Patient alone is prone to non-adherence and attrition, so he needs ON-LINE support in this HYBRID program. IDEAL—family member available = for patient’s SAFETY, especially for:

  • standing and walking exercises in cases of bilateral vestibular loss

  • Epley maneuvre—“Tumarkin-like” attack might appear at the end of the maneuver

These telemedicine solutions are not reimbursed in many countries, and this was a problem for health care providers and patients as well.

There are also some limitations of VR through telemedicine:

• Unstable internet connection

• Type of mobile phone (it has to have a mobile camera and access to the internet)

• Low technology knowledge from the patient

• Hearing impaired patient

• Light intensity in the room

• Correct positioning of the video camera, especially for repositioning maneuvers and walking exercises

Informing and counseling are crucial for coping and therapy adherence. We must explain to the patients the symptoms and inform them explicitly about the impact of and need for treatment. Do not forget that therapy adherence in almost any chronic disease = only 30–50%!!!

For better adherence and compliance of patients to this physical treatment, virtual reality programs are used more and more often, most easily based on Wii and Kinect platforms or virtual reality Googles.

Recent studies demonstrated better results with virtual reality in patients with unilateral peripheral vestibular loss and in elderly. This induces retinal slip and secondary optokinetic eye movements, which stimulate adaptation and compensation mechanisms [47, 48]. Using smartphones for delivering the virtual reality environment proved to be a valid training stimulus, which induces difficulties in postural stability control. Additionally, if a head-mounted system is used, there is a potential to reduce the VOR gain through adaptative changes in the central structures of the vestibular system [49, 50].

Benefit’s evaluation of the vestibular rehabilitation.

Physical treatment through vestibular rehabilitation has proven to be a very important instrument in recovery of the vestibular deficit. The benefit has to take into consideration both patient’s evaluation as well as health care provider’s point of view.

• Subjective evaluation of the UVL-induced handicap and treatment’s benefit includes self-evaluation questionnaires:

  • VAS—visual analog scale for symptoms associated with vestibular impairment

  • DHI—Dizziness Handicap Inventory, used for quantification of the severity of the lesion (Table 1) and also for treatment’s result (improvement with more than 18 points is considered a statistically significant improvement)

  • Activities-specific Balance Confidence (ABC) Scale

  • Anxiety/depression self-evaluation: HADS-A, HADS-D, because many patients with vestibular impairment experience anxiety, fear, low confidence in their physical independence and even depression

  • Vestibular Rehabilitation Benefit Questionnaire which was recently refined and validated

• Physical performance tests

  • BBS: Berg Balance Scale

  • SPPB: Short Physical Performance Battery

  • POMA: Performance Oriented Mobility Assessment

  • DGI: Dynamic Gait Index, very useful for fall risk assessment

  • TUG: Timed Up and Go Test

• Clinical vestibular evaluation:

  • for vestibulo-ocular reflex (VOR): presence of nystagmus, head impulse test

  • for vestibulo-spinal reflex (VSR): Romberg test, stepping test, Unipedal Stance Test (excellent predictor for falls)

• Objective vestibular evaluation:

  • CDP: computerized dynamic posturography allows assessment of the vestibulospinal reflex and also visual or proprioception dependence. Recent versions offer additional tests, such as dynamic visual acuity (DVA) and gaze stabilization test (GST)

  • vHIT: video Head Impulse Test

  • cVEMP and oVEMP: cervical and ocular Vestibular Evoked Myogenic Potentials

  • SVV: Subjective Visual Vertical

16–34p	Mild handicap
36–52p	Moderate handicap
>54p	Severe handicap

Table 1.

Severity of the vestibular lesion based on DHI score.

To summarize, vestibular rehabilitation:

• improves walking, static, and sand dynamic balance

• reduces vestibular symptoms during daily activities

• reduces anxiety and depression induced by AUVL

• increase self-confidence, movement independence, and life quality [51].

• rehab optimizes compensation, sensory substitution, and may lead to new connections and strategies

• but we have to start FAST with rehab (therapeutical window of 8 days after acute loss) for patient’s best recovery

Besides unilateral vestibular loss, many patients experience bilateral vestibular hypofunction (such as aging of the vestibular system in elderly = presbivestibulia) or even bilateral vestibular loss (bvl). They struggle to maintain balance, especially when walking in the dark or on uneven surfaces and present oscillopsia during walking or head movements. Central vestibular compensation can not occur in these cases due to bilateral impairment, so patients’ recovery is much more difficult, and imperfect. BVL leads up to 30 times higher risk of falling, significant loss of quality of life, and an increased socioeconomic burden on individuals and on society [52]. The etiologies of BVL vary from ototoxicity (e.g., aminoglycoside treatment or chemotherapy), to genetic factors (e.g., DFNA9), CANVAS or spinocerebellar ataxia, infectious causes (meningitis), autoimmunity (e.g., Cogan’s syndrome), trauma, and neurodegenerative diseases [53, 54, 55].

In some patients, there may be a transition from presbyvestibulopathy to BVP due to aging or neurodegeneration [56, 57].

New methods of treatment for bilateral vestibular loss are also available, only in clinical studies for the moment:

2.3.3 Vestibular prothesis: Balance Belt

A wearable (hip belt) medical device which provides haptic feedback to improve balance and mobility in patients with severe bilateral vestibular loss (Figure 7) [58]. Patients improved their independent balance, moved without relying on somebody else or walking cane.

Figure 7.

Balance belt.

The Balance Belt, developed by Professor Herman Kingma, contains several tiny vibration motors and an accelerometer which sense the direction the wearer is leaning toward and provides vibrational feedback to alert the wearer about their self-movement and body position. The wearer interprets the feedback subconsciously, corrects their posture, and improves their balance this way.

According to the inventor: “A sensor in the belt feels, as it were, where gravity is. If someone moves too far in the wrong direction, the belt produces vibrations. This is just enough to make sure you do not get out of balance and gain just a little bit more certainty.”

2.3.4 Vestibular implant (VI)

Vestibular implant (VI) (Figure 8) is a self-contained system that provides artificial sensation of head rotation by electrically stimulating the three semicircular canal branches of the vestibular nerve [59]. As for cochlear implant, vestibular implant is an artificial replacement of the non-functional vestibular end organ, which captures head movement through motion sensors and sends electrical signals to the vestibular nerves by electrodes that are implanted near the vestibular nerve branches that innervate the semicircular canals and the otolith organs [60, 61, 62, 63].

Figure 8.

Vestibular implant (Source: MED EL Company).

Clinical studies showed an increase in the vestibulo-ocular gain [64, 65, 66, 67], an improvement of vestibulospinal and vestibulocollic reflexes [68, 69] and restoration of the dynamic visual acuity in difficult high-frequency head movements [70, 71].

The criteria for VI-implantation should go beyond the existing criteria for BVP, in order to demonstrate significant impairment of all canals in all frequency ranges, and (on indication) the otolith organs, because implantation would destroy residual vestibular function [72].

Criteria for vestibular implant eligibility are:

1. Chronic vestibular impairment with 2 disabling symptoms of unsteadiness when walking or standing plus at least one of the following:

   • Movement-induced blurred vision or oscillopsia during walking or quick head/body movements, and/or

   • Worsening of unsteadiness in darkness and/or on uneven ground

2. Head movement induces the most severe symptoms.

3. Bilaterally reduced or absent angular VOR function documented by at least one of the following major criteria:

   • Bilaterally pathological horizontal angular VOR gain ≤0.6 and at least bilaterally one vertical angular VOR gain <0.7, measured by the video-HIT or scleral-coil technique. Angular eye velocity is measured at a fixed time (around 60 ms after onset of the impulse), minimum of seven artifact-free impulses, with peak acceleration of at least 1000/s² [73]. Only one vertical semicircular canal on each side needs to fulfill the criterion of an angular VOR gain <0.7, since it was shown that selective sparing of a single semicircular canal is possible [74] while a clinically relevant BVP is still present, making the patient probably eligible for implantation.

   • Reduced caloric response (sum of bithermal max. Peak SPV on each side ≤6°/s for 30 s water stimuli or <10°/s for 60 s water or air stimuli). Irrigations of water, lasting for ≥30 s, with a total volume of at least 250 ml and 5 min interval between successive irrigations [73]. For air stimulus, 8 l/min for at least 60 s should be used. Patients with a sum of all bithermal irrigations <20°/s still reported significant imbalance and/or oscillopsia [53, 75].

   • Reduced horizontal angular VOR gain ≤0.1 upon sinusoidal stimulation on a rotatory chair (0.1 Hz, Vmax = 50°/s) and a phase lead >68° (time constant <5 s).

     C′. Obligatory only in case of implantation of otolith structures: Bilaterally absent cVEMP and oVEMP responses.

4. In case only one or two criteria from C are matched (and also criterion C′ is matched in case of otolith stimulation), the remaining test(s) should comply with the following minor criteria:

   • Bilaterally pathological VOR gains of at least two semicircular canals <0.7, measured by the video-HIT or scleral-coil technique.

   • Reduced caloric response (sum of bithermal max. Peak SPV on each side <10°/s for water and air stimuli of ≥30 s).

   • Reduced horizontal angular VOR gain <0.2 upon sinusoidal stimulation on a rotatory chair (0.1 Hz, Vmax = 50°/s).

5. Symptoms are not better accounted for by another disease.

6. Fitting the additional requirements relevant to initial preclinical trials.

   • Age 18 years and above.

   • BVP results most likely from a peripheral origin [55].

   • An improvement in patient’s vestibular function is unlikely [76] (6 months “wait-and-see” period).

   • Patent vestibular end-organ and intact vestibular nerve [56] and no chronic otitis media.

   • Ability to use the device and follow a personalized rehabilitation program.

   • Ability to undergo the surgery [57].

7. No current psychological or psychiatric disorder that could significantly interfere with the use or evaluation of the VI [73].

SHIMP test was not included in the evaluation of the vestibular function since the clinical relevance of SHIMPs in BVP should still be determined [77].

Handicap Inventory total score of >30 would be preferred since this could show at least moderate handicap [78, 79, 80]. But this is not mandatory if we discuss about eligibility criteria for vestibular implantation.

With absent cVEMP and oVEMP responses, it is expected that the benefit of vestibular implantation will be higher than the drawbacks of the potential iatrogenically induced vestibular hypofunction due to vestibular implantation of the otolith endorgans.

Surgery for vestibular implantation implies inserting the electrodes either in the proximity of the ampullae of the semicircular canals by opening the semicircular canals or the vestibulum (intralabyrinthine approach), either in the vicinity of the vestibular nerve branches on the semicircular canals end or in the internal auditory canal (extralabyrinthine approach) [81]. Each surgical option has its risks—loss of residual hearing for the intralabyrinthine approach and exposure and damage of the facial nerve for the extralabyrinthine approach [82].

Since implantation of otolith structures [60] is almost certain to cause otolith hypofunction due to mechanical disruption of the membranous labyrinth during implantation, oVEMPS and cVEMPS were included in the implantation criteria when the otolith structures will be replaced by the vestibular implant.

3. Conclusion

Peripheral vestibular lesions are found in more than 50% of patients with vestibular impairment. First three etiologies of peripheral vestibular lesions are BPPV, vestibular neuritis and Menière’s disease, each of them with specific treatment management, different in between.

Only this is solid argument for continuously updating our knowledge in the field, in order to offer best treatment option to our patients—appropriate repositioning maneuver, acute or subacute and chronic medical treatment or vestibular rehabilitation individualized programs.

Vestibular impairment, most frequently unilateral, decrease mobility, equilibrium and impair patient’s daily activities and his job skills, with a decreased overall quality of life.

Some vestibular disorders have a negative impact upon patient’s daily mental status, like Menière’s disease with its unpredictable acute attacks. Others, like vestibular neuritis patients, have a long-lasting functional impairment and imply long-term recovery treatment (medical and physical) which will facilitate and enhance the natural recovery mechanism of central vestibular compensation.

Bilateral vestibular hypofunction (e.g., elderly) or bilateral vestibular loss is much more difficult to treat, because vestibular neuroplasticity does not work in these cases. For these patients, specific vestibular rehabilitation programs were designed, more recently with specific virtual reality exercises included for better adherence and compliance to years of rehabilitation.

Also, as research studies for the moment, specific medical devices were designed—vibrotactile Balance Belt and vestibular implant.

Conflict of interest

The author declares no conflict of interest.