Introduction to Vestibular Rehabilitation

Introduction[edit | edit source]

Ear Anatomy.png

Vestibular rehabilitation is an evidence-based approach to managing dizziness, vertigo, motion sensitivity, balance and postural control issues that occur due to vestibular dysfunction.[1]

Patients with vestibular impairment typically experience issues with gaze stability, motion stability, and balance and postural control. Vestibular rehabilitation is, therefore, focused on addressing these areas of pathology or dysfunction. However, the specific treatment approach will depend on the pathology and each patient’s unique presentation.[1] It is, therefore, essential to have a detailed understanding of the vestibular system when treating this patient group.

Epidemiology[edit | edit source]


Vestibular disturbance is a significant issue globally. It is estimated that 35.4 percent of North Americans aged over 40 have experienced some form of vestibular dysfunction. The likelihood of experiencing vestibular dysfunction increases with age.[2]

  • 80 percent of people aged over 65 years experience dizziness - in 30 to 50 percent of cases this dizziness is caused by benign paroxysmal positional vertigo (BPPV)[1]
  • 75 percent of adults aged over 70 years have a balance impairment[3]
  • Nearly 85 percent of adults aged over 80 years have vestibular dysfunction[3]

Individuals with vestibular dysfunction are eight times more likely to experience a fall,[3] which is significant as falls are associated with significant morbidity, mortality[3] and economic cost.[4] Moreover, the number of people experiencing vestibular dysfunction is expected to grow due to our ageing populations.[1]

Defining Dizziness and Vertigo[edit | edit source]

Dizziness and vertigo are not interchangeable terms:[1]

  • Dizziness is a non-specific term used to describe a variety of sensations such as light-headedness, disorientation and presyncope[5]
  • Vertigo is a specific type of dizziness where there is the illusion of movement in the environment (e.g. spinning, whirling)[1]

Vertigo is caused by both peripheral and central vestibular diseases.[6] It is often rotational (i.e. the room spins around the patient), but there can also be linear disruptions or, less commonly, the patient might feel that his / her body is moving relative to the environment.[1]

Dizziness and vertigo are both purely subjective phenomena. There is no objective means of measuring them, so the patient’s subjective history is key.[1]

Causes of Dizziness[edit | edit source]

There are many causes of dizziness including:

  • Cardiovascular dysfunction[1]
  • Neurological dysfunction[1]
    • Multiple sclerosis (MS)[8] - MS can mimic vestibular dysfunction and cause symptoms such as dizziness / vertigo
  • Vision dysfunctions[1][9]
    • Any condition that affects visual input can cause dizziness
    • These might occur in the eye (e.g. macular degeneration, cataracts), be related to the optic nerve, or be due to problems with visual processing
  • Psychogenic dizziness[1]
    • Dizziness can trigger anxiety and anxiety can cause dizziness[9]
    • It is not, however, common to see purely psychogenic dizziness and vertigo
  • Cervicogenic dizziness (CGD)
    • A clinical syndrome characterised by the presence of dizziness and associated neck pain. There are no definitive clinical or laboratory tests for CGD and therefore CGD is a diagnosis of exclusion[10]
    • NB musculoskeletal structures of the cervical spine (e.g. golgi tendon organs, joint receptors, muscle spindles) cannot typically cause sensations of vertigo[1]
  • Vestibular system disorders[1][11][12]

The following video provides additional information about some common causes of vertigo.


Signs and Symptoms of Vestibular Disorders[edit | edit source]

  • Nystagmus (involuntary eye movement)
  • Vertigo
  • Dizziness
  • Imbalance or ataxia
  • Compromised gaze stability (decreased visual acuity with head movement - i.e. the vestibular ocular reflex (VOR) is affected)

Anatomy of the Peripheral Vestibular System[edit | edit source]

The outer ear consists of the external acoustic meatus. The tympanic membrane (i.e. eardrum) separates the outer ear from the middle ear. The inner ear contains the vestibular apparatus and the cochlear.[1]

As is shown in Figure 3, the vestibular apparatus consists of:

  1. Three semicircular canals,
  2. The utricle and the saccule, which together form the otoliths.[15] The otoliths are positioned in the central chamber known as the vestibule.

The cochlear is also positioned in the inner ear and it is responsible for hearing.

Travelling within the membranous labyrinth of the inner ear is a clear, viscous fluid called endolymph:[1][15]

  • The acceleration of endolymph in the vestibular apparatus enables people to perceive balance and equilibrium
  • In the cochlear duct, endolymph plays an important role in the perception of sound

Because endolymph travels in both the vestibular apparatus and the cochlear, any conditions that cause increased endolymphatic pressure in the vestibular apparatus (e.g. Meniere’s disease) will affect the cochlear as well.[1]

Semicircular Canals[edit | edit source]

The semicircular canals are specialised mechanoreceptors that provide information about angular velocity.[16]

There are three semicircular canals on each side of the body (i.e. six in total):

  • Anterior
  • Posterior
  • Horizontal (or lateral)

The anterior and posterior canals have a conjoint canal, called the common crus.[1]

Planes of Movement[edit | edit source]

Figure 2. Semicircular Canals - Planes of Movement

The vestibular system has three planes of movement. Each plane of movement has two semicircular canals in it, so there are three coplanar pairs.[17] See Figure 2.

  • The anterior and posterior canals sit on the vertical plane
  • The anterior and posterior canals are also oriented along two diagonal planes:
    • LARP plane = left anterior right posterior plane
    • RALP plane = right anterior left posterior plane
  • The horizontal canals are positioned on a 30 degree angle (i.e. close to horizontal)

Ampullae[edit | edit source]

The ampullae is a widened area in the semicircular canals (see Figure 3). It contains the neurons that detect head movement. The neurons are embedded in a matrix of blood vessels and connective tissue called the crista ampullaris. Attached to these neurons are specialised mechanoreceptors called “hair cells”.[18] Each hair cell contains a large number of cross-linked actin filaments, which are called stereocilia. Stereocilia move in response to the acceleration of endolymph.[18] Essentially, they act as motion sensors that convert angular head movements into afferent neural discharges.[1]

Cupula[edit | edit source]

Figure 3. Ampullae and Cupula

The cupula is the gelatinous part of the crista ampullaris in which the hair cells are embedded. It extends from the crista to the roof of the ampullae.[1]

The cupula creates a fluid barrier - the endolymph cannot circulate within the cupula, but it is affected by movements of the endolymph around it:[19]

  • When an individual turns his / her head (i.e. an angular movement), the movement of the endolymph generates a force across the cupula, pushing it away from the direction the head is moving (see Figure 3)
  • This moves the hair cells in the crista

Linear accelerations, however, create an equal force on either side of the cupula, so displacement does not occur.[19] The semicircular canals are, therefore, unable to detect linear movement patterns and are also insensitive to gravity.[1]

Otoliths[edit | edit source]

Unlike the semicircular canals, the otoliths detect translational or linear movements,[19] including:[1]

  • Forward to backwards
  • Up and down
  • Side to side (not turning)
  • Static head position relative to gravity

Both the utricle and saccule contain a macula in which neuronal hair cells are anchored.[1][20] The hair cells sit under a gelatinous layer, which in turn is under the otolithic membrane.[20]

The otolithic membrane has calcium carbonate crystals, known as otoconia, embedded in it.[20]

The otolithic membrane is heavier than surrounding structures and fluids because of the weight of the otoconia. Because of this weight, when an individual tilts his / her head, gravity causes the membrane to move in relation to the macula. This displaces the hair cells and generates a receptor potential.[20]

The anatomy of the vestibular system is summarised in the following video.


Vestibular Reflexes[edit | edit source]

Vestibulo-spinal reflex (VSR)[edit | edit source]

The VSR stabilises the body. [22] However, while assessing balance will activate an individual's vestibulo-spinal reflex, it does not provide enough information about the vestibular apparatus to be relevant in this patient group.[1]

Vestibulo-Ocular Reflex (VOR)[edit | edit source]

The VOR maintains stable vision during head motion.[23] There are two components to the VOR and both work together to ensure gaze stability while the head turns.[1][22]

  • Angular VOR[22]
    • Mediated by the semicircular canals
    • Compensates for rotation
    • Primarily responsible for gaze stabilisation
  • Linear VOR[22]
    • Mediated by the otoliths
    • Compensates for translation
    • More important when looking at targets close up and when the head moves at reasonably high frequencies

Push-Pull Arrangement of the VOR[edit | edit source]

When an individual turns his / her head to the right:[1]

  • The right horizontal canal is excited and the left is inhibited (in a push-pull arrangement)
  • The right horizontal canal activates the right medial rectus and left lateral rectus muscles to pull the eyes to the left
  • The left horizontal canal inhibits the right lateral rectus and left medial rectus muscles, which allows this movement to occur

The VOR is the fastest human reflex - operating in around 14 milliseconds.[1] The reason for this speed is that the VOR pathway:[24]

  • Is relatively short
  • Uses only sensory information from the vestibular system to activate the necessary motoneurons

Because of this speed, the VOR must be very accurate (i.e 98 percent or more) to ensure that there is no blurring / skipping of the visual field when an individual moves his / her head.[1][24]

The following video provides a detailed description of the VOR.


Gain[edit | edit source]

VOR gain is defined as the ratio of eye velocity to head velocity during head movements. It is often used as a physiological measure of vestibular function and it tends to decline with age.[26]

Ideally, the gain of the VOR approximates 1.0.[26] This means that the magnitude of eye velocity should be equal to the magnitude of head velocity.[27] VOR gain is typically around 0.96 to 0.97, but it can operate anywhere from 0.5 to 2.[1] It has been proposed that a VOR gain of less than 0.68 is the cut off point between normal and too low.[26]

VOR gain is mediated by the central nervous system control (CNS) in a process called adaptation. When the CNS modifies VOR gain, it changes the sensitivity of the reflex to enable people to adapt to the environment. Thus, gaze stabilisation exercises, which form part of vestibular rehabilitation, can be thought of as adaptation exercises.[1]

Nystagmus[edit | edit source]

Nystagmus is one of the signs of vestibular dysfunction and it is defined as “a rhythmic, involuntary, rapid, oscillatory movement of the eyes.”[28]

It can result in slow or fast movements or a combination of the two.[28] Movements may be:[29]

  • Side to side (horizontal nystagmus)
  • Up and down (vertical nystagmus)
  • In a circle (rotary nystagmus)
  • Continuous or sudden[28]
  • Related to specific gaze or head positioning triggers[28]
  • Pathological or physiological (i.e. normal)[1]

While every reflex has a central and peripheral component, the saccade system (i.e. rapid eye movements) is considered more centrally mediated and the VOR is more peripherally mediated. Therefore, nystagmus can be considered a combination of peripheral and central mediated reflexes.[1]

Types of nystagmus include:

  • Jerk:
    • The eye moves slowly to the side where there is inhibition, or decreased activity, and then  "jerks" back to the centre[30]
    • Can be centrally or peripherally mediated[1]


  • The eye moves in sinusoidal pattern (i.e. like a pendulum)
  • Only slow eye movements are present - it does not typically have a fast phase
  • Centrally mediated[1]

Summary[edit | edit source]

  • Vestibular dysfunction is a significant issue particularly in older adults
  • There are many different causes of dizziness, all of which will be managed differently
  • Dizziness and vertigo are not interchangeable terms
  • Understanding the anatomy of the vestibular system is essential to creating an effective vestibular rehabilitation management plan

References[edit | edit source]

  1. 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 1.19 1.20 1.21 1.22 1.23 1.24 1.25 1.26 1.27 1.28 1.29 1.30 1.31 1.32 1.33 Tonks B. Introduction to Vestibular Rehabilitation Course. Plus. 2021.
  2. Agrawal Y, Carey JP, Della Santina CC, Schubert MC, Minor LB. Disorders of balance and vestibular function in US adults: data from the National Health and Nutrition Examination Survey, 2001-2004. Arch Intern Med. 2009;169(10):938-44.
  3. 3.0 3.1 3.2 3.3 Hall CD, Herdman SJ, Whitney SL, Cass SP, Clendaniel RA, Fife TD et al. Vestibular rehabilitation for peripheral vestibular hypofunction: An evidence-based clinical practice guideline: FROM THE AMERICAN PHYSICAL THERAPY ASSOCIATION NEUROLOGY SECTION. J Neurol Phys Ther. 2016;40(2):124-55.
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