Introduction to Vestibular Rehabilitation

 Vestibular rehabilitation is an evidence-based approach to managing dizziness, vertigo, motion

sensitivity, balance and postural control issues that occur due to vestibular dysfunction.

 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.

Epidemiology

 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.

 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)

 75 percent of adults aged over 70 years have a balance impairment

 Nearly 85 percent of adults aged over 80 years have vestibular dysfunction

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

Defining Dizziness and Vertigo

Dizziness and vertigo are not interchangeable terms:

 Dizziness is a non-specific term used to describe a variety of sensations such as light-headedness,

disorientation and presyncope.

 Vertigo is a specific type of dizziness where there is the illusion of movement in the environment
(e.g. spinning, whirling).

Vertigo is caused by both peripheral and central vestibular diseases. 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.

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

Causes of Dizziness

There are many causes of dizziness including:

 Cardiovascular dysfunction

 Stroke - recent reports suggest strokes are the underlying cause of symptoms in around 3 to 5 percent of
patients who visit emergency departments with dizziness / vertigo.
 Orthostatic hypotension

 Arrhythmias

 Neurological dysfunction

 Multiple sclerosis (MS) - MS can mimic vestibular dysfunction and cause symptoms such as
dizziness / vertigo.

 Vision dysfunctions

 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

 Dizziness can trigger anxiety and anxiety can cause dizziness

 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.
 NB musculoskeletal structures of the cervical spine (e.g. golgi tendon organs, joint
receptors, muscle spindles) cannot typically cause sensations of vertigo.

• Vestibular system disorders

 Head trauma such as whiplash or concussion

 Vestibular system degeneration (age related)
 Vestibular neuritis / labyrinthitis
 BPPV
 Endolymphatic hydrops (e.g. Meniere’s disease)
 Ototoxicity, barotrauma, acoustic neuroma

Signs and Symptoms of Vestibular Disorders

• 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).
 Vestibular Anatomy and Neurophysiology
 The vestibular system is a part of the sophisticated human postural control system, normal static
stance relies on three sensory inputs: vision, proprioception and vestibular. It is sensitive to two types
of information: the position of the head in space and sudden changes in the direction of movement of
the head. Together this information helps to orient a person's sense of balance and equilibrium.

 The vestibular system is divided into a central and peripheral system.

 The vestibular system has both a sensory and motor component to help us sense and perceive motion
and provides information about the movement of the head and its position with respect to gravity and
other inertial forces (like those generated when driving in a car). This information is used to stabilise
the eyes to maintain our gaze on targets of interest, with or without head movement.

 The vestibular system also employs complicated strategies to maintain blood pressure when one
quickly goes from supine to an erect posture. It helps us to maintain good head and body orientation
in relation to our environment, most often in an upright posture allowing us to maximise sensory
integration of our senses (see, hear, and smell).

The Peripheral Vestibular System (PVS)

 The PVS is situated in the inner ear, behind the tympanic membrane. Inputs from the PVS are
integrated by the central vestibular processor called the ‘vestibular nuclear complex’ which generates
motor commands to drive the eyes and the body. The system is normally very accurate. To maintain
accuracy, the vestibular system is monitored and calibrated by the cerebellum.
Semi-Circular Canals

 The Semi-circular canals (SCC’s) are specialised mechanoreceptors to help us access information
regarding angular velocity. The sensory input received from the SCC’s enables the Vestibular Ocular
Reflex (VOR) to generate an eye movement that matches the velocity of the head movement.
 The 3 SCC’s are positioned at right angles to each other to give us feedback in 3 different planes of
movement. Remember there are 2 ears, so effectively 6 SCC’s.

The six individual semi-circular canals become three coplanar pairs:

1. right and left lateral

2. left anterior and right posterior
3. left posterior and right anterior

 The planes of the canals are close to the planes of the extraocular muscles, so sensory neurons and
motor output neurons can give quick information to individual ocular muscles.
 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).
  Inside the canals there are hair cells in endolymph, and with head movement, the swishing of
endolymph displaces these hair cells of the coplanar pair in opposite directions with respect to their
ampullae, and neural firing increases in one vestibular nerve and decreases on the opposite side.
Endolymph displacement is proportional to angular head velocity, so the semi-circular canals
transmit a velocity signal to the brain.

Ampullae

 The ampullae is a widened area in the semi-circular canals. 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”. 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. Essentially, they act as
motion sensors that convert angular head movements into afferent neural discharges.

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.
 The cupula creates a fluid barrier - the endolymph cannot circulate within the cupula, but it is
affected by movements of the endolymph around it:
 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.
 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. The semi-circular canals are, therefore, unable to detect linear movement patterns
and are also insensitive to gravity.
Otoliths

 The Otoliths are made up of the Utricle (horizontal) and Saccule (vertical). Their job is to give us
information about linear acceleration by triggering an action potential to the brain to detect head
position. Because earth’s gravitational field is a linear acceleration field, the otoliths register tilt. For
example, as the head is tilted laterally (which is also called roll), shear force is exerted upon the
utricle, causing excitation, while shear force is lessened upon the saccule. Similar changes occur
when the head is tilted forwards or backwards (called pitch).
 Unlike the semi-circular canals, the otoliths detect translational or linear movements, including:

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

Otoconia

 Otoconia are little calcium carbonate crystals embedded in the otolithic membrane. Head tilt and
linear head motion cause displacement of the otoconial complex, producing a shearing force that
deflects the hair bundles and subsequently depolarizes the sensory hair cells. These electrical signals
are then relayed to the central nervous system (CNS) by the afferent vestibular nerve, which jointly
with other proprioceptive information, stimulate the CNS to initiate neuronal responses for
maintaining body balance.

 The correct formation and anchoring of otoconia is essential for optimal vestibular function and
maintaining body balance. Otoconia abnormalities are common and can cause vertigo and
imbalance in humans

Side Note: Benign Paroxysmal Positional Vertigo (BPPV) is thought to be caused by dislodging of calcium
carbonate crystals (otoconia) from the otolithic membrane in the utricle which migrates into one of the semi-
circular canals of the inner ear. This dislodgment physically displaces hair cells on movement and creates
persistent action potentials until the response is fatigued, generally within 30 to 60 seconds.

Dizziness is a common symptom post and the health professional needs to be able to differentiate
dizziness from vertigo. Vertigo is most often characterised with nystagmus and dizziness particularly
with positional changes of the head.

 In summary, the hair cells of the canals and otoliths convert the mechanical energy generated by
head motion into neural discharges directed to specific areas of the brainstem and the cerebellum.
With their special orientation, the SCC’s and otolithic organs can respond selectively to head motion
in particular directions. It is important to remember that the otoliths and semi-circular canals have
different fluid mechanics: SCC’s measure angular velocity whereas the otoliths measure linear
acceleration.

Planes of Movement

The vestibular system has three planes of movement. Each plane of movement has two semi-circular
canals in it, so there are three coplanar pairs.

 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)