An Overview of Vestibular Dysfunction and Rehabilitation in

Individuals with Brain Injury

Janet Callahan PT, DPT, MS, NCS

The Numbers

TBI Rates

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Brain Injury and Vestibular Dysfunction

BPPV CENTRAL PERIPHERAL

% R

ange

of

Pat

ien

ts

0

80

40

20

60

30

10

50

70

Maskell F et al, 2009

9 – 71% of patients experienced dizziness

Faaq C 2007, Smith PF 2013, Besnard S 2015, Yardley L 1998, Black O 2004, Bigelow RT 2015

• Impaired gaze stability • Impaired postural control • Impaired eye-hand coordination • Impaired executive function • Impaired spatial orientation • Impaired motion perception • Impaired attention • Impaired memory • Impaired cognition • Fatigue

Implications of Vestibular Dysfunction

Role of the Vestibular System

• Stabilize visual images on the fovea of the retina during head movements to allow clear vision

• Maintain postural stability during head movements

• Provide information used for spatial orientation – ability to maintain our body orientation and/or

posture in relation to the surrounding environment at rest and during motion

Zee D, Leigh J, Neurology of Eye Movements

Components of the Vestibular System

Hain TC, et al. Anatomy and Physiology of the Vestibular System. In Herdman SJ (ed): Vestibular Rehabilitation. FA Davis, Philadelphia, PA, 2000, p4.

Motor Neurons

Vestibular

Primary processor (Vestibular nuclear

complex)

Adaptive processor

(Cerebellum)

Eye Movements (VOR)

Postural Movements

(VSR) Proprioception

Visual

other CNS

processing

Herdman S . (2007) Vestibular Rehabilitation (3rd ed.)

Peripheral Vestibular Apparatus

• 3 Semicircular Canals – Angular acceleration

• Anterior

• Posterior

• Lateral

• 2 Otolith organs – Linear acceleration/gravity

• Utricle

• Saccule

• Work in complimentary pairs

• One side is excited while other side is inhibited

Bony Labyrinth

Membranous

Labyrinth

Perilymph

Endolymph

Semicircular Canal Receptors

CUPULA

OTOLITHS

VESTIBULAR SYSTEM

Hain TC, et al. Anatomy and Physiology of the Vestibular System. In Herdman SJ (ed): Vestibular Rehabilitation. FA Davis, Philadelphia, PA, 2000, p4.

Motor Neurons

Vestibular Primary processor (Vestibular nuclear

complex)

Adaptive processor

(Cerebellum)

Eye Movements (VOR)

Postural Movements

(VSR) Proprioception

Visual

other CNS

processing

Landing pad/relay station for all sensory inputs

Central Vestibular Projections

Vestibular Nuclear Complex Vestibulo-Cerebellum

Monitors vestibular receptor activity Calibrates the Vestibular Ocular Reflex

Fine tunes eye movements

Central Vestibular Projections

• Thalamus – Discriminates between self movement vs. that of the

environment – Multisensory integration for

postural control

• Vestibular Cortex – Junction of parietal and

insular lobe – Multisensory integration of

vestibular information with somatosensory and visual input

http://www.sciencedirect.com/science/article/pii/S1053

811911014340

VESTIBULAR SYSTEM

Hain TC, et al. Anatomy and Physiology of the Vestibular System. In Herdman SJ (ed): Vestibular Rehabilitation. FA Davis, Philadelphia, PA, 2000, p4.

Motor Neurons

Vestibular Primary processor (Vestibular nuclear

complex)

Adaptive processor

(Cerebellum)

Eye Movements (VOR)

Postural Movements

(VSR) Proprioception

Visual

other CNS

processing

Vestibular Motor Projections

Gaze stabilization

Vestibulo-Ocular Reflex

(VOR)

Postural Control

Vestibulo-Spinal Reflex

(VSR)

Via Cranial Nerve VIII to vestibular nuclear complex

At Rest

0

80-100

RIGHT LEFT

Spik

es/S

ec

What happens with head movement? S

pik

es/S

ec

0

200

RIGHT LEFT

Assymetrical input indicates to CNS that the head is moving

Right side excited Left side inhibited

Head Turn Right

What if receptor(s) or CN VIII is not functioning?

0

80-100

RIGHT LEFT

Head Turn Right

Spik

es/S

ec

CNS receives inadequate information about head movement Compensatory eye movement is absent or inadequate

Impaired gaze stability (VOR) and postural control (VSR)

Left side inhibited

What happens when the head rotates continuously? (Real or Perceived)

Nystagmus

Nystagmus

•Involuntary rhythmic conjugate eye movement •May be spontaneous, gaze-evoked or positional •Named for fast phase

PERIPHERAL •Engaged when head

rotation exceeds the limits of eye rotation to produce a slow phase eye movement

(VOR) in one direction and a fast phase saccadic “reset”

back towards primary position

•Damage to vestibular receptor or nerve

CENTRAL Occurs as a result of a

number of different brain conditions or damage to

certain brain (stem) structures

Nystagmus

VOR maintains fixation on

target

Saccadic reset to reposition eye in center of socket

Slow Phase Fast Phase

See repetitive cycles of VOR to stabilize gaze

followed by saccadic re-set

In the event of continuous head rotation…………..

Clinical Finding Central Peripheral

Complaints of Vertigo Vertigo less common. More often disequilibrium, dizziness, unsteadiness

More Common

Nystagmus: •Spontaneous •Positional •Gaze-evoked

Single Plane: (upbeating, downbeating, torsional)

Direction Changing: gaze-evoked nystagmus greater towards side of lesion

Mixed Plane: (vertical-torsional, horizontal-torsional) Non-direction changing Increases with gaze to more neurally active side Increases in direction of quick phase

Suppression of Nystagmus with Visual Fixation (no Frenzels)

NO- nystagmus remains the same or increases

YES- nystagmus decreases

Lesion Location

PERIPHERAL STRUCTURES

• Vestibular end organ

• Vestibular nerve

CENTRAL STRUCTURES • Brainstem • Cerebellum • Thalamus • Insular Cortex

Peripheral Vestibular System

Damage to Peripheral Receptor Labyrinthine Concussion

https://www2.aofoundation.org/wps/portal/surgerymobile?contentUrl=/srg/93/01

Damage to Peripheral Receptor Benign Paroxysmal Positional Vertigo

Damage to Peripheral Receptor Perilymphatic Fistula

• Damage to Round or oval window

• Sound or pressure induced vertigo and or nystagmus

• Symptoms increase with activity

• Often associated with head trauma

• Surgical repair if doesn’t seal over with bedrest

Round Window

Oval Window

Damage to Vestibular Nerve Unilateral Vestibular Hypofunction

Vestibular Nerve

Examination

Examination

• History

• Oculomotor Examination

• Vestibular System Function

• Postural Control

DIZZINESS Symptoms

• Vertigo

– Illusion of movement; Spinning

• Lightheadedness

– Feeling in head; feeling faint

• Dysequilibrium

– Off balance; unsteadiness; stagger

• Oscillopsia

– Visual blurring with head motion

Dizziness What do patients call it?

• Spinning

• Balance problems

• Fogginess

• Spaciness

• Lightheadedness

• Like being on a boat

• Rocking

• Feeling “off”

Pattern of Symptom Occurrence

• Circumstances

– Spontaneous

– Position change

– Eye, head or body movement

– Environment

– Activities

– Coughing or sneezing

• Intensity

• Duration – Intermittent

• Minutes

• Hours

– Constant

• Timing – Acute vs. Chronic

– Onset • Sudden

• Gradual

Peripheral Vestibular Dysfunction Pattern of Symptoms

Disorder Tempo Symptoms Circumstances

Vestibular Nerve Injury

Sudden onset; Acute Dizziness

(May not be noticed due to LOC)

Vertigo, disequilibrium, N/V,

oscillopsia

Spontaneous, exacerbated by head

movement

Unilateral Vestibular Hypofunction

Chronic Dizziness

Dizziness, disequilibrium

Induced by head movement, complex

environments, altered sensory

inputs

Bilateral Vestibular Hypofunction

Chronic Dizziness Lightheadedness, Dizziness,

disequilibrium

Induced by head movement, complex

environments, altered sensory

inputs

BPPV Sudden onset; Spells of dizziness lasting

seconds

Vertigo, lightheaded, N/V

Induced by positional change: lying down, sitting

up, rolling over

Eye Movements

Examination of Oculomotor Control

What is so important about the oculomotor system?

• Vestibulo-Ocular Reflex involves eye movements and is fully integrated with other oculomotor control systems

• VOR occurs in combination with pursuit, saccades and vergence eye movements

• Impairments in these oculomotor control systems = central vestibular dysfunction

Symptoms of Oculomotor Disturbances

• Blurred vision

• Double vision

• Oscillopsia

• Dysequilibrium/Falls

• Frontal headache

• Fatigue

• Difficulty reading

• Difficulty attending

• Difficulty in school

• Difficulty using computers

• Difficulty with target accuracy

• Difficulty with depth perception

Eye Movement Examination

• Alignment/Fixation

• Extraocular Movements

• Gaze Holding – End range

– 30 degrees

• Pursuit

• Saccades

• Vergence

• VOR

Ocular misalignments result in impaired eye-head coordination

HYPOTROPIA

EXOTROPIA ESOTROPIA HYPERTROPIA

Ocular Misalignments

Six Extra-ocular Muscles Controlled by Three Cranial Nerves

http://www.cs.txstate.edu/~uj1001/pictures/eye_muscles.gif

CN VI CN IV

CN III

CN III

CN III

CN III

http://quizlet.com/9891924/week-03-jack-and-his-spots-flash-cards/

Extraocular Movements

Oculomotor Nuclei within the Brainstem

Blumenfeld, 2002

Trochlear (CN IV) nucleus

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RA

IN

Extra-ocular Movements

• Determine if ROM of eyes is full and gaze is conjugate (eyes move together)

• Abnormality indicates potential cranial nerve abnormality

• Effects coordination of eyes with one another

• Results in Diplopia

Cranial Nerve Palsies

CN III Oculomotor • Lesion:

– Monocular deviation in primary gaze “down and out”

– No adduction or upward vertical eye movements

– Eyelid ptosis

– Impaired pupillary light reflex

– Diplopia worse looking away from side of lesion

• Innervates all eye muscles except lateral rectus and superior oblique

Cranial Nerve Palsies

CN IV Trochlear • Innervates Superior

Oblique • Lesion: – Monocular deviation up

and extorted

– Cannot look down and out in primary position

– Adopts head tilt to accommodate elevation and rotation

Cranial Nerve Palsies

CN VI Abducens

• Innervates lateral rectus

• Lesion:

– Esotropia in primary gaze (inward)

– Cannot Abduct

– Diplopia worse looking towards side of lesion

Right Gaze Primary Gaze Left gaze

Gaze-Evoked Nystagmus

• Peripheral

– Resting tone imbalance

– Unidirectional

– Beats in same direction no matter the eye location in socket

• Central

– Neural integrator dysfunction

– Direction changing

– Beats in direction of eye movement

Gaze-Evoked Nystagmus (Peripheral)

Gaze-Evoked Nystagmus (Central)

Impaired Pursuit

Hypermetric Saccades

Hypermetric Saccades

Vergence

• Moves eyes in opposite directions to keep images at different distances stable on the fovea

– Convergence

• visual axes comes together

– Divergence

• visual axis separate

• Impairment results in diplopia, blurring and eye strain

https://www.en.eyebrainpedia.com/vergence

Vestibular Function

Vestibulo-Ocular Reflex (VOR)

• Holds image steady on retina during head movements – Head turns left – Left lateral SCC hair cells are

excited, while right are inhibited – Vestibular nerve to vestibular

nuclei to oculomotor nuclei – Stimulates ipsilateral (left) CN III:

medial rectus and contralateral CN VI: lateral rectus

– Eyes turn right

• Impairments result in reduced gaze stability, visual blurring, impaired postural control

Head Thrust Videos

Head Thrust

Positional Provocational Testing BPPV

Herdman, SJ & Tusa, RJ. Chapter 17; Vestibular Rehabilitation (3rd edition)

Roll Test for Lateral Canals

http://www.webmd.com/hw/health_guide_atoz/zm2447.asp

Dix-Hallpike Test for Vertical Canals

Central vs. Peripheral

Clinical Finding

Central Peripheral

Saccades impaired YES NO

Smooth pursuit impaired YES (may also be impaired with advanced age)

NO

Convergence impaired YES NO

VOR impaired YES YES

Head Thrust impaired Possible (e.g vestib. nuclei) YES to side of hypofunction

VOR Cancellation impaired YES NO

Head Shaking Nystagmus + Vertical nystagmus >2-3 beats horizontal nystagmus beating suggests peripheral. Beats towards the more neurally active side.

Interpretation What does it all mean? Peripheral Dysfunction Central

Dysfunction Mixed Dysfunction

Cause BPPV Damaged Receptor

Damage to CNS

structures

Combination

Treatment Re-positioning maneuvers

Adaptation, Substitution

exercises; Postural control

training

Adaptation, Substitution

exercises; Postural control training

Adaptation, Substitution exercises;

Postural control training

Goal Eliminate Dizziness

Optimize gaze and postural

stability

Optimize gaze and postural stability

Optimize gaze and postural stability

Prognosis Very good good fair fair

Interventions and

Outcomes

Purpose of Vestibular Rehabilitation

• Exercise approach to remediate dizziness and disequilibrium symptoms associated with peripheral and/or central vestibular dysfunction

• Based on the premise that the CNS can adapt/change in response to peripheral and central vestibular dysfunction

• In cases where the CNS cannot adapt/change, vestibular rehabilitation may be directed at substituting for vestibular dysfunction

Vestibular Compensation

• Robust, multi-faceted process of re-establishing postural control, gaze stability and spatial orientation.

• Occurs as a result of neuroplasticity

• Typifies the principles of motor learning

– Appropriate stimulus

– Work at maximal level of performance

– Allow adequate success/minimize error

– Follows principles of task specificity

Vestibular Interventions

• Adaptation:

– Improve gaze stability by increasing the gain of the VOR

• Substitution:

– Use of other strategies to replace lost or compromised function

• Postural Control Retraining

• Habituation:

– Reduce sensitivity through repeated exposure

Adaptation Exercises: Gaze Stability Exercises

X1 viewing exercises:

Head moving 20 – 300 side to side/up and down while visually fixating on a stationary target

X2 viewing exercises:

Head moving 20 – 300 side to side/up and down while visually fixating on a target moving opposite head movement

Refer to Adaptation Handout

Adaptation Exercises: X1 Viewing Exercises

Adaptation Exercises: X2 Viewing Exercises

Substitution Exercises

• Purpose: To foster the use of alternative strategies to replace the lost or compromised vestibular function

• Goals: – Improve gaze stabilization

– Maximize postural stability

– Central preprogramming

– Use of other strategies:

Corrective eye saccades

Slowed head movements

Increase use of smooth pursuit

Substitution Exercises

• Visual Fixation on Stationary Object – X1 viewing at slow speed to increase use of cervico-ocular

reflex and central pre-programming

• Active Eye Movements Between 2 Targets – Facilitates use of saccadic or smooth pursuit strategies and

central pre-programming

• Remembered/Imaginary Targets – Improve voluntary control and central pre-programming

Active Eye-Head Movement Between Two Targets

• Hold 2 targets at eye level 10-12 inches apart, head in midline

• Move eyes to one target

• Maintain eyes on target and turn head to same target

• Shift eyes to 2nd target

• Move head to 2nd target

• Repeat in opposite direction

Active Eye-Head Movement Between Two Targets

Remembered Targets

• Place target directly in front of you

• While looking at the target, close eyes

• Slowly turn head away while imagining the target

• Open eyes and verify still focused on the target adjust gaze if necessary

• Repeat in multiple directions and at variable speeds

Remembered Targets

Progression of Gaze Stability Exercises

VARIABLE PROGRESSION

Duration 1 2 minutes per exercise

Frequency 2 5 times per day

Velocity Increase head speed while keeping target in focus

Target Size Large Small

Target Distance Near Far

Background Simple Complex

Position of Patient Supported sitting Walking

Support Surface Firm Compliant Wide Narrow BOS

X1 Viewing Complex Background Example

X1 Walking

©2016 Neurology Section, APTA

Clinical Practice Guideline 2016

A. Action Statement 1: EFFECTIVENESS OF VESTIBULAR REHABILITATION IN PERSONS WITH ACUTE AND SUBACUTE UNILATERAL VESTIBULAR HYPOFUNCTION. Clinicians should offer vestibular rehabilitation to patients with acute or subacute unilateral vestibular hypofunction. (Evidence quality: I; recommendation strength: Strong

A. Action Statement 2: EFFECTIVENESS OF VESTIBULAR REHABILITATION IN PERSONS WITH CHRONIC UNILATERAL VESTIBULAR HYPOFUNCTION. Clinicians should offer vestibular rehabilitation to patients with chronic unilateral vestibular hypofunction. (Evidence quality: I; recommendation strength: Strong

A. Action Statement 3: EFFECTIVENESS OF VESTIBULAR REHABILITATION IN PERSONS WITH BILATERAL VESTIBULAR HYPOFUNCTION. Clinicians should offer vestibular rehabilitation to patients with bilateral vestibular hypofunction. (Evidence quality: I; Recommendation strength: Strong)

Effectiveness of Vestibular Rehabilitation Exercises – Central Dysfunction

Brown KE et al., 2006 Retrospective Case Series: “Physical Therapy for Central Vestibular Dysfunction”

• 48 patients with central vestibular dysfunction

– Central vestibulopathy, cerebellar dysfunction, stroke, mixed central and peripheral and post-traunmatic central disorders

• Significant differences were found pre and post vestibular rehabilitation on ABC, DHI, DGI, TUG and FTSTS

• Cerebellar patients improved the least

BPPV Interventions

CRM for Posterior Canal BPPV Log Roll for Lateral Canal BPPV

Straight Head Hang for Anterior Canal

BPPV

Compliments JO Helminski

Summary

• Vestibular dysfunction can influence learning

• Oculomotor examination impairments indicate central vestibular dysfunction

• Improvements in vestibular function can lead to improved gaze stability, postural control, concentration, attention, memory etc.

I have a question

Me first

No, me first

Questions?