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Original Editor - Jess Bell based on the course by Bernard Tonks
Top Contributors - Jess Bell and Kim Jackson
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Introduction[edit | edit source]

As discussed here, there are a number of conditions that can cause dysfunction of the vestibular system. Examples of vestibular pathologies include:

  • Vestibular labyrinthitis or neuritis (also termed neuronitis)
  • Labyrinthine concussion (unilateral vestibular lesions or bilateral vestibular lesions) or post-concussion syndrome
  • Benign paroxysmal positional vertigo (BPPV)
  • Perilymphatic fistula
  • Primary endolymphatic hydrops (Meniere’s disease)
  • Secondary endolymphatic hydrops (traumatic, infections etc)
  • Utricular dysfunctions
  • Superior canal dehiscence syndrome (congenital, but trauma can also ‘activate’)
  • Central vestibulopathies (sensory integration dysfunctions)
  • Drug toxicity
  • Persistent Postural-Perceptual Dizziness (PPPD)
  • Mal de Debarquement Syndrome (MdDS)

A detailed subjective and objective assessment is necessary when treating patients with vertigo or dizziness to determine the most effective treatment for each patient.

Subjective Evaluation[edit | edit source]

When taking a subjective history, the following questions should be asked:[1]

  • How long do the episodes of dizziness or vertigo last (i.e. seconds, minutes or hours)?
  • Does the patient have vertigo or more generalised dizziness and disequilibrium (or both)?
  • Has the patient had any medical investigations or been given a diagnosis?
  • Does the patient have a history of head trauma or other precipitating factors?
  • Does the patient experience symptoms with visual tasks or in complex, motion rich environments?

It is also important to consider the following conditions or symptoms in the subjective interview.

Mal de Debarquement Syndrome (MdDS)[edit | edit source]

MdDS is a form of sensory integration dysfunction. If a patient complains of a rocking or swaying sensation (i.e. as if they are on a ship) MdDS should be considered in a differential diagnosis.[2]

The vestibular system must be able to adapt to continuous passive motion – for example while travelling at sea - and then re-adapt when back on land. In MdDS, this re-adaptation does not occur. The symptoms of rocking / swaying persist sometimes for months and occasionally for years.[3] Typically MdDS patients feel better when they are in motion.[1][2]

Motion Sickness[edit | edit source]

Asking about motion sickness in the subjective assessment of vestibular patients is relevant because a history of motion sickness indicates that:[1]

  • A patient’s central nervous system chooses strategies to manage sensory conflict that are not adaptive
  • There is a sensory mismatch between vestibular and visual cues[1][4]

Oscillopsia[edit | edit source]

Oscillopsia is the subjective illusion of visual motion  - it is caused by a malfunction of the vestibulo-ocular reflex (VOR).[5] It can only occur when an individual’s eyes are open and it frequently presents with bilateral peripheral vestibular lesions (BVL).[1]

Floating, Swimming, Spinning Inside the Head[edit | edit source]

These symptoms are frequently associated with anxiety, depression and somatoform disorders - the vestibular system does not tend to causes these types of sensations.[1]

Vertical Diplopia[edit | edit source]

Vertical diplopia is a type of double vision where the individual sees two images, which line up vertically:[1]

  • Symptoms disappear if either eye is closed
  • It is often caused by skew eye deviation and is due to an otolith dysfunction or otolith processing issue

Vertigo[edit | edit source]

Vertigo is defined as the Illusion of movement of self or the environment. It is an entirely subjective phenomenon. If vertigo is related to a dysfunction of the vestibular system, it will be due to a sudden imbalance of tonic neural output.[1]

Lightheadedness or Presyncope[edit | edit source]

These symptoms are related to orthostatic hypotension - they are not a vestibular symptom.[1]

It is important in the subjective interview to determine the circumstances which provoke symptoms. For example, find out if symptoms:[1]

  • Are provoked by certain movements of the head and body, or in situations where there is visual-vestibular-somatosensory mismatch
  • Occur in busy, noisy and motion rich environments
  • Be related to specific visual tasks and activities

For a summary of the key symptoms of dizziness and their underlying mechanisms, please see Table 1.

Table 1. Symptoms of Dizziness
Symptoms Mechanisms
Disequilibrium - imbalance or unsteadiness while standing or walking Loss of vestibulospinal, proprioceptive, visual, motor function, joint pain or instability and psychological factors
Lightheadedness or presyncope Decreased blood flow to the brain
Sense of rocking or swaying as if on a ship (MdDS) Vestibular system adapts to continuous, passive motion and must re-adapt once the environment is stable
Motion sickness Visual-vestibular mismatch
Nausea and vomiting Stimulation of medulla
Oscillopsia - illusion of visual motion Spontaneous: acquired nystagmus

Head-induced: severe, bilateral loss of VOR

Floating, swimming, rocking, and spinning inside of head Anxiety, depression, and somatoform disorders
Vertical diplopia Skew-eye deviation
Vertigo - rotation, linear movement, tilt Imbalance of neural activity to vestibular cerebral cortex

Falls[edit | edit source]

Patients with UVL do not tend to fall more than their age-matched peers. However, patients with BVLs have been found to be more at risk of falling:[1]

  • The risk of falling increases in those who have fallen more than twice in the past 6 months

Questions to ask include:[1]

  • Was the individual injured in the fall?
  • When and how did the fall occur?
  • Has the individual changed his / her lifestyle due to the fall?

Functional Status[edit | edit source]

Subjective Outcome Measurement[edit | edit source]

The Dizziness Handicap Inventory (DHI or DI) can be useful for both the subjective evaluation of vestibular patients and as an outcome measure. It enables the clinician to measure a patient’s perception of his / her disability[1] - i.e. the impact of the dizziness on his / her quality of life.[6] Items relate to functional, emotional and physical problems.[7]

A score of 16 to 34 indicates the patient perceives his/ her dizziness as mild. A score of 36 to 52 suggests moderate symptoms and a score of over 54 suggests a perception that the dizziness is severe.[1]

Psychosocial Status[edit | edit source]

Psychosocial status has to be considered due to the disruptive influence of anxiety on vestibular symptoms, which leads to diminished outcomes for patients.[1][8]

The Positive and Negative Affective Scale (PANAS) can be used for vestibular patients. It is a screening scale for the presence of anxiety or depression, but it is important to note that it does not indicate the cause of symptoms.[1]

Cognitive Vestibular Interactions[edit | edit source]

Individuals with vestibular dysfunction might also present with cognitive dysfunction[9] including decreased memory, compromised concentration and impaired abilities when multitasking.[1]

  • There are projections of pathways from the vestibular system to the cortex[10]
  • A recent study by Brandt and colleagues suggested that “moving towards a concept of higher vestibular disorders” would be helpful [10]
  • This interaction between cognitive and vestibular dysfunction probably represents problems with sensory integration (visual, vestibular)[10]

Objective Evaluation[edit | edit source]

Vision Screening[edit | edit source]

Oculomotor screen[edit | edit source]

When conducting any vision screening or testing, it is important to watch and ask the patient how must effort a task requires and the degree of symptoms provoked. The basic oculomotor screen during a vestibular assessment should include:[1]

  • Fixation in primary and eccentric gaze
  • Smooth pursuit or tracking
  • VOR cancellation
  • Saccades

Oculomotor Testing[edit | edit source]

Spontaneous Nystagmus[edit | edit source]

  • Tested in primary and eccentric gaze
  • It occurs due to the unopposed tonic neural activity of the intact side when there are lesions in the peripheral vestibular systems (acute) or central vestibular pathways[1]

Primary gaze is tested as follows: [1]

  • The patient looks forward and visually fixates on a target
  • This position is held for 10 seconds and the therapist looks for any nystagmus

Eccentric gaze:

The most common pathological type of nystagmus driven by the CNS is gaze evoked nystagmus (GEN). It is tested as follows:[1]

  • The patient to fixate on a position 30 degrees to each side, up and down (i.e. an eccentric position)
  • Each position is held for 10 seconds and the therapist looks for nystagmus
  • GEN is only present with eccentric gaze, not in primary gaze

It is important to differentiate between GEN and end point nystagmus. End point nystagmus occurs when gaze is held at the end of range. End point nystagmus is considered normal, so in order to test for GEN it is essential that the patient only holds his / her gaze 30 degrees off-centre.[1][11]

For a summary of the difference between peripheral and central nystagmus, please see Table 2.

Table 2. Peripheral versus Central Nystagmus
Findings Peripheral Central
Effect of fixation  (room light) Nystagmus is typically absent within 2-3 days in room light Nystagmus either does not change or it increases
Direction of nystagmus Usually mixed plane (horizontal and torsional) Usually single plane (sustained down beating)
Effect of gaze Nystagmus increases with gaze toward direction of quick phase Nystagmus either does not change or it reverses direction

Smooth Pursuit and VOR Cancellation[edit | edit source]

  • Slow, tracking eye movements that maintain images of smaller moving targets (20 to 30 degrees per second) on the fovea.[1][12]
  • Centrally mediated reflex[1]

Smooth Pursuit Eye Movements[edit | edit source]

  • Refixation saccades occur during target motion toward the side of the lesion
  • There may be unilateral or bilateral refixation saccades[1]

VOR Cancellation[edit | edit source]

  • Head and eyes move with a target - suppressing the VOR
  • Refixation saccades will occur during head movement toward the side of the lesion[1]

Smooth Pursuit Torsion Test[edit | edit source]

  • The smooth pursuit neck torsion test measures smooth pursuit eye movement with the head / trunk in neutral and when the trunk and neck are rotated relative to a stationary head[13]
  • Smooth pursuit neck torsion test is considered to be specific for detecting eye movement disturbances due to altered cervical sensory input[14][15]
  • A decrease in velocity gain of smooth pursuit eye movements during the test is only seen in patients with neck pain[1]

Saccadic Eye Movements[edit | edit source]

Saccades are defined as: “fast conjugate eye movements that shift the eyes from one target to another, bringing an object of interest into focus on the fovea where visual acuity is highest”.[16]

Saccades are centrally mediated – there are volitional saccades and reflexive saccades[17][18]

In order to test saccadic eye movements:[1]

  • Instruct the patient to look between two targets as quickly as possible – vertical and horizontal
  • During these fast changes in eye position, the therapist looks at the amplitude, velocity and accuracy of targeting
    • Hypometric saccade =  when the patient ‘undershoots’ the target
    • Hypermetric saccade = when the patient ‘overshoots’ the target[19]

One hypometric saccade is typically considered normal. Two or more hypometric or one or more hypermetric saccades is considered abnormal.[1]

Vestibulo-Ocular Reflex (VOR) Testing

  • The VOR is the primary mechanism for gaze stability during head movement
  • There are two tests of VOR function that can be done effectively  in the clinic without an infrared camera system
  1. The Head Thrust Test
  2. The Dynamic Visual Acuity (DVA) Test

The Head Shaking Test can also be conducted, but it works better with an infrared camera system. WEB

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 Tonks B. Vestibular Assessment Course. Physioplus, 2021.
  2. 2.0 2.1 Saha KC, Fife TD. Mal de débarquement syndrome: Review and proposed diagnostic criteria. Neurol Clin Pract. 2015;5(3):209-15.
  3. Cha YH, Brodsky J, Ishiyama G, Sabatti C, Baloh RW. Clinical features and associated syndromes of mal de debarquement. J Neurol. 2008;255(7):1038-44.
  4. Koch A, Cascorbi I, Westhofen M, Dafotakis M, Klapa S, Kuhtz-Buschbeck JP. The Neurophysiology and Treatment of Motion Sickness. Dtsch Arztebl Int. 2018;115(41):687-96.
  5. Hain TC, Cherchi M, Yacovino DA. Bilateral vestibular weakness. Front Neurol. 2018;9:344.
  6. Tamber AL, Wilhelmsen KT, Strand LI. Measurement properties of the Dizziness Handicap Inventory by cross-sectional and longitudinal designs. Health Qual Life Outcomes. 2009;7:101.
  7. Mutlu B, Serbetcioglu B. Discussion of the dizziness handicap inventory. J Vestib Res. 2013;23(6):271-7.
  8. Saman Y, Bamiou DE, Gleeson M, Dutia MB. Interactions between stress and vestibular compensation - a review. Front Neurol. 2012;3:116.
  9. Rizk HG, Sharon JD, Lee JA, Thomas C, Nguyen SA, Meyer TA. Cross-sectional analysis of cognitive dysfunction in patients With vestibular disorders. Ear Hear. 2020;41(4):1020-7.
  10. 10.0 10.1 10.2 Brandt T, Strupp M, Dieterich M. Towards a concept of disorders of "higher vestibular function". Front Integr Neurosci. 2014;8:47.
  11. Serra A, Leigh RJ. Diagnostic value of nystagmus: spontaneous and induced ocular oscillations. J Neurol Neurosurg Psychiatry. 2002;73(6):615-8.
  12. Purves D, Augustine GJ, Fitzpatrick D, et al., editors. Neuroscience. 2nd edition. Sunderland (MA): Sinauer Associates; 2001. Types of Eye Movements and Their Functions. Available from: https://www.ncbi.nlm.nih.gov/books/NBK10991/
  13. Tjell C, Rosenhall U. Smooth pursuit neck torsion test: a specific test for cervical dizziness. Am J Otol. 1998;19(1):76-81.
  14. Daly L, Giffard P, Thomas L, Treleaven J. Validity of clinical measures of smooth pursuit eye movement control in patients with idiopathic neck pain. Musculoskelet Sci Pract. 2018;33:18-23.
  15. Majcen Rosker Z, Vodicar M, Kristjansson E. Inter-visit reliability of smooth pursuit neck torsion test in patients with chronic neck pain and healthy individuals. Diagnostics (Basel). 2021;11(5):752.
  16. Termsarasab P, Thammongkolchai T, Rucker JC, Frucht SJ. The diagnostic value of saccades in movement disorder patients: a practical guide and review. J Clin Mov Disord. 2015;2:14.
  17. Patel SS, Jankovic J, Hood AJ, Jeter CB, Sereno AB. Reflexive and volitional saccades: biomarkers of Huntington disease severity and progression. J Neurol Sci. 2012;313(1-2):35-41.
  18. McDowell JE, Dyckman KA, Austin BP, Clementz BA. Neurophysiology and neuroanatomy of reflexive and volitional saccades: evidence from studies of humans. Brain Cogn. 2008;68(3):255-270.
  19. Bourrelly C, Quinet J, Goffart L. Pursuit disorder and saccade dysmetria after caudal fastigial inactivation in the monkey. J Neurophysiol. 2018;120(4):1640-54.