By Marcello Cherchi, MD PhD
For patients
We use the term “vestibular weakness” to refer to a situation in which there is diminished balance-related information traveling from the inner ear to the brain. The vast majority of such cases are caused by diseases affecting either the inner ear itself, or the nerve between the ear and the brain, or both. Some of these diseases preferentially affect just one ear, while others affect both ears.
In many instances it is possible for vestibular testing to identify that vestibular weakness is present, but that identification alone does not reveal the underlying cause. The underlying cause of vestibular weakness can sometimes be figured out from other tests, or may be suggested by a patient’s clinical history.
Most causes of vestibular weakness do not have a direct treatment — in the sense of an intervention that reverses or “undoes” the vestibular weakness.
Almost irrespective of the cause of vestibular weakness, the treatment is usually the same: vestibular physical therapy specifically targeting vestibular weakness. Such therapy usually relies on strategies such as sensory substitution, adaptation and habituation. While vestibular rehabilitation therapy does not restore inner ear function, it stands some chance of making a patient less uncomfortable, improving the level of function in daily activities, and reducing fall risk.
For practitioners
We use the term “vestibular weakness” to refer to any situation or disease process that reduces the flow of vestibular information traveling from the labyrinth to the vestibular nuclei. Such situations can be unilateral or bilateral, abrupt or gradual in onset, instantaneous or progressive, transient or irreversible. Some examples of each include:
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Usually unilateral |
Bilateral versions of usually unilateral disease |
Bilateral |
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Usually acute onset |
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Usually subacute onset |
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Usually gradual onset |
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Vestibular weakness may be suspected from the clinical history. The suspicion may increase based on physical examination findings — for example, unilateral weakness may be suspected based on the finding of spontaneous unidirectional horizontal nystagmus on video Frenzel oculography, or bilateral vestibular weakness may be suspected by low retinal gain on ophthalmoscopy or poor performance on dynamic visual acuity testing.
A practical next step is corroboration with objective vestibular testing, such as with vestibular evoked myogenic potentials, video head impulse testing, caloric testing and rotatory chair testing. In some instances it may be appropriate to check less common tests, such as fundus photography or optical coherence tomography to identify ocular torsion.
If vestibular weakness is verified, then the differential diagnosis will be narrowed by ascertaining whether the weakness is unilateral or bilateral, by the chronology (acute, subacute or gradually progressive), by other aspects of the clinical history (e.g., medications), by other otologic testing (e.g. unilateral predominantly high frequency hearing loss ipsilateral to the vestibular weakness suggests labyrinthitis; unilateral predominantly low frequency hearing loss ipsilateral to the vestibular weakness suggests Ménière’s disease) and by imaging (e.g., vestibular schwannoma).
In some situations it may be possible to identify on vestibular testing that vestibular weakness is present, yet difficult or impossible to determine the underlying etiology.
If a reversible cause of vestibular weakness is identified (such as pharmacologic vestibular suppression), then this should be treated.
If a treatable cause of vestibular weakness is identified (such as autoimmune inner ear disease), then this should be treated.
If the etiology cannot be identified, then referral to vestibular rehabilitation therapy is appropriate.
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