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Eye movements and balance 

Eye movements and balance

Eye movements and balance

Michael Strupp

and Thomas Brandt



Clinical method—expanded discussion of history-taking and clinical examination.

Treatment—pharmacological therapies for vertigo.

Specific conditions—updated notes on benign paroxysmal positioning vertigo, Menière’s disease, bilateral vestibular failure, and vestibular migraine.

Updated on 28 Nov 2012. The previous version of this content can be found here.
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date: 25 April 2017

Eye movements

The major function of eye movements is to keep the image of the visual surroundings stable on the retina, even during eye movements or head and body movements. This is achieved by (1) conjugate eye movements (both eyeballs move in parallel)—gaze-holding, smooth pursuit, saccades, vestibulo-ocular nystagmus (VOR), and optokinetic nystagmus; and (2) disconjugate eye movements—convergence and divergence.

All of these different eye movements are reflexive movements except saccades and convergence/divergence. Clinical examination of eye movements should include tests of (1) eye position (latent or manifest strabism, in particular vertical divergence/skew deviation); (2) nystagmus (in particular peripheral vestibular spontaneous nystagmus or central fixation nystagmus); (3) gaze-holding function (gaze-evoked nystagmus or endpoint nystagmus); (4) smooth pursuit (saccadic or smooth); and (5) saccades (velocity, accuracy and conjugacy). Many abnormalities of eye movements are distinctive and often indicate the site and the side of a lesion, e.g. vertical eye movements are generated and controlled in the mesencephalon, whereas horizontal eye movements are generated and controlled in the pons.

Dizziness and vertigo

Vertigo, dizziness, and disequilibrium are common complaints of patients of all ages, particularly older people, with a lifetime prevalence of about 30%. Although the anatomy and the physiology of the vestibular and ocular motor systems are complex, a correct diagnosis can be made in most patients on the basis of the patient history and the bedside examination.

Vertigo syndromes are commonly characterized by a combination of phenomena involving (1) vertigo itself—resulting from a disturbance of cortical spatial orientation; (2) nystagmus—caused by a direction-specific imbalance in the VOR, which activates brainstem neuronal circuitry; (3) postural imbalance—caused by inappropriate or abnormal activation of monosynaptic and polysynaptic vestibulospinal pathways; and (4) unpleasant autonomic responses of nausea, vomiting, and anxiety—ascending and descending vestibulo-autonomic pathways activate the medullary vomiting centre.

Clinical approach—the history is of special importance, with the patient’s symptoms giving an idea of the likely underlying cause and differentiating the different forms of peripheral and central vestibular vertigo. Patient history should focus on four aspects:

(1) Type of vertigo/dizziness (rotatory vertigo or postural imbalance; (2) duration of the symptoms (seconds, minutes, hours, days, weeks, or permanent); (3) factors that provoke, increase or alleviate the symptoms (e.g. change of head or body position, standing or walking); and (4) accompanying symptoms (in particular, brainstem or cerebellar symptoms, symptoms arising from the ear, or symptoms typical for migraine). Careful and systematic combined bedside examination of the ocular motor and vestibular systems often allows an exact topographic determination of the lesion. Additional laboratory investigations often do not contribute materially to the diagnosis.

Particular causes—more than 60% of all patients presenting with dizziness, vertigo or disequilibrium in a neurological dizziness unit will be suffering from one of the following: (1) benign paroxysmal positioning vertigo; (2) phobic postural vertigo; (3) central vestibular disorders; (4) vestibular migraine; (5) Menière’s disease; (6) vestibular neuritis.

Prognosis and treatment—many forms of vertigo have a benign cause and are characterized by spontaneous recovery of vestibular function or central compensation of a peripheral vestibular tone imbalance. Most forms of vertigo can be effectively relieved by (1) pharmacological treatment—depending on the particular cause, e.g. vestibular suppressants for symptomatic treatment, antimigraineous drugs for vestibular migraine, betahistine dihydrochloride for Menière’s disease, corticosteroids for acute vestibular neuritis, antiepileptic drugs for vestibular paroxysmia, or aminopyridines for downbeat nystagmus and episodic ataxia type 2; (2) physical therapy—liberatory manoeuvres for benign paroxysmal positioning vertigo or vestibular exercises and balance training—for uni- or bilateral vestibular failure or central forms of vertigo; (3) psychotherapy—in particular cognitive behavioural therapy for phobic postural vertigo; or (very rarely); (4) surgery for vestibular schwannoma or perilymph fistula.

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