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Treatment of Specific Types of Nystagmus

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Pediatric Ophthalmology, Neuro-Ophthalmology, Genetics

Part of the book series: Essentials in Ophthalmology ((ESSENTIALS))

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Abstract

■ The function of the ocular motor system is to hold images stable on the fovea. The vestibular system and the vestibulo-ocular reflex (VOR) also play an important role in this function. The VOR connects the peripheral vestibular endorgans – the semicircular canals and otoliths – with their appropriate pair of eye muscles via a three-neuronal arc.

■ A direct result of the inability to maintain stable foveal vision is acquired or congenital nystagmus, which causes decreased visual acuity, blurred vision, and the illusion that the observed surroundings are moving (i.e., oscillopsia).

■ Vestibular neuritis is characterized by an acute rotatory vertigo with horizontalrotatory nystagmus and ipsilateral perceptual deficits and falls. It most likely has a viral etiology. Patients with vestibular neuritis should be given cortisone (e.g., methylprednisolone) as early as possible (within the first 3 days after disease onset), since it significantly improves the long-term outcome.

■ Early physical therapy, at least two times a day, has been proven to normalize impaired body sway of patients with vestibular neuritis within 2–3 weeks. All these exercises are used to recalibrate the VOR in its three major planes of action for perfect eye–head coordination.

■ Antivertiginous drugs are contraindicated for patients with chronic dizziness or positioning vertigo, since these drugs suppress central compensation.

■ There is growing evidence that vascular compression of the trochlear nerve, as occurs in trigeminal neuralgia, must be assumed to be the underlying cause of superior oblique myokymia. Patients with longer-lasting symptoms should be administered anticonvulsants (carbamazepine, gabapentin).

■ Central vestibular disorders frequently occur as a dysfunction in the sagittal (pitch) plane. Examples are downbeat (DBN) and upbeat (UBN) nystagmus, which are caused by paramedian lesions of the ponto-medullary brainstem or the cerebellar flocculus. The pathophysiology is still not completely understood. The individual components of DBN can differ, since there are obviously several pathogeneses: a vestibular one with imbalance in the graviceptive VOR (impairment in the projection of otolithic information), or imbalance due to dysfunction of the neuronal ocular motor integrator, the saccade-burst generator, or the vertical smooth pursuit system.

■ The treatment of patients with persisting DBN and UBN should include GABAergic substances such as baclofen and clonazepam, gabapentin (probably a calcium channel blocker), and the potassium channel blocker 4-aminopyridine.

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  1. Neurologische Klinik, Universität Mainz, Langenbeckstraße 1, 55101, Mainz, Germany

    Marianne Dieterich

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  1. Marianne Dieterich
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Birgit Lorenz Francois-Xavier Borruat

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Dieterich, M. (2008). Treatment of Specific Types of Nystagmus. In: Lorenz, B., Borruat, FX. (eds) Pediatric Ophthalmology, Neuro-Ophthalmology, Genetics. Essentials in Ophthalmology. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-33679-2_16

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  • DOI: https://doi.org/10.1007/978-3-540-33679-2_16

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