A Neurobiological Approach to Acquired Nystagmus

Leigh, R. John; Das, Vallabh E.; Seidman, Scott H.

doi:10.1111/j.1749-6632.2002.tb02835.x

Cited by 41 publications

(17 citation statements)

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“…In spite of many clinical reports of downbeat nystagmus (DBN) and upbeat nystagmus (UBN) and multiple hypotheses about possible mechanisms, the pathophysiology is still under discussion [7][8][9]. In the light of several clinical findings and experimental data, a current general concept is that asymmetries in the cerebello-brainstem network that normally stabilizes vertical gaze could lead to an imbalance in structures such as (a) the vertical cerebello-vestibular Ôneural integrator', (b) the central connections of the vertical VOR including both the semicircular canal and the otolith responses, or (c) the vertical smooth pursuit system.…”

Section: Vestibular Syndromes In the Sagittal (Pitch) Planementioning

confidence: 99%

Central vestibular disorders

Dieterich

2007

J Neurol

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Dizziness or vertigo is an erroneous perception of selfmotion or object-motion as well as an unpleasant distortion of static gravitational orientation. It is caused by a mismatch between the vestibular, visual, and somatosensory systems. Thanks to their functional overlap, the three systems are able to compensate, in part, for each other's deficiencies. Thus, vertigo is not a well-defined disease entity, but rather a multisensory syndrome that results when there is a pathological dysfunction of any of the stabilizing sensory systems (e.g., central vestibular disorders, peripheral vestibular diseases with asymmetric input into the vestibular nuclei). This article provides an overview of the most important and frequent forms of central vestibular vertigo syndromes, including basilar/vestibular migraine, which are characterized by ocular motor, postural, and perceptual signs. In a simple clinical classification they can be separated according to the three major planes of action of the vestibulo-ocular reflex: yaw, roll, and pitch. A tonic imbalance in yaw is characterized by horizontal nystagmus, lateropulsion of the eyes, past-pointing, rotational and lateral body falls, and lateral deviation of the perceived straight-ahead. A tonic imbalance in roll is defined by torsional nystagmus, skew deviation, ocular torsion, tilts of head, body, and the perceived vertical. Finally, a tonic imbalance in pitch can be characterized by some forms of upbeat or downbeat nystagmus, fore-aft tilts and falls, and vertical deviation of the perceived straight ahead. The thus defined syndromes allow for a precise topographic diagnosis as regards their level and side.

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Section: Vestibular Syndromes In the Sagittal (Pitch) Planementioning

confidence: 99%

Central vestibular disorders

Dieterich

2007

J Neurol

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“…Patients with acquired fixational pendular nystagmus (APN), a very distressing oculomotor finding in multiple sclerosis (MS), often experience oscillopsia and blurred vision, all of which interfere with their ability to read, watch television, or even to visually stabilize their posture [23,26,43]. The pathophysiology and exact site of the causal lesions are not yet known [1,11,26,40].…”

Section: Introductionmentioning

confidence: 98%

Acquired pendular nystagmus in multiple sclerosis: an examiner-blind cross-over treatment study of memantine and gabapentin

Starck¹,

Albrecht²,

Pöllmann³

et al. 2009

J Neurol

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A prospective examiner-blind, cross-over study was conducted to compare the efficacy of memantine (40 or 60 mg/day) and gabapentin (1,200 mg/day) as therapy for acquired fixational pendular nystagmus (APN) in 11 patients with multiple sclerosis. APN was documented in 20 eyes by electrooculography (EOG). The primary objective of the study was an at least 50% reduction in amplitude and/or frequency of APN compared with baseline values in EOG. This aim was reached for 17 of 20 APN-affected eyes with memantine 40-60 mg and for 11 eyes with gabapentin up to 1,200 mg. A complete cessation of APN was achieved in eight eyes (four patients) with memantine 40 mg and in a further four eyes (two patients) with memantine 60 mg. One patient achieved the same benefit with memantine 40 mg and gabapentin. In two other eyes APN completely subsided with gabapentin 1,200 mg only, but not with memantine. Near visual acuity, a secondary outcome parameter, improved by at least 0.1 in 11 of 17 eyes treated with memantine and in 8 out of 16 eyes treated with gabapentin. In summary, memantine and gabapentin are safe and effective treatment options for APN.

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“…Some agents, such as cannabis and alcohol 27 , are not viable treatments during everyday activities because of their sideeffects; however, they may provide clues leading to new drug strategies. Before any agent can be regarded as an effective treatment for nystagmus, a controlled masked trial is essential 28 .…”

Section: Drug Treatments For Nystagmusmentioning

confidence: 99%