Abstract

Objective: Alexander's law (AL) states the intensity of nystagmus increases when gaze is toward the direction of the quick phase. What might be its cause? A gaze-holding neural integrator (NI) that becomes imperfect as the result of an adaptive process, or saturation in the discharge of neurons in the vestibular nuclei?Methods: We induced nystagmus in normal subjects using a rapid chair acceleration around the yaw (vertical) axis to a constant velocity of 200°/second [s] and then, 90 s later, a sudden stop to induce post-rotatory nystagmus (PRN). Subjects alternated gaze every 2 s between flashing LEDs (right/left or up/down). We calculated the change in slow-phase velocity (ΔSPV) between right and left gaze when the lateral semicircular canals (SCC) were primarily stimulated (head upright) or, with the head tilted to the side, stimulating the vertical and lateral SCC together.Results: During PRN AL occurred for horizontal eye movements with the head upright and for both horizontal and vertical components of eye movements with the head tilted. AL was apparent within just a few seconds of the chair stopping when peak SPV of PRN was reached. When slow-phase velocity of PRN faded into the range of 6–18°/s AL could no longer be demonstrated.Conclusions: Our results support the idea that AL is produced by asymmetrical responses within the vestibular nuclei impairing the NI, and not by an adaptive response that develops over time. AL was related to the predicted plane of eye rotations in the orbit based on the pattern of SCC activation.

Highlights

  • Alexander’s law (AL) is commonly shown by patients with spontaneous nystagmus (SN) due to a vestibular imbalance

  • When the TcNI is low, making the neural integrator (NI) “leaky,” the eyes drift centripetally on eccentric gaze so when a patient with SN looks in the direction of the slow phase, the SN is reduced, gaze is better stabilized, images move less on the retina, and vision is improved [2, 5]

  • When TcNI began to recover (TcNI > 5 s), the slow-phase velocity (SPV) of PRN had diminished into the range of 6– 18◦/s and AL was no longer present despite the residual PRN

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Summary

Introduction

Alexander’s law (AL) is commonly shown by patients with spontaneous nystagmus (SN) due to a vestibular imbalance. The nystagmus is more intense, with a higher velocity of the slow phase, when patients gaze in the direction of the quick phase [1]. AL has been attributed to a slowly developing, adaptive mechanism that lessens the slow-phase velocity of a pathological SN when gaze is in the direction of the slow phase [2]. According to this hypothesis, the neural circuit for eccentric gaze holding is “purposefully” impaired, causing the eyes to drift centripetally so that in one direction of gaze a bias from the centripetal drift opposes and diminishes the SN. When the TcNI is low, making the NI “leaky,” the eyes drift centripetally on eccentric gaze so when a patient with SN looks in the direction of the slow phase, the SN is reduced, gaze is better stabilized, images move less on the retina, and vision is improved [2, 5]

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