Abstract
BackgroundWhen patients with ocular motor deficits come to the clinic, in numerous situations it is hard to relate their behavior to one or several deficient neural structures. We sought to demonstrate that neuromimetic models of the ocular motor brainstem could be used to test assumptions of the neural deficits linked to a patient’s behavior.MethodsEye movements of a patient with unexplained neurological pathology were recorded. We analyzed the patient’s behavior in terms of a neuromimetic saccadic model of the ocular motor brainstem to formulate a pathophysiological hypothesis.ResultsOur patient exhibited unusual ocular motor disorders including increased saccadic peak velocities (up to ≈1000 deg/s), dynamic saccadic overshoot, left-right asymmetrical post-saccadic drift and saccadic oscillations. We show that our model accurately reproduced the observed disorders allowing us to hypothesize that those disorders originated from a deficit in the cerebellum.ConclusionOur study suggests that neuromimetic models could be a good complement to traditional clinical tools. Our behavioral analyses combined with the model simulations localized four different features of abnormal eye movements to cerebellar dysfunction. Importantly, this assumption is consistent with clinical symptoms.
Highlights
Ocular flutter is an abnormal eye movement consisting of repetitive, irregular, involuntary bursts of horizontal saccades without an intersaccadic interval [1]
The physiology of this rare disorder remains unclear. It probably results from a dysfunction of brainstem ocular motor structures, in particular the paramedian pontine reticular formation (PPRF) involved in saccade generation: excitatory burst neurons (EBN), inhibitory burst neurons (IBN) and omnipause neurons (OPN)
We sought to determine if their coexistence within a single patient implies widespread lesions or dysfunctions, or whether they could result from the alteration of a focal neural structure
Summary
Ocular flutter is an abnormal eye movement consisting of repetitive, irregular, involuntary bursts of horizontal saccades without an intersaccadic interval [1] It is generally superimposed on normal ocular motor behavior and its occurrence may be facilitated by various events, such as blinks, the triggering of normal saccades or optokinetic stimulation [2,3] and has been observed during pursuit [4]. The physiology of this rare disorder remains unclear. We sought to demonstrate that neuromimetic models of the ocular motor brainstem could be used to test assumptions of the neural deficits linked to a patient’s behavior
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