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Neuromimetic model of saccades for localizing deficits in an atypical eye-movement pathology.

Daye PM, Optican LM, Roze E, Gaymard B, Pouget P - J Transl Med (2013)

Bottom Line: We show that our model accurately reproduced the observed disorders allowing us to hypothesize that those disorders originated from a deficit in the cerebellum.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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Laboratory of Sensorimotor Research, National Institutes of Health, Bethesda, Maryland, USA. pierre.daye@gmail.com

ABSTRACT

Background: When 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.

Methods: Eye 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.

Results: Our 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.

Conclusion: Our 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.

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Related in: MedlinePlus

Model simulation: healthy subject. Upper row represents a simulation (time course of horizontal eye position) of the model when a target is presented 25 deg to the right. Same color conventions as in Figures 5–6. Lower row represents simulation of a main sequence by the model. The gray line represents a fit computed on data extracted from Figure 1 of [24]. The blue dots represent simulations of the model for a range of amplitudes between two and 40 deg in steps of one deg.
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Figure 7: Model simulation: healthy subject. Upper row represents a simulation (time course of horizontal eye position) of the model when a target is presented 25 deg to the right. Same color conventions as in Figures 5–6. Lower row represents simulation of a main sequence by the model. The gray line represents a fit computed on data extracted from Figure 1 of [24]. The blue dots represent simulations of the model for a range of amplitudes between two and 40 deg in steps of one deg.

Mentions: The upper panel of Figure 7 shows the time course of a simulated saccadic movement toward a rightward 25 deg target. Because of the undershoot, the model generated two saccades. The first saccade ended at 22.5 deg (peak velocity: 545 deg/s) and a corrective saccade of 2.5 deg (peak velocity: 138.5 deg/s) was triggered by the model of the cortex to cancel the remaining visual error.


Neuromimetic model of saccades for localizing deficits in an atypical eye-movement pathology.

Daye PM, Optican LM, Roze E, Gaymard B, Pouget P - J Transl Med (2013)

Model simulation: healthy subject. Upper row represents a simulation (time course of horizontal eye position) of the model when a target is presented 25 deg to the right. Same color conventions as in Figures 5–6. Lower row represents simulation of a main sequence by the model. The gray line represents a fit computed on data extracted from Figure 1 of [24]. The blue dots represent simulations of the model for a range of amplitudes between two and 40 deg in steps of one deg.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3672089&req=5

Figure 7: Model simulation: healthy subject. Upper row represents a simulation (time course of horizontal eye position) of the model when a target is presented 25 deg to the right. Same color conventions as in Figures 5–6. Lower row represents simulation of a main sequence by the model. The gray line represents a fit computed on data extracted from Figure 1 of [24]. The blue dots represent simulations of the model for a range of amplitudes between two and 40 deg in steps of one deg.
Mentions: The upper panel of Figure 7 shows the time course of a simulated saccadic movement toward a rightward 25 deg target. Because of the undershoot, the model generated two saccades. The first saccade ended at 22.5 deg (peak velocity: 545 deg/s) and a corrective saccade of 2.5 deg (peak velocity: 138.5 deg/s) was triggered by the model of the cortex to cancel the remaining visual error.

Bottom Line: We show that our model accurately reproduced the observed disorders allowing us to hypothesize that those disorders originated from a deficit in the cerebellum.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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Laboratory of Sensorimotor Research, National Institutes of Health, Bethesda, Maryland, USA. pierre.daye@gmail.com

ABSTRACT

Background: When 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.

Methods: Eye 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.

Results: Our 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.

Conclusion: Our 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.

Show MeSH
Related in: MedlinePlus