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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: patient saccadic average behavior. Superimposed on the patient data of Figure 4, this figure shows how the model reproduces the average behavior of the patient. Red dots represent rightward simulated saccades. Blue dots represent leftward simulated saccades. Same layout as in Figure 4.
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Figure 9: Model simulation: patient saccadic average behavior. Superimposed on the patient data of Figure 4, this figure shows how the model reproduces the average behavior of the patient. Red dots represent rightward simulated saccades. Blue dots represent leftward simulated saccades. Same layout as in Figure 4.

Mentions: Once the parameters were tuned to match this relationship, we added a 25% random gaussian noise on iFNMax, patient to account for a part of the variability observed in the patient data (noise amplitude arbitrarily chosen). Then, we simulated 117 leftward and 117 rightward saccades with varying amplitudes between 2 and 45 deg. Figure 8 shows the main sequences generated by the model. Upper panel of Figure 9 represents the saccade-amplitude vs. peak-velocity relationship while the lower panel shows the peak-velocity vs. maximum-displacement relationship. Red dots represent the rightward saccade simulations and blue dots represent the leftward saccade simulations. As expected by the tuning of the parameters, the model reproduces correctly the maximum displacement-peak velocity relationship.


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: patient saccadic average behavior. Superimposed on the patient data of Figure 4, this figure shows how the model reproduces the average behavior of the patient. Red dots represent rightward simulated saccades. Blue dots represent leftward simulated saccades. Same layout as in Figure 4.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 9: Model simulation: patient saccadic average behavior. Superimposed on the patient data of Figure 4, this figure shows how the model reproduces the average behavior of the patient. Red dots represent rightward simulated saccades. Blue dots represent leftward simulated saccades. Same layout as in Figure 4.
Mentions: Once the parameters were tuned to match this relationship, we added a 25% random gaussian noise on iFNMax, patient to account for a part of the variability observed in the patient data (noise amplitude arbitrarily chosen). Then, we simulated 117 leftward and 117 rightward saccades with varying amplitudes between 2 and 45 deg. Figure 8 shows the main sequences generated by the model. Upper panel of Figure 9 represents the saccade-amplitude vs. peak-velocity relationship while the lower panel shows the peak-velocity vs. maximum-displacement relationship. Red dots represent the rightward saccade simulations and blue dots represent the leftward saccade simulations. As expected by the tuning of the parameters, the model reproduces correctly the maximum displacement-peak velocity relationship.

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