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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: saccadic oscillations. Simulation of a rightward horizontal towards a target located 15 deg on the right of the central fixation point. Same color conventions as in Figure 6.
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Figure 10: Model simulation: saccadic oscillations. Simulation of a rightward horizontal towards a target located 15 deg on the right of the central fixation point. Same color conventions as in Figure 6.

Mentions: Figure 10 shows the model behavior when the OPN activity is not reactivated at the end of a 15 deg rightward saccade (to reproduce the patient behavior in the upper panel of Figure 6). The model starts to oscillate if the OPN are not reactivated at saccade offset. The simulated oscillation mechanism is similar to the one reported in [6] and can be reproduced by the model because of the cross-inhibition of the short-lead inhibitory burst neurons and the post-inhibitory rebound of the neurons. To generate the oscillation pattern of Figure 10, we decreased only the input gain of the OPN and we kept all the other average parameters as in Figure 9. Therefore, at the end of the saccade when the OPN should have fired to prevent the sIBNL- sIBNR circuit from oscillating, the OPN inhibition by the long-lead inhibitory burst neurons could not be stopped and an oscillatory movement started. The main differences between our simulation and the patient observation is the variable amplitude of the oscillations. To generate a variable amplitude of the oscillations, we could included some variability in the amplitude of the input gain of the OPN, but that is beyond the scope of this paper. The patient also exhibited shorter oscillatory periods. To simulate those situations, the input OPN gain must be amplified sooner. This will excite the OPN and stop the oscillations.


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: saccadic oscillations. Simulation of a rightward horizontal towards a target located 15 deg on the right of the central fixation point. Same color conventions as in Figure 6.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 10: Model simulation: saccadic oscillations. Simulation of a rightward horizontal towards a target located 15 deg on the right of the central fixation point. Same color conventions as in Figure 6.
Mentions: Figure 10 shows the model behavior when the OPN activity is not reactivated at the end of a 15 deg rightward saccade (to reproduce the patient behavior in the upper panel of Figure 6). The model starts to oscillate if the OPN are not reactivated at saccade offset. The simulated oscillation mechanism is similar to the one reported in [6] and can be reproduced by the model because of the cross-inhibition of the short-lead inhibitory burst neurons and the post-inhibitory rebound of the neurons. To generate the oscillation pattern of Figure 10, we decreased only the input gain of the OPN and we kept all the other average parameters as in Figure 9. Therefore, at the end of the saccade when the OPN should have fired to prevent the sIBNL- sIBNR circuit from oscillating, the OPN inhibition by the long-lead inhibitory burst neurons could not be stopped and an oscillatory movement started. The main differences between our simulation and the patient observation is the variable amplitude of the oscillations. To generate a variable amplitude of the oscillations, we could included some variability in the amplitude of the input gain of the OPN, but that is beyond the scope of this paper. The patient also exhibited shorter oscillatory periods. To simulate those situations, the input OPN gain must be amplified sooner. This will excite the OPN and stop the oscillations.

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