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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

General architecture of the model. This figure represents the different parts of the model and their feedforward and feedback connections. First, a target (T) appears on the retina and generates a position error (PE) sent to the cortex. Second, the cortex computes the desired eye displacement (ΔE) and sends it to the superior colliculus (SC) and the cerebellum (CBLM). Third, SC and CBLM send a drive to the brainstem which sends back an efference copy of the eye position to CBLM which controls eye displacement. CBLM also modulates the collicular activity through a facilitation signal. Finally, the brainstem sends a drive to the eye plant. Lines with arrowheads correspond to excitation, with filled circles correspond to inhibition, and with filled diamonds correspond to facilitation. Details of the brainstem connectivity are presented in Figure 2.
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Figure 1: General architecture of the model. This figure represents the different parts of the model and their feedforward and feedback connections. First, a target (T) appears on the retina and generates a position error (PE) sent to the cortex. Second, the cortex computes the desired eye displacement (ΔE) and sends it to the superior colliculus (SC) and the cerebellum (CBLM). Third, SC and CBLM send a drive to the brainstem which sends back an efference copy of the eye position to CBLM which controls eye displacement. CBLM also modulates the collicular activity through a facilitation signal. Finally, the brainstem sends a drive to the eye plant. Lines with arrowheads correspond to excitation, with filled circles correspond to inhibition, and with filled diamonds correspond to facilitation. Details of the brainstem connectivity are presented in Figure 2.

Mentions: Figure 1 shows the unilateral general organization of the model, including the feedback loops. The overall architecture is similar to [13,14]. Briefly, based on target visual information, the cortex determines the desired eye displacement and sends it to the superior colliculus (SC) and to the cerebellum (CBLM). The superior colliculus sends a drive to the brainstem that shapes the initial eye velocity while the cerebellum controls eye trajectory through a drive sent to the brainstem. The CBLM modulates the amplitude of the collicular discharge through a disfacilitation signal (diamond tipped arrow in Figure 1). The brainstem sends the motor signal to the eye plant as well as an efference copy of this signal back to the cerebellum and to the cortex (green arrows from the brainstem to CBLM and Cortex in Figure 1). At the end of the saccade, the cortex evaluates whether a visual position error remains and triggers a corrective saccade if needed.


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)

General architecture of the model. This figure represents the different parts of the model and their feedforward and feedback connections. First, a target (T) appears on the retina and generates a position error (PE) sent to the cortex. Second, the cortex computes the desired eye displacement (ΔE) and sends it to the superior colliculus (SC) and the cerebellum (CBLM). Third, SC and CBLM send a drive to the brainstem which sends back an efference copy of the eye position to CBLM which controls eye displacement. CBLM also modulates the collicular activity through a facilitation signal. Finally, the brainstem sends a drive to the eye plant. Lines with arrowheads correspond to excitation, with filled circles correspond to inhibition, and with filled diamonds correspond to facilitation. Details of the brainstem connectivity are presented in Figure 2.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 1: General architecture of the model. This figure represents the different parts of the model and their feedforward and feedback connections. First, a target (T) appears on the retina and generates a position error (PE) sent to the cortex. Second, the cortex computes the desired eye displacement (ΔE) and sends it to the superior colliculus (SC) and the cerebellum (CBLM). Third, SC and CBLM send a drive to the brainstem which sends back an efference copy of the eye position to CBLM which controls eye displacement. CBLM also modulates the collicular activity through a facilitation signal. Finally, the brainstem sends a drive to the eye plant. Lines with arrowheads correspond to excitation, with filled circles correspond to inhibition, and with filled diamonds correspond to facilitation. Details of the brainstem connectivity are presented in Figure 2.
Mentions: Figure 1 shows the unilateral general organization of the model, including the feedback loops. The overall architecture is similar to [13,14]. Briefly, based on target visual information, the cortex determines the desired eye displacement and sends it to the superior colliculus (SC) and to the cerebellum (CBLM). The superior colliculus sends a drive to the brainstem that shapes the initial eye velocity while the cerebellum controls eye trajectory through a drive sent to the brainstem. The CBLM modulates the amplitude of the collicular discharge through a disfacilitation signal (diamond tipped arrow in Figure 1). The brainstem sends the motor signal to the eye plant as well as an efference copy of this signal back to the cerebellum and to the cortex (green arrows from the brainstem to CBLM and Cortex in Figure 1). At the end of the saccade, the cortex evaluates whether a visual position error remains and triggers a corrective saccade if needed.

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