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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

Feedforward bilateral connectivity. This figure represents a detailed view of the bilateral architecture with feedforward connections. Gray boxes correspond to neural structures modeled as being unilateral. Red boxes represent right side neural structures. Blue boxes represent left side neural structures. The green shadow box represents the detailed description of the green box “brainstem” in Figure 1. Lines with arrowheads correspond to excitation, with filled circles correspond to inhibition, and with filled diamonds correspond to facilitation. No efferent-copy signals (to cortical and/or subcortical neural areas) are represented in this figure because they correspond to feedback connections.
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Figure 2: Feedforward bilateral connectivity. This figure represents a detailed view of the bilateral architecture with feedforward connections. Gray boxes correspond to neural structures modeled as being unilateral. Red boxes represent right side neural structures. Blue boxes represent left side neural structures. The green shadow box represents the detailed description of the green box “brainstem” in Figure 1. Lines with arrowheads correspond to excitation, with filled circles correspond to inhibition, and with filled diamonds correspond to facilitation. No efferent-copy signals (to cortical and/or subcortical neural areas) are represented in this figure because they correspond to feedback connections.

Mentions: 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.


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)

Feedforward bilateral connectivity. This figure represents a detailed view of the bilateral architecture with feedforward connections. Gray boxes correspond to neural structures modeled as being unilateral. Red boxes represent right side neural structures. Blue boxes represent left side neural structures. The green shadow box represents the detailed description of the green box “brainstem” in Figure 1. Lines with arrowheads correspond to excitation, with filled circles correspond to inhibition, and with filled diamonds correspond to facilitation. No efferent-copy signals (to cortical and/or subcortical neural areas) are represented in this figure because they correspond to feedback connections.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 2: Feedforward bilateral connectivity. This figure represents a detailed view of the bilateral architecture with feedforward connections. Gray boxes correspond to neural structures modeled as being unilateral. Red boxes represent right side neural structures. Blue boxes represent left side neural structures. The green shadow box represents the detailed description of the green box “brainstem” in Figure 1. Lines with arrowheads correspond to excitation, with filled circles correspond to inhibition, and with filled diamonds correspond to facilitation. No efferent-copy signals (to cortical and/or subcortical neural areas) are represented in this figure because they correspond to feedback connections.
Mentions: 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.

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