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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

Patient main sequence. Upper row represents saccade peak velocity as a function of saccade amplitude. Lower row represents saccade peak velocity as a function of saccadic maximum displacement. Gray dots correspond to the patient data. Thick colored lines represent the average behavior computed with an exponential fit. Thin colored lines represent the 95% confidence interval around the exponential fit. Red lines are used for rightward movements. Blue lines are used for leftward movements. Negative amplitudes (maximum displacements) correspond to leftward movements. Positive amplitudes (maximum displacements) represent rightward movements.
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Figure 4: Patient main sequence. Upper row represents saccade peak velocity as a function of saccade amplitude. Lower row represents saccade peak velocity as a function of saccadic maximum displacement. Gray dots correspond to the patient data. Thick colored lines represent the average behavior computed with an exponential fit. Thin colored lines represent the 95% confidence interval around the exponential fit. Red lines are used for rightward movements. Blue lines are used for leftward movements. Negative amplitudes (maximum displacements) correspond to leftward movements. Positive amplitudes (maximum displacements) represent rightward movements.

Mentions: In this section, we characterize the general saccadic behavior of the patient. The upper graph in Figure 4 shows the relationship between saccade amplitude (e.g. difference between eye position at point c and eye position at point b in Figure 5 for the first saccade) and saccade peak velocity known as the main sequence [23]. Leftward (rightward) saccades are represented with a negative (positive) amplitude. Lower graph shows the peak velocity as a function of the maximum displacement during the saccade. The maximum displacement is defined as the difference between eye position at the extrema of the position hook (reversal of the saccadic trajectory, e.g. point b in Figure 5 for the first saccade) and the eye position at the onset of the saccade (e.g. point a in Figure 5 for the first saccade). One can see that the dispersion is smaller for the peak-velocity vs. maximum-displacement relationship than for the peak-velocity vs. saccade-amplitude relationship. To test this, we fitted an exponential model to characterize the different relationships in Figure 4:


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)

Patient main sequence. Upper row represents saccade peak velocity as a function of saccade amplitude. Lower row represents saccade peak velocity as a function of saccadic maximum displacement. Gray dots correspond to the patient data. Thick colored lines represent the average behavior computed with an exponential fit. Thin colored lines represent the 95% confidence interval around the exponential fit. Red lines are used for rightward movements. Blue lines are used for leftward movements. Negative amplitudes (maximum displacements) correspond to leftward movements. Positive amplitudes (maximum displacements) represent rightward movements.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 4: Patient main sequence. Upper row represents saccade peak velocity as a function of saccade amplitude. Lower row represents saccade peak velocity as a function of saccadic maximum displacement. Gray dots correspond to the patient data. Thick colored lines represent the average behavior computed with an exponential fit. Thin colored lines represent the 95% confidence interval around the exponential fit. Red lines are used for rightward movements. Blue lines are used for leftward movements. Negative amplitudes (maximum displacements) correspond to leftward movements. Positive amplitudes (maximum displacements) represent rightward movements.
Mentions: In this section, we characterize the general saccadic behavior of the patient. The upper graph in Figure 4 shows the relationship between saccade amplitude (e.g. difference between eye position at point c and eye position at point b in Figure 5 for the first saccade) and saccade peak velocity known as the main sequence [23]. Leftward (rightward) saccades are represented with a negative (positive) amplitude. Lower graph shows the peak velocity as a function of the maximum displacement during the saccade. The maximum displacement is defined as the difference between eye position at the extrema of the position hook (reversal of the saccadic trajectory, e.g. point b in Figure 5 for the first saccade) and the eye position at the onset of the saccade (e.g. point a in Figure 5 for the first saccade). One can see that the dispersion is smaller for the peak-velocity vs. maximum-displacement relationship than for the peak-velocity vs. saccade-amplitude relationship. To test this, we fitted an exponential model to characterize the different relationships in Figure 4:

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