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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

Neuron model. Three stages composed the neuron model used in this paper. The first one is a neuronal adaptation with a gain GA and a time constant TA. In the second stage, this drive is modulated by the OPN activity. In the third stage, the modulated signal is sent to a first order transfer function (gain: α, time constant: TM) representing the membrane potential dynamics with a saturated output between 0 and dm≥0. The crossed circle represents a sum operator. The circled π represents a product.
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Figure 3: Neuron model. Three stages composed the neuron model used in this paper. The first one is a neuronal adaptation with a gain GA and a time constant TA. In the second stage, this drive is modulated by the OPN activity. In the third stage, the modulated signal is sent to a first order transfer function (gain: α, time constant: TM) representing the membrane potential dynamics with a saturated output between 0 and dm≥0. The crossed circle represents a sum operator. The circled π represents a product.

Mentions: The architecture of the brainstem connectivity used in the model is shown in Figure 2. The model architecture is an updated version of [6] which includes two new populations of neurons: the long-lead inhibitory burst neurons (LIBNR and LIBNL) and the nuclei prepositus hypoglossi (NPHR and NPHL). The activity of each brainstem neuronal population is represented in the model by the same neuron model, shown in Figure 3. This model combines a linear burster (as in [13,14]) and neuronal adaptation as in [6]. TM represents the membrane time constant, α represents the gain of the neuron, GA corresponds to the adaptation gain and TA represents the adaptation time constant. The neuronal discharge is saturated between zero and Dmax. Finally, compared to [6], the OPN activity has a multiplicative inhibitory behavior on downstream neurons instead of an additive effect. Thus, when OPN are discharging, the activity at the input of the membrane low-pass filter is equal to zero.


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)

Neuron model. Three stages composed the neuron model used in this paper. The first one is a neuronal adaptation with a gain GA and a time constant TA. In the second stage, this drive is modulated by the OPN activity. In the third stage, the modulated signal is sent to a first order transfer function (gain: α, time constant: TM) representing the membrane potential dynamics with a saturated output between 0 and dm≥0. The crossed circle represents a sum operator. The circled π represents a product.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 3: Neuron model. Three stages composed the neuron model used in this paper. The first one is a neuronal adaptation with a gain GA and a time constant TA. In the second stage, this drive is modulated by the OPN activity. In the third stage, the modulated signal is sent to a first order transfer function (gain: α, time constant: TM) representing the membrane potential dynamics with a saturated output between 0 and dm≥0. The crossed circle represents a sum operator. The circled π represents a product.
Mentions: The architecture of the brainstem connectivity used in the model is shown in Figure 2. The model architecture is an updated version of [6] which includes two new populations of neurons: the long-lead inhibitory burst neurons (LIBNR and LIBNL) and the nuclei prepositus hypoglossi (NPHR and NPHL). The activity of each brainstem neuronal population is represented in the model by the same neuron model, shown in Figure 3. This model combines a linear burster (as in [13,14]) and neuronal adaptation as in [6]. TM represents the membrane time constant, α represents the gain of the neuron, GA corresponds to the adaptation gain and TA represents the adaptation time constant. The neuronal discharge is saturated between zero and Dmax. Finally, compared to [6], the OPN activity has a multiplicative inhibitory behavior on downstream neurons instead of an additive effect. Thus, when OPN are discharging, the activity at the input of the membrane low-pass filter is equal to zero.

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