Distributed model of control of saccades by superior colliculus and cerebellum

Università degli Studi di Trieste, Trst, Friuli Venezia Giulia, Italy
Neural networks: the official journal of the International Neural Network Society (Impact Factor: 2.71). 11/1998; 11(7-8):1175-1190. DOI: 10.1016/S0893-6080(98)00071-9
Source: PubMed

ABSTRACT We investigate the role that superior colliculus (SC) and cerebellum (CBLM) might play in controlling saccadic eye movements. Even though strong experimental evidence argues for an important role for the CBLM, the most recent models of the saccadic system have relied mostly on the SC for the dynamic control of saccades. In this study, we propose that saccades are controlled by two parallel pathways, one including the SC and the other including the CBLM. In this model, both SC and CBLM provide part of the drive to the saccade. Furthermore, the CBLM receives direct feedback from the brain stem and keeps track of the residual motor error, so that it can issue appropriate commands to compensate for incorrect heading and to end the movement when the target has been foveated. We present here a distributed model that produces realistic saccades and accounts for a great deal of neurophysiological data.

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    • "As further proof of this theory, it is well known that cerebellar lesions [43, 44] induce permanent deficits, affecting dramatically the consistency [42, 45] and the accuracy of saccades [37]. While a wide range of evidence has emerged accounting for a dominant role of cerebrocerebellar interactions in motor control and its movement-related functions are the most solidly established that, recent studies have clearly suggested an influence of the cerebellum in cognitive and behavioral functions [65, 67, 70, 71], including fear and pleasure responses [72–74]. "
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    ABSTRACT: Attention allows us to selectively process the vast amount of information with which we are confronted, prioritizing some aspects of information and ignoring others by focusing on a certain location or aspect of the visual scene. Selective attention is guided by two cognitive mechanisms: saliency of the image (bottom up) and endogenous mechanisms (top down). These two mechanisms interact to direct attention and plan eye movements; then, the movement profile is sent to the motor system, which must constantly update the command needed to produce the desired eye movement. A new approach is described here to study how the eye motor control could influence this selection mechanism in clinical behavior: two groups of patients (SCA2 and late onset cerebellar ataxia LOCA) with well-known problems of motor control were studied; patients performed a cognitively demanding task; the results were compared to a stochastic model based on Monte Carlo simulations and a group of healthy subjects. The analytical procedure evaluated some energy functions for understanding the process. The implemented model suggested that patients performed an optimal visual search, reducing intrinsic noise sources. Our findings theorize a strict correlation between the "optimal motor system" and the "optimal stimulus encoders."
    02/2014; 2014(2):162423. DOI:10.1155/2014/162423
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    • "The second deficit we tried to reproduce with the model was the dynamic overshoot of the patient. Optican and colleagues have proposed that the ipsilateral cerebellar discharge is responsible for stopping the saccade through a choke signal sent to the contralateral EBN and IBN [13,14]. Hence, to model the dynamic overshoot of our patient, we increased the maximum discharge of the ipsilateral cerebellar discharge and triggered its activity sooner. "
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    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.
    Journal of Translational Medicine 05/2013; 11(1):125. DOI:10.1186/1479-5876-11-125 · 3.93 Impact Factor
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    • "The oculomotor system comprises different areas. The retina projects to the superior colliculus (Lefèvre et al., 1998), which, in turn, sends afferents to the cerebellum and the lateral intraparietal area (LIP). The LIP is connected with the frontal eye field (FEF) and the basal ganglia and superior colliculus gate input from the FEF to the LIP (Straube and Buttner, 2007). "
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    ABSTRACT: Following the fundamental recognition of its involvement in sensory-motor coordination and learning, the cerebellum is now also believed to take part in the processing of cognition and emotion. This hypothesis is recurrent in numerous papers reporting anatomical and functional observations, and it requires an explanation. We argue that a similar circuit structure in all cerebellar areas may carry out various operations using a common computational scheme. On the basis of a broad review of anatomical data, it is conceivable that the different roles of the cerebellum lie in the specific connectivity of the cerebellar modules, with motor, cognitive, and emotional functions (at least partially) segregated into different cerebro-cerebellar loops. We here develop a conceptual and operational framework based on multiple interconnected levels (a meta-levels hypothesis): from cellular/molecular to network mechanisms leading to generation of computational primitives, thence to high-level cognitive/emotional processing, and finally to the sphere of mental function and dysfunction. The main concept explored is that of intimate interplay between timing and learning (reminiscent of the "timing and learning machine" capabilities long attributed to the cerebellum), which reverberates from cellular to circuit mechanisms. Subsequently, integration within large-scale brain loops could generate the disparate cognitive/emotional and mental functions in which the cerebellum has been implicated. We propose, therefore, that the cerebellum operates as a general-purpose co-processor, whose effects depend on the specific brain centers to which individual modules are connected. Abnormal functioning in these loops could eventually contribute to the pathogenesis of major brain pathologies including not just ataxia but also dyslexia, autism, schizophrenia, and depression.
    Frontiers in Neural Circuits 11/2012; 6:116. DOI:10.3389/fncir.2012.00116 · 3.60 Impact Factor
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