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GABAAergic dysfunction in the olivary-cerebellar-brainstem network may cause eye oscillations and body tremor

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Acknowledgements

We thank the patients for participation to the study. We thank also Dr. F. Sicurelli, Prof. A. Rossi, Prof. D. Nuti, Prof. A. Federico, and Dr. F. Rossi for patients care. This study was supported by the Intramural Research Program of National Eye Institute and FP7-PEOPLE-2010-IRSES CERVISO 269263.

Conflict of interest: The authors declare no competing financial interests.

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    Other evidence from mild traumatic brain injury supports a role for altered intracortical mechanisms in the motor cortex due to impaired gamma-amino-butyric acid (GABA) receptor activity (Tremblay et al., 2011). This idea may provide a link between concussion-related cortical injury and abnormal ocular oscillations, as alterations in the sensitivity of brainstem saccadic neurons to GABA have been directly implicated in several causes of opsoclonus/ocular flutter (Petit-Pedrol et al., 2014; Pretegiani et al., 2017; Shaikh and Wilmot, 2016), and GABA receptors are present both in the forebrain and in the cerebellum. Thus, based on the likely location of injury in our patient, impaired inhibitory input from the frontal eye field to OPN may be the more likely explanation for opsoclonus than direct injury to the cerebellum—which is less common with mild traumatic brain injury (Kepski, 1983; Meabon et al., 2016).

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    However, such theories produce only sinusoidal oscillations, and are thus unable to account for the quasi-sinusoidal waveforms usually seen in O/F. Nor could they account for the gaze position-dependence of our patient. Recently, we analyzed data from two patients with opsoclonus following abuse of anabolic steroids (Pretegiani et al., 2017b). This led us to propose a new model of O/F, based on dysfunction in a circuit involving the brain stem premotor neurons (EBNs, IBNs and OPNs) and the cerebellum (oculomotor vermis and fastigial nuclei oculomotor region) (Optican and Pretegiani, 2017a).

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