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• W2069308013 endingPage "631" @default.
• W2069308013 startingPage "613" @default.
• W2069308013 abstract "The pathomechanism of downbeat nystagmus (DBN), an ocular motor sign typical for vestibulo-cerebellar lesions, remains unclear. Previous hypotheses conjectured various deficits such as an imbalance of central vertical vestibular or smooth pursuit pathways to be causative for the generation of spontaneous upward drift. However, none of the previous theories explains the full range of ocular motor deficits associated with DBN, i.e., impaired vertical smooth pursuit (SP), gaze evoked nystagmus, and gravity dependence of the upward drift. We propose a new hypothesis, which explains the ocular motor signs of DBN by damage of the inhibitory vertical gaze-velocity sensitive Purkinje cells (PCs) in the cerebellar flocculus (FL). These PCs show spontaneous activity and a physiological asymmetry in that most of them exhibit downward on-directions. Accordingly, a loss of vertical floccular PCs will lead to disinhibition of their brainstem target neurons and, consequently, to spontaneous upward drift, i.e., DBN. Since the FL is involved in generation and control of SP and gaze holding, a single lesion, e.g., damage to vertical floccular PCs, may also explain the associated ocular motor deficits. To test our hypothesis, we developed a computational model of vertical eye movements based on known ocular motor anatomy and physiology, which illustrates how cortical, cerebellar, and brainstem regions interact to generate the range of vertical eye movements seen in healthy subjects. Model simulation of the effect of extensive loss of floccular PCs resulted in ocular motor features typically associated with cerebellar DBN: (1) spontaneous upward drift due to decreased spontaneous PC activity, (2) gaze evoked nystagmus corresponding to failure of the cerebellar loop supporting neural integrator function, (3) asymmetric vertical SP deficit due to low gain and asymmetric attenuation of PC firing, and (4) gravity-dependence of DBN caused by an interaction of otolith-ocular pathways with impaired neural integrator function." @default.
• W2069308013 created "2016-06-24" @default.
• W2069308013 creator A5036924687 @default.
• W2069308013 creator A5054196251 @default.
• W2069308013 creator A5058426311 @default.
• W2069308013 creator A5089553680 @default.
• W2069308013 date "2008-05-08" @default.
• W2069308013 modified "2023-10-17" @default.
• W2069308013 title "A model-based theory on the origin of downbeat nystagmus" @default.
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• W2069308013 doi "https://doi.org/10.1007/s00221-008-1396-7" @default.
• W2069308013 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18463856" @default.
• W2069308013 hasPublicationYear "2008" @default.
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