Pathomechanism of mammalian downbeat nystagmus due to cerebellar lesion: a simple hypothesis

Abstract Most of the various hypotheses on the pathomechanism of the slight ocular upward drift in normal mammals and on the prominent downbeat nystagmus following cerebellar lesions assume an inherent vertical asymmetry in the central vestibulo–ocular pathways. In this paper we propose that this vertical asymmetry is simply based on the anatomical orientation of the six semicircular canals in the head which is right–left symmetrical but lacks symmetry in the cranio–caudal direction. Presuming that each semicircular canal elicits eye movements in a direction roughly in its anatomical plane, vectorial addition of the tonic resting activity of all six canals leads to a cancellation of horizontal and torsional eye movement components but leaves an important vertical (slow phase) upward component. This peripheral vestibular bias is centrally cancelled by floccular and parafloccular inhibitory pathways which are related to the smooth pursuit system, but becomes disinhibited in the presence of posterior cerebellar lesions.