It is suggested that the main types of spontaneous vertical nystagmus due to focal central lesions result from a primary dysfunction of the SVN–VTT pathway. This becomes hypoactive after pontine or caudal medullary lesions, thereby eliciting UBN, and hyperactive after floccular lesions, thereby eliciting DBN. Finally, since gravity influences UBN and DBN and may facilitate the downward vestibular system and restrain the upward vestibular system, it is hypothesized that the excitatory SVN–VTT pathway, along with its specific floccular inhibition, has developed to counteract the gravity pull.
Pierrot Deseilligny, C, and DMilea. “Vertical nystagmus: clinical facts and hypotheses.” Brain 128.6 (2005):1237-1246.