Figure 80: Vascular Distribution and Anatomy Relevant to the Medial Medullary Syndrome

This axial section of the medulla highlights those structures that, when damaged, are often responsible for spontaneous upbeat nystagmus (UBN). The nucleus of Roller and nucleus intercalatus normally have an inhibitory influence over the cerebellar flocculus, and when there is a lesion of Roller/intercalatus, there is less inhibition of the flocculus. The Purkinje cells of the flocculus normally inhibit the anti-gravity or upward anterior semicircular canal (SCC) pathways. With a lesion of Roller/intercalatus, the flocculus will over-inhibit the anterior SCC pathways, causing relative activation of the posterior SCC pathways which will generate a downward slow phase. The fast/position-reset phase will be upward, and these alternating slow (downward) and fast (upward) phases are responsible for UBN. Involvement of the inferior cerebellar peduncle (ICP) and caudal aspect of the vestibular nucleus (medial vestibular nucleus [MVN]) is common in the lateral medullary syndrome (see "Vascular distribution and anatomy relevant to the lateral medullary (Wallenberg) syndrome" figure).