Daniel R. Gold, DO, Departments of Neurology, Ophthalmology, Neurosurgery, Otolaryngology - Head & Neck Surgery, Emergency Medicine, and Medicine, The Johns Hopkins School of Medicine
This is a video of two patients who suffered small strokes involving the right medial medulla, and who presented with acute vertigo and oscillopsia. The first patient in the video had pure upbeat nystagmus, while the second patient had upbeat-torsional (towards the right ear) nystagmus in addition to gaze-evoked, direction-changing nystagmus (also a central sign in patients with the acute vestibular syndrome). Spontaneous vertical nystagmus is almost always central in origin. While medications like 4-aminopyridine or baclofen may occasionally be helpful to alleviate upbeat nystagmus (UBN), fortunately the upbeat will almost always eventually by itself over weeks or months. UBN from pontomedullary pathology is usually the result of: • Damage to the nucleus intercalatus/nucleus of Roller: • Results in increased activation of flocculus, decreased anterior canal [AC] tone and relative increase in posterior canal [PC] pathway tone -> downward drift and upward (upbeat) fast phase • Damage to the cell groups of the paramedian tracts - Involved in vertical gaze holding • Damage to the ventral tegmental tract (VTT) - Carries AC fibers or upward pathways so that damage to the VTT causes decreased anterior canal [AC] tone and relative increase in posterior canal [PC] pathway tone -> downward drift and upward (upbeat) fast phase. The second patient's gaze-evoked nystagmus is almost certainly the result of damage to the nucleus prepositus hypoglossi (NPH)- medial vestibular nucleus (MVN) complex, as these structures are responsible for horizontal gaze holding.
Spencer S. Eccles Health Sciences Library, University of Utah