Research advances on mechanism and lesion location of vertical nystagmus / 临床耳鼻咽喉头颈外科杂志

Vertical nystagmus is a vertical nystagmus caused by structural abnormalities and/or dysfunction of the central vestibular system and observed in situ in the center of the eyeball. There are two kinds of nystagmus （UBN） and downbeat nystagmus （DBN） according to the direction of nystagmus. The diagnosis of UBN is mainly made by naked eye or electronystagmography/viewer. It is a common neuro-ophthalmologic sign in the field of vestibular medicine. In this paper, the mechanism of vertical nystagmus formation and the location of lesions were briefly introduced, in order to provide help for the diagnosis and treatment of Vertigo.

Research advances on mechanism and lesion location of vertical nystagmus / 临床耳鼻咽喉头颈外科杂志

Summary@#Vertical nystagmus is a vertical nystagmus caused by structural abnormalities and/or dysfunction of the central vestibular system and observed in situ in the center of the eyeball. There are two kinds of nystagmus （UBN） and downbeat nystagmus （DBN） according to the direction of nystagmus. The diagnosis of UBN is mainly made by naked eye or electronystagmography/viewer. It is a common neuro-ophthalmologic sign in the field of vestibular medicine. In this paper, the mechanism of vertical nystagmus formation and the location of lesions were briefly introduced, in order to provide help for the diagnosis and treatment of Vertigo.

Primary Position Upbeat Nystagmus during an Acute Attack of Multiple Sclerosis

BACKGROUND AND PURPOSE: Ocular manifestation is one of the frequent signs of an acute attack in multiple sclerosis (MS), although primary position upbeat nystagmus (PPUN) is rare. The purpose of this study is to determine the incidence of PPUN in MS and to determine the lesions that are responsible for this sign. METHODS: The medical records of 120 MS patients with acute brain lesions were reviewed over a consecutive period of 9 years; of these, 6 patients were found to have PPUN. Other ocular motor abnormalities were analyzed in combination with upbeat nystagmus, video-oculographic findings, and lesions detected on brain MRI. RESULTS: Lesions in the pontine tegmentum involving the medial longitudinal fasciculus (MLF) and ventral tegmental tract (VTT) were the most common, being observed in three of the six patients with PPUN. One patient exhibited caudal medullary lesions bilaterally affecting the paramedian portion of the posterior tegmentum, and two patients exhibited multiple lesions involving the pons with the cerebral peduncle or medulla. In five patients, other ocular motor dysfunctions, such as gaze-evoked nystagmus (n=3) and internuclear ophthalmoplegia (n=1), were found in combination with upbeat nystagmus. CONCLUSIONS: PPUN is an infrequent, ocular manifestation noted during an acute attack of MS, and was observed in 5% of the present cases. Brainstem lesions in these cases primarily involved the pontine tegmentum and the caudal medulla. These findings support the theory that upbeat nystagmus is attributable to damage to the upward vestibulo-ocular reflex pathway related to the vestibular nucleus, VTT, and interconnecting pathways.

Transient Upbeat Nystagmus Due to Unilateral Pontine Infarction

Upbeat nystagmus has been described in bilateral lesions of the medulla, the ventral tegmentum, the anterior cerebellar vermis, the adjacent brachium conjunctivum, and the midbrain. Imbalance of the vertical vestibulo- ocular reflex (VOR) favoring the downward VOR activity would therefore result in upbeat nystagmus. We report a patient with transient upbeat nystagmus due to unilateral pontine infarction that may have disrupted bilateral upward VOR pathways running in the ventral tegmental tracts.

Upbeat Nystagmus: Clinicoanatomical Correlations in 15 Patients

BACKGROUND AND PURPOSE: The mechanism of upbeat nystagmus is unknown and clinicoanatomical correlative studies in series of patients with upbeat nystagmus are limited. METHODS: Fifteen patients with upbeat nystagmus received full neuro-ophthalmological evaluation by the senior author. Nystagmus was observed using video Frenzel goggles and recorded with video-oculography. Brain lesions were documented with MRI. RESULTS: Lesions responsible for nystagmus were found throughout the brainstem, mainly in the paramedian area: in the medulla (n=8), pons (n=3), pons and midbrain with or without cerebellar lesions (n=3), and midbrain and thalamus (n=1). Underlying diseases comprised cerebral infarction (n=10), multiple sclerosis (n=2), cerebral hemorrhage (n=1), Wernicke encephalopathy (n=1), and hydrocephalus (n=1). Upbeat nystagmus was mostly transient and showed occasional evolution during the acute phase. In one patient with a bilateral medial medullary infarction, the upbeat nystagmus changed into a hemiseesaw pattern with near complete resolution of the unilateral lesion. Gaze and positional changes usually affected both the intensity and direction of the nystagmus. A patient with a cervicomedullary lesion showed a reversal of upbeat into downbeat nystagmus by straight-head hanging and leftward head turning while in the supine position. Gaze-evoked nystagmus (n=7), ocular tilt reaction (n=7), and internuclear ophthalmoplegia (n=4) were also commonly associated with upbeat nystagmus. CONCLUSIONS: In view of the responsible lesions and associated neuro-ophthalmological findings, upbeat nystagmus may be ascribed to damage to the pathways mediating the upward vestibulo-ocular reflex or the neural integrators involved in vertical gaze holding.