English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Dear Editor, Nystagmus may be classified into jerky or pendular according to the presence of quick phases. In a single patient with acquired nystagmus the nystagmus is almost always either jerky or pendular. To the best of our knowledge, only a few cases of combined jerky and pendular nystagmus involving different axes of rotation have been described in patients with central myelin disorders. Moreover, no correlation between the nystagmus patterns and involved structures has been reported.1 We report a patient with upbeat jerky and pendular horizontal-torsional nystagmus. This suggests the presence of different mechanisms for generating ocular oscillations in different eye-movement planes in a single patient. A 21-year-old woman with no past neurological history developed headache and vomiting along with right-side hypesthesia and paresthesia, and severe gait imbalance from a medullary hemorrhage, probably due to cavernous hemangioma (Fig. 1A and B). About 1 year later she began to suffer from dizziness and oscillopsia with a rather abrupt onset, and was referred for evaluation of abnormal eye movements that had been newly detected. The physical examination performed at that time showed spontaneous upbeat jerky nystagmus and horizontal-torsional pendular nystagmus, but without palatal tremor (Fig. 1C, Supplementary Video 1 in the online-only Data Supplement). The nystagmus was not modulated by the gaze, saccades, or smooth pursuit, but decreased after turning the head to either side while supine, and during straight-head hanging and Dix-Hallpike maneuvers. Horizontal saccades were hypermetric, and smooth pursuit was impaired in both horizontal directions and upward. The findings of bedside head impulse tests were normal, and a neurological examination was otherwise unremarkable. Gabapentin was ineffective in reducing the nystagmus. Her condition deteriorated in a stepwise manner, and she finally became wheelchair-bound. Even though upbeat nystagmus has been reported in lesions involving various areas of the brainstem and cerebellum, in the medulla it has been ascribed to damage to the perihypoglossal nuclei, the cell groups of the paramedian tracts (PMTs), or the medial longitudinal fasciculus.1 The perihypoglossal nuclei include the nucleus prepositus hypoglossi (NPH), nucleus of Roller, and nucleus intercalatus (NI), and are important for gaze holding. Of these, the NI seems mostly responsible for upbeat nystagmus since it is involved in processing the vertical eye position through its projections to the cerebellar flocculus. The PMT cell groups might provide the cerebellum with motor feedback signals essential for maintaining the gaze position, and are another possible neural substrate responsible for upbeat nystagmus in the medulla.2 The vestibulo-ocular reflex pathways from both anterior semicircular canals may also cause upbeat nystagmus when they are damaged in the rostral medulla.3 Given the transient suppression and phase shift (resetting) of acquired pendular nystagmus following a saccade, especially for larger saccades4 in multiple sclerosis, acquired pendular nystagmus has been hypothesized as arising in the neural integrators that receive Sang-Won Han Hyo-Jung Kim Jeong-Yoon Choi Xu Yang Dong-Eog Kim Ji-Soo Kim

Combined Jerky and Pendular Nystagmus in Medullary Hemorrhage