Upbeat Nystagmus

2011 ◽  
pp. 118-121
Author(s):  
Matthew J. Thurtell ◽  
Robert L. Tomsak ◽  
Robert B. Daroff

Upbeat nystagmus is a less common type of central vestibular nystagmus that is often transient. However, it can be persistent and responsible for visual symptoms. We review the characteristics and causes of upbeat nystagmus in this chapter. We also discuss the management of upbeat nystagmus occurring in the setting of Wernicke’s encephalopathy.

2016 ◽  
Vol 75 (6) ◽  
pp. 505-510
Author(s):  
Atsushi Ochiai ◽  
Hideaki Naganuma

2010 ◽  
Vol 298 (1-2) ◽  
pp. 145-147 ◽  
Author(s):  
Byoung-Soo Shin ◽  
Sun-Young Oh ◽  
Ji Soo Kim ◽  
Hyung Lee ◽  
Eui-Jung Kim ◽  
...  

2011 ◽  
Vol 65 (3) ◽  
pp. 160-163 ◽  
Author(s):  
L. Abouaf ◽  
A. Vighetto ◽  
E. Magnin ◽  
A. Nove-Josserand ◽  
S. Mouton ◽  
...  

2019 ◽  
pp. 151-154
Author(s):  
Matthew J. Thurtell ◽  
Robert L. Tomsak

Upbeat nystagmus is a less common type of central vestibular nystagmus that is often transient. It is a vertical jerk-waveform nystagmus with downward slow phases and upward quick phases. In this chapter, we begin by reviewing the clinical features of upbeat nystagmus. Since it can be produced by lesions in a variety locations in the brainstem and cerebellum, we next describe the symptoms and signs that can help to localize the causative lesion. We list the causes of upbeat nystagmus. We then discuss the clinical and imaging findings in Wernicke encephalopathy, which is a common cause of upbeat nystagmus, and we review the management of Wernicke encephalopathy. Lastly, we briefly discuss the medical treatment options for persistent upbeat nystagmus.


1999 ◽  
Vol 41 (2) ◽  
pp. 21-23
Author(s):  
Takeshi YONEDA ◽  
Sayo TAGASHIRA ◽  
Akiko KITA ◽  
Megumi MATSUURA ◽  
Kanji TAKATSUGU

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Chikanori Tsutsumi ◽  
Toshiya Abe ◽  
Tomohiko Shinkawa ◽  
Hideyuki Watanabe ◽  
Kazuyoshi Nishihara ◽  
...  

Abstract Background Wernicke’s encephalopathy (WE) is an acute neuropsychiatric disorder resulting from thiamine (vitamin B1) deficiency, frequently associated with chronic alcoholism and total parenteral nutrition without thiamine. However, only a few reports have focused on the relationship between WE and subtotal stomach-preserving pancreatoduodenectomy (SSPPD). Case presentation A 71-year-old woman underwent SSPPD for an adenocarcinoma of the ampulla of Vater. Although there had been no evidence of recurrence, the patient was treated with antibiotics for cholangitis at 12 and 31 months, respectively, post-surgery. Thereafter, the patient presented with vomiting and disorientation 33 months after surgery. Although she was admitted and underwent closer inspection by a neurologist and a psychiatrist, the exact cause of these syndromes remained unknown. The psychiatrist measured thiamine concentration to examine the cause of disorientation. After 6 days, her level of consciousness worsened. Magnetic resonance imaging of the head showed symmetrically multiple abnormal hyperintense signals on fluid-attenuated inversion-recovery and diffusion weighted image, compatible with WE. An administration of intravenous thiamine was immediately initiated. After 8 days of the measurement of the thiamine level, the patient’s serum thiamine level was found to be 6 µg/mL (reference range, 24–66 µg/mL). Accordingly, the patient was diagnosed with WE. Shortly after starting the treatment, blood thiamine value reached above normal range with significant improvement of her confusional state. However, short-term memory and ataxia remained. Conclusions Development of WE after SSPPD is uncommon. However, to prevent an after-effect, the possibility of development of WE after SSPPD should be recognized.


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