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Show Nonconvulsive Status Epilepticus Presenting as Epileptic Nystagmus in a Patient With Herpes Encephalitis Ju-Hee Lee, MD, Do-Hyun Nam, MD, Sun-Young Oh, MD, Byung-Soo Shin, MD, Man-Wook Seo, MD, Seul-Ki Jeong, MD, Jun-Young Lee, MD Abstract: Epileptic nystagmus (EN) is characterized by rhythmic ocular oscillations or quick, repetitive eye move-ments secondary to seizure activity. The fast component of EN is known to be contralateral to the epileptogenic focus. There are few reports EN occurring patients in nonconvul-sive status epilepticus (NCSE). We report such a patient in the setting of herpes encephalitis. Journal of Neuro-Ophthalmology 2012;32:249-251 doi: 10.1097/WNO.0b013e3182413679 © 2012 by North American Neuro-Ophthalmology Society Epileptic nystagmus (EN) is an uncommon phenomenon characterized by rhythmic ocular oscillations or quick repetitive ocular movements secondary to seizure activity (1-4). First described at 1954 with corresponding electroen-cephalography (EEG) (5), EN has been observed in 10% of 42 cases with occipital lobe epilepsy (6) and described as a lateralizing sign of focal epilepsy in adults and in children (7). The epileptic focus of EN is located in the cortical areas of the brain controlling conjugated saccadic eye movements (1,8-11). In previous reports, the direction of the fast com-ponent of EN was contralateral to the seizure focus. Nonconvulsive status epilepticus (NCSE) is defined as one of 2 events lasting longer than 30 minutes: either continuous seizure activity or 2 or more sequential seizures without full recovery of consciousness between seizures and without clinical signs of seizure activity between sequential episodes. Confusion, personality change, dysphasia, and subtle motor activity may be some of the presenting signs (12). There are few reports of EN in NCSE (4), and we describe a patient with herpes simplex encephalitis presenting with EN. CASE REPORT A 19-year-old girl was admitted to hospital for headache, fever, and altered mental status, which occurred several days previously. With onset of symptoms, she com-plained of a right homonymous hemianopia, and her mental status deteriorated steadily into stuporous state. At the time of initial examination, she was afebrile. Cerebrospinal fluid examination revealed white blood cell count of 19/mm3 and herpes simplex virus IgG titer of 2.6 IU/mL. Brain MRI demonstrated high signal inten-sities involving portions of the left temporal and occipital lobes (Fig. 1). Diagnosed with herpes encephalitis, the patient was given intravenous acyclovir. Despite treatment, she contin-ued to deteriorate clinically. She had no response to painful stimuli and developed spontaneous conjugate right-beating nystagmus with tonic deviation toward the right side. The slow component of nystagmus did not cross the midline. Her head paroxysmally deviated to the right along with her eyes and showed episodic bilateral eyelid elevation. EEG revealed spiky rhythmic alpha activity in the left posterior region of the head, which evolved into repetitive sharp waves (Fig. 2). We felt that the patient had NCSE with EN and administered intravenous phenytoin and lorazepam. This led to almost immediate suppression of ictal activity and disappearance of nystagmus with progressive improve-ment of cognitive function. DISCUSSION Depending on the clinical characteristics of EN, there are 3 different mechanisms for generation of this eye move-ment disorder. First, EN may be due to epileptic discharges in the cortical saccade regions of the frontal Department of Neurology, Research Institute of Clinical Medicine, Chonbuk National University, Chonbuk National University Hospital, Jeonju, South Korea. The authors report no conflicts of interest. Address correspondence to Jun-Young Lee, MD, Department of Neurology, Research Institute of Clinical Medicine, Chonbuk National University, Chonbuk National University Hospital, 634-18 Geumam-dong, Dukjingu, Jeonju 561-712, South Korea; E-mail: everblue0912@hanmail.net Lee et al: J Neuro-Ophthalmol 2012; 32: 249-251 249 Clinical Observation Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. eye field (frontal precentral sulcus), the parietal eye field (anterior angular sulcus), or posterior parietal cortex (inferior parietal lobule) (4). Activation of these regions induces nystagmus with the fast phase beating opposite to the side of the epileptic focus. This is followed by an ipsilateral centripetal slow drift of the eyes that do not cross the midline (8,13). Second, EN may be caused by epileptic discharges in the tempero-parieto-occipital junc-tion. Activation of this region induces ipsilateral smooth pursuit eye movements, which cross the midline (11). This is followed by secondary, reflexive contraversive saccades. Third, EN may arise from epileptic discharges in the op-tokinetic region, a projection from temporal-occipital cor-tex to the nucleus of the optic tract (11). In our patient, EN onset was probably due to the first mechanism. This is supported by the MRI findings and the tonic deviation of the eyes to the right, the slow phase of the nystagmus that did not cross the midline, and the onset of ictal discharges localized over the parieto-occipital electrodes. Despite many cases of EN, it has infrequently been associated with NCSE (4). This may in part be due to the lack of diagnostic criteria for NCSE (14), particularly when dealing with an obtunded/comatose patient. NCSE should be considered in any patient with unexplained altered men-tal status or coma with or without abnormal motor activity. This diagnosis requires a high index of suspicion and must be verified with an EEG (15). FIG. 1. Axial (A) and coronal (B) FLAIR MRI show an area of high signal involving the left hippocampus and parahippocampal and lingual gyri. FIG. 2. EEG shows spiky rhythmic alpha activity in the left posterior head region, which evolved into repetitive sharp waves. Nystagmus was observed in the right frontopolar channel (boxed recordings). 250 Lee et al: J Neuro-Ophthalmol 2012; 32: 249-251 Clinical Observation Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. REFERENCES 1. Garcia-Pastor A, Lopez-Esteban P, Peraita-Adrados R. Epileptic nystagmus: a case study video-EEG correlation. Epileptic Disord. 2002;4:23-28. 2. Gire C, Somma-Mauvais H, Nicaise C, Roussel M, Garnier JM, Farnarier G. Epileptic nystagmus: electroclinical study of a case. Epileptic Disord. 2001;3:33-37. 3. Weber YG, Roesche J, Lerche H. 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