Epileptic Nystagmus and Vertigo Associated with Bilateral Temporal and Frontal Lobe Epilepsy

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Demerol and nexium nystagmus

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Epileptic nystagmus is defined as a quick, repetitive jerky movement of the eyeball associated with seizure activity. In cases of epileptic nystagmus associated with ictal discharge from multiple brain areas, localization of the exact epileptogenic zone could be extremely difficult.

During episodes of epilepsy, patients suffer from diverse visual symptoms such as illusion, hallucination, and visual loss and oculomotor signs tonic eye deviation, eyelid blinking, or myoclonus [ 1 ]. Epileptic nystagmus EN is defined as a quick, repetitive jerky movement of the eyeball associated with seizure activity [ 2 ]. Because EN is a rare accompanying demerol and nexium nystagmus of epilepsy, fewer than 50 cases of EN have been reported [ 3 ], demerol and nexium nystagmus.

A number of different cortical regions could induce EN. However, cases of EN due to ictal discharge from the posterior temporo-parietal-occipital region or occipital lobe have been reported [ 3 ]. In addition, there is still significant controversy regarding the exact pathophysiologic mechanism of EN. Clinically, epilepsy associated with simultaneous ictal discharge from multiple cortical lesions is not uncommon. In cases of EN associated with this multiple discharge, localization of the exact epileptogenic zone inducing EN could be difficult.

Therefore, we report on this case with a review of relevant literature, demerol and nexium nystagmus. A nine-year-old female visited our outpatient clinic demerol and nexium nystagmus from intermittent, rotatory vertigo for one year. Initially, she experienced a dizzy spell two or three times a week.

The duration of vertigo was less than one minute. During vertigo attack, there was no loss of consciousness, visual loss or hallucination, or any orbital discomfort. However, there was no improvement of the attacks of dizziness, demerol and nexium nystagmus.

Since then, her father has reported observation of rapid, demerol and nexium nystagmus, jerky movements of the eyeball during vertigo attack. There were no accompanying neurologic, ophthalmologic, or audiologic complaints.

Her father reported that he had experienced several attacks of generalized tonic-clonic seizure. In order to rule out the peripheral cause of vertigo, we performed head shake test, demerol and nexium nystagmus, head impulse test, Dix-Hallpike test and head rolling test. We also performed video nystagmography, caloric test and posturography during the interictal period.

Results of all these examinations were normal during the interictal period. Results of neurologic examination were normal during interictal phase. However, during the ictal phase, horizontal rapid left-beating nystagmus was observed for approximately 20 seconds. The rapid phase of nystagmus was left-sided, and the slow phase was right-sided without crossing the midline Video clip 1, Supplementary material. There was no cognitive impairment, gaze deviation, cortical blindness, or visual hallucination during episodes of EN.

No specific findings were observed on magnetic resonance imaging MRI. Her ophthalmologic examination for visual acuity and visual field showed normal findings. Interictal electroencephalography EEG showed no abnormal epileptic activity. Frequent ictal episodes were monitored during a 12 hour video EEG. During the left-beating nystagmus, the ictal EEG pattern showed rhythmic fast frequency spikes discharges initially in the right temporal regions Fig. It was then followed by demerol and nexium nystagmus fast spikes in bilateral frontal areas Fig.

Ictal electroencephalography shows A initial rhythmic fast spikes with discharges in the right temporal area arrow during the onset of nystagmus and vertigo and B continued rhythmic fast spikes in bilateral temporal regions arrow.

Which were followed by C rhythmic fast frequency spikes in the bilateral frontal area arrow. After two weeks of treatment, she no longer complained of vertigo attack. Vertigo is not a common complaint in the pediatric population, therefore, few studies of pediatric vertigo have been reported, compared to studies demerol and nexium nystagmus the adult population [ 4 ].

EN is an uncommon ictal phenomenon characterized by repetitive jerking movements of the eye due to seizures [ 5 ]. It usually presents as binocular horizontal nystagmus and other symptoms and signs such as episodic gaze deviation, visual hallucinations, demerol and nexium nystagmus blindness, and vertigo may be associated or not.

Age onset of EN has been reported from 10 postnatal days to 75 years [ 5 ]. However, vertigo due to epilepsy in pediatric patients is very rare [ 5 ]. Therefore, it is difficult for physicians to suspect EN clinically as the possible cause of pediatric vertigo.

In patients with epileptic seizures, vertigo is known to be induced by temporal lobe epilepsy [ 6 ]. According to Bense et al. In our case, dizzy spells preceded EN for approximately 10 months. Therefore, we could suppose demerol and nexium nystagmus epileptic discharge from the temporal lobe, cortical saccade region or PIVC could be responsible for the birth control pills and weight vertigo in our patient.

In most cases of EN, several oculomotor signs, including gaze deviation, blindness, or eye blinking are observed along with nystagmus [ 5 ]. However, in our case, there were absolutely no accompanying oculomotor signs, except nystagmus. Although many patients with EN have a brain anomaly, such as hemorrhage, tumor, cortical dysplasia, or cortical atrophy [ 5 ], in our case, MRI finding was completely normal.

Under these conditions, definite diagnosis of EN would be quite difficult. EN could be classified as two types according to their pathophysiologic mechanisms. In type I, the cortical saccade region including the frontal eye field, supplementary eye field, parietal eye field, and posterior parietal lobule is activated for production of epileptic discharge, demerol and nexium nystagmus, and contributes to nystagmus with a contralateral fast component [ 8 ].

In our case, as there was a left-sided fast component and right-sided slow component of nystagmus, right type I contralateral and right type II ipsilateral could both be responsible for the pathophysiologic mechanism. The main difference between each type is that the slow component does not cross the midline in type I, while the slow component crosses the midline in type II [ 89 ]. In our case, as the slow component of nystagmus did not cross the midline, the right cortical saccade region should be responsible for EN.

Although, in our case, we observed discharges from multiple brain areas during the ictal phase, we could suppose that discharges from the right temporal area should be responsible for the EN. In fact, initial ictal discharges started from the right temporal region, spreading to other brain areas.

Therefore, in such a confusing case, thorough understanding of the pathophysiologic mechanism of EN could be helpful in localizing the brain area responsible for nystagmus and dizziness.

Further imaging modality, such as single photon emission computer tomography SPECTcould be considered for better localization of epileptic lesions [ 2 ]. Previous researchers reported that eyeball movements could cause artifacts to readings of EEG [ 11 ]. However, in our case, ictal discharge preceded nystagmus. Therefore, EEG artifact caused by nystagmus could be ruled out. In conclusion, putting clinical findings, characteristics of nystagmus, and EEG findings together, we could induce a possible focus demerol and nexium nystagmus EN among multiple brain lesions in the bilateral hemisphere.

As an ENT doctor, we should suspect brain lesions in cases with prolonged, unexplained vertigo refractory to conventional medication, such as in our case. And we should also perform several studies, demerol and nexium nystagmus, including MRI and EEG, in cases with seizure activity and atypical nystagmus which could not be explained by peripheral neuropathy.

And, if EEG shows abnormal findings, such as ictal discharge, further imaging study, such as SPECT could be considered for better localization of the lesion. No potential conflict of interest to this article was reported.

During the ictal phase, horizontal rapid left-beating nystagmus was observed for approximately 20 seconds. The rapid phase of nystagmus was left-sided, and the slow phase was right-sided without crossing the midline. Accompanying videos can be found in the journal homepage http: National Center for Biotechnology InformationU.

Journal List Clin Exp Otorhinolaryngol v. Published online Nov Find articles by Kyu-Sung Kim. Find articles by Young Hyo Kim. Find articles by Yoonseok Hwang. Find articles by Ben Kang. Find articles by Dong Hyun Kim. Find articles by Young Se Demerol and nexium nystagmus. This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License http: This article has been cited by other articles in PMC.

Abstract Epileptic nystagmus is defined as a quick, demerol and nexium nystagmus, repetitive jerky movement of the eyeball associated with seizure activity. Epilepsy, demerol and nexium nystagmus, Pathologic nystagmus, Vertigo, Electroencephalography, demerol and nexium nystagmus.

Open in a separate window. DISCUSSION Vertigo is not a common complaint in the pediatric population, therefore, few studies of pediatric vertigo have been reported, compared to studies of the adult population [ 4 ]. Footnotes No potential conflict of interest to this article was reported.

Click here to view. Neuro-ophthalmologic manifestations of epilepsy. Lateralizing value of epileptic nystagmus. The spectrum of vertigo in children. Arch Otolaryngol Head Neck Surg. Multisensory cortical signal increases and decreases during vestibular galvanic stimulation fMRI J Neurophysiol. Neurophysiologic and clinical correlations of epileptic nystagmus. Epileptic nystagmus in infancy.

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Demerol and nexium nystagmus

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