• Annals of Clinical Neurophysiology
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• v.13 no.1
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• pp.26-30
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• 2011

Although the pathophysiologic mechanism is unknown, there has been long-running debate on whether periodic discharges such as periodic lateralized epileptiform discharges (PLEDs) and generalized periodic epileptiform discharges are an ictal or interictal EEG pattern. The goal of this review is to give evidence that such periodic discharges on EEG are not ictal phenomenon and just represent underlying acute brain damage. This review includes coma with epileptiform EEG pattern and its prognostic and therapeutic implications. Based on previous reports, rather than taking the view PLEDs represent either an underlying ictal process or an electrographic correlate of neuronal injury, it would be more reasonable that PLEDs are considered as a dynamic pathophysiological state in which unstable neurobiological processes create an ictal-interictal continuum.

• Journal of Ginseng Research
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• v.33 no.1
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• pp.48-54
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• 2009

Epileptifrom discharges were induced in the telencephalon of the adult zebrafish via perfusion with pentylenetetrazole (PTZ), bicuculline methiodide, kainic acid-treated artificial cerebrospinal fluid (aCSF), and $Mg^{2+}$-free aCSF. Ginseng total saponin [GTS ($50{\mu}g/ml$)] was shown to attenuate the occurrence rate of epilpetiform discharges by 50-75%, compared to the control. Ginsenoside $Rg_1$ ($130{\mu}M$) reduced the epileptiform discharges in the isolated telencephalon and delayed the occurrence of behavioral seizures observed from the adult zebrafish placed in the PTZ (10 mM)-containing aquarium water. However, Re was not effective in the suppression of epileptiform discharges and behavioral seizures. These results indicate that $Rg_1$ may be useful in the control of epileptiform discharges and effective in controlling behavioral seizures, and that the zebrafish can be used as a model animal for the testing of potential anticonvulsant drugs.

• Annals of Clinical Neurophysiology
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• v.13 no.1
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• pp.21-25
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• 2011

Periodic lateralized epileptiform discharges (PLEDs) had been debated whether it is ictal or non-ictal phenomenon. As most of PLEDs occur in patients with acute structural lesions, some epileptologists prefer PLEDS as a non-ictal phenomenon, rather an obscure epiphenomenon of etiological diseases. But, almost half of the patients with PLEDs do not have acute structural lesions in the brain and metabolic disorders or old CNS lesions may cause PLEDs and even more, no brain lesion was identified in some patients. There are many data supporting PLEDs as ictal phenomena. Occurrence of PLEDs usually accompanied by decreased mentality and is improved as PLEDs disappeared. Current SPECT study showed marked hyperperfusion in the lesion side of PLEDs, that is striking evidence of PLEDs as ictal phenomena. Also careful review of EEG with PLEDs revealed it is a dynamic process rather than a static state. Despite of these evidences, as PLEDs are an end-stage of animal status epilepticus models, it may be a transition of ictal to interictal state.

• Annals of Clinical Neurophysiology
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• v.19 no.1
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• pp.58-63
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• 2017

Studies of interictal epileptiform discharges are essential for improving the diagnosis, classification, and management of epilepsy. In this case series we sought to identify the clinical and neurophysiological significance of bifid spikes, whose pattern bears a strong resemblance to the cardiac M pattern. We hypothesize that, analogous to the cardiac M pattern, the cerebral M pattern is generated by a conduction defect associated with asynchronous spatiotemporal averaging of electrical signals in the cortex, resulting in the signals reaching the scalp with different latencies. Unlike the cardiac M pattern, the pathology underlying the cerebral M pattern is unknown, although congenital CNS anomalies may be a culprit.

• Annals of Clinical Neurophysiology
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• v.8 no.1
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• pp.81-83
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• 2006

Periodic lateralized epileptiform discharges(PLEDs) are usually seen in acute and subacute cerebral lesions. Occasionally PLEDs could be observed in persistent structural lesions. We observed PLEDs-plus in a patient with right basal ganglionic hemorrhage, at 10 months and 13 months after the stroke. The patients suffered two seizures 3 months and 5 days before recording of EEG. PLEDs-plus may persist as an interictal abnormal finding and the rhythmic discharge of that may be increased by a seizure.

• Journal of Yeungnam Medical Science
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• v.24 no.2
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• pp.107-118
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• 2007

Background : It is well known that non-rapid eye movement(NREM) sleep activates the occurrence of interictal epileptiform discharges(IED) in many epileptic syndromes. We performed this study to assess the effect of NREM sleep on IED in epileptic patients with organic brain lesions. Materials and Methods : We analyzed awake and sleep electroencephalopathy(EEG) recorded simultaneously after partial sleep deprivation in 50 patients. We calculated the awake and sleep spike index (ASI and SSI, spikes/epoch), and the percentage increase of ASI and SSI during sleep. Results : In the 50 patients, the IEDs were recorded exclusively during the awake state in 1 (2%) patient, and during the sleep state in 13(26%) patients. The SSI was higher in 44 (88%) patients, and the ASI was higher in 5 (10%) patients. The mean ASI and the SSI in patients with organic brain lesions were $0.058{\pm}0.121$ and $0.148{\pm}0.187$, and it was $0.081{\pm}0.150$ and $0.174{\pm}0.226$ in patients without organic brain lesions. There were significant increases in the spike index (P<0.05) during NREM sleep in both groups (n=36), but no significant difference in the percent increase of spike index (P>0.05). Conclusion : The IEDs were activated significantly during NREM sleep both in patients with and without organic brain lesions, but there were no differences in the degree of activation in both groups. The activating effect of NREM sleep was not correlated with clinical factors such as, frequent nocturnal seizures, frequent generalized tonic clonic seizures, type of epilepsy and taking anticonvulsants. We conclude that the routine EEG used to evaluate epileptiform discharges in epileptic patients should include sleep recordings after partial sleep deprivation.

• Archives of Pharmacal Research
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• v.27 no.5
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• pp.524-530
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• 2004

Epilepsy or the occurrence of spontaneous recurrent epileptiform discharges (SREDs, seizures) is one of the most common neurological disorders. Shift in the balance of brain between excitatory and inhibitory functions due to different types of structural or functional alterations may cause epileptiform discharges. N-Methyl-D-aspartate (NMDA) receptor dysfunctions have been implicated in modulating seizure activities. Seizures and epilepsy are clearly dependent on elevated intracellular calcium concentration ([C $a^{2+}$]$_{i}$ ) by NMDA receptor activation and can be prevented by NMDA antagonists. This perturbed [C $a^{2+}$]$_{i}$ levels is forerunner of neuronal death. However, therapeutic tools of elevated [C $a^{2+}$]$_{i}$ level during status epilepticus (SE) and SREDs have not been discovered yet. Our previous study showed fast inhibition of ginseng total saponins and ginsenoside R $g_3$ on NMDA receptor-mediated [C $a^{2+}$]$_{i}$ in cultured hippocampal neurons. We, therefore, examined the direct modulation of ginseng on hippocampal neuronal culture model of epilepsy using fura-2-based digital $Ca^{2+}$ imaging and neuronal viability assays. We found that ginseng total saponins and ginsenoside R $g_3$ inhibited $Mg^{2+}$ free-induced increase of [C $a^{2+}$]$_{i}$ and spontaneous [C $a^{2+}$]$_{i}$ oscillations in cultured rat hippocampal neurons. These results suggest that ginseng may playa neuroprotective role in perturbed homeostasis of [C $a^{2+}$]$_{i}$ and neuronal cell death via the inhibition of NMDA receptor-induced SE or SREDs.d SE or SREDs..

• Korean Journal of Clinical Laboratory Science
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• v.49 no.3
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• pp.294-299
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• 2017

The aim of this study was to detect the status of epilepticus and seizure based on the initial patterns observed in the first 30 minutes of continuous electroencephalogram (cEEG) monitoring. An cEEG was recorded digitally using electrodes applied according to the International 10~20 System. The EEG data were reviewed from January 2014 to December 2015. The baselines of the EEG patterns were characterized by lateralized periodic discharges, generalized periodic discharges, burst suppression, focal epileptiform, asymmetric background, generalized slowing, and generalized periodic discharges with a triphagic wave. The etiology was classified into five categories. The subjects of this study were 128 patients (age: $56.9{\pm}17.5years$, male:female, 74:54). The mean cEEG monitoring duration was $5.5{\pm}5.1$ (min:max, 1:33) days. The EEG pattern categories included lateralized periodic discharges (N=7), generalized periodic discharges (N=10), burst suppression (N=6), focal epileptiform (N=19), asymmetric background (N=24), generalized slowing (N=51), and generalized periodic discharges with a triphagic wave (N=11). The etiological classifications of the patients with status epilepticus were remote symptomatic (N=4), remote symptomatic with acute precipitant (N=9), acute symptomatic (N=6), progressive encephalopathy (N=2), and febrile seizure (N=1). cEEG monitoring was found to be useful for the diagnosis of non-convulsive epileptic seizures or status epilepticus. The seizure was confirmed by the EEG pattern.

• Annals of Clinical Neurophysiology
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• v.11 no.1
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• pp.16-23
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• 2009

Background: The intermittent delta activity in electroencephalographies (EEGs) of patients with focal brain lesions has been reported to be a marker of an epileptogenic focus. This study investigated the concordance between the current source distribution (CSD) of the interictal epileptiform discharges (IEDs) and that of the background delta frequency bands (DFBs) of the scalp EEG. Methods: We collected scalp EEGs of 13 patients with focal epilepsy that contained uniregional IEDs and unilateral delta to theta slow waves. We applied a distributed source model using LORETA$^{(R)}$ to determine the CSD of the peak points of the IEDs and the DFBs of the background activity. Results: The CSDs of the DFBs were ipsilateral to the CSDs of the peak point of the averaged IEDs in ten patients, and bilateral with ipsilateral predominance in three patients. In the cases with an ipsilateral CSD of the DFB, 8 of 10 patients had concordance of the CSD localization between the averaged IED and the DFB. In the cases with bilateral CSD of the DFB, 2 of 3 patients had concordance of the CSD localization between the averaged IED and the DFB. Conclusions: The CSD localization and lateralization appear to be concordant between the IEDs and the DFB of background activity in epileptic patients. Therefore, the CSD of the DFB in EEGs with visually observable slow activities may predict those of IEDs.

• Clinical and Experimental Pediatrics
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• v.55 no.5
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• pp.159-163
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• 2012

Most children with epilepsy are of normal intelligence. However, a significant subset will have temporary or permanent cognitive impairment. Factors that affect cognitive function are myriad and include the underlying neuropathology of the epilepsy, seizures, epileptiform discharges, psychosocial problems, age at seizure onset, duration of epilepsy, and side effects associated with antiepileptic drugs. This review article discusses cognitive function in children with idiopathic epilepsy and the effects of antiepileptic drugs on cognitive function in children.