Nonconvulsive status epilepticus (NCSE) is an unusual complication in patients treated with cefepime. An 82-year-old woman on maintenance hemodialysis was given cefepime for pneumonia. Her level of consciousness decreased since the administration of cefepime, and she was diagnosed with NCSE based on electroencephalography (EEG) findings. After discontinuation of cefepime, improvement was seen both in the level of consciousness and EEG findings. Clinicians should be aware of cefepime-induced NCSE, particularly in patients with renal failure.

Nonconvulsive status epilepticus usually presents with altered mentation without distinct manifestations of seizures. It may be related with various medical disorders. Hashimoto’s encephalopathy is characterized by various neurological manifestations accompanied by high titers of anti-thyroid antibodies. Here, we report a patient with nonconvulsive status epilepticus caused by Hashimoto’s encephalopathy who showed a dramatic response to steroids.

Background
: We studied EEG changes during pilocarpine-induced status epilepticus(SE), a widely used model whose EEG characteristics have not been fully described previously. Method : Male Sprague-Dawley rats weighing 250-350 grams were used as subjects. SE was induced 5-7 days after placement of chronic epidural electrodes, using 360-380mg/Kg pilocarpine IP. Rats were observed with continuous EEG recording following pilocarpine injection until end of the SE episode. Results : SE occurred in 10/12 rats studied. SE began with a series of discrete seizures 11.1?.93 minutes after pilocarpine injection. 5.2?.71 seizures occurred over 10.9?.62 minutes, until the EEG converted to a waxing and waning pattern, during which the amplitude and frequency of epileptiform activity increased. After 1.4?.82 minutes, a pattern of continuous high amplitude rapid spiking was established. Continuous spiking continued for 3.4?.48 hours with a very gradual decline in amplitude and frequency, until periodic epileptiform discharges(PEDs) began to occur. The EEG consisted primarily of PEDs for another 7.4?.09 hours, until electrographic generalized seizures beganto occur. These continued for 5.8?.82 hours until death. Duration of SE was 17.0?.88 hours. Flat periods were a prominent feature during all EEG patterns in this model. Conclusion : EEG features distinctive in pilocarpine SE(but not unique to it) include flat periods during all patterns and resumption of continuous spiking episodes after the onset of PEDs. The sequence of discrete seizures to waxing and waning to continuous spiking to PEDs was identical to that which has been described in humans and other animal models.

Backgrounds and Objectives: Despite of enormous clinical and laboratory researches focused on the useful markersin status epilepticus(SE), clinically applicable methods are not yet available. Although ketogenic diet (KD) is an oldmethod of treating epilepsies, its outstanding antiepileptic effect in some epileptic patients needs re-evaluation of thismethods. This study was performed to evaluate the effect of KD on the change of nitric oxide(NO) during the SE.Methods: After the determination of critical EEG stages in the pilocarpine-induced SE model, serum NO levels weremeasured with Griess reaction. Open cardiac puncture was done immediately after the four different EEG stages of SEin the KD rats and regular diet (RD) rats. Cessation of SE was done with the 10~20 mg/Kg of diazepam i.p. injection ineach stages of SE in KD and RD rats.Results: Pilocarpine-induced SE showed reliable EEG and behavioral patterns in all rats. Also, KD did not affect theSE induced by pilocarpine in terms of the SE induction time and SE severity. Serum NO was consistently higher in KDrats than RD rats in all SE stages.Conclusions: KD significantly increases NO during the pilocarpine-induced SE. These finding might contribute theneuroprotective effect of KD in the SE.

Periodic lateralized epileptiform discharges (PLEDs) had been debated whether it is ictal or non-ictal phenomenon. As mostof 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 acutestructural lesions in the brain and metabolic disorders or old CNS lesions may cause PLEDs and even more, no brain lesionwas identified in some patients. There are many data supporting PLEDs as ictal phenomena. Occurrence of PLEDs usuallyaccompanied by decreased mentality and is improved as PLEDs disappeared. Current SPECT study showed marked hyperperfusionin the lesion side of PLEDs, that is striking evidence of PLEDs as ictal phenomena. Also careful review of EEGwith PLEDs revealed it is a dynamic process rather than a static state. Despite of these evidences, as PLEDs are an end-stageof animal status epilepticus models, it may be a transition of ictal to interictal state.

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