Highlights Seizures are known to be one of the neurological complications of thyrotoxicosis. We report unusual bitemporal independent 3-Hz spike-wave activity in a patient with IGE and Graves disease. We speculate that thyroid dysfunction superimposed on IGE thalamocortical network oscillations resulted in this EEG pattern.

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We describe a case of surgical treatment of intractable temporal epilepsy in a female patient with congenital middle cranial fossa encephalocele. We present clinical-anamnestic and neuroimaging data as well as the microscopic and macroscopic pictures of encephalocele. We analyze outcomes of surgery for this pathology, which have been reported in the literature. To date, there have been a few articles on this subject in the domestic literature. The development of neuroimaging techniques and a growing number of verified encephalocele cases promote the widespread use of surgery for treatment of intractable epilepsy. Congenital encephalocele should be considered in the differential diagnosis of intractable temporal epilepsy, and, if verified, surgical treatment is the method of choice in most cases.

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Both non-epileptic sleep disturbances and epilepsy are common in patients with mucopolysaccharidoses (MPS), so diagnosis of sleep-related hypermotor epilepsy in these patients is a tackling issue. We present a case of an adult patient with MPS IIIB (Sanfilippo syndrome), who presented with numerous nocturnal events of sudden awakening and hypermotor behavior, which had been previously regarded as parasomnias. Overnight video-EEG captured numerous stereotypical seizures with ictal pattern in the frontal regions, which led the diagnosis of SHE. The patient was started with carbamazepine, which resulted in a substantial reduction in the number of seizures. Our report provides further support for use of overnight video-EEG in the differential diagnosis of sleeprelated disorders in MPS, yet true incidence of SHE in MPS patients remains unknown.

Cefepime is a fourth-generation cephalosporin antibiotic widely used in clinical practice for various organ systems pathology treatment. The article describes the clinical observation of a patient who, 3 days after cefepime administration, had a decrease in the level of consciousness, regarded as encephalopathy. Cefepime-induced neurotoxicity is characterized by toxic encephalopathy, which manifests 2–6 days after the start of the treatment with this drug and disappears 1–3 days after its withdrawal. Electroencephalography (EEG) abnormalities include generalized periodic discharges (GPR) of triphasic morphology or a pattern corresponding to the criteria for non-convulsive status epilepticus (BSES). In our observation, the EEG recorded stimulus-induced GPRs of triphasic morphology with a frequency of 1.5 Hz; a test with intravenous administration of an antiepileptic drug (levetiracetam) was negative. A day after the withdrawal of cefepime, the patient’s level of consciousness returned to the initial level, and on the EEG periodic discharges completely regressed. Thus, cefepime may cause encephalopathy in patients with rhythmic or intermittent EEG activity, especially in the presence of a stimulus-induced component. In some cases, the use of cefepime may develop epileptic seizures and BSES.

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Sleep is an important activator of epileptiform activity, with epileptiform discharge (ED) probability varying among sleep stages. The aim of our study was to analyze the association between epileptiform activity and sleep stages or wakefulness in adults with temporal discharges. We analyzed 32 long-term overnight EEG recordings. All focal discharges were marked, and the entire sleep was staged. Absolute general epileptiform discharge index (EDI), defined as a ratio of total ED number to the full recording time in hours, as well as absolute EDIs for REM, N1, N2 and N3 stages were calculated. The majority of patients (28) had the highest EDI in N3. EDI increased significantly while sleep progressed to deeper stages, reaching its peak in N3. In REM sleep, EDI sharply declined (p < 0.01) reaching the levels of wakefulness. Increasing synchronization of cortical neurons is thought to be the major mechanism of EDI rise in NREM sleep. Hence, N3 seems to be the most sensitive stage to capture EDs, which highlights the importance of deep sleep recording in patients with temporal epilepsy.