BACKGROUND Various anticonvulsant medications have been associated with paradoxical aggravation of epileptic seizures in therapeutic doses and toxic concentrations. Lamotrigine has been reported to exacerbate seizures and myoclonic seizures in generalized epilepsy in a child with localization-related epilepsy. OBJECTIVE To describe lamotrigine intoxication paradoxically producing status epile...

background: in this study, we compared the efficacy and safety of propofol and midazolam in treatment of children’s refractory status epilepticus.   methods: we recruited 32 patients with refractory status epilepticus. of those, 16 were treated primarily with midazolam and 16 received propofol.   results: we achieved complete seizure control in 6 (38%) patients treated by midazolam, and in 10 (...

BACKGROUND Transient imaging abnormalities, including changes on diffusion-weighted imaging (DWI), may be seen in status epilepticus. These abnormalities can be followed by hippocampal sclerosis. CASE REPORT We report a 15-year-old lady with focal non convulsive status epilepticus (NCSE) and focal slowing on EEG. DWI exhibited abnormal hyperintense signals in bilateral temporal and insular co...

Electroencephalography is a useful tool in the diagnosis and management of status epilepticus (SE) and it can also give prognostic information. It can help to confirm that an episode of SE has ended. It can identify the patients who have unsuspected subclinical seizures. There is a wide range of presentations of SE. Nearly all types of seizures have the potential of occurring in a repeated or c...

Nonconvulsive status epilepticus (NCSE) poses a significant multidimensional challenge for emergency and intensive care physicians as well as neurologists [1, 2]. This primarily starts with the diagnosis and related detection and confirmation of NCSE, and continues through optimal therapy and difficult prognosis [3]. Although a convulsive status epilepticus (CSE) needs only to be distinguished ...

The epileptic semiology of 19 patients (from 15 families) with mitochondrial disease due to mutations in the POLG1 gene is presented. The patients were either homozygous for the 1399G > A (p.A467T) or 2243G > C (p.W748S) mutations or compound heterozygotes for these two mutations. While the clinical features have been reviewed, detailed analysis of their epilepsy is presented for the first time...