Seizure

The EEG phenomenon of ESES was first described in 1971 in a case series of 6 children with epilepsy who were found to have continuous spike-wave discharges in non–rapid eye movement sleep, with resolution upon awakening. [1] CSWS is a specific clinical syndrome, defined in 1989 as an epileptic encephalopathy during childhood that shows continuous EEG abnormalities during non-REM sleep (often shows ESES), in association with a variety of seizure types, including nocturnal convulsions, atypical absence seizures, and epileptic negative ...

Temporal lobe encephaloceles (TEs) are defined as a pathological herniation of brain parenchyma through a dural and/or bony defect in the middle cranial fossa [1,2]. Their aetiology remains controversial. Most TEs seem to be congenital, although symptomatic forms have been reported, and are typically associated with local inflammation, trauma, neoplasia or idiopathic intracranial hypertension [3–5].

Developmental and epileptic encephalopathy with suppression burst (DEE-SB) is a severe disorder in which cognitive, sensory, and motor development are impaired by recurrent clinical seizures or prominent interictal epileptiform discharges during the neonatal or early infantile period. The key electroencephalogram (EEG) finding is the suppression-burst pattern. Seizures are highly intractable, and in previous reports, antiepileptic medications have demonstrated only limited effectiveness in seizure control [1,2].

Over the last few years Seizure – European Journal of Epilepsy has published many articles on Psychogenic Nonepileptic Seizures (PNES). For example, six articles with “PNES” in their title were identified since January 2019, i.e. in the last five months [1–6]. “PNES” is now the most common term in the neurology literature for naming a psychiatric disorder characterized by the production of clinical seizures without electroencephalographic changes. This disorder has been misnamed over the centuries with different terms, such as ...

Dissociative seizures—also referred to as psychogenic non-epileptic seizures— account for about 20% of referrals to seizure clinics [1]. Traditionally, neurologists have viewed their role as limited to the diagnosis of dissociative seizures rather than the treatment of this disorder [2]. While there is currently no clear evidence base, expert opinion has favoured psychotherapeutic treatments [3], although most patients perceive their dissociative seizures as a problem which is largely “physical” [4].

Focal (partial onset) seizures are often treated similarly in children over 4 years of age and in adolescent or adult patients [1,2]. As in adults, over 25% of children have inadequate seizure control on currently available antiepileptic drugs (AEDs), or have experienced significant adverse drug effects [3,4]. In general, there are fewer data from randomized controlled trials to guide the treatment of epilepsy in pediatric patients compared with adults [5].

Diffuse gliomas are the most common primary brain tumor in adults, affecting about 20,000 people in the US each year [1]. Epileptic seizures often develop in patients with gliomas (40%–70%) and approximately 30% are pharmaco-resistant even after glioma resection [2,3]. There is an abundance of literature supporting the association between tumor grade and histopathology and glioma-related epilepsy [3,4]. However, recent studies suggest that epileptogenesis is also influenced by tumor molecular genetic markers [4–7].

Monitoring seizures with long-term video-electroencephalography (EEG) in the epilepsy monitoring unit (EMU) is one of the most useful diagnostic tools in the epileptologist’s armamentarium. While clinically useful and largely safe, this procedure is not risk-free. Adverse events reported by epilepsy centers include falls, status epilepticus, postictal psychosis, fractures, infections, and the most feared complication, sudden unexpected death in epilepsy (SUDEP) [1]. A large retrospective study noted a SUDEP risk of 1.2 per 10,000 inpatient video-EEG monitoring admissions [2].

Watanabe et al. reported focal epilepsy of infants with favorable outcome [1,2], and proposed an epilepsy syndrome called benign partial epilepsy in infancy [3]. Benign partial epilepsy in infancy was renamed benign infantile epilepsy (BIE) or benign familial infantile epilepsy (BFIE), if familial, and it has been described in the international classification of epilepsy [4]. Additionally, an association of BIE with paroxysmal kinesigenic dyskinesia (PKD) has been reported and called infantile convulsions and choreoathetosis [5].

We read with great interest the paper entitled “Compound heterozygous SZT2 mutations in two siblings with early-onset epilepsy, intellectual disability and macrocephaly” by Domingues et al. [1].