About this Research Topic
Self-limited focal childhood epilepsy (SELFE) is currently a highly debated hot topic, being the focus of several papers. These conditions account for 15-20% of childhood epilepsies and raise many unresolved questions both from conceptual and therapeutic aspects. In 2012, an international symposium in London dealt with SELFE, calling them a “lost tribe” of epileptological taxonomies. Several years later, the time is ripe to re-discuss the accumulated data and views about this enigmatic group.
An ILAE task force has recently proposed a new nomenclature for ordering the overlapping and contradictory designations. This will help communication between specialists and allow more accurate definitions and classifications of the involved conditions. This is of paramount importance because we lack consensus about several syndromes’ inclusion.
These epilepsies interfere with childhood cognitive development, and it has been found that cognitive deterioration likely starts before clinical epilepsy-onset. The causative role of epilepsy (mainly interictal discharges) or a common developmental abnormality underlying both an early cognitive impairment and a later epilepsy can be raised. At the severe end of the spectrum (ESES/LKS), epilepsy likely has a role in cognitive decay.
The goal of this Research Topic is to offer a proper occasion to discuss crucial questions, provide a new impetus and bring together those involved. Thus, Topic Editors welcome any types of manuscripts supported by the journal, comprised of original research article, brief research article, review, mini-review, and meta-analysis, pertaining, but not limited to, the following themes:
- The relationship between cognitive and epileptic symptoms.
- The diverging localization and timing of epileptic (ictal and interictal) features and neuropsychological symptoms.
- The involvement of the perisylvian language network. Does it really host SELFE and is it really hijacked by the epileptic process as the system epileptic approach of epileptogenesis would dictate?
- The roles of the centro-temporal spikes (CTS) (+ripples) across the spectrum. CTS is a shared interictal epileptiform potential marking the severity of the involved conditions, together with pathological ripples in sleep.
- The link between CTS and early drivers of synapting plasticity, such as “delta-brush” and “sharp-wave ripple”.
- The pathophysiology of the transformation of the CTS (IEDs) to ESES discharges, which may highlight epileptic progression and epileptogenesis in general.
- The chameleon like changes (transformations) of syndromes within the spectrum.
- Taxonomical aspects and the relationship with other epilepsies’ mechanism of cessation in adolescence (the problem of time window).
- The mechanism of EE-SWAS regression.
- Further research on the relation of genetic, clinical, and EEG data.
An ILAE task force has recently proposed a new nomenclature for ordering the overlapping and contradictory designations. This will help communication between specialists and allow more accurate definitions and classifications of the involved conditions. This is of paramount importance because we lack consensus about several syndromes’ inclusion.
These epilepsies interfere with childhood cognitive development, and it has been found that cognitive deterioration likely starts before clinical epilepsy-onset. The causative role of epilepsy (mainly interictal discharges) or a common developmental abnormality underlying both an early cognitive impairment and a later epilepsy can be raised. At the severe end of the spectrum (ESES/LKS), epilepsy likely has a role in cognitive decay.
The goal of this Research Topic is to offer a proper occasion to discuss crucial questions, provide a new impetus and bring together those involved. Thus, Topic Editors welcome any types of manuscripts supported by the journal, comprised of original research article, brief research article, review, mini-review, and meta-analysis, pertaining, but not limited to, the following themes:
- The relationship between cognitive and epileptic symptoms.
- The diverging localization and timing of epileptic (ictal and interictal) features and neuropsychological symptoms.
- The involvement of the perisylvian language network. Does it really host SELFE and is it really hijacked by the epileptic process as the system epileptic approach of epileptogenesis would dictate?
- The roles of the centro-temporal spikes (CTS) (+ripples) across the spectrum. CTS is a shared interictal epileptiform potential marking the severity of the involved conditions, together with pathological ripples in sleep.
- The link between CTS and early drivers of synapting plasticity, such as “delta-brush” and “sharp-wave ripple”.
- The pathophysiology of the transformation of the CTS (IEDs) to ESES discharges, which may highlight epileptic progression and epileptogenesis in general.
- The chameleon like changes (transformations) of syndromes within the spectrum.
- Taxonomical aspects and the relationship with other epilepsies’ mechanism of cessation in adolescence (the problem of time window).
- The mechanism of EE-SWAS regression.
- Further research on the relation of genetic, clinical, and EEG data.
Keywords: Self-limited Focal Childhood Epilepsies, Perisylvian epileptic network, centrotemporal spikes, Rolandic epilepsy, neuropsycological deficits, atypical Rolandic epilepsy, electrical status epilepticus in sleep (ESES), Landau-Kleffner syndrome
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