To send content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about sending content to .
To send content items to your Kindle, first ensure email@example.com
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about sending to your Kindle.
Note you can select to send to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be sent to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Apart from age of presentation, the electro-clinical syndromes are elaborated by a distinctive and recognizable set of features including the type of seizure(s) and the electrographic traits which aggregate together.1 Imaging findings can be considered. Neurodevelopmental and psychiatric comorbidities of varying degree are often associated. Causation may be included in the classification system. According to the 2017 position paper of the ILAE Commission for Classification and Terminology, the etiology of epilepsy may be structural, genetic, infectious, metabolic, or immune. Causation may also be unknown (formerly cryptogenic).2 Idiopathic and self-limited (formerly benign) epilepsies occur in children with a normal neurological examination and normal neuro-imaging, in whom there may be a familial predisposition. The term idiopathic (as opposed to genetic) is still preferred by some in respect of four well-recognized idiopathic generalized epilepsy syndromes (IGEs): childhood absence epilepsy (CAE), juvenile absence epilepsy (JAE), juvenile myoclonic epilepsy (JME), and generalized tonic–clonic seizures alone (formerly generalized tonic–clonic seizures on awakening). Although monogenic or more complex genetic or environmental susceptibility factors may be implicated in these epilepsies, the mechanisms are not always fully elucidated. The attribution to genetic causation may incorrectly suggest a high rate of inheritance. Benign focal epilepsies, such as benign or childhood epilepsy with centrotemporal spikes (CECTS) and the occipital lobe epilepsies of Panayiotopoulos and Gastaut are, again according to the position paper, termed self-limited as the term benign does not seem to fully address the developmental impact of these transient epilepsies.2 The epileptic encephalopathies, recognized as a distinct category, comprise a polymorphous group of epilepsy syndromes in which the epileptic activity itself contributes to cognitive and behavioral impairments above and beyond what might be expected from the underlying pathology alone.1 There is abundant epileptiform activity and inherently there is the idea that limiting or suppressing the activity will improve the neurodevelopmental outlook.
Email your librarian or administrator to recommend adding this to your organisation's collection.