There is an increased risk of unprovoked seizures in ADHD children, especially for iADHD whereas benign centro-temporal seizures and related IEDs would prevail in hADHD. Potential pathogenetic factors include neurotrasmitters alterations, genetic, environmental and iatrogenic factors. A higher rate of cognitive dysfunction, language and learning disabilities is shared by ADHD and epilepsy. Also epileptiform EEG (IEDs) abnormalities occur more frequently in ADHD with a mean of 15% against a background incidence of 2-3% in normal school-aged children. Although rarely pursued during sleep, epileptic activity/abnormalities (EAS) is more frequent and severe during SWS even in children with no seizure history and none or sporadic IEDS while awake. Focal abnormalities, right sided or bilateral, prevail over generalized ones, involving, in order, centro-temporal, frontal and parieto-temporal areas. They interfere with developing cognitive abilities and strongly relate to learning disability, contributing to attention impairment. Specific cognitive deterioration has been reported with severe IEDs even in the absence of clinical seizures, warranting specific AE treatment to ameliorate the cognitive domain. Informed therapeutic choices need to be cautions to avoid iatrogenic further damage from “old” or cognitive unfriendly drugs such as CBZ or TPM, whereas LEV, LTG and VPA hold favourable profiles. Also disorders of arousal (DOA) occur more frequently in ADHD children, representing a common dysmaturative factor expressing vulnerability to SWS fragmentation. A thorough differential diagnosis of nocturnal paroxysmal events is mandatory and a role for drugs acting as sleep stabilizers could prevent both seizures and/or other paroxysmal nocturnal events.
Nocturnal epileptiform activity in patients with ADHD
SILVESTRI, Rosalia
2010-01-01
Abstract
There is an increased risk of unprovoked seizures in ADHD children, especially for iADHD whereas benign centro-temporal seizures and related IEDs would prevail in hADHD. Potential pathogenetic factors include neurotrasmitters alterations, genetic, environmental and iatrogenic factors. A higher rate of cognitive dysfunction, language and learning disabilities is shared by ADHD and epilepsy. Also epileptiform EEG (IEDs) abnormalities occur more frequently in ADHD with a mean of 15% against a background incidence of 2-3% in normal school-aged children. Although rarely pursued during sleep, epileptic activity/abnormalities (EAS) is more frequent and severe during SWS even in children with no seizure history and none or sporadic IEDS while awake. Focal abnormalities, right sided or bilateral, prevail over generalized ones, involving, in order, centro-temporal, frontal and parieto-temporal areas. They interfere with developing cognitive abilities and strongly relate to learning disability, contributing to attention impairment. Specific cognitive deterioration has been reported with severe IEDs even in the absence of clinical seizures, warranting specific AE treatment to ameliorate the cognitive domain. Informed therapeutic choices need to be cautions to avoid iatrogenic further damage from “old” or cognitive unfriendly drugs such as CBZ or TPM, whereas LEV, LTG and VPA hold favourable profiles. Also disorders of arousal (DOA) occur more frequently in ADHD children, representing a common dysmaturative factor expressing vulnerability to SWS fragmentation. A thorough differential diagnosis of nocturnal paroxysmal events is mandatory and a role for drugs acting as sleep stabilizers could prevent both seizures and/or other paroxysmal nocturnal events.Pubblicazioni consigliate
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