Stimulants are an effective treatment frequently prescribed for attention-deficit-hyperactivity disorder (ADHD), but they commonly are believed to lower the threshold for seizures. Although several studies have revealed that stimulants do not exacerbate well-controlled epilepsy, there is a paucity of data about seizure risk in nonepileptic children treated with stimulants. Two hundred thirty-four children (179 males, 9.1 +/- 3.6 years of age; 55 females, 9.6 +/- 3.9 years of age) with uncomplicated ADHD received electroencephalograms (EEGs) performed in our institution. Thirty-six patients (15.4%) demonstrated epileptiform abnormalities, and 198 (84.6%) demonstrated normal or nonepileptiform EEGs. Rolandic spikes accounted for 40% of the abnormal EEGs and 60% of those with focal abnormalities. Stimulant therapy was elected by 205 of 234 patients (87.6%). Seizures occurred only in the treated group, in one of 175 patients with a normal EEG (incidence 0.6%, 95% confidence intervals 0%-1.7%) and three of 30 treated patients with epileptiform EEGs (incidence 10%, 95% confidence interval 0%-20.7%). Seizures occurred in two of 12 children (16.7%) with rolandic spikes. These data suggest that a normal EEG can be used to assign children with ADHD to a category of minimal risk for seizure. In contrast, an epileptiform EEG in neurologically normal children with ADHD predicts considerable risk for the eventual occurrence of seizure. The risk, however, is not necessarily attributable to stimulant use.
"First, methylphenidate is as effective in alleviating ADHD symptoms in patients who have associated epilepsy as it is in patients with ADHD without epilepsy   . Furthermore, available data do not indicate loss of seizure control with methylphenidate in patients with well-controlled epilepsy [20,27–29], and the limited data suggesting otherwise are not conclusive . While it is well established that children with comorbid ADHD and difficult-to-treat epilepsies face educational, physical, social, and emotional difficulties that directly impact quality of life  , it is "
"These older studies estimated the incidences of paroxysmal EEG in ADHD (or former diagnostic classes of ADHD) between 12 and 15% (Capute, Niedermeyer. & Richardson, 1968; Hemmer, Pasternak, Zecker, & Trommer, 2001; Satterfield et al., 1973) to approximately 30% (Hughes, DeLeo, & Melyn, 2000), which is high compared to 1 to 2% in normal populations (Goodwin, 1947; Richter, Zimmerman, Raichle, & Liske, 1971). Note that these individuals did not present with convulsions and thus did not have a clinical diagnosis of epilepsy but simply exhibited a paroxysmal EEG in the absence of convulsions. "
[Show abstract][Hide abstract] ABSTRACT: This review article summarizes some recent developments in psychiatry such as personalized medicine, employing biomarkers and endophenotypes, and developments collectively referred to as neuromodulation with a focus on ADHD. Several neurophysiological subtypes in ADHD and their relation to treatment outcome are reviewed. In older research the exist-ence of an ‘‘abnormal EEG’’ or ‘‘paroxysmal EEG’’ was often reported, most likely explained by the high occurrence of this EEG subtype in autism, as the diagnosis of autism was not coined until 1980. This subgroup might respond best to anticonvulsant treatments, which requires more specific research. A second subgroup is a beta-excess or beta-spindling sub-group. This group responds well to stimulant medication, albeit several studies suggesting that neurophysiologically this might represent a different subgroup. The third subgroup con-sists of the ‘‘impaired vigilance’’ subgroup with the often-reported excess frontal theta or excess frontal alpha. This subgroup responds well to stimulant medication. Finally, it is pro-posed that a slow individual alpha peak frequency is an endophenotype related to treatment resistance in ADHD. Future studies should incorporate this endophenotype in clinical trials to further investigate new treatments for this substantial subgroup of patients, such as NIRS-biofeedback, transcranial Doppler sonography biofeedback, hyperbaric oxygen therapy, or medications such as nicotine and piracetam.
Journal of Neurotherapy 04/2012; 16(2):123-141. DOI:10.1080/10874208.2012.677664
"Moreover , reported prevalences vary significantly, between 0.6% and 7.0% (Eeg-Olofsson et al., 1971; Cavazzuti et al.,1980; Okubo et al., 1994). Mainly based on these studies several authors recently suggested an increased prevalence of epileptiform EEG discharges in children with behavioral disturbances including attention deficit hyperactivity disorder (ADHD) (Hemmer et al., 2001; Richer et al., 2002; Holtmann et al., 2003). As a consequence, the authors at least discuss that these children might benefit from anticonvulsive therapy (Laporte et al., 2002). "
[Show abstract][Hide abstract] ABSTRACT: Data on epileptiform electroencephalography (EEG) discharges in healthy children are limited, with published studies dating back more than 20 years. Moreover, analyses have been performed exclusively using paper-recorded EEG, and reported prevalences differ significantly. With recent reports using these data as reference suggesting an increased prevalence of epileptiform EEG discharges in children with behavioral disturbances, acquisition of exact prevalence data has become even more critical. The aim of our study was to analyze the frequency of epileptiform EEG discharges in healthy children using digitally recorded EEG (DEEG) and to compare these data to those of previously published studies.
Prospective analysis of DEEG was performed in 382 healthy children (226 male, 156 female) ages 6-13 years admitted to our hospital for minor head trauma. Recording was carried out for a minimum of 20 min including hyperventilation and photic stimulation. Analysis was carried out by two board-certified clinical neurophysiologists.
Epileptiform EEG discharges were detected in 25 of 382 children (11 of 226 male, 14 of 156 female) corresponding to an overall prevalence of 6.5%. Of these 25 children, 4 had either generalized or bifrontal spikes, 12 showed constant localized focal discharges, and 9 showed multifocal discharges. Compared to previous studies using non-DEEG recording, the prevalence of epileptiform EEG discharges in our population was significantly higher. No significant difference was found when comparing our data to prevalences recently reported in children with behavioral disturbances using DEEG.
Our study further highlights the urgent need to reevaluate the prevalence of epileptiform EEG discharges in healthy children using DEEG recordings in a large cohort.
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