Stimulant therapy and seizure risk in children with ADHD
ABSTRACT 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.
- SourceAvailable from: Martijn Arns
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- "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. "
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
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- "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). "
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.Epilepsia 12/2009; 51(7):1185-8. DOI:10.1111/j.1528-1167.2009.02411.x · 4.58 Impact Factor
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- "Gonzáles-Heydrich et al., 2007 75 Oostrom et al., 2003 47 Holtmann e Schmidt, 2003 31 Hesdorffer et al., 2004 17 Duane, 2003 55 Dunn et al., 2005 46 Schubert, 2005 36 Dunn et al., 2009 6 Pellock, 2004 2 Schreibman et al., 2009 21 Bechtel et al., 2009 22 Hermann et al., 2007 20 Gilby, 2009 16 Zhang et al., 2009 52 Kanner, 2008 10 Fonseca et al., 2008 27 Kavros et al., 2008 35 Fonseca et al., 2007 40 Silvestri et al., 2007 33 Holtmann et al., 2006 26 Tan e Appleton, 2005 14 Duane, 2003 55 Sánchez-Carpintero e Neville, 2003 7 Holtmann et al., 2003 25 Deputy, 2002 28 Richer et al., 2002 29 Oostrom et al., 2002 41 Baglieto et al., 2001 39 Hemmer et al., 2001 24 Austin et al., 2001 49 Hughes et al., 2000 32 Fastenau et al., 2004 48 Borgatti et al., 2004 53 Becker et al., 2004 30 Stella e Maciel, 2003 54 Hernandez et al., 2003 51 McAfee et al., 2008 69 Baptista Neto et al., 2008 70 Torres et al., 2008 65 Aldenkamp et al., 2006 59 Feltz-Cornelis et al., 2006 74 Nicolai et al., 2006 23 Gucuyener et al., 2003 "
ABSTRACT: OBJECTIVE: To investigate in the literature elements that explain the association between the attention deficit hyperactivity disorder (ADHD) and epilepsy and to provide clinical guidelines for the management of patients that share these disorders. METHODS:Review of literature of the last 10 years in MedLine and Lilacs databases. The keywords used were "attention deficit hyperactivity disorder", "ADHD" and "epilepsy. RESULTS: Symptoms of ADHD are more frequent in idiopathic epilepsies. Several factors may contribute to this comorbidity: 1) common genetic environment; 2) participation of neurotransmitters norepinephrine and dopamine in ADHD and in neuronal excitability modulation; 3) the underlying brain structural abnormalities found in epileptic patients with ADHD; 4)the chronic effects of seizures and of the epileptiform interictal EEG discharges in attention; 5) the cognitive side effects of antiepileptic drugs. CONCLUSIONS: Recents evidences suggest that seizures and ADHD may have common neurobiological bases. Researches that investigate dysfunctions in cerebral cathecholamines pathways and the role of the interictal epileptiform discharges in the generation of the sintoms are essencial to understand these mechanisms. Treatment for ADHD with stimulant drugs are safe and effective in most epileptic patients.Jornal brasileiro de psiquiatria 12/2009; 59(2):146-155. DOI:10.1590/S0047-20852010000200011