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Effects of lamotrigine on attention-deficit hyperactivity disorder in pediatric epilepsy patients.

ABSTRACT: The purpose of this study was to investigate the effects of lamotrigine for the treatment of attention-deficit hyperactivity disorder (ADHD) symptoms in children with epilepsy.Pediatric patients newly diagnosed with epilepsy (n=90 [61 boys and 29 girls]; mean age, 9.1±3.4 years) were enrolled. All patients were evaluated with the Korean ADHD rating scale (K-ARS)-IV before treatment with lamotrigine and after doses had been administered. The mean interval of ADHD testing was approximately 12.3 months. The initial dosage of lamotrigine was 1 mg/kg/day (maximum 25 mg/day for the first 2 weeks), and increased by 1 mg/kg every 2 weeks until titrated up to 7 mg/kg/day (or maximum 200 mg/day).The mean ADHD test score of the 90 subjects was 17.0±1.8 at baseline. It was slightly reduced to 15.6±1.7 after lamotrigine monotherapy (P >0.01). Prior to treatment, a total of 31 patients (34.4%) met the diagnostic criteria for ADHD according to Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision, Of these 31 patients, 27 (87.1%) had significantly improved ADHD scores with lamotrigine monotherapy (28.0±1.6 reduced to 18.1±2.6, P<0.001). Among these 27 patients, 25 (92.6%) showed normalized electroencephalogram (EEG) and 26 (96.3%) achieved total freedom from seizures within 12 months of the initiation of lamotrigine monotherapy.The results from our study show that lamotrigine had a positive effect in pediatric epilepsy patients by reducing ADHD symptoms, preventing seizures, and normalizing EEG. However, further research is required to determine whether lamotrigine is efficacious against ADHD symptoms independent of its effects on epileptic seizures.

SUBMITTER: Han SA

PROVIDER: S-EPMC5500387 | biostudies-other | 2017 Jun

REPOSITORIES: biostudies-other

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Project description:The purpose of this study was to assess the efficacy and safety of edivoxetine (LY2216684), a selective norepinephrine reuptake inhibitor, in pediatric patients with attention-deficit/hyperactivity disorder (ADHD).A fixed-dose, randomized, double-blind, 8 week study was conducted in patients 6-17 years of age, who were randomized by two strata: 1) Patients with prior stimulant use randomized to placebo, edivoxetine 0.1?mg/kg/day, 0.2?mg/kg/day, or 0.3?mg/kg/day arms in a 1:1:1:1 ratio; 2) Stimulant-naïve patients randomized to placebo, edivoxetine 0.1mg/kg/day, 0.2?mg/kg/day, 0.3?mg/kg/day, or osmotic-release oral system methylphenidate (OROS MPH) (18-54?mg/day based on body weight) arms in a 1:1:1:1:1 ratio. The primary efficacy measure was baseline-to-week 8 change of ADHD Rating Scale (ADHD-RS) total score for edivoxetine 0.2?mg/kg/day and 0.3?mg/kg/day.A total of 340 patients were randomized to placebo (n=78); edivoxetine 0.1?mg/kg/day (n=76), 0.2?mg/kg/day (n=75), or 0.3?mg/kg/day (n=75); or OROS MPH (n=36). In the stimulant-naïve stratum, the positive control, OROS MPH, was significantly superior to placebo in mean ADHD-RS total score change at end-point (-19.46, p=0.015). The edivoxetine 0.2?mg/kg/day and 0.3?mg/kg/day arms had statistically significantly greater improvement than the placebo arm in mean ADHD-RS total score change at end-point (placebo -10.35; edivoxetine 0.2?mg/kg/day -16.09, p<0.010; edivoxetine 0.3?mg/kg/day -16.39, p<0.010) and Clinical Global Impressions-Improvement score (placebo 3.05; edivoxetine 0.1?mg/kg/day 3.01, p=0.860; edivoxetine 0.2?mg/kg/day 2.54, p=0.013; edivoxetine 0.3?mg/kg/day 2.53, p=0.013). In the overall efficacy-analyses data set (n=270), the effect size estimates for edivoxetine doses 0.1?mg/kg/day, 0.2?mg/kg/day and 0.3?mg/kg/day at the week 8 time point were 0.17, 0.51, and 0.54, respectively (for the stimulant-naïve stratum, the effect size estimate for OROS MPH was 0.69). Compared with placebo, edivoxetine treatment was associated with statistically significant increases in blood pressure and pulse (p<0.050), and a smaller increase or slight decrease in weight.Edivoxetine at doses of 0.2?mg/kg/day and 0.3?mg/kg/day demonstrated efficacy in ADHD treatment, despite the presence of a sizeable placebo response. No unexpected adverse events were identified. Clinical Trial Registry identifier: NCT00922636.

Project description:BackgroundEpilepsy and attention-deficit/hyperactivity disorder (ADHD) are strongly associated; however, the underlying factors contributing to their co-occurrence remain unclear. A shared genetic liability has been proposed as one possible mechanism. Therefore, our goal in this study was to investigate the familial coaggregation of epilepsy and ADHD and to estimate the contribution of genetic and environmental risk factors to their co-occurrence.MethodsWe identified 1,899,654 individuals born between 1987 and 2006 via national Swedish registers and linked each individual to his or her biological relatives. We used logistic regression to estimate the association between epilepsy and ADHD within individual and across relatives. Quantitative genetic modeling was used to decompose the cross-disorder covariance into genetic and environmental factors.ResultsIndividuals with epilepsy had a statistically significant increased risk of ADHD (odds ratio [OR] = 3.47, 95% confidence interval [CI] = 3.33-3.62). This risk increase extended to children whose mothers had epilepsy (OR = 1.85, 95% CI = 1.75-1.96), children whose fathers had epilepsy (OR = 1.64, 95% CI = 1.54-1.74), full siblings (OR = 1.56, 95% CI = 1.46-1.67), maternal half siblings (OR = 1.28, 95% CI = 1.14-1.43), paternal half siblings (OR = 1.10, 95% CI = 0.96-1.25), and cousins (OR = 1.15, 95% CI = 1.10-1.20). The genetic correlation was 0.21 (95% CI = 0.02-0.40) and explained 40% of the phenotypic correlation between epilepsy and ADHD, with the remaining variance largely explained by nonshared environmental factors (49%, nonshared environmental correlation = 0.36, 95% CI = 0.23-0.49). The contribution of shared environmental factors to the cross-disorder overlap was not statistically significant (11%, shared environmental correlation = 0.32, 95% CI = -0.16-0.79).ConclusionsThis study demonstrates a strong and etiologically complex association between epilepsy and ADHD, with shared familial factors and risk factors unique to the individual contributing to co-occurrence of the disorders. Our findings suggest that epilepsy and ADHD may share less genetic risk as compared with other neurodevelopmental disorders.

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Effects of lamotrigine on attention-deficit hyperactivity disorder in pediatric epilepsy patients.

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