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Pre-Existing Comorbid Emotional Symptoms Moderate Short-Term Methylphenidate Adverse Effects in a Randomized Trial of Children with Attention-Deficit/Hyperactivity Disorder.

ABSTRACT: Objective: We sought to ascertain whether baseline anxiety/depression and oppositional defiant disorder (ODD) symptoms impacted the experience of short-term methylphenidate (MPH) adverse effects (AEs) in 7- to 11-year-old children with attention-deficit/hyperactivity disorder (ADHD) (n = 171) undergoing a double-blind MPH crossover trial. Method: The Vanderbilt ADHD Diagnostic Parent Rating Scale measured baseline child anxiety/depression and ODD symptomology. The parent-completed Pittsburgh Side Effect Rating Scale assessed the AEs of anxiety, sadness, and irritability at baseline, on placebo, and on three MPH dosages. For each AE, we evaluated comorbidity main effects, dose main effects, and comorbidity × dose interactions. Results: Baseline anxiety/depression × dose and ODD × dose interactions were significant for the AEs of anxiety, sadness, and irritability. Compared with premedication baseline, these AEs attenuated on MPH for children with initially higher comorbidity symptoms, whereas those with initially lower comorbidity symptoms tended toward no change or increasing AE levels. Conclusion: Premedication anxiety/depressive and ODD symptoms may be important predictors of short-term MPH emotional AEs.

SUBMITTER: Froehlich TE

PROVIDER: S-EPMC7153644 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Sleep-Associated Adverse Events During Methylphenidate Treatment of Attention-Deficit/Hyperactivity Disorder: A Meta-Analysis.

Project description:ObjectiveSleep disturbances are a feature of attention-deficit/hyperactivity disorder (ADHD) and an adverse event (AE) of methylphenidate treatment. The authors sought to clarify methylphenidate-associated sleep problems and how studies are affected by confounding factors.Data sourcesPublished studies in English collected via online databases and unpublished data from www.clinicaltrials.gov and US Food and Drug Administration websites. Sources were searched from inception to August 2017.Study selectionIncluded were blinded placebo-controlled studies of youth with ADHD conducted in naturalistic settings, leading to 35 studies yielding 75 observations of sleep-related AEs. These studies comprised 3,079 drug-exposed and 2,606 placebo-treated patients.Data extractionTwo PhD-level reviewers reviewed each study for inclusion. Four PhD/PharmD-level reviewers extracted data in duplicate. Discrepancies were resolved by discussion or, if needed, by the senior author.ResultsIncreased pooled relative risks (RRs) were found for methylphenidate-associated sleep-related AEs for insomnia (general), initial insomnia, middle insomnia, combined insomnia, and sleep disorder. Several sample or study design features were significantly associated with the RR for sleep-related AEs and the methylphenidate formulation studied (P < .05). After correction for confounding variables, significant differences among drugs were found for initial insomnia, insomnia (general), and sleep disorder (P < .0001) as the other categories could not be tested due to insufficient studies. The findings also show that the RR and its interpretation are constrained by the placebo AE rate.ConclusionsSeveral types of insomnia and sleep problems are associated with methylphenidate treatment. Study design and sample features influence the RR statistic. By showing that the rate of placebo AEs impacts the RR, this study provides the field with a useful covariate for adjusting RR statistics.

| S-EPMC8074661 | biostudies-literature

Effect of methylphenidate on gene expression profiles of Attention Deficit Hyperactivity Disorder patients and unaffected controls.

Project description:Attention deficit hyperactivity disorder (ADHD) is a common psychiatric condition of children with a prevalence of 5-10% worldwide. Up to 30% of adults with a history of childhood ADHD maintain symptoms in later life; these adult ADHD patients are severely impaired in social and professional life due to persistence of ADHD core symptoms like impulsivity, attention deficit and hyperactivity as well as frequently observed co-morbidities like alcohol and drug abuse, major depression, bipolar and personality disorders. Pharmaceutical treatment options include methylphenidate (MPH), which is amongst others an inhibitor of the dopamine transporter and therefore increases dopamine levels in the brain. However, not all ADHD patients are MPH responders with clinical features to distinguish responders and non-responders being not at hand so far. Likewise, neurobiological reasons for drug response are still elusive. Here, we examined the global transcriptional response of MPH on lymphoblastoid cell lines (LCLs) derived from ADHD patients and unaffected controls.

2014-09-05 | E-GEOD-52889 | biostudies-arrayexpress

Effect of methylphenidate on gene expression profiles of Attention Deficit Hyperactivity Disorder patients and unaffected controls.

2014-09-05 | GSE52889 | GEO

Integrative genomic analysis of methylphenidate response in attention-deficit/hyperactivity disorder.

Project description:Methylphenidate (MPH) is the most frequently used pharmacological treatment in children with attention-deficit/hyperactivity disorder (ADHD). However, a considerable interindividual variability exists in clinical outcome. Thus, we performed a genome-wide association study of MPH efficacy in 173 ADHD paediatric patients. Although no variant reached genome-wide significance, the set of genes containing single-nucleotide polymorphisms (SNPs) nominally associated with MPH response (P?<?0.05) was significantly enriched for candidates previously studied in ADHD or treatment outcome. We prioritised the nominally significant SNPs by functional annotation and expression quantitative trait loci (eQTL) analysis in human brain, and we identified 33 SNPs tagging cis-eQTL in 32 different loci (referred to as eSNPs and eGenes, respectively). Pathway enrichment analyses revealed an over-representation of genes involved in nervous system development and function among the eGenes. Categories related to neurological diseases, psychological disorders and behaviour were also significantly enriched. We subsequently meta-analysed the association with clinical outcome for the 33 eSNPs across the discovery sample and an independent cohort of 189 ADHD adult patients (target sample) and we detected 15 suggestive signals. Following this comprehensive strategy, our results provide a better understanding of the molecular mechanisms implicated in MPH treatment effects and suggest promising candidates that may encourage future studies.

| S-EPMC5789875 | biostudies-literature

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Project description: Not available

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Methylphenidate for children and adolescents with attention deficit hyperactivity disorder (ADHD).

Project description: Not available

| S-EPMC8763351 | biostudies-literature

Improvements in Irritability with Open-Label Methylphenidate Treatment in Youth with Comorbid Attention Deficit/Hyperactivity Disorder and Disruptive Mood Dysregulation Disorder.

Project description:OBJECTIVE:The purpose of this open-label study was to examine the effects of long-acting methylphenidate (MPH) treatment on irritability and related emotional symptoms associated with disruptive mood dysregulation disorder (DMDD) in youth with comorbid attention-deficit/hyperactivity disorder (ADHD). METHODS:The sample included 22 medication-free male and female subjects (ages 9-15) who met criteria for both DMDD and ADHD. Participants underwent a 4-week trial of long-acting MPH treatment (Concerta®), with weekly dosing increases until a therapeutic dose was reached. Repeated measures t-tests were used to compare pre- and posttreatment ratings of primary and secondary measures. The primary outcome was self-report irritability. Secondary outcomes included parent and child ratings of emotional frequency, emotional lability, and negative affect (NA). Multiple regression was used to examine the impact baseline hyperactivity, age, gender, race, socioeconomic status, or comorbid diagnosis had on treatment outcomes. RESULTS:Significant improvements (medium to large effect sizes) in child-rated irritability as well as parent and child ratings of emotional lability, NA, and anger were found. As anticipated, ADHD symptoms also improved. While a majority of the sample saw improvement in child-rated irritability (71%), symptoms worsened a small proportion (19%), and an even smaller portion experienced no change (10%). No demographics, psychiatric comorbidities, or severity of ADHD symptoms influenced treatment outcomes. CONCLUSIONS:Study findings suggest that MPH treatment significantly improved mood and emotional symptoms associated with DMDD comorbid with ADHD. These findings, coupled with good tolerability in this open-label pilot study supports further research into the use of MPH as a first-line treatment for DMDD. Future work examining MPH treatment of youth with DMDD with and without comorbid ADHD is needed.

| S-EPMC6016730 | biostudies-literature

Methylphenidate normalizes frontocingulate underactivation during error processing in attention-deficit/hyperactivity disorder.

Project description:Children with attention-deficit/hyperactivity disorder (ADHD) have deficits in performance monitoring often improved with the indirect catecholamine agonist methylphenidate (MPH). We used functional magnetic resonance imaging to investigate the effects of single-dose MPH on activation of error processing brain areas in medication-naive boys with ADHD during a stop task that elicits 50% error rates.Twelve medication-naive boys with ADHD were scanned twice, under either a single clinical dose of MPH or placebo, in a randomized, double-blind design while they performed an individually adjusted tracking stop task, designed to elicit 50% failures. Brain activation was compared within patients under either drug condition. To test for potential normalization effects of MPH, brain activation in ADHD patients under either drug condition was compared with that of 13 healthy age-matched boys.During failed inhibition, boys with ADHD under placebo relative to control subjects showed reduced brain activation in performance monitoring areas of dorsomedial and left ventrolateral prefrontal cortices, thalamus, cingulate, and parietal regions. MPH, relative to placebo, upregulated activation in these brain regions within patients and normalized all activation differences between patients and control subjects. During successful inhibition, MPH normalized reduced activation observed in patients under placebo compared with control subjects in parietotemporal and cerebellar regions.MPH normalized brain dysfunction in medication-naive ADHD boys relative to control subjects in typical brain areas of performance monitoring, comprising left ventrolateral and dorsomedial frontal and parietal cortices. This could underlie the amelioration of MPH of attention and academic performance in ADHD.

| S-EPMC3139835 | biostudies-literature

Pharmacogenetics of methylphenidate in childhood attention-deficit/hyperactivity disorder: long-term effects.

Project description:Attention-deficit/hyperactivity disorder (ADHD) is a common neurodevelopmental disorder in which a significant proportion of patients do not respond to treatment. The objective of this study was to examine the role of genetic risk variants in the response to treatment with methylphenidate (MPH). The effectiveness of MPH was evaluated based on variations in the CGI-S and CGAS scales over a 12-month treatment period using linear mixed effects models. A total of 208 ADHD patients and 34 polymorphisms were included in the analysis. For both scales, the response was associated with time, extended-release MPH/both formulations, and previous MPH treatment. For the CGI-S scale, response was associated with SLC6A3 rs2550948, DRD4 promoter duplication, SNAP25 rs3746544, and ADGRL3 rs1868790. Interactions between the response over time and SLC6A3 and DRD2 were found in the CGI-S and CGAS scales, respectively. The proportion of the variance explained by the models was 18% for the CGI-S and 22% for the CGAS. In this long-term study, the effects of SLC6A3, DRD4, SNAP25, and ADGRL3 on response to treatment reflect those observed in previous studies. In addition, 2 previously unreported interactions with response to treatment over a 12-month period were found (SLC6A3 and DRD2).

| S-EPMC5583388 | biostudies-literature

Individualizing the dosage of Methylphenidate in children with attention deficit hyperactivity disorder.

Project description:BackgroundAttention deficit hyperactivity disorder (ADHD) is one of the most common childhood mental health disorders. Stimulant drugs as the most commonly used treatment and first-line therapy for ADHD have side effects. One of the newest approaches to select the best choices and optimize dosages of medications is personalized medicine.MethodsThis historical cohort study was carried out on the data taken from the period of 2008 to 2015. Eligible subjects were included in the study randomly. We used mixed-effects logistic regression models to personalize the dosage of Methylphenidate (MPH) in ADHD. The patients' heterogeneity was considered using subject-specific random effects, which are treated as the realizations of a stochastic process. To recommend a personalized dosage for a new patient, a two-step procedure was proposed. In the first step, we obtained estimates for population parameters. In the second step, the dosage of the drug for a new patient was updated at each follow-up.ResultsOf the 221 children enrolled in the study, 169 (76.5%) were male and 52 (23.5%) were females. The overall mean age at the beginning of the study is 82.5 (± 26.5) months. In multivariable mixed logit model, three variables (severity of ADHD, time duration receiving MPH, and dosage of MPH) had a significant relationship with improvement. Based on this model the personalized dosage of MPH was obtained.ConclusionsTo determine the dosage of MPH for a new patient, the more the severity of baseline is, the more of an initial dose is required. To recommend the dose in the next times, first, the estimation of random coefficient should be updated. The optimum dose increased when the severity of ADHD increased. Also, the results show that the optimum dose of MPH as one proceeds through the period of treatment will decreased.

| S-EPMC7065304 | biostudies-literature

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