EEG correlates of methylphenidate response in ADHD: association with cognitive and behavioral measures.

J Clin Neurophysiol

Department of Psychiatry and Biobehavioral Sciences, UCLA Neuropsychiatric Institute, Los Angeles, CA 90024, USA.

Published: February 2005


Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

The authors examined the association between EEG correlates of medication response and concomitant cognitive and behavioral changes among children with attention-deficit hyperactivity disorder (ADHD). Subjects were 36 children with ADHD, aged 8 to 12 years. EEG activity was recorded from nine active electrodes during placebo and medication conditions. Medication administration resulted in increased alpha activity in central and parietal regions during both the baseline and cognitive activation conditions. Children who were medication responders exhibited increased frontal beta activity whereas nonresponders showed decreased beta activity in the same region. Increased frontal beta activity was significantly correlated with medication-related improvement in performance on Conners'Continuous Performance Test and parent behavior ratings in attention and hyperactivity. Decreased right frontal theta activity was associated with improvements in parent-rated attention, but not in CPT performance. Stimulant medication increases beta activity in children with ADHD, particularly in frontal regions. Increased cortical arousal and activation in the frontal cortex is strongly associated with sustained attention and response inhibition and with parent-rated attention and hyperactivity/impulsivity.

Download full-text PDF

Source
http://dx.doi.org/10.1097/01.wnp.0000150890.14421.9aDOI Listing

Publication Analysis

Top Keywords

beta activity
16
eeg correlates
8
cognitive behavioral
8
children adhd
8
increased frontal
8
frontal beta
8
parent-rated attention
8
activity
7
medication
5
frontal
5

Similar Publications

Background: Alzheimer's disease (AD) patients and animal models exhibit an altered gut microbiome that is associated with pathological changes in the brain. Intestinal miRNA enters bacteria and regulates bacterial metabolism and proliferation. This study aimed to investigate whether the manipulation of miRNA could alter the gut microbiome and AD pathologies.

View Article and Find Full Text PDF

Epidemiology, resistance profiles, and risk factors of multidrug- and carbapenem-resistant Serratia marcescens infections: a retrospective study of 242 cases.

BMC Infect Dis

September 2025

Department of Laboratory Medicine, Affiliated Hospital of Medical School, Nanjing Drum Tower Hospital, Nanjing University, Nanjing, China.

Background: Serratia marcescens is an opportunistic pathogen increasingly associated with healthcare-associated infections and rising antimicrobial resistance. The emergence of multidrug-resistant (MDR) and carbapenem-resistant S. marcescens (CRSM) presents significant therapeutic challenges.

View Article and Find Full Text PDF

Forkhead-box-protein P3 (FOXP3) is a key transcription factor in T regulatory cells (Tregs). However, its expression and significance in non-immune stromal cells in the tumor microenvironment remain unclear. Here, we demonstrated FOXP3 expression in stromal fibroblasts of mouse and human gastrointestinal tumors.

View Article and Find Full Text PDF

Upon DNA virus infection, cGAS senses viral DNA and triggers MITA (also called STING)-dependent induction of type I interferons (IFN-Is) and other cytokines/chemokines. IFN-Is further activate STAT1/2 to induce interferon-stimulated genes (ISGs) and the innate antiviral response. How the innate antiviral response is silenced in uninfected cells and efficiently mounts upon viral infection is not fully understood.

View Article and Find Full Text PDF

G protein-coupled receptors (GPCRs) engage multiple transducers to regulate distinct physiological processes. These transducers include various G proteins subtypes, GPCR kinases (GRKs), and β-arrestins. In addition to promoting receptor desensitization, β-arrestins serve as scaffolds for signaling via non-G protein pathways.

View Article and Find Full Text PDF