Purpose: This retrospective multicenter study aimed to assess the efficacy and safety of brivaracetam (BRV) in pediatric epilepsy.
Methods: Our cohort consisted of 93 children (mean age 11.5 ± 7.5 years) with a wide spectrum of pediatric epilepsy, including epileptic encephalopathy and generalized epilepsy. Of these, 61 (60.4%) were diagnosed with focal epilepsy, 19 (15.8%) with generalized epilepsy, and 16 (15.8%) with combined epilepsy, while 8 patients (7.9%) had an unknown epilepsy type. The cohort included rare epilepsy syndromes: 8 patients with Lennox-Gastaut syndrome, 3 with Dravet syndrome, and 1 with Rasmussen syndrome. Patients had a history of various antiseizure medications (ASMs) (6.42 ± 3.15), and on average, were being treated with more than two (2.57 ± 1.16) drugs at the time of BRV deployment.
Results: Retention rates were high, with 80.6% of patients adhering to treatment at 3 months, 66.7% at 6 months, and 45.2% at 12 months. In 29 patients (30.1%), BRV was added in an overnight switch from levetiracetam (LEV), resulting in a reduction of behavioral adverse effects (AEs) in 5 patients (17.2%). The response rate was 25.8% at 3 months, 16.1% at 6 months, and 17.2% at 12 months, with no responders in the epileptic encephalopathy group. Therapy tolerance was notable, with 70 patients (75.3%) reporting no AEs. Transient AEs occurred in 10 patients (10.7%), and in 13 cases (14.0%), the AEs warranted dose adjustment or discontinuation of BRV.
Conclusion: Approximately one-fifth of pediatric patients with drug-resistant epilepsy responded to BRV, with the best response observed in patients with focal seizures. However, the impact on patients with epileptic encephalopathy was limited.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.seizure.2024.08.022 | DOI Listing |
Pediatr Res
January 2025
Center for Genetic Medicine, Children's National Research Institute, Washington, DC, USA.
Background: Prenatally transmitted viruses can cause severe damage to the developing brain. There is unexplained variability in prenatal brain injury and postnatal neurodevelopmental outcomes, suggesting disease modifiers. Of note, prenatal Zika infection can cause a spectrum of neurodevelopmental disorders, including congenital Zika syndrome.
View Article and Find Full Text PDFCNS Neurosci Ther
January 2025
Jiujiang Clinical Precision Medicine Research Center, Jiujiang, Jiangxi, China.
Background: Adenosine deaminase action on RNA 1 (ADAR1) can convert the adenosine in double-stranded RNA (dsRNA) molecules into inosine in a process known as A-to-I RNA editing. ADAR1 regulates gene expression output by interacting with RNA and other proteins; plays important roles in development, including growth; and is linked to innate immunity, tumors, and central nervous system (CNS) diseases.
Results: In recent years, the role of ADAR1 in tumors has been widely discussed, but its role in CNS diseases has not been reviewed.
Neurochem Res
January 2025
Department of Physiology, Faculty of Medicine, University of Ondokuz Mayıs, Samsun, Türkiye.
In the present study, the effects of the acetylcholinesterase (AChE) enzyme inhibitor rivastigmine (RIVA) on spike-wave discharges (SWDs), memory impairment, anxiety-like behavior, and the transient receptor potential vanilloid 1 (TRPV1) gene expression were investigated in genetic absence epileptic Wistar Albino Glaxo/Rijswijk (WAG/Rij) rats. After tripolar electrodes were implanted on the WAG/Rij rats' skulls, single doses of 0.125, 0.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Memory and Aging Center, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA.
Background: Patients with Alzheimer's Disease and related dementias associated with the accumulation of pathological tau (tauopathies) in neurons have an increased incidence of epileptic episodes and sub-clinical epileptiform activity. This neuronal hyperexcitability represents some of the earliest changes in patient brains, is associated with more severe symptoms, and presents an opportunity for early therapeutic intervention. Despite these provocative observations, the molecular details of how tau and neuronal excitability are connected in tauopathies remain unknown.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of California Los Angeles, Los Angeles, CA, USA.
Background: Epileptic activity is increasingly recognized as a contributor to Alzheimer's Disease (AD) pathology. In AD models, endogenous tau contributes to epileptic activity and associated cognitive deficits through mechanisms that are not fully understood. Increased attention is being directed towards tau's interactions with proteins that regulate neuronal activity, particularly tau's proline rich domain and its binding to SH3-containing proteins.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!