Objective: To provide further data around magnetoencephalographic (MEG) findings in early-onset autism spectrum disorders (ASD).
Methods: Thirty-six children (mean age 7 years) diagnosed of PDD (DSM-IV, ICD-10) were studied. There were 22 children with autistic disorder, 9 with Asperger's syndrome, and 5 with pervasive developmental disorder not otherwise specified (PDD-NOS). According to the Childhood Autism Rating Scale (CARS), the autistic disorder was mild to moderate in 11, and severe in 11. Neuroimaging studies using three-dimensional MRI as well as simultaneous MEG-EEG and fusion techniques through magnetic source imaging (MSI) were performed, with the aid of anesthesia in non-cooperative patients.
Results: Most patients had no EEG abnormalities. All ASD children showed common specific abnormalities in the shape of low amplitude monophasic and biphasic spikes (isolated or short bursts) as well as acute waves, predominantly distributed in the perisylvian areas. In Asperger's syndrome, epileptiform spikes were mostly found in the right hemisphere. No lateralized epileptiform activity was observed in non-Asperger's autistic patients.
Conclusions: MEG epileptiform activity is frequently documented in children with early-onset ASD.
Significance: Subclinical epileptiform activity is present especially in the perisylvian regions for many patients with ASD.
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http://dx.doi.org/10.1016/j.clinph.2007.11.007 | DOI Listing |
Epilepsia
January 2025
Epilepsy Unit, Hôpital Gui de Chauliac, Montpellier, France.
Contemporary studies report nonconvulsive status epilepticus (NCSE) in Creutzfeldt-Jakob disease (CJD), based on benzodiazepine (BZP)-responsive epileptiform discharges on the electroencephalogram (EEG), with the following false syllogism: (1) intravenous (IV) administration of BZPs usually suppress ictal activity in NCSE; (2) in CJD, periodic sharp wave complexes (PSWCs) are suppressed by IV BZPs; (3) therefore, these patients have NCSE. This is a simplistic and invalid conclusion, because authors of 20th-century science reports have clearly shown that IV BZPs, short-acting barbiturates, and drugs with no antiseizure effects, such as chloral hydrate and IV naloxone, suppress PSWCs, but patients fall asleep with no clinical improvement. In contrast, IV methylphenidate transiently improves both the EEG and clinical states.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Vanderbilt University Medical Center, Nashville, TN, USA.
Background: Manganese (Mn) is an essential metal that serves as a cofactor for metalloenzymes important in moderating the glutamate/glutamine cycle and other oxidative stress pathways. Typically, Mn is acquired through the diet, however, Mn overexposure can arise through drinking inadequately treated well water or inhalation of Mn-containing industrial byproducts. Mn toxicity disrupts dopaminergic neurotransmission resulting in a Parkinsonian disorder referred to as manganism.
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.
Alzheimers Dement
December 2024
University of California San Francisco, San Francisco, CA, USA.
Background: Neural circuit hyperexcitability and impaired excitation-to-inhibition (E/I) activity is believed to be a key contributor to synaptic and network degeneration in Alzheimer's disease (AD). Extensive preclinical research on transgenic animal models of AD have demonstrated neuronal and circuit level E/I imbalance mediated by amyloid-beta (Aβ) and tau proteins. Synaptic and network deficits are also integral changes of aging.
View Article and Find Full Text PDFAdv Sci (Weinh)
December 2024
Institute for Translational Brain Research, State Key Laboratory of Medical Neurobiology, MOE Frontiers Center for Brain Science, Institute of Pediatrics, National Children's Medical Center, Children's Hospital, Fudan University, Shanghai, 200032, China.
Focal cortical dysplasia (FCD) is a highly heterogeneous neurodevelopmental malformation, the underlying mechanisms of which remain largely elusive. In this study, personalized dorsal and ventral forebrain organoids (DFOs/VFOs) are generated derived from brain astrocytes of patients with FCD type II (FCD II). The pathological features of dysmorphic neurons, balloon cells, and astrogliosis are successfully replicated in patient-derived DFOs, but not in VFOs.
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