We evaluated the incidence of de novo nonepileptic seizures (NES), confirmed by EEG monitoring, after cranial surgery for intractable epilepsy in 228 surgery patients. Eight patients (3.5%) developed de novo NES at 6 weeks to 6 years (mean, 23 months) after surgery. Six had undergone a resection and two complete callosotomy. They did not differ from a larger surgical group with respect to sex, side of surgery, age at onset, or duration of epilepsy, Full Scale Intelligence Quotient, seizure outcome, or preoperative interictal dysphoric disorder (IDD), but there was a significant excess of postoperative IDD and operative complications (bone flap infections); the callosotomy patients had marked hemisphere disconnection syndromes. Repeat EEG videotelemetry monitoring is important to detect postoperative NES so that inappropriate therapeutic measures may be avoided. Risk factors may be exacerbation or persistence of IDD and surgical complications. The etiology of NES is discussed.
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http://dx.doi.org/10.1006/ebeh.2000.0124 | DOI Listing |
Epileptic Disord
December 2024
Department of Pediatric Epileptology, Functional Neurology and Sleep Disorders, Hôpital Femme Mère Enfant, University Hospitals of Lyon (HCL), Member of ERN EpiCARE, Lyon, France.
Pediatr Neurol
November 2024
Centre de recherche Azrieli du CHU Sainte-Justine, Montreal, Québec, Canada; Department of Pediatrics, University of Montreal, Montreal, Québec, Canada. Electronic address:
Int J Mol Sci
July 2024
Unit of Cell Biology and Diagnosis of Mitochondrial Disorders, Laboratory of Medical Genetics, Bambino Gesù Children's Hospital IRCCS, 00146 Rome, Italy.
Mitochondrial fission and fusion are vital dynamic processes for mitochondrial quality control and for the maintenance of cellular respiration; they also play an important role in the formation and maintenance of cells with high energy demand including cardiomyocytes and neurons. The (dynamin-1 like) gene encodes for the DRP1 protein, an evolutionary conserved member of the dynamin family that is responsible for the fission of mitochondria; it is ubiquitous but highly expressed in the developing neonatal heart. De novo heterozygous pathogenic variants in the gene have been previously reported to be associated with neonatal or infantile-onset encephalopathy characterized by hypotonia, developmental delay and refractory epilepsy.
View Article and Find Full Text PDFNeurohospitalist
July 2024
Department of Neurology, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA.
Multiple medications are known to increase epileptogenicity in patients with and without an underlying seizure disorder. Paradoxically, some of these medications include anti-seizure medications (ASMs) and other medications, such as psychotropics, that act on the central nervous system (CNS). This article aims to discuss 3 clinical cases that highlight the gamut of epileptogenic reactivity secondary to CNS drugs ranging from increased epileptogenicity in the form of interictal epileptiform discharges (IEDs) without seizures, increased epileptogenicity on electroencephalogram (EEG) with associated non-epileptic movement disorders, and frank, seizures.
View Article and Find Full Text PDFHeliyon
January 2024
Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, 610041, China.
Background: Leigh syndrome (LS) is a heterogeneous neurodegenerative disease that is the most common manifestation of mitochondrial disease in children.
Methods: We report a case of Leigh syndrome with paroxysmal body swing in a 1-year-old boy.
Results: The boy presented with paroxysmal body swing, and the electroencephalogram showed no epileptic discharge during the paroxysmal episode.
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