Background: Gastroesophageal reflux disease (GERD) can mimic epileptic seizure, and may be misdiagnosed as epilepsy. On the other hand, GERD can be more commonly seen in children with neurological disorders such as cerebral palsy (CP); this co-incidence may complicate the management of patients by mimicking refractory seizures.
Objective: The purpose of our study was to evaluate the clinical features, definite diagnoses and treatment approaches of the patients with clinically suspected GERD who were referred to the division of pediatric neurology with a suspected diagnosis of epileptic seizure. We also aimed to investigate the occurrence of GERD in children with epilepsy and/or CP.
Methods: Fifty-seven children who had a final diagnosis of GERD but were initially suspected of having epileptic seizures were assessed prospectively.
Results: All patients were assigned to 3 groups according to definite diagnoses as follows: patients with only GERD who were misdiagnosed as having epileptic seizure (group 1: n=16; 28.1%), those with comorbidity of epilepsy and GERD (group 2: n=21; 36.8%), and those with the coexistence of GERD with epilepsy and CP (group 3: n=20; 35.1%). Five patients (8.8%) did not respond to anti-reflux treatment and laparoscopic reflux surgery was performed. The positive effect of GERD therapy on paroxysmal nonepileptic events was observed in 51/57 (89.5%) patients.
Conclusions: GERD is one of the important causes of paroxysmal nonepileptic events. In addition, GERD must be kept in mind at the initial diagnosis and also in the long-term management of patients with neurological disorders such as epilepsy and CP.
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http://dx.doi.org/10.1016/j.braindev.2015.09.009 | DOI Listing |
Hum Mol Genet
January 2025
Department of Cell & Developmental Biology, Vanderbilt University School of Medicine, 1161 21st Ave S, Nashville, Tennessee, 37232, United States of America.
Tuberous Sclerosis Complex (TSC) is a debilitating developmental disorder characterized by a variety of clinical manifestations. While benign tumors in the heart, lungs, kidney, and brain are all hallmarks of the disease, the most severe symptoms of TSC are often neurological, including seizures, autism, psychiatric disorders, and intellectual disabilities. TSC is caused by loss of function mutations in the TSC1 or TSC2 genes and consequent dysregulation of signaling via mechanistic Target of Rapamycin Complex 1 (mTORC1).
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December 2024
Clinical Research, National Institute of Neurology and Neurosurgery, Mexico City, MEX.
Anti-NMDA (N-methyl-D-aspartate) receptor encephalitis (ANRE) is a rare autoimmune condition targeting brain receptors, often linked to ovarian tumors in young women. In severe cases, it can lead to status epilepticus, but in sporadic cases, it may progress to super-refractory status epilepticus (SRSE), a dangerous state of continuous or repetitive seizures demanding urgent medical attention that continues or recurs more than 24 hours after the initiation of anesthetic therapy. We present a case report of anti-NMDA receptor limbic encephalitis-triggered SRSE terminated with vagus nerve stimulation (VNS) and titrated to high stimulation parameters in the immediate postoperative period.
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January 2025
Department of Neurology, Huashan Hospital, Fudan University and Institute of Neurology, Fudan University, Shanghai, China.
We report a case of optic neuritis (ON) secondary to autoimmune encephalitis (AE) in a patient with concomitant antibodies to N-methyl-D-aspartate receptor (NMDAR), gamma-aminobutyric acid-B receptor (GABAR), and myelin oligodendrocyte glycoprotein (MOG). The patient exhibited a constellation of symptoms, including vision loss, seizures, mental and behavioral disorders, cognitive impairment, and speech abnormalities. At the two-year follow-up, the patient's symptoms had abated entirely.
View Article and Find Full Text PDFThe hippocampus forms memories of our experiences by registering processed sensory information in coactive populations of excitatory principal cells or ensembles. Fast-spiking parvalbumin-expressing inhibitory neurons (PV INs) in the dentate gyrus (DG)-CA3/CA2 circuit contribute to memory encoding by exerting precise temporal control of excitatory principal cell activity through mossy fiber-dependent feed-forward inhibition. PV INs respond to input-specific information by coordinating changes in their intrinsic excitability, input-output synaptic-connectivity, synaptic-physiology and synaptic-plasticity, referred to here as experience-dependent PV IN plasticity, to influence hippocampal functions.
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January 2025
Hainan General Hospital and Hainan Affiliated Hospital of Hainan Medical University, Haikou, China.
Protein lactylation is a new form of post-translational modification that has recently been proposed. Lactoyl groups, derived mainly from the glycolytic product lactate, have been linked to protein lactylation in brain tissue, which has been shown to correlate with increased neuronal excitability. Ischemic stroke may promote neuronal glycolysis, leading to lactate accumulation in brain tissue.
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