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Objective: Patients with functional seizures frequently present to emergency departments, and often have unsatisfactory/negative experiences there. It has been proposed that many of these visits are preventable, but the patient perspectives have not been well-studied.
Methods: Past (≥1 appointment, discharged and no longer engaged with the clinic) and present (≥1 appointment, still engaged with the clinic) patients of the Alfred Hospital Functional Seizures clinic without comorbid epilepsy with an established diagnosis of functional seizure were invited to complete a survey on reasons for attending an emergency department and experiences of emergency care. Themes were identified using descriptive content analysis.
Results: There were 229 eligible patients, and 94 participants returned the survey (41 % response rate), of whom 58 (62 %) had presented to an emergency department at least once with functional seizures since their diagnosis. The most frequent reason for seeking emergency care was a change in seizure symptomatology (47 %), followed by medical investigation (16 %). Most (62 %) did not make the decision to go to the emergency department themselves, with family members the most reported decision-makers. Almost a quarter (24 %) felt that presenting to emergency was unavoidable. Themes of validation, medical attention, and knowledge/expertise were identified by individuals as useful when attending emergency departments; and a lack of these features featured heavily in responses regarding concerns about (and negative experiences of) seeking treatment for functional seizures in emergency departments.
Conclusions: The minority of patients make the decision to seek emergency department care themselves with a functional seizure. Further education of ED professionals, including guidelines for screening and quality of care measures, could help to address the needs of people who present to ED with functional seizures.
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http://dx.doi.org/10.1016/j.yebeh.2025.110609 | DOI Listing |
Br J Pharmacol
September 2025
Department of Physiology and Medical Physics, RCSI University of Medicine and Health Sciences, Dublin, Ireland.
Background And Purpose: Neuroinflammation is increasingly recognised to contribute to drug-resistant epilepsy. Activation of ATP-gated P2X7 receptors has emerged as an important upstream mechanism, and increased P2X7 receptor expression is present in the seizure focus in rodent models and patients. Pharmacological antagonists of P2X7 receptors attenuate seizures in rodents, but this has not been explored in human neural networks.
View Article and Find Full Text PDFBMJ Case Rep
September 2025
Gandhi Medical College and Hospital, Secunderabad, Telangana, India
Fahr's syndrome is a rare neurological condition marked by unusual calcifications in the basal ganglia and other brain regions, often resulting from metabolic disorders, such as hypoparathyroidism. Secondary hypoparathyroidism, a frequent complication of total thyroidectomy, can lead to Fahr's syndrome, manifesting as movement disorders, seizures, psychiatric symptoms and indications of calcium deficiency. This case report discusses a woman in her mid-30s who developed Fahr's syndrome due to secondary hypoparathyroidism after total thyroidectomy.
View Article and Find Full Text PDFNeurobiol Dis
September 2025
Department of Neuroscience, Developmental and Regenerative Biology, The University of Texas at San Antonio, San Antonio, TX, USA; Brain Health Consortium, The University of Texas at San Antonio, San Antonio, TX, USA. Electronic address:
Temporal lobe epilepsy is associated with aberrant neurogenesis and ectopic migration of adult-born granule cells (abGCs), yet the molecular mechanisms driving these changes remain poorly defined. Using a pilocarpine-induced mouse model of temporal lobe epilepsy and chemogenetic silencing of abGCs via Designer Receptors Exclusively Activated by Designer Drugs (DREADDs), we previously demonstrated that abGC inhibition reduces both ectopic migration and seizure susceptibility. To identify underlying molecular regulators, we performed RNA sequencing of FACS-isolated abGCs and identified Rrm2 and Timp3 as top candidate genes modulated by seizure activity and neuronal silencing.
View Article and Find Full Text PDFNeurobiol Dis
September 2025
Department of Neurology, the First Affiliated Hospital of Chongqing Medical University, Chongqing Key Laboratory of Major Neurological and Mental Disorders, Chongqing Key Laboratory of Neurology, Chongqing, China. Electronic address:
Ubiquilin 4 (UBQLN4) is an important molecule that regulates protein degradation through the ubiquitin-proteasome pathway. This study found that UBQLN4 expression is significantly reduced in a chronic epilepsy mouse model induced by kainic acid, primarily localized in neurons and widely distributed at excitatory post-synapses. Experiments involving adeno-associated virus-mediated overexpression or knockdown of UBQLN4 indicate that a reduction in UBQLN4 increases susceptibility to and severity of epilepsy, while its overexpression has a protective effect.
View Article and Find Full Text PDFExp Neurol
September 2025
Department of Human Genetics, Emory University School of Medicine, Atlanta, GA, USA. Electronic address:
Synapse refinement through the elimination of excess synapses is crucial for proper neuronal circuitry during development and adulthood, and the phagocytic activity of astrocytes plays an important role in this process. Failure to remove excess synapses can lead to neurological and neurodevelopmental disorders like epilepsy and autism spectrum disorder (ASD). The adhesion G protein-coupled receptor BAI1/ADGRB1 contributes to phagocytosis in various tissues, including the clearance of apoptotic myoblasts in skeletal muscle and epithelial cells in the intestine.
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