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Objectives: To examine the relationship between clinical, psychological, and cognitive characteristics of adults with functional seizures.
Methods: This study describes baseline characteristics of one-hundred and seven participants with a documented diagnosis of functional seizures recruited to the Re-PROGRAM randomised controlled trial. Participants completed a semi-structured interview, neuropsychological assessment, and questionnaire measures via Telehealth.
Results: Participants reported low levels of trust in body sensations, high levels of negative ruminative thinking, dissociation, somatisation, anxiety, depression, severe levels of functional impairment, and poor quality of life. At a group level, they had normal neurocognitive function, including mental control, processing speed, attention, and executive function. Anxiety (73%), depression (68%), post-traumatic stress disorder (49%), migraine (63%) and chronic pain (52%) were common comorbidities. Forty-three percent reported a family history of dementia. Somatic symptoms were associated with depression, anxiety, dissociation, ruminative negative thinking, and lower scores on the 'Not-distracting' interoception scale. Poorer psychosocial functioning was associated with depression and dissociation. Reduced mental quality of life was associated with higher levels of depression, anxiety, dissociation, ruminative negative thinking, and lower scores on the 'Trusting' interoception scale. There were no associations between the clinical or psychological variables and seizure frequency or seizure classification. Neither cognitive impairment nor failure on effort testing were associated with the clinical or psychological factors, quality of life or psychosocial functioning.
Significance: This study highlights the burden of psychiatric and physical comorbidity; and the relationship between psychological factors and functional impairment in a large cohort of patients with functional seizures despite normal cognitive function.
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http://dx.doi.org/10.1016/j.yebeh.2024.110117 | DOI Listing |
CNS Neurosci Ther
September 2025
Department of Functional Neurosurgery, Beijing Institute of Functional Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China.
Aim: A total of 30% of individuals with epilepsy are resistant to drug treatment. Deep brain stimulation (DBS) of the anterior nucleus of the thalamus (ANT) shows promise for treating drug-resistant epilepsy (DRE), but further research is needed to optimize DBS parameters, including stimulation frequency. This study aimed to reveal the optimal frequency for ANT-DBS by testing the real-time effects of various stimulation frequencies on the ANT among patients undergoing stereoelectroencephalography (SEEG) electrode implantation.
View Article and Find Full Text PDFBr 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.
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