Objective: This nationwide population-based cohort study evaluated the effects of nonapnea sleep disorders (NSDs) on the development of epilepsy.
Methods: We identified 63,865 patients aged ≥20years, diagnosed with NSDs (ICD-9-CM: 307.4 or 780.5), and without coding for apnea-related sleep disorders (ICD-9-CM: 780.51, 780.53, or 780.57) during 2000-2003 as the NSD cohort. In addition, we enrolled a comparison cohort of 127,728 patients. We calculated the adjusted hazard ratio (aHR) for developing epilepsy (ICD-9-CM: 345) after adjustment for age, sex, comorbidities, and drug use. A Kaplan-Meier analysis was used to measure the cumulative incidence of epilepsy between the 2 groups until the end of 2011.
Results: The cumulative incidence of epilepsy was significantly higher in the NSD cohort than in the comparison cohort. The aHR for developing epilepsy in the NSD cohort was 1.52 (95% CI=1.37-1.69). The risk of developing epilepsy was higher among males (aHR=1.41) than among females. The age-stratified effects of NSDs on developing epilepsy were the highest among patients aged ≥65years. When comorbidities and NSDs coexisted, the risk of epilepsy was specifically increased in patients having an NSD and stroke (aHR: 8.61, 95% CI: 7.43-9.98) in addition to brain tumors (aHR: 7.66, 95% CI: 5.06-11.6).
Conclusion: This study indicated that patients with NSDs have a higher risk of developing epilepsy and that the risk is much higher among men and older patients. These findings suggest that NSDs constitute a predisposing, possibly independent factor for developing subsequent epilepsy in adulthood.
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http://dx.doi.org/10.1016/j.ypmed.2016.08.034 | DOI Listing |
J Pediatr Endocrinol Metab
December 2024
Pediatric Endocrinology Clinic, Bilkent City Hospital, Ankara, Türkiye.
Objectives: Hypothalamic hamartoma (HH) is a rare condition that causes epilepsy and central precocious puberty (CPP) at an early age. In this report, we describe a child with CPP secondary to HH and discuss the current literature.
Case Presentation: A 26-month-old girl was brought to our hospital for evaluation of breast enlargement.
Exp Neurol
December 2024
Neuroscience Department, U.S. Army Medical Research Institute of Chemical Defense (USAMRICD), Aberdeen Proving Ground, MD, United States of America. Electronic address:
Exposure to organophosphorus nerve agents irreversibly inhibits acetylcholinesterase and may lead to cholinergic crisis and seizures. Although benzodiazepines are the standard of care after nerve agent-induced status epilepticus, when treatment is delayed for up to 30 min or more, refractory status epilepticus can develop. Adult male rodents are often utilized for evaluation of therapeutic efficacy against nerve agent exposure.
View Article and Find Full Text PDFBiosens Bioelectron
December 2024
2020 X-Lab, Shanghai Institute of Microsystem and Information Technology, Chinese Academy of Sciences, Shanghai, 200050, China; Center of Materials Science and Optoelectronics Engineering, University of Chinese Academy of Sciences, Beijing, 100049, China; State Key Laboratory of Transducer Technology, Shanghai Institute of Microsystem and Information Technology, Chinese Academy of Sciences, Shanghai, 200050, China; School of Graduate Study, University of Chinese Academy of Sciences, Beijing, 100049, China. Electronic address:
Anti-seizure medications and deep brain stimulation are widely used therapies to treat seizures; however, both face limitations such as resistance and the unpredictable nature of seizures. Recent advancements, including responsive neural stimulation and on-demand drug release, have been developed to address these challenges. However, a gap remains, as electrical stimulation provides only transient effects while medication has a delayed onset.
View Article and Find Full Text PDFEur J Med Genet
December 2024
Rare Diseases and Medical Genetics Unit, Bambino Gesù Children's Hospital, IRCSS, Rome, Italy.
O'Donnell-Luria-Rodan (ODLURO) syndrome is an autosomal dominant neurodevelopmental disorder mainly characterized by global development delay/intellectual disability, white matter abnormalities, and behavioral manifestations. It is caused by pathogenic variants in the KMT2E gene. Here we report seven new patients with loss-of-function KMT2E variants, six harboring frameshift/nonsense changes, and one with a 7q22.
View Article and Find Full Text PDFAm J Hum Genet
December 2024
Department of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, the Second Affiliated Hospital, Guangzhou Medical University, Guangzhou 510260, Guangdong, China. Electronic address:
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