2,481 results match your criteria: "Posttraumatic Epilepsy"

Posttraumatic epilepsy (PTE) is considered to be one of the most severe and enduring outcomes that can arise from traumatic brain injury (TBI). The authors' study aims to create and authenticate a prognostic model for forecasting the PTE occurrence after TBI. The clinical prognostic model was developed in 475 people who had a TBI history in Nanning using a multivariate logistic regression model.

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Toll-like receptors (TLRs) are activated by endogenous molecules released from damaged cells and contribute to neuroinflammation following traumatic brain injury (TBI) and epilepsy. TLR1/2 agonist tri-palmitoyl-S-glyceryl-cysteine (Pam3cys) is a vaccine adjuvant with confirmed safety in humans. We assessed impact of TLR1/2 postconditioning by Pam3cys on epileptogenesis and neuroinflammation in male rats, 6, 24, and 48 h after mild-to-moderate TBI.

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Article Synopsis
  • The study aims to systematically review existing data to better understand how long it typically takes for post-traumatic epilepsy (PTE) to develop after a mild traumatic brain injury (mTBI) like a concussion.
  • Researchers will conduct a thorough search of medical literature, assess the risk of bias in the studies, and combine their findings using meta-analysis techniques to draw clearer conclusions about incidence and latency.
  • This research aims to enhance early detection and intervention strategies for PTE, ultimately improving patient care and quality of life for individuals affected by mTBI.
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Background: Decompressive craniectomy (DC) is a surgical procedure to treat refractory increase in intracranial pressure. DC is frequently succeeded by cranioplasty (CP), a reconstructive procedure to protect the underlying brain and maintain cerebrospinal fluid flow dynamics. However, complications such as seizures, fluid collections, infections, and hydrocephalus can arise from CP.

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Posttraumatic epilepsy: Integrating clinical, inflammatory, and genetic profiles in traumatic brain injury patients.

Epilepsy Res

September 2024

Laboratory of Neurobiology, Department of Physiology, Universidade Federal de São Paulo, São Paulo, Brazil; Instituto D'Or de Pesquisa e Ensino, São Paulo, São Paulo, Brazil.

Objective: This study aims to assess the clinical, inflammatory, and genetic profiles of traumatic brain injury (TBI) patients over a 2-year follow-up period, focusing on the development of posttraumatic epilepsy (PTE).

Methods: Fifty-nine patients with acute TBI were recruited in the emergency unit of a hospital in Brazil. Clinical data and blood samples were collected after 10 days of hospitalization for posterior genetic profile (Apolipoprotein E- ApoE and Glutamic Acid Descarboxylase-GAD sequencing) analyses.

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Inflammasomes at the crossroads of traumatic brain injury and post-traumatic epilepsy.

J Neuroinflammation

July 2024

The Department of Neuroscience, School of Translational Medicine, Monash University, 99, Commercial Road, Melbourne, Australia.

Post-traumatic epilepsy (PTE) is one of the most debilitating consequences of traumatic brain injury (TBI) and is one of the most drug-resistant forms of epilepsy. Novel therapeutic treatment options are an urgent unmet clinical need. The current focus in healthcare has been shifting to disease prevention, rather than treatment, though, not much progress has been made due to a limited understanding of the disease pathogenesis.

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Background: Conducting mild traumatic brain injury (mTBI) longitudinal studies across multiple sites is a challenging endeavor which has been made more challenging because of COVID-19.

Objective: This article briefly describes several concerns that need to be addressed during the conduct of research to account for COVID-19's impact.

Methods: The recent actions and steps taken by the Long-term Impact of Military-relevant Brain Injury Consortium (LIMBIC)-Chronic Effects of Neurotrauma Consortium (CENC) researchers are reviewed.

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Objective: To examine the efficacy and safety of perampanel (PER) in patients with post-stroke epilepsy (PSE), brain tumor-related epilepsy (BTRE), and post-traumatic epilepsy (PTE) using Japanese real-world data.

Methods: The prospective post-marketing observational study included patients with focal seizures with or without focal to bilateral tonic-clonic seizures who received PER combination therapy. The observation period was 24 or 52 weeks after the initial PER administration.

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Diagnosing a non-epileptic seizure is difficult in the absence of a video electroencephalogram. The expert commission of the international league against epilepsy proposes a diagnostic approach allowing the diagnosis to be made according to a degree of certainty with or in the absence of a video electroencephalogram. Our objective was to determine the hospital frequency of psychogenic non-epileptic seizures in the absence of video-electroencephalogram.

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Background: Post-traumatic epilepsy (PTE) is a well-known complication of traumatic brain injury (TBI). Although several risk factors have been identified, prediction of PTE is difficult. Changing demographics and advances in TBI treatment may affect the risk of PTE.

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Anti-HMGB1 mAb Therapy Reduces Epidural Hematoma Injury.

Int J Mol Sci

May 2024

Department of Translational Research & Drug Development, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 7008558, Japan.

Article Synopsis
  • Epidural and subdural hematomas often occur due to traumatic brain injuries, and while surgery is the main treatment, it's important to prevent complications like post-traumatic epilepsy.* -
  • In a study with rats, researchers found that a monoclonal antibody targeting high mobility group box-1 (HMGB1) effectively reduced inflammation and the release of inflammatory markers after a hematoma occurred.* -
  • The study suggests that using anti-HMGB1 therapy could help minimize brain inflammation and protect neural tissue, making it a potential addition to treatment protocols for epidural hematomas.*
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Neuroprotective effects of naltrexone in a mouse model of post-traumatic seizures.

Sci Rep

June 2024

Stead Family Department of Pediatrics , Carver College of Medicine, University of Iowa, 25 South Grand Ave, 2040 MedLabs, Iowa City, IA, 52242, USA.

Article Synopsis
  • Traumatic Brain Injury (TBI) can cause brain inflammation that may lead to epilepsy, which is having seizures.
  • Researchers tested a medicine called naltrexone, usually used to help with drug addiction, to see if it could stop brain inflammation and seizures after TBI.
  • They found that naltrexone helped reduce inflammation and prevent seizures in mice that got TBI, making it a potential new treatment for this problem.
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Post-epileptic seizure posttraumatic stress Disorder: A mediation analysis.

Epilepsy Behav

August 2024

CHRU de Nancy, Département de Neurologie, Nancy, France; Pôle Hospitalo-Universitaire de Psychiatrie D'Adultes Du Grand Nancy, Centre Psychothérapique de Nancy, Laxou, France. Electronic address:

Objective: Previous studies investigated the varying prevalence of post-epileptic seizure posttraumatic stress disorder (PS-PTSD). The current study aimed first to compare the profiles of patients with and without PS-PTSD and, second, to study the interaction between other past traumatic experiences, subjective ictal anxiety, psychiatric comorbidities, and PS-PTSD in people with epilepsy (PWE).

Methods: We conducted an observational study, investigating past traumatic experiences and PS-PTSD through standardized scales (CTQ-28, LEC-5 and PCL-5).

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Post-Traumatic Stress-Disorder in Epilepsy: Meta-analysis of current evidence.

Epilepsy Behav

August 2024

Neurology, Epilepsy and Movement Disorders Unit, Bambino Gesù Children's Hospital, IRCCS, Full Member of European Reference Network on Rare and Complex Epilepsies, EpiCARE, Rome, Italy.

Epilepsy, a chronic neurological condition characterized by unpredictable seizures, poses considerable challenges, including disability, stigma, and increased mortality. Psychiatric comorbidities are prevalent in 20-30% of epilepsy patients, notably mood or anxiety disorders, psychotic symptoms, and personality disorders. Trauma and childhood adversities are pivotal risk factors for psychopathology, yet the link between Post-Traumatic Stress Disorder (PTSD) and epilepsy remains underexplored.

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Traumatic brain injury (TBI) is the primary cause of child mortality and disability worldwide. It can result in severe complications that significantly impact children's quality of life, including post-traumatic epilepsy (PTE). An increasing number of studies suggest that TBI-induced oxidative stress and neuroinflammatory sequelae (especially, inflammation in the hippocampus region) may lead to the development of PTE.

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Introduction: Post-traumatic seizures (PTSs) contribute to morbidity after traumatic brain injury (TBI). Early PTS are rare in combat casualties sustaining TBI, but the prevalence of late PTS is poorly described. We sought to define the prevalence and risk factors of late PTS in combat casualties with computed tomography evidence of TBI.

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Traumatic brain injury (TBI) is often followed by post-traumatic epilepsy (PTE), a condition often difficult to treat and leading to a substantial decline in quality of life as well as increased long-term mortality. The latent period between TBI and the emergence of spontaneous recurrent seizures provides an opportunity for pharmacological intervention to prevent epileptogenesis. Biomarkers capable of predicting PTE development are urgently needed to facilitate clinical trials of putative anti-epileptogenic drugs.

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This study is aimed at investigating epileptic seizures, one of the consequences of traumatic brain injury (TBI). Immediate and early post-traumatic seizures, as well as late post-traumatic epileptic seizures or post-traumatic epilepsy, can have different pathogenetic bases. The following key risk factors associated with post-traumatic epilepsy are known: duration of unconsciousness, gunshot wounds, intracranial hemorrhage, diffuse axonal injury, prolonged (more than 3 days) post-traumatic amnesia, acute subdural hematoma with surgical evacuation, immediate and early post-traumatic epileptic seizures, fracture of the skull bones.

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Objective: The mechanistic target of rapamycin (mTOR) pathway has been implicated in promoting epileptogenesis in animal models of acquired epilepsy, such as posttraumatic epilepsy (PTE) following traumatic brain injury (TBI). However, the specific anatomical regions and neuronal populations mediating mTOR's role in epileptogenesis are not well defined. In this study, we tested the hypothesis that mTOR activation in dentate gyrus granule cells promotes neuronal death, mossy fiber sprouting, and PTE in the controlled cortical impact (CCI) model of TBI.

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Pathophysiology, Diagnosis, Prognosis, and Prevention of Poststroke Epilepsy: Clinical and Research Implications.

Neurology

June 2024

From the Department of Neurology (T.T., M.I., K.F.), National Cerebral and Cardiovascular Center, Osaka, Japan; Department of Neurology (N.K.M.), Yale University School of Medicine, New Haven, CT; Department of Clinical & Experimental Epilepsy (M.J.K.), UCL Queen Square Institute of Neurology, London, United Kingdom; Moscow Research and Clinical Center for Neuropsychiatry (A.G.), Pirogov Russian National Research Medical University, Russia; and Department of Epilepsy, Movement Disorders and Physiology (A.I.), Kyoto University Graduate School of Medicine, Japan.

Poststroke epilepsy (PSE) is associated with higher mortality and poor functional and cognitive outcomes in patients with stroke. With the remarkable development of acute stroke treatment, there is a growing number of survivors with PSE. Although approximately 10% of patients with stroke develop PSE, given the significant burden of stroke worldwide, PSE is a significant problem in stroke survivors.

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Objective: The increased amplitude of ictal activity is a common feature of epileptic seizures, but the determinants of this amplitude have not been identified. Clinically, ictal amplitudes are measured electrographically (using, e.g.

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Objective: Posttraumatic epilepsy (PTE) significantly impacts morbidity and mortality, yet local PTE data remain scarce. In addition, there is a lack of evidence on cognitive comorbidity in individuals with PTE in the literature. We sought to identify potential PTE predictors and evaluate cognitive comorbidity in patients with PTE.

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Deep brain stimulation of the amygdala for treatment-resistant combat post-traumatic stress disorder: Long-term results.

J Psychiatr Res

July 2024

Department of Neurosurgery, UCLA, 300 Stein Plaza Driveway Suite 420, Los Angeles, CA, 90095, USA; Southwest VA Epilepsy Center of Excellence, 11301 Wilshire Blvd, Bldg 500 (10H2), Los Angeles, CA, USA, 90073. Electronic address:

Deep brain stimulation (DBS) holds promise for neuropsychiatric conditions where imbalance in network activity contributes to symptoms. Treatment-resistant Combat post-traumatic stress disorder (TR-PTSD) is a highly morbid condition and 50% of PTSD sufferers fail to recover despite psychotherapy or pharmacotherapy. Reminder-triggered symptoms may arise from inadequate top-down ventromedial prefrontal cortex (vmPFC) control of amygdala reactivity.

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Hospital-acquired infections as a risk factor for post-traumatic epilepsy: A registry-based cohort study.

Epilepsia Open

August 2024

Department of Neuroscience, School of Translational Medicine, Monash University, Melbourne, Victoria, Australia.

Objective: Hospital-acquired infections are a common complication for patients with moderate or severe traumatic brain injury (TBI), contributing to morbidity and mortality. As infection-mediated immune responses can predispose towards epilepsy, we hypothesized that post-injury hospital-acquired infections increase the risk of post-traumatic epilepsy (PTE).

Methods: A retrospective cohort study of adults with moderate to severe TBI was conducted using data from the Victorian State Trauma Registry in Australia.

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