Patients with epilepsy have 20-fold risk of sudden death when compared to the general population. Uncontrolled seizures is the most consistent risk factor, and death often occurs at night or in relation to sleep. We examined seizure-related respiratory disturbances in sleep versus wakefulness,
OBJECTIVE
Hypoxia-inducible factor-1α (HIF-1α) is involved in critical aspects of cell survival in response to hypoxia and regulates vascular endothelial growth factor (VEGF) expression. Previous experimental and human studies in epilepsy show up-regulation of VEGF following seizures, although
To investigate potentially high-risk cardiac arrhythmias (PHAs) following focal to bilateral tonic-clonic seizures (FBTCSs) and generalized tonic-clonic seizures (GTCSs) and to study the association of PHAs with seizure characteristics and the severity of associated ictal respiratory
Sudden unexpected death in epilepsy (SUDEP) has been recognised for centuries. The precise frequency of occurrence is not well defined. Education of medical professionals is needed, so that death certificates and coronial inquests may appropriately, correctly and consistently record SUDEP as the
OBJECTIVE
Autonomic effects of seizures, including cardiorespiratory abnormalities, may be involved in sudden unexpected death in epilepsy (SUDEP). The purpose of this study was to determine the prevalence and risk factors for ictal hypoxemia (oxygen saturation <90%) and ictal bradycardia (heart
Immediately preceding sudden unexpected death in epilepsy (SUDEP), patients experienced a final generalized tonic-clonic seizure (GTCS), rapid ventilation, apnea, bradycardia, terminal apnea, and asystole. Whether a progressive pathophysiology develops and increases
Cerebral oximetry has not been explored in patients experiencing seizures in the epilepsy monitoring unit (EMU). The purpose of our study was to evaluate the feasibility of periictal measurement of cerebral oxygenation using noninvasive cerebral tissue oximetry and to determine whether there was
OBJECTIVE
To estimate the incidence of ictal hypoxemia (IH) and to identify clinical and study-related factors modulating the estimate.
METHODS
We searched articles recording concurrent peri-ictal and ictal EEG and Sp02 in adults and children with epilepsy. Studies reporting the total number of
To seek a neuropathologic signature of sudden unexpected death in epilepsy (SUDEP) in a postmortem cohort by use of immunohistochemistry for specific markers of inflammation, gliosis, acute neuronal injury due to hypoxia, and blood-brain barrier (BBB) disruption, enabling the generation of
Epidemiological evidence associating ictal hypoventilation during focal seizures with a heightened risk for subsequent sudden unexpected death in epilepsy (SUDEP) is lacking. We describe a patient with temporal lobe epilepsy with two focal seizures recorded in the epilepsy monitoring unit that were
A recent article by Farrell et al. characterizes the phenomenon, mechanisms, and treatment of a local and severe hypoperfusion/hypoxia event that occurs in brain regions following a focal seizure. Given the well-established role of cerebral ischemia/hypoxia in brain damage and behavioral dysfunction
CONCLUSIONS
There is increasing evidence that periictal respiratory disturbances are an important contributor to the pathophysiological changes leading to sudden unexpected death in epilepsy (SUDEP). In patients with SUDEP occurring in epilepsy monitoring units, respiratory disturbances occurred
Sudden unexpected death in epilepsy is a major cause of premature death in people with epilepsy. We aimed to assess whether structural changes potentially attributable to sudden death pathogenesis were present on magnetic resonance imaging in people who subsequently died of sudden unexpected death
Objectives: Hypoxia, or abnormally low blood-oxygen levels, often accompanies seizures and may elicit brain structural changes in people with epilepsy which contribute to central processes underlying sudden unexpected death in epilepsy
Sudden unexpected death in epilepsy (SUDEP) represents one of the most severe consequences of drug-resistant epilepsy, for which no evidence-based prevention is available. Development of effective prevention will depend on the following: (1) better understanding of the pathophysiology of SUDEP to
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