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sudden unexpected death in epilepsy/serotonina

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Sudden unexpected death in epilepsy (SUDEP) is a critical issue in epilepsy, and DBA/1 mice are a useful animal model of this devastating epilepsy sequela. The serotonin hypothesis for SUDEP proposes that modifying serotonergic function significantly alters susceptibility to

Serotonin and sudden unexpected death in epilepsy.

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Epilepsy is a highly prevalent disease characterized by recurrent, spontaneous seizures. Approximately one-third of epilepsy patients will not achieve seizure freedom with medical management and become refractory to conventional treatments. These patients are at greatest risk for sudden unexpected

Sudden Unexpected Death in Epilepsy: Risk Factors, Biomarkers and Prevention.

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Sudden unexpected death in epilepsy (SUDEP) is one of the most important direct epilepsy-related causes of death, with an incidence in adults of 1.2 per 1000 person years. Generalized tonic-clonic seizures have consistently emerged as the leading risk factor for SUDEP, particularly when such

Pediatric Sudden Unexpected Death in Epilepsy: What Have we Learned from Animal and Human Studies, and Can we Prevent it?

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Several factors, such as epilepsy syndrome, poor compliance, and increased seizure frequency increase the risks of sudden unexpected death in epilepsy (SUDEP). Animal models have revealed that the mechanisms of SUDEP involve initially a primary event, often a seizure of sufficient type and severity,

From unwitnessed fatality to witnessed rescue: Pharmacologic intervention in sudden unexpected death in epilepsy.

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The mechanisms of sudden unexpected death in epilepsy (SUDEP) have been difficult to define, as most cases occur unwitnessed, and physiologic recordings have been obtained in only a handful of cases. However, recent data obtained from human cases and experimental studies in animal models have

Abnormal serotonin receptor expression in DBA/2 mice associated with susceptibility to sudden death due to respiratory arrest.

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Previous studies indicate that DBA/2 mice may be a useful model of human sudden unexpected death in epilepsy (SUDEP), since these mice exhibit generalized convulsive seizures followed by respiratory arrest (RA). Respiratory deficits, following generalized convulsive seizures, are observed prior to

Sudden unexpected death in epilepsy: ongoing challenges in finding mechanisms and prevention.

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Purpose/aim of the study: To summarize recent studies on the pathophysiology and preventive strategies for SUDEP. METHODS Databases and literature review. RESULTS Patients with epilepsy have a significantly higher risk of death than the general population. Sudden unexpected death in epilepsy (SUDEP)

Sudden unexpected death in epilepsy.

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Sudden unexpected death in epilepsy (SUDEP) is a significant cause of death for people with epilepsy. Recent research suggests that multiple factors may contribute and that both cardiac and respiratory mechanisms are involved. Both human and animal data suggest that specific genetic factors might

Treatments for the prevention of Sudden Unexpected Death in Epilepsy (SUDEP).

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BACKGROUND Sudden Unexpected Death in Epilepsy (SUDEP) is defined as sudden, unexpected, witnessed or unwitnessed, non-traumatic or non-drowning death of people with epilepsy, with or without evidence of a seizure, excluding documented status epilepticus and in whom postmortem examination does not

The association of serotonin reuptake inhibitors and benzodiazepines with ictal central apnea.

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Ictal (ICA) and postconvulsive central apnea (PCCA) have been implicated in sudden unexpected death in epilepsy (SUDEP) pathomechanisms. Previous studies suggest that serotonin reuptake inhibitors (SRIs) and benzodiazepines (BZDs) may influence breathing. The aim of this study was to

Postictal serotonin levels are associated with peri-ictal apnea.

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To determine the relationship between serum serotonin (5-HT) levels, ictal central apnea (ICA), and postconvulsive central apnea (PCCA) in epileptic seizures.

METHODS
We prospectively evaluated video EEG, plethysmography, capillary oxygen saturation
DBA/1 mice are susceptible to audiogenic seizure-induced respiratory arrest (S-IRA), leading to death, which is a model of human sudden unexpected death in epilepsy (SUDEP). Female DBA/1 mice exhibited 71% susceptibility to S-IRA on the third daily test when seizure testing began at postnatal day

Decreased serotonin synthesis is involved in seizure-induced respiratory arrest in DBA/1 mice.

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A known cause of seizure-induced respiratory arrest is the deficiency in serotonergic neurotransmission. Tryptophan hydroxylase-2 (TPH2) is the rate-limiting enzyme of central serotonin (5-hydroxytryptamine) synthesis which converts l-tryptophan to 5-hydroxytryptophan. A recent study revealed a
DBA/1 mice are a chronically susceptible model of sudden unexpected death in epilepsy (SUDEP) that exhibit chronic audiogenic generalized convulsive seizures (GCSs), leading to death from respiratory arrest (RA) if not resuscitated. Serotonin (5-HT) normally enhances respiration in response to

Serotonin neurones have anti-convulsant effects and reduce seizure-induced mortality.

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Sudden unexpected death in epilepsy (SUDEP) is the leading cause of death in patients with refractory epilepsy. Defects in central control of breathing are important contributors to the pathophysiology of SUDEP, and serotonin (5-HT) system dysfunction may be involved. Here we examined the effect of
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