sudden unexpected death in epilepsy/potasio

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The role of P-glycoprotein (P-gp) and inwardly rectifying potassium (Kir) channels in sudden unexpected death in epilepsy (SUDEP).

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Sudden unexpected death in epilepsy (SUDEP) is the major cause of death that affects patients with epilepsy. The risk of SUDEP increases according to the frequency and severity of uncontrolled seizures; therefore, SUDEP risk is higher in patients with refractory epilepsy (RE), in whom most

Scn2a deletion improves survival and brain-heart dynamics in the Kcna1-null mouse model of sudden unexpected death in epilepsy (SUDEP).

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People with epilepsy have greatly increased probability of premature mortality due to sudden unexpected death in epilepsy (SUDEP). Identifying which patients are most at risk of SUDEP is hindered by a complex genetic etiology, incomplete understanding of the underlying pathophysiology and lack of

[A case of sudden unexpected death in epilepsy 3 years after the onset of acute encephalitis with refractory, repetitive partial seizures].

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Acute encephalitis with refractory, repetitive partial seizures (AERRPS) is a peculiar form of encephalitis mainly affecting children. Although not usually lethal, we report a case of sudden unexpected death in epilepsy (SUDEP) 3 years after the onset of AERRPS. A 6-year-old boy was admitted to our

Pharmacogenetics of KCNQ channel activation in 2 potassium channelopathy mouse models of epilepsy.

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Antiseizure drugs are the leading therapeutic choice for treatment of epilepsy, but their efficacy is limited by pharmacoresistance and the occurrence of unwanted side effects. Here, we examined the therapeutic efficacy of KCNQ channel activation by retigabine in preventing seizures and neurocardiac

Biochemical findings in sudden unexpected death in epilepsy: Hospital based case-control study.

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A review study on the biochemistry of epilepsy showed that in epileptic patients, serum glucose and cholesterol concentrations are low, sodium is unaffected, potassium increases, glucose is high and mild hypocalcemia. We have conducted a biochemical study on sudden unexpected death in

The Kv1.1 null mouse, a model of sudden unexpected death in epilepsy (SUDEP).

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OBJECTIVE Kv1.1 potassium channel null mouse (NULL) exhibits spontaneous seizure-related bradycardia, dies following seizure, and has been proposed as a model for vagus-mediated SUDEP. We characterized the cardiac events surrounding sudden unexpected death in epilepsy (SUDEP) in NULL during terminal

Altered A-type potassium channel function in the nucleus tractus solitarii in acquired temporal lobe epilepsy.

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Sudden unexpected death in epilepsy (SUDEP) is among the leading causes of death in people with epilepsy. Individuals with temporal lobe epilepsy (TLE) have a high risk for SUDEP because the seizures are often medically intractable. Neurons in the nucleus tractus solitarii (NTS) have been implicated

New onset seizures in a patient with Long QT Syndrome (LQTS2) and a pathogenic carboxyl-terminus frameshift variant of the KCNH2 gene.

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In patients with Long QT Syndrome (LQTS), mutations in the potassium channel KCNH2 gene increase seizure susceptibility with missense mutations involving the pore region of the gene acting as a positive predictor of seizures. Seizures are less commonly reported in patients with carboxyl

The changes of ERG channel expression after administration of antiepileptic drugs in the hippocampus of epilepsy gerbil model.

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Ether-a-go-go (ERG) K(+) channel is a channel of potassium inward rectification. ERG channelopathy may be a cause of sudden unwanted death. The purpose of our study is to assess the effect of antiepileptic drugs on the expression of ERG K(+) channel in the hippocampus using seizure resistant (SR)

Developmental and epilepsy spectrum of KCNB1 encephalopathy with long-term outcome

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Objective: We aimed to delineate the phenotypic spectrum and long-term outcome of individuals with KCNB1 encephalopathy. Methods: We collected genetic, clinical,

Kv1.1 Channelopathies: Pathophysiological Mechanisms and Therapeutic Approaches.

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Kv1.1 belongs to the Shaker subfamily of voltage-gated potassium channels and acts as a critical regulator of neuronal excitability in the central and peripheral nervous systems. KCNA1 is the only gene that has been associated with episodic ataxia type 1 (EA1), an autosomal dominant

Neuro-Glial Network Model Of Postictal Generalized EEG Suppression (PGES).

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Over the past couple of decades, glial cells have been highlighted as active agents in hyperexcitability of neuronal networks, specifically playing key roles in seizure onset and termination. In particular, microglia have been suggested to have both neuroprotective and neurotoxic effects on the

Acquired cardiac channelopathies in epilepsy: Evidence, mechanisms, and clinical significance.

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There is growing evidence that cardiac dysfunction in patients with chronic epilepsy could play a pathogenic role in sudden unexpected death in epilepsy (SUDEP). Recent animal studies have revealed that epilepsy secondarily alters the expression of cardiac ion channels alongside abnormal cardiac

Spreading depolarization in the brainstem mediates sudden cardiorespiratory arrest in mouse SUDEP models.

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Cardiorespiratory collapse after a seizure is the leading cause of sudden unexpected death in epilepsy (SUDEP) in young persons, but why only certain individuals are at risk is unknown. To identify a mechanism for this lethal cardiorespiratory failure, we examined whether genes linked to increased

Lamotrigine in idiopathic epilepsy - increased risk of cardiac death?

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OBJECTIVE Lamotrigine (LTG) has recently been shown to inhibit the cardiac rapid delayed rectifier potassium ion current (Ikr). Ikr-blocking drugs may increase the risk of cardiac arrhythmia and sudden unexpected death. With this background, it may be of importance that in our outpatient clinic

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