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quinidine/epileptisk anfald
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KCNT1-positive epilepsy of infancy with migrating focal seizures successfully treated with nonnarcotic antitussive drugs after treatment failure with quinidine: A case report
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Background: Epilepsy of infancy with migrating focal seizures (EIMFS) is one of the early-onset epileptic encephalopathies resistant to antiepileptic drugs, therefore carrying an extremely poor neurodevelopmental outcome. KCNT1, encoding for a sodium-activated
The P-glycoprotein inhibitor quinidine decreases the threshold for bupivacaine-induced, but not lidocaine-induced, convulsions in rats.
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OBJECTIVE
To examine whether inhibition of P-glycoprotein (P-gp) activity by quinidine affects the central nervous system toxicity of lidocaine and racemic bupivacaine (bupivacaine).
METHODS
Forty male Sprague-Dawley rats were randomly divided into four groups (n = 10). Fifteen minutes following
Two South Indian Children with KCNT1-Related Malignant Migrating Focal Seizures of Infancy - Clinical Characteristics and Outcome of Targeted Treatment with Quinidine.
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KCNT1 gene encodes a sodium-gated potassium channel subunit that plays an important role in regulating excitability in neurons. Quinidine is a partial antagonist of this channel. We report the clinical characteristics of two south Indian children with KCNT1-related epileptic
Effect of dextromethorphan/quinidine on pentylenetetrazole- induced clonic and tonic seizure thresholds in mice.
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INTRODUCTION
This study aimed to investigate the effects of dextromethorphan (DM) or dextromethorphan/quinidine (DM/Q) against pentylenetetrazole (PTZ)- induced seizure threshold in mice and the probable involvement of N-methyl D-aspartate (NMDA), sigma-1 and serotonin 1AEarly Treatment with Quinidine in 2 Patients with Epilepsy of Infancy with Migrating Focal Seizures (EIMFS) Due to Gain-of-Function KCNT1 Mutations: Functional Studies, Clinical Responses, and Critical Issues for Personalized Therapy.
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Epilepsy of infancy with migrating focal seizures (EIMFS) is a rare early-onset developmental epileptic encephalopathy resistant to anti-epileptic drugs. The most common cause for EIMFS is a gain-of-function mutation in the KCNT1 potassium channel gene, and treatment with the KCNT1 blocker quinidine
A quinidine non responsive novel KCNT1 mutation in an Indian infant with epilepsy of infancy with migrating focal seizures.
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Epilepsy of infancy with migrating focal seizures {a.k.a malignant migrating partial seizures of infancy (MMPSI)} is an uncommon epileptic encephalopathy with a poor prognosis. Migrating focal seizures with autonomic features, developmental stagnation and refractoriness to treatment are its key
Targeted treatment of migrating partial seizures of infancy with quinidine.
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Migrating partial seizures of infancy is an early onset epileptic encephalopathy syndrome that is typically resistant to treatment. The most common cause is a gain of function mutation in the potassium channel KCNT1. The antiarrhythmic drug quinidine is a partial antagonist of KCNT1 and hence may be
On the anticonvulsive effect of quinidine. I. Experimental investigation of somatomotor, vegetative and bioelectrical aspects of convulsive seizures elicited by electroshocks.
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Corrigendum to "Does age affect response to quinidine in patients with KCNT1 mutations? Report of three new cases and review of the literature" [Seizure 55 (February) (2018) 1-3].
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[11C]quinidine and [11C]laniquidar PET imaging in a chronic rodent epilepsy model: impact of epilepsy and drug-responsiveness.
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BACKGROUND
To analyse the impact of both epilepsy and pharmacological modulation of P-glycoprotein on brain uptake and kinetics of positron emission tomography (PET) radiotracers [(11)C]quinidine and [(11)C]laniquidar.
METHODS
Metabolism and brain kinetics of both [(11)C]quinidine and
Lack of selectivity for ventricular and ischaemic tissue limits the antiarrhythmic actions of lidocaine, quinidine and flecainide against ischaemia-induced arrhythmias.
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The antiarrhythmic effectiveness, electrocardiographic and haemodynamic properties of three representative class I antiarrhythmics have been investigated in anaesthetized rats. Quinidine, lidocaine and flecainide were chosen as representatives of class Ia, Ib and Ic, respectively. Lidocaine showed
Concurrent Quinidine and Phenobarbital in the Treatment of a Patient with 2 KCNT1 Mutations.
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Epilepsy of infancy with migrating focal seizures is a devastating pediatric neurologic disorder that often results in treatment-resistant seizure activity and developmental delay. The condition has been associated with mutations in the KCNT1 gene that cause a gain of function in neuronal
Unexceptional seizure potential of tramadol or its enantiomers or metabolites in mice.
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Tramadol is one of the most widely used centrally acting analgesics worldwide. Because of its multimodal analgesic mechanism (opioid plus nonopioid), the adverse effects profile of tramadol, similar to its analgesic profile, can be atypical compared with single-mechanism opioid analgesics. The
Excitatory effects of gap junction blockers on cerebral cortex seizure-like activity in rats and mice.
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OBJECTIVE
The role of gap junctions in seizures is an area of intense research. Many groups have reported anticonvulsant effects of gap junction blockade, strengthening the case for a role for gap junctions in ictogenesis. The cerebral cortex is underrepresented in this body of research. We have
Do traditional anti-seizure drugs have a future? A review of potential anti-seizure drugs in clinical development.
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Currently information is available for 20 potential anti-seizure drugs in clinical development. They include candidates with mechanisms of action similar to those of marketed AEDs (allopregnanolone, brivaracetam, ganaxolone, ICA-105665, NS1209, selurampanel); those with new mechanisms of action
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