Publications by authors named "J N P Zwemmer"

Article Synopsis
  • - The study evaluates how the quality of MRI scans (specifically signal-to-noise ratio and spatial resolution) affects the detection of focal cortical dysplasia (FCD) using a software called Morphometric Analysis Program v2018 (MAP18) in patients with epilepsy.
  • - Researchers conducted a retrospective analysis on 30 MRI scans and artificially reduced the SNR and SR, discovering that lower quality led to significant declines in detecting FCD clusters and their characteristics.
  • - The findings indicate that low-quality MRI scans can hinder FCD detection, suggesting that ensuring high-quality imaging is crucial before conducting further analysis, as missing FCD can lead to ongoing seizures.
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Introduction: The standard treatment for patients with focal drug-resistant epilepsy (DRE) who are not eligible for open brain surgery is the continuation of anti-seizure medication (ASM) and neuromodulation. This treatment does not cure epilepsy but only decreases severity. The PRECISION trial offers a non-invasive, possibly curative intervention for these patients, which consist of a single stereotactic radiotherapy (SRT) treatment.

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Background And Objectives: The efficacy of deep brain stimulation of the anterior nucleus of the thalamus (ANT DBS) in patients with drug-resistant epilepsy (DRE) was demonstrated in the double-blind Stimulation of the Anterior Nucleus of the Thalamus for Epilepsy randomized controlled trial. The Medtronic Registry for Epilepsy (MORE) aims to understand the safety and longer-term effectiveness of ANT DBS therapy in routine clinical practice.

Methods: MORE is an observational registry collecting prospective and retrospective clinical data.

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Objective: No international guideline is available for minimum safety measures at epilepsy monitoring units (EMUs), although recommendations for preferred practices exist. These are mostly based on expert opinion, without evidence of effectiveness. We do not apply all of these preferred practices at our EMU setting.

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Studies in rodents suggest that flumazenil is a P-glycoprotein substrate at the blood-brain barrier. This study aimed to assess whether [C]flumazenil is a P-glycoprotein substrate in humans and to what extent increased P-glycoprotein function in epilepsy may confound interpretation of clinical [C]flumazenil studies used to assess gamma-aminobutyric acid A receptors. Nine drug-resistant patients with epilepsy and mesial temporal sclerosis were scanned twice using [C]flumazenil before and after partial P-glycoprotein blockade with tariquidar.

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