Disease-Modification in Epilepsy by Nonpharmacological Methods.
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ABSTRACT:
SUBMITTER: Jones NC
PROVIDER: S-EPMC5967595 | biostudies-literature | 2018 Jan-Feb
REPOSITORIES: biostudies-literature
Publications
Disease-Modification in Epilepsy by Nonpharmacological Methods.
Epilepsy currents 20180101 1
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Project description:BackgroundBlinding is a cornerstone of treatment evaluation. Blinding is more difficult to obtain in trials assessing nonpharmacological treatment and frequently relies on "creative" (nonstandard) methods. The purpose of this study was to systematically describe the strategies used to obtain blinding in a sample of randomized controlled trials of nonpharmacological treatment.Methods and findingsWe systematically searched in Medline and the Cochrane Methodology Register for randomized controlled trials (RCTs) assessing nonpharmacological treatment with blinding, published during 2004 in high-impact-factor journals. Data were extracted using a standardized extraction form. We identified 145 articles, with the method of blinding described in 123 of the reports. Methods of blinding of participants and/or health care providers and/or other caregivers concerned mainly use of sham procedures such as simulation of surgical procedures, similar attention-control interventions, or a placebo with a different mode of administration for rehabilitation or psychotherapy. Trials assessing devices reported various placebo interventions such as use of sham prosthesis, identical apparatus (e.g., identical but inactivated machine or use of activated machine with a barrier to block the treatment), or simulation of using a device. Blinding participants to the study hypothesis was also an important method of blinding. The methods reported for blinding outcome assessors relied mainly on centralized assessment of paraclinical examinations, clinical examinations (i.e., use of video, audiotape, photography), or adjudications of clinical events.ConclusionsThis study classifies blinding methods and provides a detailed description of methods that could overcome some barriers of blinding in clinical trials assessing nonpharmacological treatment, and provides information for readers assessing the quality of results of such trials.
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Project description:Gene therapy has been suggested as a plausible novel approach to achieve seizure control in patients with focal epilepsy that do not adequately respond to pharmacological treatment. We investigated the seizure-suppressant potential of combinatorial neuropeptide Y and Y2 receptor single vector gene therapy based on adeno-associated virus serotype 1 (AAV1) in rats. First, a dose-response study in the systemic kainate-induced acute seizure model was performed, whereby the 1012 genomic particles (gp)/mL titer of the vector was selected as an optimal concentration. Second, an efficacy study was performed in the intrahippocampal kainate chronic model of spontaneous recurrent seizures (SRSs), designed to reflect a likely clinical scenario, with magnetic resonance image (MRI)-guided focal unilateral administration of the vector in the hippocampus during the chronic stage of the disease. The efficacy study demonstrated a favorable outcome of the gene therapy, with a 31% responder rate (more than 50% reduction in SRS frequency) and 13% seizure-freedom rate, whereas no such effects were observed in the control animals. The inter-SRS and SRS cluster intervals were also significantly prolonged in the treated group compared to controls. In addition, the SRS duration was significantly reduced in the treated group but not in the controls. This study establishes the SRS-suppressant ability of the single vector combinatorial neuropeptide Y/Y2 receptor gene therapy in a clinically relevant chronic model of epilepsy.
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Project description:IntroductionAlzheimer's disease (AD) poses an increasing global health challenge and is marked by gradual cognitive deterioration, memory impairment, and neuroinflammation. Innovative therapeutic approaches as non-pharmacological protocol are urgently needed with side effect risk of drugs. Microcurrent therapy, a non-invasive modality involving low-level electrical currents, has emerged as a potential solution to address AD's complex pathogenesis. This study investigates the optimal application of microcurrent therapy as a clinical protocol for AD, utilizing a comprehensive approach that integrates behavioral assessments and neuroinflammation evaluation in a mouse model of dementia.Methods and resultsThe results reveal that microcurrent therapy holds promise in ameliorating memory impairment and reducing neuroinflammation in AD. Behavioral assessments, including the Novel Object Recognition Test (NOR) and Radial Arm Maze Test (RAM), demonstrated improved cognitive function following microcurrent therapy. Furthermore, microcurrent therapy inhibited expression of neuroinflammatory proteins, including ionized calcium binding adaptor molecule 1 (Iba1), and glial fibrillary acidic protein (GFAP) in current-treated group. Mechanistic insights suggest that microcurrent therapy may modulate neuroinflammation through the regulation of MAPK signaling pathways.ConclusionThis study emphasizes the prospect of microcurrent therapy as a safe and efficacious non-pharmacological strategy for Alzheimer's disease (AD), providing optimism to the countless individuals impacted by this debilitating ailment. These results contribute to the developments of an innovative clinical protocol for AD and recovery from neurological injury, underscoring the significance of investigating unconventional therapeutic approaches for addressing this complex condition.
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Project description:Epilepsy is a prevalent neurological disorder afflicting nearly 50 million people worldwide. The disorder is characterized clinically by recurrent spontaneous seizures attributed to abnormal synchrony of brain neurons. Despite advances in the treatment of epilepsy, nearly one-third of patients are resistant to current therapies, and the underlying mechanisms whereby a healthy brain becomes epileptic remain unresolved. Therefore, researchers have a major impetus to identify and exploit new drug targets. Here we distinguish between epileptic effectors, or proteins that set the seizure threshold, and epileptogenic mediators, which control the expression or functional state of the effector proteins. Under this framework, we then discuss attempts to regulate the mediators to control epilepsy. Further insights into the complex processes that render the brain susceptible to seizures and the identification of novel mediators of these processes will lead the way to the development of drugs to modify disease outcome and, potentially, to prevent epileptogenesis.
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Project description:This SuperSeries is composed of the following subset Series: GSE6771: Temporal Cortex Control (mesial temporal lobe epilepsy control) GSE6773: Temporal neocortex mesial temporal lobe epilepsy GSE6774: Temporal Cortex Control (Alzheimer's disease control) GSE6775: Temporal Cortex Alzheimer's Disease GSE6777: Cerebellum Alzheimer's Disease GSE6778: Cerebellum Control (Alzheimer's disease control) Keywords: SuperSeries Refer to individual Series
2007-01-23 | E-GEOD-6834 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below.
2007-01-23 | GSE6834 | GEO
Project description:ObjectivesWearable technology is increasingly used to monitor neurological disorders. The purpose of this systematic review was to synthesize knowledge from quantitative and qualitative clinical researches using wearable sensors in epilepsy, Parkinson's disease (PD), and stroke.MethodsA systematic literature search was conducted in PubMed and Scopus spanning from 1995 to January 2017. A synthesis of the main findings, reported adherence to wearables and missing data from quantitative studies, is provided. Clinimetric properties of measures derived from wearables in laboratory, free activities in hospital, and free-living environment were also evaluated. Qualitative thematic synthesis was conducted to explore user experiences and acceptance of wearables.ResultsIn total, 56 studies (50 reporting quantitative and 6 reporting qualitative data) were included for data extraction and synthesis. Among studies reporting quantitative data, 5 were in epilepsy, 21 PD, and 24 studies in stroke. In epilepsy, wearables are used to detect and differentiate seizures in hospital settings. In PD, the focus is on quantification of cardinal motor symptoms and medication-evoked adverse symptoms in both laboratory and free-living environment. In stroke upper extremity activity, walking and physical activity have been studied in laboratory and during free activities. Three analytic themes emerged from thematic synthesis of studies reporting qualitative data: acceptable integration in daily life, lack of confidence in technology, and the need to consider individualization.ConclusionsWearables may provide information of clinical features of interest in epilepsy, PD and stroke, but knowledge regarding the clinical utility for supporting clinical decision making remains to be established.
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Project description: Not available
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Project description:There is a substantial body of evidence that spontaneous recurrent seizures occur in a subset of patients with Alzheimer disease (AD), especially the familial forms that have an early onset. In transgenic mice that simulate these genetic forms of AD, seizures or reduced seizure threshold have also been reported. Mechanisms underlying the seizures or reduced seizure threshold in these mice are not yet clear and are likely to be complex, because the synthesis of amyloid β (Aβ) involves many peptides and proteases that influence excitability. Based on transgenic mouse models of AD where Aβ and its precursor are elevated, it has been suggested that seizures are caused by the downregulation of the Nav1.1 sodium channel in a subset of GABAergic interneurons, leading to a reduction in GABAergic inhibition. Another mechanism of hyperexcitability appears to involve tau, because deletion of tau reduces seizures in some of the same transgenic mouse models of AD. Therefore, altered excitability may be as much a characteristic of AD as plaques and tangles-especially for the familial forms of AD.
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