eHealth Literacy (eHL) is a set of competencies and skills encompassing the knowledge, comfort and perceived ability to identify, evaluate and apply electronic health information to health problems. Given its role in the appropriate use of health technologies, ensuring equitable access to health information and improving patient outcomes, this study aims to systematically retrieve, qualitatively and quantitative pool and critically appraise available experimental evidence on the effectiveness of eHL interventions across different population groups. Following the PRISMA guidelines, we conducted a systematic review in PubMed/Medline, Scopus, Web of Science, Embase, Cochrane Library and ClinicalTrials.gov, including original experimental studies quantifying the effectiveness of interventions aimed at increasing eHL, as assessed by the eHealth Literacy Scale (eHEALS) or other validated scales. We performed a random-effects model meta-analysis comparing changes in eHL levels before and after the interventions, and between the intervention and control groups. Heterogeneity was assessed using I2 statistics. Out of the 504 studies retrieved, 15 studies conducted between 2011 and 2023 met the inclusion criteria. Target populations of eHL interventions included adults in 7 studies, older people in 5 and young people in 4. The meta-analysis included 10 studies that used the eHEALS. Participants showed a mean increase in eHEALS scores of 5.81 points (95% CI = 3.36–8.26, N = 1025) following the eHL interventions compared to the pre-intervention period. In the analysis between the intervention and control groups, we found a statistically significant difference in eHL improvement in favour of the intervention group, with mean eHEALS scores 3.62 points (95% CI = 1.63–5.60, N = 1258) higher in the intervention group than in the control groups. Subgroup analyses by intervention type, stratified by Collaborative Learning (CL) or Individualistic Learning (IL) showed significant increases in eHealth Literacy in the pre-post intervention analysis (CL: UMD = 5.19, CI = 0.01–10.38, N = 402; IL: UMD = 6.05; CI = 3.14–8.97, N = 623) and in the intervention vs. control analysis in the IL group (DMD = 4.98; CI = 1.77–8.12, N = 540). Our findings support the effectiveness of tailored interventions in significantly enhancing eHL, providing key insights for evidence-based intervention design targeted to different population groups.
Epilepsy is increasingly conceptualized as a network disorder. In this cross-sectional mega-analysis, we integrated neuroimaging and connectome analysis to identify network associations with atrophy patterns in 1021 adults with epilepsy compared to 1564 healthy controls from 19 international sites. In temporal lobe epilepsy, areas of atrophy colocalized with highly interconnected cortical hub regions, whereas idiopathic generalized epilepsy showed preferential subcortical hub involvement. These morphological abnormalities were anchored to the connectivity profiles of distinct disease epicenters, pointing to temporo-limbic cortices in temporal lobe epilepsy and fronto-central cortices in idiopathic generalized epilepsy. Negative effects of age on atrophy further revealed a strong influence of connectome architecture in temporal lobe, but not idiopathic generalized, epilepsy. Our findings were reproduced across individual sites and single patients and were robust across different analytical methods. Through worldwide collaboration in ENIGMA-Epilepsy, we provided deeper insights into the macroscale features that shape the pathophysiology of common epilepsies.
Abstract Drug-resistant focal epilepsy is often caused by focal cortical dysplasias (FCDs). The distribution of these lesions across the cerebral cortex and the impact of lesion location on clinical presentation and surgical outcome are largely unknown. We created a neuroimaging cohort of patients with individually mapped FCDs to determine factors associated with lesion location and predictors of postsurgical outcome. The Multi-centre Epilepsy Lesion Detection (MELD) project collated a retrospective cohort of 580 patients with epilepsy attributed to FCD from 20 epilepsy centres worldwide. MRI-based maps of individual FCDs with accompanying demographic, clinical and surgical information were collected. We mapped the distribution of FCDs, examined for associations between clinical factors and lesion location, and developed a predictive model of postsurgical seizure freedom. FCDs were non-uniformly distributed, concentrating in the superior frontal sulcus, frontal pole and temporal pole. Epilepsy onset was typically before age 10. Earlier epilepsy onset was associated with lesions in primary sensory areas while later epilepsy onset was associated with lesions in association cortices. Lesions in temporal and occipital lobes tended to be larger than frontal lobe lesions. Seizure freedom rates varied with FCD location, from around 30% in visual, motor and premotor areas to 75% in superior temporal and frontal gyri. The predictive model of postsurgical seizure freedom had a positive predictive value of 70% and negative predictive value of 61%. FCD location is an important determinant of its size, the age of epilepsy onset and the likelihood of seizure freedom post-surgery. Our atlas of lesion locations can be used to guide the radiological search for subtle lesions in individual patients. Our atlas of regional seizure freedom rates and associated predictive model can be used to estimate individual likelihoods of postsurgical seizure freedom. Data-driven atlases and predictive models are essential for evidence-based, precision medicine and risk counselling in neurology.
Conventional Ultrasound (US) Doppler methods for blood flow imaging are limited to velocity estimations only in the axial direction, i.e. along the beam direction. Transverse oscillations (TO) methods extend blood investigations towards multidimensional estimates, and detailed descriptions of complex and fast blood flows are achievable by high frame-rate (HFR) imaging methods. In this work, TO are coupled with plane-waves (PWs) to reconstruct radio-frequency (RF) images with bi-directional oscillations in the pulse-echo field. The achieved RF images are exploited by a 2D phase-based displacement estimator to produce 2D-vector flow maps. A preliminary simulation study confirmed the capability of the method to produce the designed oscillations in the RF pulse-echo fields as well as the possibility to obtain 2D-vector maps with errors lower than 10% in many different conditions.
A bstract Temporal lobe epilepsy with hippocampal sclerosis (TLE-HS) is associated with a complex genetic architecture, but the translation from genetic risk factors to brain vulnerability remains unclear. Here, we examined associations between epilepsy-related polygenic risk scores for HS (PRS-HS) and brain structure in a large sample of neurotypical children, and correlated these signatures with case-control findings in in multicentric cohorts of patients with TLE-HS. Imaging-genetic analyses revealed PRS-related cortical thinning in temporo-parietal and fronto-central regions, strongly anchored to distinct functional and structural network epicentres. Compared to disease-related effects derived from epilepsy case-control cohorts, structural correlates of PRS-HS mirrored atrophy and epicentre patterns in patients with TLE-HS. By identifying a potential pathway between genetic vulnerability and disease mechanisms, our findings provide new insights into the genetic underpinnings of structural alterations in TLE-HS and highlight potential imaging-genetic biomarkers for early risk stratification and personalized interventions.
Abstract The common human epilepsies are associated with distinct patterns of reduced cortical thickness, detectable on neuroimaging, with important clinical consequences. To explore underlying mechanisms, we layered MRI-based cortical structural maps from a large-scale epilepsy neuroimaging study onto highly spatially-resolved human brain gene expression data, identifying >2,500 genes overexpressed in regions of reduced cortical thickness, compared to relatively-protected regions. The resulting set of differentially-expressed genes shows enrichment for microglial markers, and in particular, activated microglial states. Parallel analyses of cell-specific eQTLs show enrichment in human genetic signatures of epilepsy severity, but not epilepsy causation. Post mortem brain tissue from humans with epilepsy shows excess activated microglia. In an experimental model, depletion of activated microglia prevents cortical thinning, but not the development of chronic seizures. These convergent data strongly implicate activated microglia in cortical thinning, representing a new dimension for concern and disease modification in the epilepsies, potentially distinct from seizure control.
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