Epilepsy is a significant public health problem. More than 50 million people worldwide live with epilepsy, and over three-quarters of them are in low- and middle-income countries. The situation in Chad regarding people with epilepsy is challenging to assess, starting from the shortage of scientific data, the inadequacy of technical facilities, the lack of human resources, and the inadequacy of government action. The Ministry of Health and Chadian Society of Neurology are looking forward to prioritizing epilepsy as well as improving the living conditions of persons with this disease.
The epilepsy treatment issue is also problematic. Most of the patients are either off treatment or under-medicated. Few antiseizure medications (ASMs) are available, notably carbamazepine, phenobarbital, and valproic acid. Epilepsy remains little-known and does not seem to be a priority for decision-makers. We describe the current situation in Chad, to improve the conditions under which epilepsy is treated.
Epilepsies is a chronic brain problem that is common in poorer settings. The daily lives of people with epilepsy are chaotic in Chad. The challenges are numerous, particularly those related to health infrastructures, due to the lack of adequate diagnostic means and the lack of neurologists. The cultural and language challenges, especially since epilepsy is still considered the devil's disease and the name differs according to the dialects. Stigmatization is also frequent and is often responsible for school dropout, refusal, or dismissal from work. Care and prevention are daily challenges that require government action. Social coverage is insufficient and almost absent in rural areas. It is urgent to prioritize epilepsy in future action plans and also to increase awareness of the conditions to overcome these challenges.
Newer glucose-lowering drugs (GLDs) protect against cerebrovascular, neurodegenerative, and neuroinflammatory pathologies. Therefore, we performed a meta-analysis of randomized controlled trials (RCTs) comparing newer GLDs to placebo that assessed long-term cardiovascular and renal outcomes to analyze their potential to prevent late-onset seizures and epilepsy, separately and as a combined outcome. A comprehensive MEDLINE and CENTRAL databases search for DPP-4 inhibitors, GLP-1 receptor agonists, and SGLT2 inhibitor RCTs, which reported adverse effects, including seizures and epilepsy on clinicaltrials.gov, yielded 413 studies. Of them, 27 studies with almost 200 000 patients (mean age 64.9 years, 65.6% males) were included. We calculated relative risk (RR) and odds ratio (OR) using the Mantel–Haenszel method and Peto's method. Patients taking newer GLDs had a 24% lower risk of late-onset seizures and epilepsy, combined, (RR: 0.76, 95% CI: 0.62–0.95) and 22% lower risk of late-onset seizures only (RR = 0.78; 95% CI = 0.60–1.00), compared to patients on placebo. This seizure and epilepsy prevention benefit was only noted among patients taking GLP-1 receptor agonists. Stroke incidence was comparable between newer GLDs and placebo group. GLP-1 receptor agonists like Semaglutide significantly reduce late-onset seizures and epilepsy, and their anti-epileptogenic potential in older adults needs further exploration.
Our analysis 27 clinical trials and nearly 200 000 patients evaluated the potential of newer glucose-lowering drugs (GLDs) to prevent late-onset seizures and epilepsy in older adults. The study found that newer GLDs, especially GLP-1 receptor agonists like Semaglutide, reduced the combined risk of seizures and epilepsy by 24% compared to placebo. These findings suggest that newer GLDs may offer prevention against the development of seizures and epilepsy in older adults. However, further research is needed to confirm their anti-epileptogenic effects.
Hybrid depth electrodes are increasingly being used for epilepsy monitoring and human neurophysiology research. Microwires extending from the tip of the Behnke-Fried (BF) electrode into (sub)cortical areas allow to isolate single neurons and perform microstimulation. Conventional CT or MRI visualize the entire microwire bundle as an artifact extending from the BF electrode tip with low resolution, without proper identification of individual microwires. We illustrate the first direct visualization method of individual microwires using high-resolution photon-counting CT (PCCT). Coregistration of the PCCT scan with a preoperative MRI can visualize individual wires directly in cortex, which is an advantage as it provides feedback on the accuracy of the implantation method and can guide future implantations. This PCCT technique allows for accurately depicting individual microwires which could be relevant for neuroscientific research through improved visualization and implantation of specific cortical and subcortical brain areas.
Researchers are using hybrid depth electrodes to study epilepsy and brain activity. These electrodes, called Behnke-Fried (BF) electrodes, have microwires at the tip that can record single neurons and stimulate brain areas. Regular CT or MRI scans do not show the individual microwires clearly. The authors use a new high-resolution photon-counting CT (PCCT) technique, which can show each individual microwire in the brain. By combining PCCT with MRI, the authors can precisely see where the microwires are located. This could improve future implantation surgeries and brain research.
Clinical studies indicated a link between DTI imaging characteristics and epilepsy, but the causality of this connection had not been established. Therefore, we employed the Mendelian randomization analysis method to determine the causal relationship between DTI imaging characteristics and epilepsy.
We used Mendelian randomization analysis to identify the causal relationship between brain structure and the risk of epilepsy. GWAS data of DTI phenotypes, focal epilepsy, and genetic generalized epilepsy (GGE) were utilized in the analysis.
Our study found that DTI imaging phenotypes had a causal risk relationship with epilepsy. These phenotypes had a statistical impact on the risk of epilepsy seizures. There were differences in DTI phenotype causality between GGE and focal epilepsy, which were associated with the clinical phenotype differences of the two types of epilepsy.
Our study demonstrated that the diagnosis of subtypes could be assisted by comparing the differences in DTI phenotypes of specific brain regions. This meant that by studying the changes in brain regions before the onset of epilepsy, we might be able to intervene in epilepsy at an earlier stage.
Our study used Mendelian randomization to explore the causal relationship between brain structure, as seen in DTI imaging, and epilepsy. We found that specific DTI phenotypes are linked to an increased risk of epilepsy seizures, with notable differences between genetic generalized epilepsy and focal epilepsy. This suggested that analyzing DTI phenotypes could help in diagnosing and potentially intervening in epilepsy earlier by finding brain changes before seizures begin.
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