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This book presents scientific evidence about epilepsy along with straightforward guidance and recommendations. Responses to frequently asked questions and clarification of uncertainties are provided to empower patients to optimize their medical, psychological and social care. This book helps mediate between patients and health care professionals and can assist both sides to understand the condition of epilepsy at all levels. The information provided in the book empowers patients to share decision making with their carers and clinicians and enables them to make informed decisions, by taking into account the best scientific evidence, as well as the patients' values and preferences. The Epilepsy Book: A Companion for Patients is ideal for patients with epilepsy and their carers, and will also be of interest to health care professionals, medical students and teachers. Thalia Valeta's approach to epilepsy facilitates deeper understanding of the unmet needs and expectations of patients.

Purpose of ReviewFor millennia, there has been interest in the use of cannabis for the treatment of epilepsy. However, it is only recently that appropriately powered controlled studies have been completed. In this review, we present an update on the research investigating the use of cannabidiol (CBD), a non-psychoactive component of cannabis, in the treatment of epilepsy.Recent FindingsWhile the anticonvulsant mechanism of action of CBD has not been entirely elucidated, we discuss the most recent data available including its low affinity for the endocannabinoid receptors and possible indirect modulation of these receptors via blocking the breakdown of anandamide. Additional targets include activation of the transient receptor potential of vanilloid type-1 (TRPV1), antagonist action at GPR55, targeting of abnormal sodium channels, blocking of T-type calcium channels, modulation of adenosine receptors, modulation of voltage-dependent anion selective channel protein (VDAC1), and modulation of tumor necrosis factor alpha release. We also discuss the most recent studies on various artisanal CBD products conducted in patients with epilepsy in the USA and internationally. While a high percentage of patients in these studies reported improvement in seizures, these studies were either retrospective or conducted via survey. Dosage/preparation of CBD was either unknown or not controlled in the majority of these studies. Finally, we present data from both open-label expanded access programs (EAPs) and randomized placebo-controlled trials (RCTs) of a highly purified oral preparation of CBD, which was recently approved by the FDA in the treatment of epilepsy. In the EAPs, there was a significant improvement in seizure frequency seen in a large number of patients with various types of treatment-refractory epilepsy. The RCTs have shown significant seizure reduction compared to placebo in patients with Dravet syndrome and Lennox-Gastaut syndrome. Finally, we describe the available data on adverse effects and drug-drug interactions with highly purified CBD. While this product is overall well tolerated, the most common side effects are diarrhea and sedation, with sedation being much more common in patients taking concomitant clobazam. There was also an increased incidence of aspartate aminotransferase and alanine aminotransferase elevations while taking CBD, with many of the patients with these abnormalities also taking concomitant valproate. CBD has a clear interaction with clobazam, significantly increasing the levels of its active metabolite N-desmethylclobazam in several studies; this is felt to be due to CBD’s inhibition of CYP2C19. EAP data demonstrate other possible interactions with rufinamide, zonisamide, topiramate, and eslicarbazepine. Additionally, there is one case report demonstrating need for warfarin dose adjustment with concomitant CBD.SummaryUnderstanding of CBD’s efficacy and safety in the treatment of TRE has expanded significantly in the last few years. Future controlled studies of various ratios of CBD and THC are needed as there could be further therapeutic potential of these compounds for patients with epilepsy.

The identification of potential therapeutic agents for the treatment of epilepsy requires the use of seizure models. Except for some early treatments, including bromides and phenobarbital, the antiseizure activity of all clinically used drugs was, for the most part, defined by acute seizure models in rodents using the maximal electroshock and subcutaneous pentylenetetrazole seizure tests and the electrically kindled rat. Unfortunately, the clinical evidence to date would suggest that none of these models, albeit useful, are likely to identify those therapeutics that will effectively manage patients with drug resistant seizures. Over the last 30 years, a number of animal models have been developed that display varying degrees of pharmacoresistance, such as the phenytoin- or lamotrigine-resistant kindled rat, the 6-Hz mouse model of partial seizures, the intrahippocampal kainate model in mice, or rats in which spontaneous recurrent seizures develops after inducing status epilepticus by chemical or electrical stimulation. As such, these models can be used to study mechanisms of drug resistance and may provide a unique opportunity for identifying a truly novel antiseizure drug (ASD), but thus far clinical evidence for this hope is lacking. Although animal models of drug resistant seizures are now included in ASD discovery approaches such as the ETSP (epilepsy therapy screening program), it is important to note that no single model has been validated for use to identify potential compounds for as yet drug resistant seizures, but rather a battery of such models should be employed, thus enhancing the sensitivity to discover novel, highly effective ASDs. The present review describes the previous and current approaches used in the search for new ASDs and offers some insight into future directions incorporating new and emerging animal models of therapy resistance.

Lennox-Gastaut syndrome is one of the most severe epileptic encephalopathies of childhood onset. The cause of this syndrome can be symptomatic (ie, secondary to an underlying brain disorder) or cryptogenic (ie, has no known cause). Although Lennox-Gastaut syndrome is commonly characterised by a triad of signs, which include multiple seizure types, slow spike-wave complexes on electroencephalographic (EEG) recordings, and impairment of cognitive function, there is debate with regard to the precise limits, cause, and diagnosis of the syndrome. Tonic seizures, which are thought to be a characteristic sign of Lennox-Gastaut syndrome, are not present at onset and the EEG features are not pathognomonic of the disorder. There are few effective treatment options for the multiple seizures and comorbidities, and the long-term outlook is poor for most patients. Probably as a result of the complexity of the disorder, only a few randomised trials have studied Lennox-Gastaut syndrome, and thus many of the drugs that are more commonly used have little or no supporting evidence base from controlled trials. In this Review, we discuss the main issues with regard to the diagnosis and treatment options available. We also suggest key considerations for future trials and highlight the importance of a comprehensive approach to the assessment and management of this syndrome.

A central role for neuroinflammation in epileptogenesis has recently been suggested by several investigations. This systematic review explores the role of inflammatory mediators in epileptogenesis, its association with seizure severity, and its correlation with drug-resistant epilepsy (DRE). The study analysed articles published in JCR journals from 2019 to 2024. The search strategy comprised the MESH, free terms of “Neuroinflammation”, and selective searches for the following single biomarkers that had previously been selected from the relevant literature: “High mobility group box 1/HMGB1”, “Toll-Like-Receptor 4/TLR-4”, “Interleukin-1/IL-1”, “Interleukin-6/IL-6”, “Transforming growth factor beta/TGF-β”, and “Tumour necrosis factor-alpha/TNF-α”. These queries were all combined with the MESH terms “Epileptogenesis” and “Epilepsy”. We found 243 articles related to epileptogenesis and neuroinflammation, with 356 articles from selective searches by biomarker type. After eliminating duplicates, 324 articles were evaluated, with 272 excluded and 55 evaluated by the authors. A total of 21 articles were included in the qualitative evaluation, including 18 case–control studies, 2 case series, and 1 prospective study. As conclusion, this systematic review provides acceptable support for five biomarkers, including TNF-α and some of its soluble receptors (sTNFr2), HMGB1, TLR-4, CCL2 and IL-33. Certain receptors, cytokines, and chemokines are examples of neuroinflammation-related biomarkers that may be crucial for the early diagnosis of refractory epilepsy or may be connected to the control of epileptic seizures. Their value will be better defined by future studies.

Purpose of ReviewDiagnostic delay is an increasingly recognized issue in epilepsy. At the same time, there is a clear disparity between public awareness of epilepsy and that of other public health issues. A contributing factor for this seems to be a lack of studies testing interventions designed to improve seizure recognition. In this review, we summarize the main findings from recent studies investigating diagnostic delay in epilepsy, highlighting causes, consequences, and potential interventions in future research that may improve quality of care in this population.Recent FindingsBuilding on prior evidence, diagnostic delay in patients with new-onset focal epilepsy has been identified as an important problem for patients with epilepsy. Such delay in diagnosis can lead to delayed treatment and potentially preventable morbidity and mortality including motor vehicle accidents. Nonmotor seizure semiology appears to be a major contributor for delay; such seizures are largely unrecognized when patients present to emergency departments for care. Improving recognition and diagnosis of recurrent nonmotor seizures in emergency departments represents a significant opportunity for improving time to diagnosis, particularly when patients present following a first lifetime motor seizure and meet diagnostic criteria for epilepsy.SummaryDiagnostic delay in epilepsy is a significant public health issue and recent studies have highlighted potential areas for intervention.

Epilepsy is a common neurological disorder, and its diagnosis mainly relies on the analysis of electroencephalogram (EEG) signals. However, the raw EEG signals contain limited recognizable features, and in order to increase the recognizable features in the input of the network, the differential features of the signals, the amplitude spectrum and the phase spectrum in the frequency domain are extracted to form a two-dimensional feature vector. In order to solve the problem of recognizing multimodal features, a neural network model based on a multimodal dual-stream network is proposed, which uses a mixture of one-dimensional convolution, two-dimensional convolution and LSTM neural networks to extract the spatial features of the EEG two-dimensional vectors and the temporal features of the signals, respectively, and combines the advantages of the two networks, using the hybrid neural network to extract both the temporal and spatial features of the signals at the same time. In addition, a channel attention module was used to focus the model on features related to seizures. Finally, multiple sets of experiments were conducted on the Bonn and New Delhi data sets, and the highest accuracy rates of 99.69% and 97.5% were obtained on the test set, respectively, verifying the superiority of the proposed model in the task of epileptic seizure detection.

Both invasive and non-invasive electroencephalographic (EEG) recordings from the human brain have an increasingly important role in neuroscience research and are candidate modalities for medical brain–machine interfacing. It is often assumed that the major artifacts that compromise non-invasive EEG, such as caused by blinks and eye movement, are absent in invasive EEG recordings. Quantitative investigations on the signal quality of simultaneously recorded invasive and non-invasive EEG in terms of artifact contamination are, however, lacking. Here we compared blink related artifacts in non-invasive and invasive EEG, simultaneously recorded from prefrontal and motor cortical regions using an approach suitable for detection of small artifact contamination. As expected, we find blinks to cause pronounced artifacts in non-invasive EEG both above prefrontal and motor cortical regions. Unexpectedly, significant blink related artifacts were also found in the invasive recordings, in particular in the prefrontal region. Computing a ratio of artifact amplitude to the amplitude of ongoing brain activity, we find that the signal quality of invasive EEG is 20 to above 100 times better than that of simultaneously obtained non-invasive EEG. Thus, while our findings indicate that ocular artifacts do exist in invasive recordings, they also highlight the much better signal quality of invasive compared to non-invasive EEG data. Our findings suggest that blinks should be taken into account in the experimental design of ECoG studies, particularly when event related potentials in fronto-anterior brain regions are analyzed. Moreover, our results encourage the application of techniques for reducing ocular artifacts to further optimize the signal quality of invasive EEG.

Epilepsy is a complex disease in the brain. Complete control of seizure has always been a challenge in epilepsy treatment. Currently, clinical management primarily involves pharmacological and surgical interventions, with the former being the preferred approach. However, antiepileptic drugs often exhibit low bioavailability due to inherent limitations such as poor water solubility and difficulty penetrating the blood–brain barrier (BBB). These issues significantly reduce the drugs’ effectiveness and limit their clinical application in epilepsy treatment. Additionally, the diagnostic accuracy of current imaging techniques and electroencephalography (EEG) for epilepsy is suboptimal, often failing to precisely localize epileptogenic tissues. Accurate diagnosis is critical for the surgical management of epilepsy. Thus, there is a pressing need to enhance both the therapeutic outcomes of epilepsy medications and the diagnostic precision of the condition. In recent years, the advancement of nanotechnology in the biomedical sector has led to the development of nanomaterials as drug carriers. These materials are designed to improve drug bioavailability and targeting by leveraging their large specific surface area, facile surface modification, ability to cross the BBB, and high biocompatibility. Furthermore, nanomaterials have been utilized as contrast agents in imaging and as materials for EEG electrodes, enhancing the accuracy of epilepsy diagnoses. This review provides a comprehensive examination of current research on nanomaterials in the treatment and diagnosis of epilepsy, offering new strategies and directions for future investigation.