Pathogenesis of seizures and epilepsy after stroke

Stroke is the most frequent cause of secondary epilepsy in the elderly. The incidence of cerebral stroke is increasing with the extension of life expectancy, and the prevalence of post-stroke epilepsy (PSE) is rising. There are various seizure types after stroke, and the occurrence of epilepsy is closely related to the type and location of stroke. Moreover, the clinical treatment of post-stroke epilepsy is difficult, which increases the risk of disability and death, and affects the prognosis and quality of life of patients. Now seizure and epilepsy after stroke is more and more get the attention of the medical profession, has been more and more researchers have devoted to seizures after stroke and PSE clinical and basic research, and hope to get a scientific and unified guideline, to give timely and effective treatment, but the exact pathophysiologic mechanism has not yet formed a unified conclusion. It has been found that ion channels, neurotransmitters, proliferation of glial cells, genetics and other factors are involved in the occurrence and development of PSE. In this review, we discuss the pathogenesis of early-onset epileptic seizures and late-onset epilepsy after stroke, in order to provide a basis for clinicians to understand the disease, and expect to provide ideas for future exploration.

Research progress on the prediction of post-stroke epilepsy

Epilepsy is a common neurological disease that not only causes difficulties in the work and life activities of patients, but also brings complex social problems. Cerebrovascular disease is currently the main cause of epilepsy in the elderly. With the increased survival rate of patients after stroke, the incidence of epilepsy after stroke has also increased. Effective prediction of epilepsy after stroke is extremely crucial for the prognosis of patients, the initiation of antiepileptic therapy and the reduction of epileptic seizures. In this review, we summarize and compare the current models for the prediction of epilepsy after stroke, including the SeLECT prediction model, Post-Stroke Epilepsy Risk Scale (PoSERS), CAVE score, electroencephalogram (EEG) prediction model, and Scandinavian Stroke Scale (SSS) score, in order to provide reference for clinical practice and future research. Prediction models can be selected based on the clinical classification of cerebrovascular events. The SeLECT score prognostic model is a better choice for ischemic stroke, especially for the exclusive prediction of mild post stroke epilepsy. The CAVE score model is suitable for intra-cerebral hemorrhage patients. It is simple and offers high correlation between the risk factors and epilepsy. The PoSERS score simultaneously predicts ischemic and hemorrhagic stroke, and is superior to other methods in specificity as well as positive and negative prediction rate. The SSS score, which only measures stroke severity, is not strictly considered as a mature predictor, but it can be used as a first step screening tool. A growing number of large studies are under the way to identify risk factors of poststroke epilepsy (PSE) and to improve the inclusion of predictive indicators. New and advanced findings by EEG recordings may further improve the prediction of PSE.

Potential Therapeutic Role of Carnitine and Acetylcarnitine in Neurological Disorders

Background: Current therapy of neurological disorders has several limitations. Although a high number of drugs are clinically available, several subjects do not achieve full symptomatic remission. In recent years, there has been an increasing interest in the therapeutic potential of L-carnitine (LCAR) and acetyl-L-carnitine (ALCAR) because of the multiplicity of actions they exert in energy metabolism, as antioxidants, neuromodulators and neuroprotectors. They also show excellent safety and tolerability profile. Objective: To assess the role of LCAR and ALCAR in neurological disorders. Methods: A meticulous review of the literature was conducted in order to establish the linkage between LCAR and ALCAR and neurological diseases. Results: LCAR and ALCAR mechanisms and effects were studied for Alzheimer’s disease, depression, neuropathic pain, bipolar disorder, Parkinson’s disease and epilepsy in the elderly. Both substances exert their actions mainly on primary metabolism, enhancing energy production, through β-oxidation, and the ammonia elimination via urea cycle promotion. These systemic actions impact positively on the Central Nervous System state, as Ammonia and energy depletion seem to underlie most of the neurotoxic events, such as inflammation, oxidative stress, membrane degeneration, and neurotransmitters disbalances, present in neurological disorders, mainly in the elderly. The impact on bipolar disorder is controversial. LCAR absorption seems to be impaired in the elderly due to the decrease of active transportation; therefore, ALCAR seems to be the more effective option to administer. Conclusions: ALCAR emerges as a simple, economical and safe adjuvant option in order to impair the progression of most neurological disorders.