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A variety of acute brain insults can induce epileptogenesis, a complex process that results in acquired epilepsy. Despite advances in understanding mechanisms of epileptogenesis, there is currently no approved treatment that prevents the development or progression of epilepsy in patients at risk. The current concept of epileptogenesis assumes a window of opportunity following acute brain insults that allows intervention with preventive treatment. Recent results suggest that injury-induced epileptogenesis can be a much more rapid process than previously thought, suggesting that the 'therapeutic window' may only be open for a brief period, as in stroke therapy. However, experimental data also suggest a second, possibly delayed process ("secondary epileptogenesis") that influences the progression and refractoriness of the epileptic state over time, allowing interfering with this process even after onset of epilepsy. In this review, both methodological issues in preclinical drug development and novel targets for antiepileptogenesis will be discussed. Several promising drugs that either prevent epilepsy (antiepileptogenesis) or slow epilepsy progression and alleviate cognitive or behavioral comorbidities of epilepsy (disease modification) have been described in recent years, using diverse animal models of acquired epilepsy. Promising agents include TrkB inhibitors, losartan, statins, isoflurane, anti-inflammatory and anti-oxidative drugs, the SV2A modulator levetiracetam, and epigenetic interventions. Research on translational target validity and on prognostic biomarkers that can be used to stratify patients (or experimental animals) at high risk of developing epilepsy will hopefully soon lead to proof-of-concept clinical trials with the most promising drugs, which will be essential to make prevention of epilepsy a reality.
This article was published in the following journal.
The lack of early biomarkers of epileptogenesis precludes a sound prediction of epilepsy development after acute brain injuries and of the natural course of the disease thus impairing the development ...
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OBJECTIVES: I. Determine the chromosomal regions that contain genes that raise the risk of epilepsy in families by performing genetic linkage analysis of idiopathic/cryptogenic epilepsy.
Rationale : Persons with epilepsy have a greater risk of incurring accidental injury and a higher mortality risk than the general population. The main objective of the study is to underst...
Preclinical testing of drugs in experimental animals or in vitro for their biological and toxic effects and potential clinical applications.
Specific practices for the prevention of disease or mental disorders in susceptible individuals or populations. These include HEALTH PROMOTION, including mental health; protective procedures, such as COMMUNICABLE DISEASE CONTROL; and monitoring and regulation of ENVIRONMENTAL POLLUTANTS. Primary prevention is to be distinguished from SECONDARY PREVENTION and TERTIARY PREVENTION.
The prevention of recurrences or exacerbations of a disease that already has been diagnosed. This also includes prevention of complications or after-effects of a drug or surgical procedure.
Dietary recommendations that promote reduction in or prevention of high blood pressure. Recommendations include increasing intake of fruits and vegetables, and high-fiber, low-fat foods and reducing the intake of DIETARY SODIUM and high fat foods.
Treatments which are undergoing clinical trials or for which there is insufficient evidence to determine their effects on health outcomes; coverage for such treatments is often denied by health insurers.
Epilepsy is defined as a disorder of brain function characterized by recurrent seizures that have a sudden onset. (Oxford Medical Dictionary). A seizure is caused by a sudden burst of excess electrical activity in the brain, causing a tempora...
Neurology - Central Nervous System (CNS)
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