XXXX and neuroprotection: an illustrated review.

@entity1 @entity3877 @entity410 @entity131 @entity1372 @entity519 @entity1315 @entity302 @entity460 @entity528 @entity159 @entity130
Multiple types of insults, such as @entity159 , @entity519 and @entity130 , may alter the central nervous system. Strategies to protect the brain against insults remain a very difficult and challenging problem. Damage to the central nervous system can be modulated via excessive excitatory and reduced inhibitory neurotransmission. In addition, increased @entity1372 and @entity460 loading through impaired voltage-sensitive channels, as well as alterations in the acid-base balance can contribute to both excitotoxic and apoptotic cell death. @entity302 treatment has always been related to neuroprotection, since it aims to reduce the duration or totally suppress @entity410 . Although the debate on the capacity of simple @entity410 to induce @entity528 is still ongoing, no doubt persists on the disastrous effects of prolonged episodes of status. The next step would be to prevent @entity302 . Several animal models have been used to study the various aspects of the epileptogenic process. In @entity1 , one of the most compelling examples of a series of epileptogenic events is @entity1315 ( @entity1315 ). @entity1315 is often attributed to @entity410 in childhood resulting in @entity3877 . However, the relationship between @entity1315 , @entity410 in childhood and @entity131 may not be apparent as initially believed. Furthermore, it is well recognized that in a number of @entity1 there is a delay from a specific insult to the onset of @entity410 . This "latent period" could be an opportunity for effective intervention, provided that the underlying mechanisms are understood and that appropriate means for a beneficial modification of the disease process become available. The present review discusses the various steps of @entity1315 and provides illustrations of the various mechanisms implicated in @entity528 . Data from animal models is also presented and illustrated with video sequences. Finally, on the basis of what is known on mechanisms of action of available antiepileptic drugs, some suggestions are put forward. Basic science and research are guided by clinical queries and from ongoing dialogue. The present illustrated review deals with only a small part of the important amount of work related to @entity302 and neuroprotection. As such it is necessarily schematic or even simplistic. The review is designed to inform clinicians about the basic issues related to the subject, thus allowing them to follow the ongoing debate and participate with pertinent questions. (Published with video sequences).
