Introduction A major difficulty in a discussion of epileptogenic mechanisms involved in symptomatic epilepsy is the fact that there is often disagreement about what constitutes “epileptogenesis” and what we mean by “symptomatic epilepsy.” It is therefore helpful to consider some components of these concepts – not so much to express any consensus definitions, but rather to provide a working starting point for the discussion. Epileptogenesis There is a current belief that “epileptogenic” mechanisms are different from the mechanisms that have been studied/identified underlying seizure genesis and initiation (or, indeed, those processes involved in maintaining the epileptic state). In that sense, the term, “epileptogenesis” certainly implies the existence of an epileptic state (chronic spontaneous seizure discharge? reduced seizure threshold?) – a state that follows, in a causal manner, from a previously occurring initiating “insult” or condition. Further, the term “epileptogenesis” suggests a time interval between the physical insult (or the onset of an epileptogenic state) and the resultant epileptic condition. This temporal delay is an important aspect of the epileptogenic concept, since we generally use the term “epileptogenesis” to describe a process that requires time. Further, reference to such an epileptogenic process assumes that in some earlier time in the life of the individual, the brain abnormality underlying seizure activity was not present, and that the structural changes (molecular or more grossly morphologic) leading to the epileptic state appeared gradually; that is, there is a time at which the epilepsy-inducing abnormalities begin to appear but the epilepsy is not yet present.
|Original language||English (US)|
|Title of host publication||The Causes of Epilepsy: Common and Uncommon Causes in Adults and Children|
|Publisher||Cambridge University Press|
|Number of pages||8|
|ISBN (Print)||9780511921001, 9780521114479|
|State||Published - Jan 1 2011|
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