Underlying @entity6795 as Risk Factor for XXXX : An Animal Study.

@entity1 @entity1545 @entity131 @entity410 @entity6795 @entity302 @entity35 @entity6349
UNASSIGNED: @entity131 ( @entity131 ) is a significant risk factor for development of @entity302 in @entity1 . It is unclear, however, why some @entity1 are at an increased risk of becoming @entity302 , while others recover from the @entity131 @entity410 -free. We previously showed that the presence of a proepileptic pathology increases the risk of @entity302 in an animal model of @entity6795 ( @entity6795 ) after a secondary insult, which we described as the "second hit". Here we sought to evaluate the prevalence of @entity302 activity and @entity410 in @entity6795 after a moderate @entity131 to determine the influence of @entity6349 pathology on @entity131 -induced epileptogenesis. @entity6795 was generated in @entity35 through in utero irradiation (the "first hit"). Nondysplastic and @entity6795 @entity35 were surgically implanted with EEG electrodes. Craniotomies were performed over the pre-central cortex, and @entity35 were given a moderate @entity131 using the lateral fluid percussion injury device. @entity35 were monitored with chronic EEG and video. EEG data were analyzed for the occurrence of interictal spikes and @entity302 EEG @entity410 patterns. Brains were harvested and evaluated histologically. Spontaneous @entity410 are more prominent and occur earlier in @entity35 with @entity6795 after a moderate @entity131 compared with nondysplastic control @entity35 . All of the @entity6795 animals exhibited interictal spiking after @entity131 , while only a portion of nondysplastic animals produced spikes. These results suggest that the presence of a proepileptic pathology may increase the risk for the development of @entity302 after @entity131 . Diagnosis and treatment of @entity131 may depend on underlying pathologies contributing to @entity302 after a @entity1545 .
