Intracranial pressure elevation after XXXX in @entity35 : @entity2657 is not the only cause, and short-duration mild @entity2332 is a highly effective preventive therapy.

@entity1 @entity64 @entity2657 @entity428 @entity4 @entity1188 @entity35 @entity2332 @entity385
In both the @entity1 and animal literature, it has largely been assumed that @entity4 is the primary cause of @entity428 ( @entity428 ) elevation after @entity64 and that more @entity4 equates to higher @entity428 . We recently demonstrated a dramatic @entity428 elevation 24 hours after small @entity385 in @entity35 , with minimal @entity4 . This @entity428 elevation was completely prevented by short-duration moderate @entity2332 soon after @entity64 . Here, our aims were to determine the importance of @entity4 in @entity428 elevation after @entity64 and whether mild @entity2332 could prevent the @entity428 rise. @entity64 was performed in @entity35 . @entity428 was monitored and short-duration mild (35   C) or moderate (32.5   C) @entity2332 , or normothermia (37   C) was induced after @entity64 onset. @entity4 was measured in three studies, using wet-dry weight calculations, T2-weighted magnetic resonance imaging, or histology. @entity428 increased 24 hours after @entity64 onset in all normothermic animals. Short-duration mild or moderate @entity2332 prevented this rise. No correlation was seen between   @entity428 and @entity4 or @entity1188 volumes. Calculated rates of @entity4 growth were orders of magnitude less than normal cerebrospinal fluid production rates. These data challenge current concepts and suggest that factors other than @entity2657 are the primary cause of the @entity428 elevation 24 hours after @entity64 onset.
