Update on Pharmacology: The Role of Progesterone in Traumatic Brain Injury
Tamara R. Espinoza MD
Mel B. Glenn MD; (Editor)
David W. Wright MD

$3.95 		Journal of Head Trauma Rehabilitation
December 2011 
Volume 26  Number 6
Pages 497 - 499
 
  PDF Version Available!

ABSTRACT
WITHIN the last 20 years, a significant body of literature has advanced our understanding of the pathophysiologic mechanisms that result from traumatic brain injury (TBI). Most importantly, we now recognize that brain injuries cause both central and systemic effects. For example, a number of studies have demonstrated increased release of proinflammatory cytokines and augmented oxidative stress reactions in peripheral tissues after isolated head injury.1,2 Thus, effective treatment modalities are those that work at multiple sites and levels of injury to enhance repair and regenerative mechanisms while limiting the destructive local and systemic processes that result from TBI.Progesterone is a steroid hormone well known for its role in the menstrual cycle. It is produced not only by the ovaries and placenta in females but also by the adrenal glands and the brain of both sexes. Its production in the brain, by oligodendrocytes and other cell types, provides clues to its critical role in neural homeostasis.3 Indeed, the 10-fold increase of progesterone during fetal growth is thought by some experts to be primarily for neuronal development. Within the last 20 years, preclinical research has repeatedly shown that progesterone has potent neuroprotective properties. There is evidence that it also plays a much broader role in correcting and maintaining homeostasis after physiologic stress and injury beyond the central nervous system.4 Most significantly, it exerts its effects through multiple proteomic and receptor-mediated systems, making it more robust than other therapies attempted previously.Progesterone initially became of interest in TBI after female rats with experimentally induced brain injury were noted to have improved outcomes and better recovery when compared with their male counterparts.5 In an early study, Roof et al6 measured cerebral edema after TBI in rats under 3 hormonal conditions: adult males with low levels of estrogen and progesterone, females in proestrus

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