Faculty Book
HELEN M. BRAMLETT, Ph.D.
Assistant Professor, Neurological Surgery
The Pathophysiology and Treatment of CNS Injury
Research
Interests
My research interest is understanding the pathophysiology of traumatic injury leading to the use of therapeutic strategies targeting specific mechanisms of damage. My laboratory focuses on three areas of traumatic research. Hormonal influences on traumatic brain and spinal cord injury, progressive tissue damage after traumatic injury and mechanisms involved in the exacerbation of tissue damage following trauma and secondary hypoxia.
Several recent studies have reported on the efficacy of hormones in treating stroke and traumatic brain injury (TBI). The mechanisms of action that hormones are working through are now being elucidated. We have recently demonstrated endogenous neuroprotection from hormones in intact females compared to males and ovariectomized animals on histopathological outcome measures. We are now focusing on the influence of the inflammatory response on outcome following TBI and the effect that hormones play in this response. In addition to studies in TBI, we are also studying the effects of hormones in attenuating damage and improving behavioral outcome after spinal cord injury (SCI). Based on the findings from these studies, it may be advantageous to use estrogen in combination with other growth factors to facilitate regeneration after SCI. Estrogen has been shown to produce proliferation of Schwann cells as well as neurite growth.
Our laboratory and others have recently demonstrated chronic atrophy at one year following TBI. However, it is unknown what is causing this continued gray and white matter tissue loss. Is it due to the initial injury or are there active processes ongoing that continue to degrade the tissue? Current studies in the laboratory are designed to determine what mechanisms may be contributing to this progressive damage in order to design appropriate treatment strategies to halt this loss.
One problem that arises in studying TBI is using a model that is clinically relevant. There is an ongoing debate on whether simple models or complicated models of TBI should be utilized in the laboratory. Secondary hypoxia and hypotension frequently occur clinically after TBI. Several laboratories are employing this paradigm to study the pathophysiology of this complicated model. We have recently documented an exacerbation of histopathological damage as well as behavioral deficits following TBI and secondary hypoxia. However, specific mechanisms that may be contributing to this injury pattern have not been studied in depth. We are currently concentrating on obtaining evidence for aggravated vascular dysfunction leading to an enhanced inflammatory response following TBI and secondary hypoxia.
Video Introduction
Atkins CM, Oliva AA Jr., Alonso OF, Pearse DD, Bramlett HM, Dietrich WD.(2007) Modulation of the cAMP signaling pathway after traumatic brain injury. Exp Neurol. 208(1):145-158.
Atkins CM, Oliva AA Jr., Alonso OF, Chen S, Bramlett HM, Hu BR, Dietrich WD. (2007) Hypothermia treatment potentiates ERK1/2 activation after traumatic brain injury.Eur J Neurosci. 26(4):810-9.
Dietrich WD, Bramlett HM. (2007) Hyperthermia and central nervous system injury. Prog. Brain Res.162:201-17.
Bramlett HM, Dietrich WD.(2007) Progressive damage after brain and spinal cord jury:pathomechanisms and treatment strategies. Prog Brain Res.161:125-41.
Urrea C, Castellanos DA, Sagen J, Tsoulfas P, Bramlett HM, Dietrich WD.(2007) Widespread cellular proliferation and focal neurogenesis after traumatic brain injury in the rat. Restor Neurol Neurosci. 25(1):65-76.
Truettner JS, Hu B, Alonso OF, Bramlett HM, Kokame K, Dietrich D. (2007) Subcellular stress response after traumatic brain injury. J Neurotrauma.(4):599-612.
Rodriguez-Paez AC, Brunschwig JP, Bramlett HM. (2005) Light and electron microscopic assessment of progressive atrophy following moderate traumatic brain injury in the rat. Acta Neuropathol. 109(6):603-16.
Suzuki T, Bramlett HM, Ruenes G, Dietrich WD. (2004) The effects of early post-traumatic hyperthermia in female and ovariectomized rats. J Neurotrauma. (7):842-53.
Bramlett HM, Dietrich WD. (2002) Quantitative structural changes in white and gray matter 1 year following traumatic brain injury in rats. Acta Neuropathol 103:607-614.
Bramlett HM, Dietrich WD (2001) Neuropathological protection after traumatic brain injury in intact female rats versus males or ovariectomized females. J Neurotrauma 18:891-900.
Matsushita Y, Bramlett HM, Alonso O, Dietrich WD (2001) Post-traumatic hypothermia is neuroprotective in a model of traumatic brain injury complicated by a secondary hypoxic insult. Crit Care Med 29(11):2060-6.
Matsushita Y, Bramlett HM, Kuluz JW, Alonso O, Dietrich WD (2001) Delayed hemorrhagic hypotension exacerbates the hemodynamic and histopathological consequences of traumatic brain injury in rats. J Cereb Blood Flow Metab 21(7):847-56.
Bramlett HM, Green EJ, Dietrich WD (1999) Exacerbation of cortical and hippocampal CA1 damage due to posttraumatic hypoxia following moderate fluid-percussion brain injury in rats. J Neurosurg 91:653-659.
Bramlett HM, Dietrich WD, Green EJ (1999) Secondary hypoxia following moderate fluid percussion brain injury in rats exacerbates sensorimotor and cognitive deficits. J Neurotrauma 16:1035-1047.
Last updated: November 19, 2007
Back to the Faculty Page
