Expertise
Pathophysiology of CNS injury and repair
Testing novel therapeutic strategies targeting specific mechanisms of damage.
Investigating the importance of targeted temperature management in brain injury
Evaluating cell therapies and proneurogenic compounds to promote reparative processes.
Functional recovery after CNS injury.
Dr. Bramlett is an internationally recognized with over 20 years’ experience in the field of CNS injury including the pathophysiology and treatment of traumatic brain and spinal cord injury.
The main focus of my laboratory is investigating 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: 1) neuroprotective strategies for traumatic injury, 2) progressive damage after trauma and 3) secondary injury mechanisms of traumatic brain injury (TBI).
Our laboratory has been investigating the therapeutic potential of hypothermia for many years. Current studies are involved in clarifying the importance of targeted temperature management and inflammatory markers of secondary brain injury.
We have previously shown that therapeutic hypothermia reduces blood brain barrier breakdown as well as diffuse axonal injury. Most recently, we have determined that hypothermia also modulates the innate immune response through reducing inflammasome activation and subsequent caspase-1 production.
Our laboratory and others have documented in a clinically relevant model of TBI that there is progressive atrophy of brain structures following injury. 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.
Another area of active investigation includes the study of posttraumatic seizure activity as a clinically relevant secondary injury mechanisms. Our laboratory has developed strategies for acute and chronic EEG monitoring to assess both convulsive and nonconvulsive seizure patterns after TBI.