Within the Translational Neurotrauma Research Program, research efforts focus on restorative and regenerative treatments for acquired neurological conditions, such as traumatic brain injury. In particular, scientific aims target circuit disruption that contributes to lasting neurological symptoms. In response to neurotrauma, brain circuits dismantle over a short period of time, due to mechanical forces and ensuing enzymatic activity. Thereafter, the brain repairs, rebuilds and reorganizes itself, but not necessarily reconstituting the original template. Instead, circuits can become rewired, thereby processing information differently. In this way, new neurological symptoms and morbidities emerge after acute neurological insults. Pharmacological and rehabilitative therapies can mitigate circuit dismantling and promote adaptive circuit reorganization, thereby preserving function and quality of life.
With a focus on Neurotrauma, particularly traumatic brain injury, we often hear that after a diffuse brain injury (e.g. concussion) that one should not be allowed to sleep OR be awoken every two hours OR let the person sleep. Previously, none of these approaches had been tested by primary evidence. This past year, we completed a series of studies to investigate whether brain injury induces sleep, whether chronic sleep issues may emerge, the consequences of disrupting sleep and the impact of over-the-counter anti-inflammatory treatment.
Diffuse Brain Injury
Sensory sensitivity leads to agitation and irritation to light and sound in those living with brain injury. Our diffuse brain injury model shows rodents develop sensory sensitivity to somatic whisker stimulation over 1 month post-injury. This morbidity correlates with plastic changes in the whisker circuit associated with synaptogenesis and inflammation. Our research investigates interventions to mitigate these processes in rodents, while imaging brain-injured patients with light sensitivity.