Affiliations: [a]
Barrow Neurological Institute at Phoenix Children’s Hospital – Phoenix, AZ, USA
| [b] Department of Child Health, University of Arizona College of Medicine – Phoenix, AZ, USA
| [c] Phoenix VA Healthcare System – Phoenix, AZ, USA
| [d] Neuroscience Program, Arizona State University – Tempe, AZ, USA
| [e] Core Medical Group, Manchester, NH, USA
| [f] Spinal Cord and Brain Injury Research Center, University of Kentucky Chandler Medical Center – Lexington, KY, USA
Correspondence:
[*]
Corresponding author: Theresa Currier Thomas, PhD, Assistant Professor, Translational Neurotrauma Research Program Department of Child Health, University of Arizona, College of Medicine – Phoenix, Barrow Neurological Institute at Phoenix Children’s Hospital, 425N. 5th St., 3rd floor ABC-1 Building, Phoenix, AZ 85004, USA. Tel.: +1 602 827 2505; Fax: +1 602 827 2257; E-mails: theresathomas@email.arizona.edu; tdcurr00@gmail.com.
Note: [1] denotes that authors contributed equally to data collection, data interpretation, and manuscript preparation.
Abstract: Background:As rehabilitation strategies advance as therapeutic interventions, the modality and onset of rehabilitation after traumatic brain injury (TBI) are critical to optimize treatment. Our laboratory has detected and characterized a late-onset, long-lasting sensory hypersensitivity to whisker stimulation in diffuse brain-injured rats; a deficit that is comparable to visual or auditory sensory hypersensitivity in humans with an acquired brain injury. Objective:We hypothesize that the modality and onset of rehabilitation therapies will differentially influence sensory hypersensitivity in response to the Whisker Nuisance Task (WNT) as well as WNT-induced corticosterone (CORT) stress response in diffuse brain-injured rats and shams. Methods:After midline fluid percussion brain injury (FPI) or sham surgery, rats were assigned to one of four rehabilitative interventions: (1) whisker sensory deprivation during week one or (2) week two or (3) whisker stimulation during week one or (4) week two. At 28 days following FPI and sham procedures, sensory hypersensitivity was assessed using the WNT. Plasma CORT was evaluated immediately following the WNT (aggravated levels) and prior to the pre-determined endpoint 24 hours later (non-aggravated levels). Results:Deprivation therapy during week two elicited significantly greater sensory hypersensitivity to the WNT compared to week one (p < 0.05), and aggravated CORT levels in FPI rats were significantly lower than sham levels. Stimulation therapy during week one resulted in low levels of sensory hypersensitivity to the WNT, similar to deprivation therapy and naïve controls, however, non-aggravated CORT levels in FPI rats were significantly higher than sham. Conclusion:These data indicate that modality and onset of sensory rehabilitation can differentially influence FPI and sham rats, having a lasting impact on behavioral and stress responses to the WNT, emphasizing the necessity for continued evaluation of modality and onset of rehabilitation after TBI.
