Hypothesis
- HRV will be lower (suggesting lower parasympathetic contribution) in TBI-exposed, compared to non-TBI-exposed and unexposed.
- In the TBI-exposed group, HRV will negatively correlate with markers of systemic inflammation and neurodegeneration.
- In the TBI-exposed group, the link between HRV and neurodegeneration will be mediated by levels of systemic inflammation markers.
- In the TBI-exposed group, HRV will be correlated to emotional outcomes and overall functional outcomes.
Summary
To investigate autonomic function after TBI, and its relationship to systemic inflammation and brain outcomes.
Aims:
- To investigate if the autonomic function is different after TBI.
- To investigate whether autonomic function in a TBI group is related to systemic inflammation.
- To investigate whether autonomic function in a TBI group is related to neurodegeneration.
- To investigate whether any link between autonomic function and neurodegeneration is mediated by systemic inflammatory markers.
- To investigate whether autonomic function in a TBI group is related to functional outcomes.
Hypotheses:
- HRV will be lower (suggesting lower parasympathetic contribution) in TBI-exposed, compared to non-TBI-exposed and unexposed.
- In the TBI-exposed group, HRV will negatively correlate with markers of systemic inflammation and neurodegeneration.
- In the TBI-exposed group, the link between HRV and neurodegeneration will be mediated by levels of systemic inflammation markers.
- In the TBI-exposed group, HRV will be correlated to emotional outcomes and overall functional outcomes.
Keywords
Traumatic Brain Injury, TBI, Heart Rate Variability, Inflammation, Autonomic