Hypothesis

1. HRV will be lower (suggesting lower parasympathetic contribution) in TBI-exposed, compared to non-TBI-exposed and unexposed.
2. In the TBI-exposed group, HRV will negatively correlate with markers of systemic inflammation and neurodegeneration.
3. In the TBI-exposed group, the link between HRV and neurodegeneration will be mediated by levels of systemic inflammation markers.
4. 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:

1. To investigate if the autonomic function is different after TBI.
2. To investigate whether autonomic function in a TBI group is related to systemic inflammation.
3. To investigate whether autonomic function in a TBI group is related to neurodegeneration.
4. To investigate whether any link between autonomic function and neurodegeneration is mediated by systemic inflammatory markers.
5. To investigate whether autonomic function in a TBI group is related to functional outcomes.

Hypotheses:

1. HRV will be lower (suggesting lower parasympathetic contribution) in TBI-exposed, compared to non-TBI-exposed and unexposed.
2. In the TBI-exposed group, HRV will negatively correlate with markers of systemic inflammation and neurodegeneration.
3. In the TBI-exposed group, the link between HRV and neurodegeneration will be mediated by levels of systemic inflammation markers.
4. 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

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