Acute Injury Markers in mTBI

Mild traumatic brain injury (mTBI) is the most common neurologic disorder. One out of 4 patients develops long-lasting cognitive and emotional complaints that interfere with daily functioning. Therefore, mTBI poses a significant public health burden. Over the years multifactorial models have been developed, which aid in the prediction of outcome after mTBI. It has been shown that in addition to acute injury related factors, such as loss of consciousness and amnesia, outcome is strongly influenced by pre-existent psychological factors, for instance coping style and emotion regulation. Despite these scientific efforts, persistent complaints are still rather unpredictable in individual patients, for whom injury mechanisms are often comparable. So far, little is known about the influence of physiological effects of the injury, such as cellular injury, neuroinflammation, and acute stress, on outcome after mTBI. Previous functional MRI (fMRI) research has demonstrated that persistent complaints after mTBI are related to alterations in neural networks. Therefore, a pivotal question is whether acute physiological effects lead to disturbances in neural networks that are important for emotion regulation, and if there is an interaction with pre-existent personality, coping style, and stress levels, This topic has never been touched upon, and therefore forms a gap in mTBI research. With the current study, we aim to conduct biochemical, psychometric and MRI-experiments in order to disentangle the interaction(s) between (acute) physiological and (long-term) psychological consequences of TBI. Hopefully, this will lead to a better understanding of the etiology of persistent complaints and poor outcome, and to starting points for the development of tailored pharmacological and/or psychological treatments for patients with mTBI.

Primary Objective: • To investigate whether or not persistent complaints and poor outcome after mTBI be explained by an interaction between physiological and psychological factors. In other words, the aim is to investigate whether a more optimal model based on a combination of abovementioned factors can be developed, in comparison to models based on either physiological or psychological factors. Secondary Objective(s): • To identify specific patterns of brain specific protein, cortisol and cytokine release and HRV, as markers of acute brain damage or alteration of physiological processes in patients with mTBI. • To determine if patients with mTBI differ in cortisol and cytokine release from patients with another stressful condition (i.e. orthopedic injury), and healthy controls. • To find possible relationships between acute physiological disturbances (inflammation, stress) and altered activity/connectivity of neural networks in mTBI, and to determine whether or not this is related to psychological factors.

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