An integrated perspective linking physiological and psychological consequences of mild traumatic brain injury

Abstract

Despite the often seemingly innocuous nature of a mild traumatic brain injury (mTBI), its consequences can be devastating, comprising debilitating symptoms that interfere with daily functioning. Currently, it is still difficult to pinpoint the exact cause of adverse outcome after mTBI. In fact, extensive research suggests that the underlying etiology is multifactorial. In the acute and early sub-acute stages, the pathophysiology of mTBI is likely to be dominated by complex physiological alterations including cellular injury, inflammation, and the acute stress response, which could lead to neural network dysfunction. In this stage, patients often report symptoms such as fatigue, headache, unstable mood and poor concentration. When time passes, psychological processes, such as coping styles, personality and emotion regulation, become increasingly influential. Disadvantageous, maladaptive, psychological mechanisms likely result in chronic stress which facilitates the development of long-lasting symptoms, possibly via persistent neural network dysfunction. So far, a systemic understanding of the coupling between these physiological and psychological factors that in concert define outcome after mTBI is lacking. The purpose of this narrative review article is to address how psychophysiological interactions may lead to poor outcome after mTBI. In addition, a framework is presented that may serve as a template for future studies on this subject.

White matter microstructure of the neural emotion regulation circuitry in mild traumatic brain injury

“…Remarkably, in the group without symptoms, the microstructure of the right UF was changed as compared to the group with symptoms, and to a lesser extent also compared to HC, although these effects were not as extensive as for the group with frontal CT lesions. These findings provide further support for the hypothesis that the presence of symptoms is not related to micro-structural injury in emotion regulation tracts, but to preexistent psychological characteristics instead, as was suggested by our previous research (van der Horn, Out, et al, 2019). Although highly speculative, it is tantalizing to elaborate on a possible protective effect of compromised UF microstructure regarding the development of persistent symptoms via the presence of less emotional awareness.…”

“…The frontal lobe is vulnerable to TBI (Bigler, 2007). Since the frontal lobe contains areas that are important for regulating negative emotions, it is plausible that injury to the connecting white matter tracts might cause problems with psychological adaptation to symptoms and changes in daily functioning after mTBI (van der Horn, Out, et al, 2019). To investigate microstructural connectivity within the frontal emotion regulation circuitry across the entire spectrum of mTBI, we carefully selected patients with uncomplicated mTBI who did and did not report symptoms, as well as a group of patients with macroscopic lesions in the frontal areas, as measured with CT.…”

“…Many patients with mild traumatic brain injury (mTBI) develop persistent symptoms, however, it is still difficult to explain these symptoms for the individual patient (Mayer et al, 2017;van der Horn, Out, et al, 2019;van der Naalt et al, 2017). Computed tomography (CT) and conventional MRI-scans provide insufficient explanations in this respect (Jacobs et al, 2010;Karr et al, 2020;van der Horn et al, 2018;van der Naalt et al, 2017).…”

Mental Fatigue after Mild Traumatic Brain Injury in Relation to Cognitive Tests and Brain Imaging Methods

“…The assessment and definition of symptoms after an mTBI varies between studies, and symptoms are also common in the population irrespective of whether it is a case of an mTBI. The interaction between pre-and post-biological and psychological factors results in a complex model [13,14], and there is limited evidence for variables as predictors of fatigue [14]. However, in many studies, mental fatigue is not recognized as a separate factor, despite being one of the most distressing and long-lasting symptoms following mTBI [15,16], having an impact on well-being and quality of life [2].…”

Sex-Dependent Pathology in the HPA Axis at a Sub-acute Period After Experimental Traumatic Brain Injury

“…HPA axis dysregulation and affective symptoms following acquired brain injury, including TBI and stroke, have become increasingly acknowledged in clinical studies (14,32,37,(76)(77)(78)(79)(80). Despite the prevalence and late-onset nature of affective symptoms after TBI (and stroke), few studies have evaluated the longitudinal pathology and HPA axis regulation for underlying pathology (42, [81][82][83][84][85][86].…”