Traumatic Brain Injury: A Case Study

Introduction

The influence of exercise and its beneficial impact on cardiovascular health has been observed in multiple epidemiological and mechanistic studies (1). In addition to the cardiovascular health benefits of exercise, there has been a positive correlation with exercise and improvements in glucose regulation, weight control, and even clinical depression (1). The impact of exercise has helped promote the positive prognoses of several pathologies; more recently, exercise has even demonstrated beneficial influences associated with an increase in cognition and memory (1). Studies have been conducted to ascertain correlations between exercise and improvements in cognition. One such study compared the levels of physical activity and cognitive

The purpose of FPI administration was specifically to study the changes in BDNF and CREB levels on the hippocampus, with cognitive performance improvements being observed via the Morris water maze (2). The cognition of the rodent models with FPI improved as the study progressed and the levels of BDNF and CREB also subsequently increased in rats that had a delay in exercise after the initial injury administered (2). The increase in both CREB and BDNF with improved cognitive performance shows the potential impact of BDNF on injured hippocampi after the administration of exercise

The patients with Parkinson’s were given a high intensity exercise to measure the binding potential of 18F-fallypride, a measure of the amount of D2 receptors available (11). In addition, the turning performance of the patients was observed to measure changes in coordination. The induction of exercise with individuals with Parkinson’s showed enhanced performance in the turning task administered. Through examination of this task, the postural control of the exercise patient was seen to improve. Subsequently, there was also an increase the 18F-fallypride binding potential, hence, an increase expression of D2 dopamine receptors. A major characteristic of Parkinson’s disease is the loss of dopamine, causing an over activation of the indirect striatopallidal pathway via D2 (11). The over activation of this pathway results in the disproportionate activation of the direct striatopallidal pathway which results in hypokinesia (10). Exercise may induce more efficient dopamine signaling and, therefore, reduce the inappropriate activation of the indirect striatopallidal pathway, thereby ameliorating the effects of the imbalance (11). These studies show an improvement in motor control and behavior as well as physiological change associated with the increase in