The brain consists of only two percent of the entire body weight but due to its high metabolic rate, it requires a fifth of the total cardiac output. The cerebral vasculature has a number of mechanisms that allow for a constant supply of blood with nutrients and oxygen to the cerebral tissue under varying conditions. These are mainly divided into two groups. In the first group is the myogenic mechanism whereby the larger arterioles contract under increasing systemic pressure and the second mechanism is termed functional hyperemia, which describes the local vessel dilation and constriction due to neuronal activity. This latter mechanism, also known as neurovascular coupling, has shown to be increasingly important in the investigation of reduced perfusion. There is now growing evidence for the relationship between how the brain regulates its blood supply locally and neurological disorders such as dementia in older brains and cerebral palsy in younger brains.

A disordered functional hyperemia is associated with several pathologies such as hyper- tension, Alzheimers disease, cortical spreading depression, and ischemic stroke. All of these pathologies start with an altered relationship between neural activity and the cerebral blood flow (CBF). These alterations perturb the delivery of substrates to active brain cells and impair the removal of waste products from cerebral metabolism. It is likely that this disruption contributes to brain dysfunction. Increasing understanding of neural interactions highlights the importance of vascular pathology in cerebral diseases.

Significant progress has been made in both experimental and modeling fronts. As with all models, there must be a substantial data set with which validation studies can be implemented. A substantial amount of experiment has been done on animal models, notably mice and rat. However there are clear differences in the makeup of a number of important parameters between rodent and human populations. In the end, human validation is necessary. For this to be accomplished appropriately, the complex cellular model must be scaled up to allow comparisons.

The focused program shall consist of four related workshops in Neurovascular Coupling and Related Phenomena. The topic of the first workshop is cortical spreading depression (CSD), a pathological condition in the cortex. Most of the experimental and theoretical studies to-date have focused on the two major components of brain tissue itself (neurons and glial cells) without taking the effect of cerebral blood flow (CBF) into account. Recent work has suggested that CBF and neurovascular coupling, or more specifically the failure of neurovascular coupling, play essential roles in the instigation and propagation of CSD, which will be the subject of the second workshop. The third workshop is on perinatal brain development and specifically the modeling and detection of inflammation and acidemia in fetal brain, a condition related to hypoxia and the reduction of oxygen supply. It is believed that a more accurate detection algorithm will depend on the mechanisms of fetal neurovascular coupling. Finally, at a more fundamental level, to understand and model brain homeostasis, one needs to have a deep understanding on the mechanisms of ion transport and the functions of ion channels and pumps. The fourth and final workshop of the program is on the mathematical and computational models for transport of ionic particles in a biological environment.