Stroke and Cerebrovascular Center
Stroke and Cerebrovascular Center Research
Search Stroke and Cerebrovascular Center
MIT Collaborative Research
MOBERG
NICP
MEDIUM: A Model for Cerebral Fluid Dynamics Using Imaging
Supported by: Department
Principal Investigator at BMC: James Holsapple, MD
Primary Research Contact: Brandon Finn, BA (617-638-8650)
The cranium contains three major fluid spaces: the cerebrospinal fluid space, the intravascular fluid space, and the interstitial fluid space of the brain parenchyma. Currently, the functional interaction of these three fluid spaces in health and disease is poorly understood. For example, the cerebral perfusion pressure (CPP) is defined as arterial blood pressure (ABP, upstream pressure) minus intracranial pressure (ICP, external pressure) or the jugular venous pressure (JVP, the downstream pressure) depending on which is higher. From a fluid dynamic perspective, defining the perfusion pressure as the upstream pressure minus the outside pressure (ICP) implies flow limitation through collapsible vessels, where along the anatomy of the cerebral vasculature such flow limitation occurrences have not been identified. This suggests that it might be in some cases more accurate to use the upstream pressure minus the downstream pressure (ABP-JVP) to get a better understanding of how circulating blood is changing pressure.
Our current understanding of the CPP mechanism is that the body can auto-regulate this pressure while in the range of 50-150 mmHg. While in this range, if the CPP begins to decrease, there is vasodilation of cerebral resistance vessels, a decrease in cerebrovascular resistance, and an increase in the cerebral blood volume which then helps to stabilize the CPP. In the setting of acute neurological insult, the body loses the ability to auto-regulate CPP, however, the exact loss of function mechanism is not fully understood. It is clear that injury resulting in blood loss (hypotension) will lower the ABP therefore resulting in a decreased CPP. Injury resulting in intracranial hemorrhage will increase the ICP, therefore, resulting in a decreased CPP. Little research has been done on the role JVP has in this mechanism.
The interactions among the different cerebrospinal fluid spaces can be investigated through realistic biomechanical models that represent the biomechanical properties of each fluid space. Such multiscale models have been built for other organ systems (e.g., the heart, lung, kidney) and have provided significant insights into the normal physiology of these organ systems and aberrations under pathological conditions. Similarly detailed and anatomically correct multiscale models of cerebrovascular and cerebrospinal fluid function currently do not exist. Here, we seek access to a series of de-identified imaging studies of the brain of ischemic stroke patients to develop anatomically realistic renderings of the cerebral arterial system, the cerebral venous system, and the cerebrospinal fluid system. Such renderings will help characterize the normal variations seen in subjects as well as changes seen in disease processes. This analysis will also result in a better understanding of the mechanism that dictates flow dynamics in regard to acute neurological insult.
Enrollment Criteria
In order to be eligible to participate in this study, an individual must meet all of the following criteria:
Age > 18 years
Stroke related to venous thrombosis, vasculitis or stroke of other determined etiology
Completed CTA/V, MRI/MRA and/or MRV
An individual who meets any of the following criteria will be excluded from participation in this study:
Status: Actively enrolling patients