Cerebral Hemodynamics through Intracrnial Pressure

Abstract: Traumatic Brain Injury (TBI) continues to be a major problem worldwide. Today, intensive care of patients with TBI is mainly focused on preventing and treating secondary brain injuries. High pressure inside the intracranial cavity has been found to be an important feature of disturbed cerebral dynamics and secondary injuries. Thus, invasive measurement of intracranial pressure (ICP) is today a well established routine in modern neuro-intensive care. Variations in ICP can be regarded as a response of the cerebrospinal system to different stimuli, including homeostatic mechanisms which attempt to maintain the cerebral equilibrium. Nevertheless, the autoregulatory processes and their functionality may also be affected by ICP. This study is an attempt to investigate the cerebral hemodynamics through analysis of ICP and other biomedical measurements available, such as arterial blood pressure and electrocardiography. The study is mainly conducted by analysing biomedical data through mathematical modelling, model-based frameworks, and simulations. This thesis focuses on the dynamics of intracranial pressure in either presence or absence of cerebral autoregulation. A model-based framework which describes the relationship between arterial distensibility and compliance was developed to study variations in the mechanical properties of distant cerebral artries/arteriols. The measurements of pulse wave propagation velocity as well as transfer function between arterial blood pressure and intracranial pressure were utilized as the key elements of the study. Using the aforementioned model, it was shown that variations in the level of ICP may arise from different states of cerebral autoregulation and the associated regime within the cerebral vasculature. The state of Cerebral Blood Flow (CBF) autoregulation during plateau waves of ICP was taken as a subsequent focus of the study. The investigation was conducted by applying the mathematical models of cerebral hemodynamics to the measurements from a TBI patient. Considering the mechanical properties of the cerebrovascular system, the study examined models of impaired as well as intact CBF autoregulation as the possible options. Although the intact autoregulatory mechanism could simulate elevated ICP waves, a large time constant of regulation far from the reported response times in human was needed. The assumption of an exhausted autoregulatory mechanism, however, led to the results pointing to a partial collapse within the cerebral arterial-arteriolar path. Finally, the origin of plateau waves of ICP was investigated by reviewing the phenomenon from a new perspective. The estimation of the baroreceptor reflex index was utilised to locate the source of bradycardia during ICP plateau waves. The result suggested that an activation of the Cushing reflex when the cerebral arterial-arteriolar segment suffers from a partial collapse may lead to the generation of these waves. Furthermore, a negative correlation between cerebral perfusion pressure (CPP) and CBF was recognised associated to this circumstance. It is concluded that a CPP-oriented treatment of TBI patients who demonstrate ICP plateau waves may not lead to the expected regulation of CBF.