Abstract
During each heart beat, the cerebrospinal fluid (CSF) flows back and forth between the cranium and spinal canal. This pulsatile flow is driven by the pulsatile blood flow to the cranial vault and is modulated by the biomechanical properties of the craniospinal system (e.g., intracranial and spinal canal compliances). Considerable effort has been made over the last eight decades, primarily using invasive techniques, to understand the dynamics of the CSF pulsation and the role of each of the system’s sub-compartments in modulation of the CSF pulsation. Even with the significant technical advances in both invasive and non-invasive modalities over the recent years, there are still conflicting observations and interpretations regarding the role of the spinal canal compartment in regulating CSF volumes and pressures in the healthy and in several related neurological disorders such as idiopathic intracranial hypertension (IIH) and Chiari-malformations Type I. Anatomically, it is expected that the mechanical compliance (the ability to accommodate additional volume without a large increase in pressure) of spinal canal compartment is larger than that of cranial compartment since the spinal canal is less confined by the spinal column bony structures compared to the cranial vault. Yet, reports by other groups suggest reversed cranio-spinal compliance distribution. This project employs novel noninvasive tools to quantify the craniospinal compliance distribution to investigate the influence of spinal canal compliance on the CSF dynamics in healthy and in impaired CSF dynamics related pathologies. In vivo quantitative characterization of the subject-specific biomechanics is achieved by ombining an MR imaging and a lumped parameter modeling. The model applied in this work is different from other modeling studies of craniospinal system in the manner it considers the influence of spinal canal compliance on the CSF flow dynamics. The model was validated by comparing the model derived results with invasive measurements based on CSF infusion. In addition, the reproducibility of estimated parameters was tested using repeated MR scans from a craniospinal flow phantom and from healthy subjects. Application of this methodology to MRI data from healthy subjects and from patients with obesity-related idiopathic intracranial hypertension suggests, for the first time, a spinal canal involvement in the pathophysiology of IIH. The spinal canal compliance contribution to the overall craniospinal compliance is reduced in IIH compared to the healthy obese female subjects. In addition, modeling of the dynamic interplay between the cranial and spinal compliances explains the reason for the large pressure fluctuations documented in IIH. Furthermore, the modeling results even explain why obesity-related IIH and Chiari malformations occur at higher frequencies in females than in males.