Neurosurgery practice · 2025
Cerebrospinal Fluid Flow and Vorticity in Hydrocephalus on 4-Dimensional Flow MRI.
СтатьяНазвание и аннотация: Перевод в очереди
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Yamada Shigeki, Okada Ko, Ito Hirotaka, Fujinami Ryota, Yamanaka Tomoyasu, Yamada Hiroshi, Tanikawa Motoki, Iseki Chifumi, Watanabe Yoshiyuki, Ii Satoshi, Otani Tomohiro, Wada Shigeo, Oshima Marie, Mase Mitsuhito
Аннотация
BACKGROUND AND OBJECTIVES: The pathophysiology of obstructive hydrocephalus caused by cerebral aqueduct obstruction or stenosis, as well as communicating hydrocephalus with oscillating cerebrospinal fluid (CSF) flow and vortices in the third ventricle (3V), remains unclear. In addition, clear criteria for selecting between ventriculoperitoneal shunting (VPS) and endoscopic third ventriculostomy (ETV) have yet to be established. This study aimed to investigate the utility of 4-dimensional flow MRI for assessing CSF dynamics to enhance our understanding of hydrocephalus pathophysiology and guide treatment selection.
METHODS: Using 4-dimensional flow MRI (velocity encoding = 5 cm/s), we evaluated CSF dynamics before and after VPS and ETV in patients with obstructive and communicating hydrocephalus, focusing on velocity vectors, streamlines, and vorticity.
RESULTS: In obstructive hydrocephalus due to cerebral aqueduct obstruction, we initially expected a complete absence of CSF circulation in the 3V and cerebral aqueduct before ETV. However, slow flow was observed around the foramen of Monro and even within the obstructed aqueduct. After ETV, rapid CSF flow with vortex formation was observed in the 3V. In obstructive hydrocephalus, while VPS reduced ventricular size, it did not enhance CSF movement in the 3V. In communicating hydrocephalus with third ventricular floor ballooning, rapid CSF flow and abnormal vortices in the 3V persisted after ETV; however, these abnormalities were mitigated by VPS.
CONCLUSION: These findings suggest that both CSF stagnation and abnormal vortices in the 3V contribute to the pathophysiology of obstructive and communicating hydrocephalus. Therefore, treatment strategies should prioritize interventions that optimize CSF flow dynamics.
METHODS: Using 4-dimensional flow MRI (velocity encoding = 5 cm/s), we evaluated CSF dynamics before and after VPS and ETV in patients with obstructive and communicating hydrocephalus, focusing on velocity vectors, streamlines, and vorticity.
RESULTS: In obstructive hydrocephalus due to cerebral aqueduct obstruction, we initially expected a complete absence of CSF circulation in the 3V and cerebral aqueduct before ETV. However, slow flow was observed around the foramen of Monro and even within the obstructed aqueduct. After ETV, rapid CSF flow with vortex formation was observed in the 3V. In obstructive hydrocephalus, while VPS reduced ventricular size, it did not enhance CSF movement in the 3V. In communicating hydrocephalus with third ventricular floor ballooning, rapid CSF flow and abnormal vortices in the 3V persisted after ETV; however, these abnormalities were mitigated by VPS.
CONCLUSION: These findings suggest that both CSF stagnation and abnormal vortices in the 3V contribute to the pathophysiology of obstructive and communicating hydrocephalus. Therefore, treatment strategies should prioritize interventions that optimize CSF flow dynamics.