Abstract
INTRODUCTION: Leukoaraiosis (LA) or white matter disease is a significant component of vascular dementia. There is a large overlap noted between normal-pressure hydrocephalus (NPH) and LA. A previously reported lumped parameter modelling study of NPH led to novel findings in this disease. Given the overlap between LA and NPH, the purpose of the current study is to perform a lumped parameter study into LA to see if the vascular pathophysiology is similar to NPH. METHODS: A lumped parameter model originally developed to study normal-pressure hydrocephalus was extended to investigate LA. The model was constrained by the known cerebral blood flow and cerebral blood volumes found in LA, as derived from the literature. RESULTS: Similar to NPH, in LA, the model predicted a balanced increase in arterial and venous outflow resistance, with the resulting ischemia affecting the white matter rather than the grey matter. However, unlike NPH, in LA, the findings are irreversible, most likely due to structural venous wall changes. CONCLUSIONS: The model suggests that the vascular physiology of LA maybe similar to NPH. A common pathophysiology is discussed based on a pulsation-induced increase in the venous outflow resistance.