Temporal evolution of neuronal necrosis following ischemic injury in the middle cerebral artery territory:deep watershed versus territorial infarct subtypes on MR perfusion and spectroscopic imagings

博士 === 國立臺灣大學 === 電機工程學研究所 === 90 === The subtypes of cerebral infarction, the cerebral watershed infarction (WI) and the territorial thromboembolic infarction (TI), present different apparent diffusion coefficient (ADC) evolution. The difference may originate from the different hemodyna...

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Bibliographic Details
Main Authors: Yi-Jui Liu, 劉益瑞
Other Authors: Hsiao-Wen Chung
Format: Others
Language:en_US
Published: 2002
Online Access:http://ndltd.ncl.edu.tw/handle/81855980032981065342
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Summary:博士 === 國立臺灣大學 === 電機工程學研究所 === 90 === The subtypes of cerebral infarction, the cerebral watershed infarction (WI) and the territorial thromboembolic infarction (TI), present different apparent diffusion coefficient (ADC) evolution. The difference may originate from the different hemodynamic condition involved. Therefore, it should help us to understand the mechanism in ischemic infarction by investigating the hemodynamic evolution of different infarction types. In this study, we attempt to prove the hypothesis that : 1. The differences between the evolution of deep watershed infarct and territorial thromboembolic infarct are associated with different time course of hemodynamic changes; 2. The difference of pathophysiology may result in various evolution of neuronal necrosis. We prospectively enrolled 25 patients, who had ischemic injuries of middle cerebral arterial territories and received only conservative treatments, in longitudinal MR study. They were divided into TI (n=16) and WI (n=9) groups. Each patient underwent up to five MR studies from hyperacute to late chronic stages of cerebral infarcts following stroke ictus. Dynamic susceptibility-contrast MR imaging was performed to yield the relative cerebral blood volume (rCBV). Chemical shift imaging was utilized to evaluate neuronal necrosis by measuring the relative levels of N-acetylaspartate (rNAA) and lactate (rLac) of the ischemic brain tissues. For TI patients, rCBV followed a progressively increasing pattern from initial hypo-perfusion (0.46±0.28) to peak hyper-perfusion at early chronic stage (1.23±0.34). rNAA dropped to 0.40±0.24 during acute stroke and lost completely in 4 days post ictus. WI patients showed consistent hyper-perfusion throughout all stages, with residual rNAA (0.53±0.25) present even at one month after symptom onset. For TI patients, rLac was significantly higher than WI at acute stage of stroke (P < 0.01). Repeated-measure analysis of variance indicated that differences in the temporal changes of both cerebral perfusion and brain metabolites between TI and WI were statistically significant (P < 0.001). It is concluded that different types of cerebral infarcts ( TI and WI ) are associated with different patterns of evolutions in hemodynamics and neuronal necrosis.