Bayesian Estimation of CBF Measured by DSC-MRI in Patients with Moyamoya Disease: Comparison with 15O-Gas PET and Singular Value Decomposition.

BACKGROUND AND PURPOSE: CBF analysis of DSC perfusion using the singular value decomposition algorithm is not accurate in patients with Moyamoya disease. This study compared the Bayesian estimation of CBF against the criterion standard PET and singular value decomposition methods in patients with Moyamoya disease. MATERIALS AND METHODS: Nineteen patients with Moyamoya disease (10 women; 22-52 years of age) were evaluated with both DSC and 15O-gas PET within 60 days. DSC-CBF maps were created using Bayesian analysis and 3 singular value decomposition analyses (standard singular value decomposition, a block-circulant deconvolution method with a fixed noise cutoff, and a block-circulant deconvolution method that adopts an occillating noise cutoff for each voxel according to the strength of noise). Qualitative and quantitative analyses of the Bayesian-CBF and singular value decomposition-CBF methods were performed against 15O-gas PET and compared with each other. RESULTS: In qualitative assessments of DSC-CBF maps, Bayesian-CBF maps showed better visualization of decreased CBF on PET (sensitivity = 62.5%, specificity = 100%, positive predictive value = 100%, negative predictive value = 78.6%) than a block-circulant deconvolution method with a fixed noise cutoff and a block-circulant deconvolution method that adopts an oscillating noise cutoff for each voxel according to the strength of noise (P < .03 for all except for specificity). Quantitative analysis of CBF showed that the correlation between Bayesian-CBF and PET-CBF values (ρ = 0.46, P < .001) was similar among the 3 singular value decomposition methods, and Bayesian analysis overestimated true CBF (mean difference, 47.28 mL/min/100 g). However, the correlation between CBF values normalized to the cerebellum was better in Bayesian analysis (ρ = 0.56, P < .001) than in the 3 singular value decomposition methods (P < .02). CONCLUSIONS: Compared with previously reported singular value decomposition algorithms, Bayesian analysis of DSC perfusion enabled better qualitative and quantitative assessments of CBF in patients with Moyamoya disease.

Noninvasive Evaluation of CBF and Perfusion Delay of Moyamoya Disease Using Arterial Spin-Labeling MRI with Multiple Postlabeling Delays: Comparison with 15O-Gas PET and DSC-MRI.

BACKGROUND AND PURPOSE: Arterial spin-labeling MR imaging with multiple postlabeling delays has a potential to evaluate various hemodynamic parameters. To clarify whether arterial spin-labeling MR imaging can identify CBF and perfusion delay in patients with Moyamoya disease, we compared arterial spin-labeling, DSC, and 15O-gas PET in terms of their ability to identify these parameters. MATERIALS AND METHODS: Eighteen patients with Moyamoya disease (5 men, 13 women; ages, 21-55 years) were retrospectively analyzed. CBF values of pulsed continuous arterial spin-labeling using 2 postlabeling delays (short arterial spin-labeling, 1525 ms; delayed arterial spin-labeling, 2525 ms) were compared with CBF values measured by 15O-gas PET. All plots were divided into 2 groups by the cutoff of time-based parameters (the time of the maximum observed concentration, TTP, MTT, delay of MTT to cerebellum, and disease severity [symptomatic or not]). The ratio of 2 arterial spin-labeling CBFs (delayed arterial spin-labeling CBF to short arterial spin-labeling CBF) was compared with time-based parameters: time of the maximum observed concentration, TTP, and MTT. RESULTS: The short arterial spin-labeling-CBF values were significantly correlated with the PET-CBF values (r = 0.63; P = .01). However, the short arterial spin-labeling-CBF value dropped in the regions with severe perfusion delay. The delayed arterial spin-labeling CBF overestimated PET-CBF regardless of the degree of perfusion delay. Delayed arterial spin-labeling CBF/short arterial spin-labeling CBF was well correlated with the time of the maximum observed concentration, TTP, and MTT (ρ = 0.71, 0.64, and 0.47, respectively). CONCLUSIONS: Arterial spin-labeling using 2 postlabeling delays may detect PET-measured true CBF and perfusion delay in patients with Moyamoya disease. Provided its theoretic basis and limitations are considered, noninvasive arterial spin-labeling could be a useful alternative for evaluating the hemodynamics of Moyamoya disease.

Optical analysis of developmental changes in synaptic potentiation in the neonatal rat corticostriatal projection.

We applied voltage-sensitive dye imaging to neonatal rat cortical slice preparations and analyzed developmental changes in synaptic plasticity, long-term potentiation (LTP), in the corticostriatal projection. Coronal slice preparations were dissected from postnatal 1- to 21-day (P1-P21) rats, and the transmembrane voltage-related optical signals evoked by cortical stimulation were recorded using a 464ch optical recording system with the voltage-sensitive absorption dye. In the striatum, the optical signal was composed of a fast spike-like signal followed by a slow signal, which corresponded to an action potential and an excitatory postsynaptic potential (EPSP), respectively. The slow signal could be detected at the P1 stage, suggesting that the EPSP is already expressed in the corticostriatal projection at least at early stages after birth. On the other hand, the slow signal was potentiated with a single shot of tetanic stimulation and the potentiation lasted at least 1 h, which is considered to correspond to long-term potentiation. With ontogenetic examinations, we found that (1) the EPSP could be potentiated with tetanic stimulation from the P9 stage and that (2) after the LTP induction, the potentiation was maintained for a longer time in the postnatal 3W stage than in the 2W stage. These results suggest that characteristics of LTP change dynamically during postnatal development.

Chronological changes of perihematomal edema of human intracerebral hematoma.

Recent investigations have indicated the importance of secondary brain damage in the pathophysiology of intracerebral hemorrhage (ICH), which includes ischemic brain damage and edema formation around a hematoma. The purpose of the current study is to investigate chronological changes of perihematomal edema in patients with human ICH and also the correlation between volume of perihematomal edema and neurological status. Fourteen patients with medium-sized putaminal hemorrhage (29.4 +/- 13.2 ml) without hematoma enlargement were included in this study. To investigate chronological changes of perihematomal edema, we performed CT scans prospectively on the day of hemorrhage and repeated them on days 1, 3, 7, 14, and 28. We evaluated the patients neurologically using the NIH stroke scale on the day a CT scan was performed. The volume of perihematomal edema in human ICH increased rapidly three days after hemorrhage and the score on the NIH stroke scale showed a deterioration. The volume of perihematomal edema then increased slowly until day 14 after hemorrhage, and decreased thereafter. Despite progression of perihematomal edema, the score on the NIH stroke scale improved gradually after day 3.

Correlation between cardiac output and cerebral blood flow following subarachnoid hemorrhage.

The authors examined the correlations between cerebral blood flow (CBF) during the stage of vasospasm following subarachnoid hemorrhage and four parameters, namely, cardiac output (cardiac index), mean arterial blood pressure, age, and the Glasgow coma scale score. Forty-two patients who were diagnosed to have subarachnoid hemorrhage were included in this study, and 50 measurements were performed between day 5 and 12 following the subarachnoid hemorrhage. The CBF was measured by stable xenon-enhanced CT and the mean values of four CBF maps were corrected for a PaCO2 of 34 mm Hg (CBF34). The cardiac output and cardiac index were continuously monitored during the CBF measurement. The correlation coefficients of cardiac index, mean arterial blood pressure, age, and GCS against CBF34 were, respectively, 0.436, 0.227, 0.037, and 0.225, and the p values were, respectively, 0.002, 0.074, 0.789, and 0.087. The CBF34 was positively correlated with only the cardiac index and not with any of the other three parameters. Therefore, an increase in the cardiac output is apparently associated with an increase in the CBF during the stage of vasospasm following subarachnoid hemorrhage. Furthermore, we measured the CBF and cerebral perfusion pressure before and after increasing cardiac output in three patients during the stage of vasospasm. The CBF increased by 22.5% +/- 2.9 (SD), with a 42.0% +/- 16.4 increase in the cardiac index, however, no significant change in cerebral perfusion pressure was observed. Therefore, the increase in CBF associated with the increase in cardiac output seems to be attributable to a reduction in the cerebrovascular resistance.