Longitudinal MRI studies in the isoflurane-anesthetized rat: long-term effects of a short hypoxic episode on regulation of cerebral blood flow as assessed by pulsed arterial spin labelling

2008 ◽  
Vol 21 (7) ◽  
pp. 696-703 ◽  
Author(s):  
Susanne Wegener ◽  
Eric C. Wong
Neuroscience ◽  
2020 ◽  
Vol 436 ◽  
pp. 27-33
Author(s):  
Fangshi Zhao ◽  
Weitao Zhang ◽  
Dan Zhu ◽  
Xiaoyi Wang ◽  
Wen Qin ◽  
...  

Brain ◽  
2019 ◽  
Vol 142 (4) ◽  
pp. 1108-1120 ◽  
Author(s):  
Henri J M M Mutsaerts ◽  
Saira S Mirza ◽  
Jan Petr ◽  
David L Thomas ◽  
David M Cash ◽  
...  

Abstract Genetic forms of frontotemporal dementia are most commonly due to mutations in three genes, C9orf72, GRN or MAPT, with presymptomatic carriers from families representing those at risk. While cerebral blood flow shows differences between frontotemporal dementia and other forms of dementia, there is limited evidence of its utility in presymptomatic stages of frontotemporal dementia. This study aimed to delineate the cerebral blood flow signature of presymptomatic, genetic frontotemporal dementia using a voxel-based approach. In the multicentre GENetic Frontotemporal dementia Initiative (GENFI) study, we investigated cross-sectional differences in arterial spin labelling MRI-based cerebral blood flow between presymptomatic C9orf72, GRN or MAPT mutation carriers (n = 107) and non-carriers (n = 113), using general linear mixed-effects models and voxel-based analyses. Cerebral blood flow within regions of interest derived from this model was then explored to identify differences between individual gene carrier groups and to estimate a timeframe for the expression of these differences. The voxel-based analysis revealed a significant inverse association between cerebral blood flow and the expected age of symptom onset in carriers, but not non-carriers. Regions included the bilateral insulae/orbitofrontal cortices, anterior cingulate/paracingulate gyri, and inferior parietal cortices, as well as the left middle temporal gyrus. For all bilateral regions, associations were greater on the right side. After correction for partial volume effects in a region of interest analysis, the results were found to be largely driven by the C9orf72 genetic subgroup. These cerebral blood flow differences first appeared approximately 12.5 years before the expected symptom onset determined on an individual basis. Cerebral blood flow was lower in presymptomatic mutation carriers closer to and beyond their expected age of symptom onset in key frontotemporal dementia signature regions. These results suggest that arterial spin labelling MRI may be a promising non-invasive imaging biomarker for the presymptomatic stages of genetic frontotemporal dementia.


2021 ◽  
Vol 5 (1) ◽  
Author(s):  
Adnan Bibic ◽  
Tea Sordia ◽  
Erik Henningsson ◽  
Linda Knutsson ◽  
Freddy Ståhlberg ◽  
...  

Abstract Background Our aim was to introduce damaged red blood cells (RBCs) as a tool for haemodynamic provocation in rats, hypothesised to cause decreased cerebral blood flow (CBF) and prolonged water capillary transfer time (CTT), and to investigate whether expected changes in CBF could be observed and if haemodynamic alterations were reflected by the CTT metric. Methods Damaged RBCs exhibiting a mildly reduced deformability were injected to cause aggregation of RBCs. Arterial spin labelling (ASL) magnetic resonance imaging experiments were performed at 9.4 T. Six datasets (baseline plus five datasets after injection) were acquired for each animal in a study group and a control group (13 and 10 female adult Wistar rats, respectively). For each dataset, ASL images at ten different inversion times were acquired. The CTT model was adapted to the use of a measured arterial input function, implying the use of a realistic labelling profile. Repeated measures ANOVA was used (alpha error = 0.05). Results After injection, significant differences between the study group and control group were observed for relative CBF in white matter (up to 20 percentage points) and putamen (up to 18–20 percentage points) and for relative CTT in putamen (up to 35–40 percentage points). Conclusions Haemodynamic changes caused by injection of damaged RBCs were observed by ASL-based CBF and CTT measurements. Damaged RBCs can be used as a tool for test and validation of perfusion imaging modalities. CTT model fitting was challenging to stabilise at experimental signal-to-noise ratio levels, and the number of free parameters was minimised.


Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Alexander Razumovsky ◽  
Melissa Rampino ◽  
Efim Kouperberg ◽  
Donna M Neuges ◽  
Thomas J DeGraba ◽  
...  

Service members (SMs) suffer from repeated exposure to concussions or mild TBI, which can disrupt cerebral blood flow. This effect is seen in the acute phase of TBI, but the development of vascular wall abnormalities, which can lead to luminal narrowing and abnormally elevated cerebral blood flow velocities (CBFV), has not been studied in the post concussive phase. The purpose of this study was to evaluate the transcranial Doppler (TCD) determined incidence of abnormal cerebral hemodynamics in patients with long-term effects of mTBI. Material and Methods: TCD recordings of mean CBFV in cm/sec and Pulsatility Indices (PI) were recorded from 431 SMs (9 females; ages 24-54, mean age 39.2 ± 6.4 years) who were admitted to the National Intrepid Center of Excellence 4-week Interdisciplinary Outpatient Program. TCD data were analyzed to determine whether SMs exhibited abnormal CBFV s in the middle cerebral artery, internal carotid artery (ICA), and basilar artery. All subjects consented to protocol #362504 prior to any data collection or analysis. Two standard deviation from the mean CBFV in any direction labeled as an abnormal and PI was assumed normal with values between 0.7 and 0.9 Patients with one or more vessels with abnormal CBFV’s and PI’s were labeled as abnormal. Results: Average time since last TBI was 5.1 ± 3.4 years. We observed abnormal CBFV values in 33% of SMs. 149 (35%) and 48 (11%) demonstrated abnormally high CBFV and PIs in one or more vessels, respectively. Abnormal CBFV was observed most frequently in the ICA (48%). Majority of studied patients had patchy pattern of abnormal data presented in one or few vessels. The presence of abnormal cerebral hemodynamics was inversely related to the time since the last mTBI exposure: the likelihood of abnormal CBFV values deceased with increasing time since last head injury was sustained but was still present. Conclusions: Our data reveal that a large proportion of SMs have elevated CBFVs following mTBI exposure in many years after last mTBI. We believe that head injuries due to combat and training blast and blunt force trauma exposure cause early atherosclerotic or fibrotic changes in the large vessel walls of the Circle of Willis, which results in vascular lumen narrowing and increased CBFV’s.


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