Contribution of cerebral blood flow autoregulation to spontaneous low-frequency oscillations in regional cerebral hemodynamics in the resting state

2010 ◽  
Vol 68 ◽  
pp. e177-e178
Author(s):  
Naoki Tanaka ◽  
Kyoko Yamazaki ◽  
Takusige Katura ◽  
Atsushi Maki
2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Jing Lin ◽  
Dilong Wang ◽  
Linfang Lan ◽  
Yuhua Fan

White matter lesions (WMLs), also known as leukoaraiosis (LA) or white matter hyperintensities (WMHs), are characterized mainly by hyperintensities on T2-weighted or fluid-attenuated inversion recovery (FLAIR) images. With the aging of the population and the development of imaging technology, the morbidity and diagnostic rates of WMLs are increasing annually. WMLs are not a benign process. They clinically manifest as cognitive decline and the subsequent development of dementia. Although WMLs are important, their pathogenesis is still unclear. This review elaborates on the advances in the understanding of the pathogenesis of WMLs, focusing on anatomy, cerebral blood flow autoregulation, venous collagenosis, blood brain barrier disruption, and genetic factors. In particular, the attribution of WMLs to chronic ischemia secondary to venous collagenosis and cerebral blood flow autoregulation disruption seems reasonable. With the development of gene technology, the effect of genetic factors on the pathogenesis of WMLs is gaining gradual attention.


2007 ◽  
Vol 293 (1) ◽  
pp. R243-R250 ◽  
Author(s):  
Caroline A. Rickards ◽  
Kathy L. Ryan ◽  
William H. Cooke ◽  
Keith G. Lurie ◽  
Victor A. Convertino

We tested the hypothesis that breathing through an inspiratory threshold device (ITD) during progressive central hypovolemia would protect cerebral perfusion and attenuate the reporting of presyncopal symptoms. Eight human subjects were exposed to lower-body negative pressure (LBNP) until the presence of symptoms while breathing through either an active ITD (−7 cmH2O impedance) or a sham ITD (0 cmH2O). Cerebral blood flow velocity (CBFV) was measured continuously via transcranial Doppler and analyzed in both time and frequency domains. Subjects were asked to report any subjective presyncopal symptoms (e.g., dizziness, nausea) at the conclusion of each LBNP exposure. Symptoms were coincident with physiological evidence of cardiovascular collapse (e.g., hypotension, bradycardia). Breathing on the active ITD increased LBNP tolerance time (mean ± SE) from 2,014 ± 106 s to 2,259 ± 138 s ( P = 0.006). We compared CBFV responses at the time of symptoms during the sham ITD trial with those at the same absolute time during the active ITD trial (when there were no symptoms). While there was no difference in mean CBFV at these time points (sham, 44 ± 4 cm/s vs. active, 47 ± 4; P = 0.587), total oscillations (sum of high- and low-frequency spectral power) of CBFV were higher ( P = 0.004) with the active ITD (45.6 ± 10.2 cm/s2) than the sham ITD (22.1 ± 5.4 cm/s2). We conclude that greater oscillations around the same absolute level of mean CBFV are induced by inspiratory resistance and may contribute to the delay in symptoms and cardiovascular collapse that accompany progressive central hypovolemia.


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