scholarly journals Total Cerebral Blood Flow in Relation to Cognitive Function: The Rotterdam Scan Study

2008 ◽  
Vol 28 (10) ◽  
pp. 1652-1655 ◽  
Author(s):  
Mariëlle MF Poels ◽  
Mohammad Arfan Ikram ◽  
Meike W Vernooij ◽  
Gabriel P Krestin ◽  
Albert Hofman ◽  
...  

Cerebral hypoperfusion has been associated with worse cognitive function. We investigated the association between cerebral blood flow and cognition and whether this association is independent of brain volume. In 892 participants, aged 60 to 91 years, of the population-based Rotterdam Scan study, we measured total cerebral blood flow (tCBF) and brain volume using magnetic resonance imaging. Lower tCBF was associated with worse information-processing speed, executive function, and global cognition. However, after correcting tCBF for brain volume, these associations disappeared. The association between tCBF and cognition may be mediated or confounded by brain atrophy. Future studies on tCBF should take into account brain atrophy.

2020 ◽  
pp. 0271678X2094861
Author(s):  
Rashid Ghaznawi ◽  
Maarten HT Zwartbol ◽  
Nicolaas PA Zuithoff ◽  
Jeroen de Bresser ◽  
Jeroen Hendrikse ◽  
...  

Global cerebral hypoperfusion may be involved in the aetiology of brain atrophy; however, long-term longitudinal studies on this relationship are lacking. We examined whether reduced cerebral blood flow was associated with greater progression of brain atrophy. Data of 1165 patients (61 ± 10 years) from the SMART-MR study, a prospective cohort study of patients with arterial disease, were used of whom 689 participated after 4 years and 297 again after 12 years. Attrition was substantial. Total brain volume and total cerebral blood flow were obtained from magnetic resonance imaging scans and expressed as brain parenchymal fraction (BPF) and parenchymal cerebral blood flow (pCBF). Mean decrease in BPF per year was 0.22% total intracranial volume (95% CI: –0.23 to –0.21). Mean decrease in pCBF per year was 0.24 ml/min per 100 ml brain volume (95% CI: –0.29 to –0.20). Using linear mixed models, lower pCBF at baseline was associated with a greater decrease in BPF over time ( p =  0.01). Lower baseline BPF, however, was not associated with a greater decrease in pCBF ( p =  0.43). These findings indicate that reduced cerebral blood flow is associated with greater progression of brain atrophy and provide further support for a role of cerebral blood flow in the process of neurodegeneration.


2015 ◽  
Vol 35 (11) ◽  
pp. 1882-1887 ◽  
Author(s):  
Hazel I Zonneveld ◽  
Elizabeth A Loehrer ◽  
Albert Hofman ◽  
Wiro J Niessen ◽  
Aad van der Lugt ◽  
...  

The question remains whether reduced cerebral blood flow (CBF) leads to brain atrophy or vice versa. We studied the longitudinal relation between CBF and brain volume in a community-dwelling population. In the Rotterdam Study, 3011 participants (mean age 59.6 years (s.d. 8.0)) underwent repeat brain magnetic resonance imaging to quantify brain volume and CBF at two time points. Adjusted linear regression models were used to investigate the bidirectional relation between CBF and brain volume. We found that smaller brain volume at baseline was associated with a steeper decrease in CBF in the whole population (standardized change per s.d. increase of total brain volume (TBV) = 0.296 (95% confidence interval (CI) 0.200; 0.393)). Only in persons aged ≥ 65 years, a lower CBF at baseline was associated with steeper decline of TBV (standardized change per s.d. increase of CBF = 0.003 (95% CI −0.004; 0.010) in the whole population and 0.020 (95% CI 0.004; 0.036) in those aged ≥65 years of age). Our results indicate that brain atrophy causes CBF to decrease over time, rather than vice versa. Only in persons aged >65 years of age did we find lower CBF to also relate to brain atrophy.


2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Qian Liu ◽  
Mohammad Iqbal H. Bhuiyan ◽  
Ruijia Liu ◽  
Shanshan Song ◽  
Gulnaz Begum ◽  
...  

Abstract Background Chronic cerebral hypoperfusion (CCH) causes white matter damage and cognitive impairment, in which astrogliosis is the major pathology. However, underlying cellular mechanisms are not well defined. Activation of Na+/H+ exchanger-1 (NHE1) in reactive astrocytes causes astrocytic hypertrophy and swelling. In this study, we examined the role of NHE1 protein in astrogliosis, white matter demyelination, and cognitive function in a murine CCH model with bilateral carotid artery stenosis (BCAS). Methods Sham, BCAS, or BCAS mice receiving vehicle or a selective NHE1 inhibitor HOE642 were monitored for changes of the regional cerebral blood flow and behavioral performance for 28 days. Ex vivo MRI-DTI was subsequently conducted to detect brain injury and demyelination. Astrogliosis and demyelination were further examined by immunofluorescence staining. Astrocytic transcriptional profiles were analyzed with bulk RNA-sequencing and RT-qPCR. Results Chronic cerebral blood flow reduction and spatial working memory deficits were detected in the BCAS mice, along with significantly reduced mean fractional anisotropy (FA) values in the corpus callosum, external capsule, and hippocampus in MRI DTI analysis. Compared with the sham control mice, the BCAS mice displayed demyelination and axonal damage and increased GFAP+ astrocytes and Iba1+ microglia. Pharmacological inhibition of NHE1 protein with its inhibitor HOE642 prevented the BCAS-induced gliosis, damage of white matter tracts and hippocampus, and significantly improved cognitive performance. Transcriptome and immunostaining analysis further revealed that NHE1 inhibition specifically attenuated pro-inflammatory pathways and NADPH oxidase activation. Conclusion Our study demonstrates that NHE1 protein is involved in astrogliosis with pro-inflammatory transformation induced by CCH, and its blockade has potentials for reducing astrogliosis, demyelination, and cognitive impairment.


2007 ◽  
Vol 28 (3) ◽  
pp. 633-639 ◽  
Author(s):  
Auke PA Appelman ◽  
Yolanda van der Graaf ◽  
Koen L Vincken ◽  
Audrey M Tiehuis ◽  
Theo D Witkamp ◽  
...  

We investigated whether total cerebral blood flow (CBF) was associated with brain atrophy, and whether this relation was modified by white matter lesions (WML). Within the Second Manifestations of ARTerial disease-magnetic resonance (SMART-MR) study, a prospective cohort study among patients with arterial disease, cross-sectional analyses were performed in 828 patients (mean age 58±10 years, 81% male) with quantitative flow, atrophy, and WML measurements on magnetic resonance imaging (MRI). Total CBF was measured with MR angiography and was expressed per 100 mL brain volume. Total brain volume and ventricular volume were divided by intracranial volume to obtain brain parenchymal fraction (BPF) and ventricular fraction (VF). Lower BPF indicates more global brain atrophy, whereas higher VF indicates more subcortical brain atrophy. Mean CBF was 52.0±10.2 mL/min per 100 mL, mean BPF was 79.2±2.9%, and mean VF was 2.03±0.96%. Linear regression analyses showed that lower CBF was associated with more subcortical brain atrophy, after adjusting for age, sex, vascular risk factors, intima-media thickness, and lacunar infarcts, but only in patients with moderate to severe WML (upper quartile of WML): Change in VF per s.d. decrease in CBF 0.18%, 95% CI: 0.02 to 0.34%. Our findings suggest that cerebral hypoperfusion in the presence of WML may be associated with subcortical brain atrophy.


2021 ◽  
Author(s):  
Kristina E. Almby ◽  
Martin H. Lundqvist ◽  
Niclas Abrahamsson ◽  
Sofia Kvernby ◽  
Markus Fahlström ◽  
...  

While Roux-en-Y Gastric Bypass (RYGB) surgery in obese individuals typically improves glycemic control and prevents diabetes, it also frequently causes hypoglycemia. Previous work showed attenuated counter-regulatory responses following RYGB. The underlying mechanisms as well as the clinical consequences are unclear. <p>In this study, 11 non-diabetic subjects with severe obesity were investigated pre- and post-RYGB during hyperinsulinemic hypoglycemic clamps. Assessments were made of hormones, cognitive function, cerebral blood flow by arterial spin labeling, brain glucose metabolism by FDG PET and activation of brain networks by functional MRI. Post- vs pre-surgery, we found a general increase of cerebral blood flow but a decrease of total brain FDG uptake during normoglycemia. During hypoglycemia, there was a marked increase in total brain FDG uptake and this was similar for post- and pre-surgery, whereas hypothalamic FDG uptake was reduced. During hypoglycemia, attenuated responses of counterregulatory hormones and improvements in cognitive function were seen post-surgery. In early hypoglycemia, there was increased activation post- vs pre-surgery of neural networks in CNS regions implicated in glucose regulation such as the thalamus and hypothalamus. The results suggest adaptive responses of the brain that contribute to lowering of glycemia following RYGB, and the underlying mechanisms should be further elucidated.</p>


2007 ◽  
Vol 28 (2) ◽  
pp. 412-419 ◽  
Author(s):  
Meike W Vernooij ◽  
Aad van der Lugt ◽  
Mohammad Arfan Ikram ◽  
Piotr A Wielopolski ◽  
Henri A Vrooman ◽  
...  

Reduced cerebral perfusion may contribute to the development of cerebrovascular and neurodegenerative diseases. Little is known on cerebral perfusion in the general population, as most measurement techniques are too invasive for application in large groups of healthy individuals. Total cerebral blood flow (tCBF) can be noninvasively measured by magnetic resonance imaging (MRI) but is highly correlated with brain volume. We calculated total brain perfusion by dividing tCBF by brain volume, and we investigated determinants of total brain perfusion in comparison with tCBF. Secondly, we studied whether persons with a low tCBF or low total brain perfusion have a larger volume of white matter lesions (WML). This study is based on 892 persons aged 60 to 91 years from the Rotterdam Study, a population-based cohort study. We performed two-dimensional (2D) phase-contrast MRI for tCBF measurement. Brain volume and WML volume were quantitatively assessed. Cardiovascular determinants were assessed by interview and physical examination. We assessed associations between cardiovascular determinants and flow measures with linear regression models, adjusted for age and sex. Associations between tCBF or total brain perfusion and WML volume were assessed using general linear models. We found that determinants of tCBF and total brain perfusion differed largely due to the large influence of brain volume on tCBF values. Persons with low total brain perfusion had a significantly larger WML volume compared with those with high total brain perfusion. Prospective studies are required to unravel whether hypoperfusion contributes to WML formation or that tissue damage, manifested by WML, leads to brain hypoperfusion.


2019 ◽  
pp. 185-188
Author(s):  
Peter Novak

This case presents a patient with extreme fatigue and excessive sleepiness. The tilt test provoked decline in cerebral blood flow velocity (CBFv) associated with decline in end tidal CO2, indicative of hypocapnic cerebral hypoperfusion (HYCH). There was also mild small fiber neuropathy affecting predominantly autonomic fibers associated with mild autonomic dysfunction.


2019 ◽  
pp. 157-162
Author(s):  
Peter Novak

The tilt test showed orthostatic cerebral hypoperfusion syndrome (OCHOS) with intermittent reduction in cerebral blood flow velocity and vision loss. OCHOS is associated with reduced orthostatic cerebral blood flow velocity without orthostatic hypotension or arrhythmia.


2019 ◽  
pp. 153-156
Author(s):  
Peter Novak

The tilt test showed severe orthostatic cerebral hypoperfusion syndrome (OCHOS) with reduced cerebral blood flow velocity. OCHOS is associated with reduced orthostatic cerebral blood flow velocity without orthostatic hypotension or arrhythmia.


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