Cerebral Autoregulation and Syncope

Folino, Antonio Franco

doi:10.1016/j.pcad.2007.01.001

Cited by 70 publications

(33 citation statements)

References 243 publications

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“…A previous SPECT study performed in pediatric patients showed that subjects with a positive tilt test had regional differences in brain perfusion, with significantly lower perfusion of the right peri-insular, posterior parietal and temporal regions compared to negative tilt test patients [17] and the reduction in rCBF in these specific areas is known to be a direct effect of the enhanced vagal reflex that leads to syncope. An rCBF decrease confined to the right insula is known to be the final trigger responsible for the reduction of heart rate and blood pressure [12]. These findings were reproduced in this study.…”

Section: Discussionsupporting

confidence: 87%

Cerebral blood flow abnormalities in patients with neurally mediated syncope

et al. 2010

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The aim of this study is to investigate regional cerebral blood flow (rCBF) in patients with syncope. We compared brain single photon emission computed tomography (SPECT) images of neurally mediated syncope patients with those of age/sex matched healthy volunteers. (99m)Tc-ethylcysteinate dimer (ECD) brain SPECT was performed in 35 patients (M/F = 17/18, mean 36.6 years) with syncope during the asymptomatic period, and in 35 healthy volunteers. For statistical parametric mapping (SPM) analysis, all SPECT images were spatially normalized to the standard SPECT template and then smoothed using a 14-mm full width at half maximum Gaussian kernel. The mean duration of syncope history was 4.9 years and the mean number of syncope episodes was 6.3. In all patients, syncope or presyncope episodes occurred during head-up tilt tests, and all were the vasodepressive type. SPM analysis of brain SPECT images showed significantly decreased rCBF in the right anterior insular cortex, left parahippocampal gyrus, bilateral fusiform gyri, bilateral middle and inferior temporal gyri, left lingual gyrus, bilateral precuneus and bilateral posterior lobes of the cerebellum in syncope patients at a false discovery rate corrected p < 0.05. There were no brain regions that showed increased rCBF in syncope patients. Furthermore, we found a negative correlation between the total number of syncopal episodes and the rCBF of the right prefrontal cortex, and between the duration of syncope history and the rCBF of the right cingulate gyrus at uncorrected p < 0.001. Decreases of rCBF in multiple brain regions may be responsible for autonomic dysregulation and improper processing of emotional stress in neurally mediated syncope patients, and frequent syncope episodes may lead to frontal dysfunction.

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Section: Discussionsupporting

confidence: 87%

Cerebral blood flow abnormalities in patients with neurally mediated syncope

et al. 2010

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“…The first is autoregulation, which is primarily at the level of the smaller arterioles 6. The cerebrovasculature is capable of self-regulating vascular tone in response to changes in arterial CO 2 concentration 7, blood pressure 8, endothelial nitric oxide production 9 or pH 10.…”

Section: The Neurovascular Unitmentioning

confidence: 99%

Immunotherapy, Vascular Pathology, and Microhemorrhages in Transgenic Mice

Wilcock

Colton²

2009

CNSNDDT

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Alzheimer's disease (AD) is a progressive, neurodegenerative disorder that results in severe cognitive decline. Amyloid plaques are a principal pathology found in AD and are composed of aggregated amyloid-beta (Aß) peptides. According to the amyloid hypothesis, Aß peptides initiate the other pathologies characteristic for Alzheimer's disease including cognitive deficits. Immunotherapy against Aß is a potential therapeutic for the treatment of humans with AD. While anti-Aß immunotherapy has been shown to reduce amyloid burden in mouse models and now in humans, immunotherapy also exacerbates vascular pathologies. Cerebral amyloid angiopathy (CAA), that is, the accumulation of amyloid in the cerebrovasculature, is increased with immunotherapy in humans with AD and in mouse models of amyloid deposition. CAA persists in the brains of clinical trial patients that show removal of parenchymal amyloid. Mouse model studies also show that immunotherapy results in multiple small bleeds in the brain, termed microhemorrhages. The neurovascular unit is a term used to describe the cerebrovasculature and its associated cellsastrocytes, neurons, pericytes and microglia. CAA affects brain perfusion and there is now evidence that the neurovascular unit is affected in Alzheimer's disease when CAA is present. Understanding the type of damage to the neurovascular unit caused by CAA in AD and the underlying cause of microhemorrhage after immunotherapy is essential to the success of therapeutic vaccines as a treatment for Alzheimer's disease. The neurovascular unitThe brain's high energy demands require a disproportionate blood supply. While the brain only composes 2% of the total body weight, it receives 15% of the cardiac output and consumes 20% of the oxygen utilized by the entire body. Maintenance and control of this blood supply requires communication between multiple components of the brain and cerebrovasculature. The cellular interface between the parenchyma of the brain and the circulating blood is composed of the blood vessel itself, perivascular neurons, pericytes, perivascular microglia and astrocytic end-feet and has been termed the neurovascular unit (NVU) 1 . The vascular component of the NVU includes the penetrating arteries that arise from the pial arteries on the surface of the brain, the arterioles and cerebral capillaries. Figure 1 summarizes the structures of the NVU. The larger arteries are composed of an endothelial layer, a smooth muscle layer and the adventitia composed of collagen, fibroblasts and perivascular nerves. Virchow-Robin spaces are CSF-filled spaces that separate the penetrating vessel from the brain. Astrocytic end-feet are located on the brain side of this space and impinge upon the pia mater that separates the fluid filled space from the adventitia of the blood vessel 2 . As the arteries branch and become smaller arterioles, the Virchow-Robin spaces shrink and disappear. At this point the astrocytic end-feet directly attach to the basement membrane of the vasculature 3 . The arterioles lose...

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“…Orthostatic tolerance depends on physical factors such as height, plasma volume, arterial and cardiopulmonary baroreflex sensitivity, cardiac filling, or stroke volume [18,[24][25][26]. Furthermore, brain blood flow is a critical factor for syncope [27,28]. A higher BP during HUT should be advantageous for maintaining the arterial BP in the brain above the lowest limit of the BP range for autoregulation (60-140 mmHg for mean BP [27]).…”

Section: Responses To Hutmentioning

confidence: 99%

“…Furthermore, brain blood flow is a critical factor for syncope [27,28]. A higher BP during HUT should be advantageous for maintaining the arterial BP in the brain above the lowest limit of the BP range for autoregulation (60-140 mmHg for mean BP [27]). Thus, our observations suggest that the nurses had higher orthostatic tolerance than the control subjects, at least in the early stage of HUT.…”

Section: Responses To Hutmentioning

confidence: 99%

Arterial blood pressure response to head-up tilt test and orthostatic tolerance in nurses

Onizuka

Niimi²,

Sato

et al. 2015

Environ Health Prev Med

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Objectives High tolerance to postural changes was examined in nurses. Methods Twelve female nurses and 12 healthy controls underwent a 70°head-up tilt (HUT) test for 10 min. Blood pressure (BP), heart rate (HR), pulse pressure, and hormone levels were measured. Baroreceptor sensitivity (BRS) was calculated using a sequence technique. Results HR increased during HUT in both subject groups, with no difference between groups. Systolic BP was rapidly increased by HUT in both subject groups, and was higher in the nurse group than in the control group during the first 2 min of HUT. Pulse pressure decreased during 1-2.5 min of HUT in the control group, but there was no decrease in the nurse group. BRS was decreased by HUT in the nurse group, while it tended to be decreased in the control group. Both during baseline and HUT, BRS was lower in the nurse group than in the control group. Plasma noradrenaline increased with HUT, and the increase was greater in the nurse group than in the control group. Conclusions Although nurse subjects had a lower BRS during HUT than control subjects, they were able to effectively maintain BP during HUT, suggesting that nurse subjects had higher orthostatic tolerance. The better maintenance of BP in nurse subjects appeared to be associated with a compensatory mechanism other than the arterial baroreflex and/or a hemodynamic mechanism.

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Cerebral Autoregulation and Syncope

Cited by 70 publications

References 243 publications

Cerebral blood flow abnormalities in patients with neurally mediated syncope

Cerebral blood flow abnormalities in patients with neurally mediated syncope

Immunotherapy, Vascular Pathology, and Microhemorrhages in Transgenic Mice

Arterial blood pressure response to head-up tilt test and orthostatic tolerance in nurses

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