Abnormal cerebrovascular regulation in hypertensive patients.

Griffith, D N; James, I M; Newbury, P A; Woollard, M L

doi:10.1136/bmj.2.6139.740

Cited by 11 publications

(3 citation statements)

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“…According to a report by Tominaga et al, 12 the resting CBF values and cerebrovascular CO2 reactivity were similar in the normotensive and the hypertensive patients. Griffith et al 13 reported normal CBF and a decrease in vasoreactivity in hypertensive patients. In contrast, Rodriguez et al 14 and Nobili et al 15 reported that the CBF decreased in the hypertensive patients without any neurological symptoms, but there was no description of white matter lesions in these studies, and it was difficult to evaluate the hemodynamics in deep white matter due to methodological problems.…”

Section: Discussionmentioning

confidence: 99%

Cerebral blood flow and vascular response to hypercapnia in hypertensive patients with leukoaraiosis

et al. 1996

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Both arteriosclerosis and leukoaraiosis have a close relationship with hypertension, but the relationship between cerebral hemodynamics and leukoaraiosis in hypertensive patients has not been fully examined. To clarify this issue, we measured the regional cerebral blood flow (rCBF) and cerebrovascular response to hypercapnia in hypertensive patients with various degrees of leukoaraiosis. The subjects consisted of 7 normotensive normal controls and 17 hypertensive patients. The hypertensive patients were divided into three groups according to the severity of white matter lesions (leukoaraiosis) on MRI and the presence of dementia, namely, (1) negative or mild leukoaraiosis without dementia, (2) moderate to severe leukoaraiosis without dementia and (3) severe leukoaraiosis with dementia. Both the rCBF and the cerebrovascular response to hypercapnia were measured by the O-15 H2O bolus-injection method and positron emission tomography. The rCBF in hypertensive patients without dementia did not decrease when compared with the normotensive controls, but the rCBF in hypertensive patients with dementia markedly decreased in the cerebral cortices and white matter. On the other hand, the cerebrovascular response to hypercapnia declined with the severity of leukoaraiosis, and it decreased most severely in patients with severe leukoaraiosis and dementia. Our results indicate that the reduction in the cerebral hemodynamic reserve capacity has a close relationship with the severity of leukoaraiosis in hypertensive patients, although the rCBF is maintained in hypertensive patients without dementia, and suggest that arteriosclerotic change reduces cerebrovascular CO2 response and causes a leukoaraiosis in hypertensive patients.

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Section: Discussionmentioning

confidence: 99%

Cerebral blood flow and vascular response to hypercapnia in hypertensive patients with leukoaraiosis

et al. 1996

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“…Non-genetic risk factors such as hypertension and diabetes compromise vascular reactivity. Hypertension reduces cerebrovascular reactivity in humans (Griffith et al, 1978; Maeda et al, 1994). Hypertension causes deterioration of cerebrovascular function through physical pressure load and angiotensin-mediated signal transduction.…”

Section: Short-term Modification By Vascular Factorsmentioning

confidence: 99%

Roles of vascular and metabolic components in cognitive dysfunction of Alzheimer disease: short- and long-term modification by non-genetic risk factors

Sato

Morishita

2013

Front. Aging Neurosci.

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It is well known that a specific set of genetic and non-genetic risk factors contributes to the onset of Alzheimer disease (AD). Non-genetic risk factors include diabetes, hypertension in mid-life, and probably dyslipidemia in mid-life. This review focuses on the vascular and metabolic components of non-genetic risk factors. The mechanisms whereby non-genetic risk factors modify cognitive dysfunction are divided into four components, short- and long-term effects of vascular and metabolic factors. These consist of (1) compromised vascular reactivity, (2) vascular lesions, (3) hypo/hyperglycemia, and (4) exacerbated AD histopathological features, respectively. Vascular factors compromise cerebrovascular reactivity in response to neuronal activity and also cause irreversible vascular lesions. On the other hand, representative short-term effects of metabolic factors on cognitive dysfunction occur due to hypoglycemia or hyperglycemia. Non-genetic risk factors also modify the pathological manifestations of AD in the long-term. Therefore, vascular and metabolic factors contribute to aggravation of cognitive dysfunction in AD through short-term and long-term effects. β-amyloid could be involved in both vascular and metabolic components. It might be beneficial to support treatment in AD patients by appropriate therapeutic management of non-genetic risk factors, considering the contributions of these four elements to the manifestation of cognitive dysfunction in individual patients, though all components are not always present. It should be clarified how these four components interact with each other. To answer this question, a clinical prospective study that follows up clinical features with respect to these four components: (1) functional MRI or SPECT for cerebrovascular reactivity, (2) MRI for ischemic lesions and atrophy, (3) clinical episodes of hypoglycemia and hyperglycemia, (4) amyloid-PET and tau-PET for pathological features of AD, would be required.

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“…Here there is almost always a secondary rise in intracranial pressure and "re¬ flex" systemic hypertension.13 Because cerebral arterial perfusion is a function of the difference between systemic arterial pressure and intracranial pressure, a fall in sys¬ temic BP will compromise cerebral perfusion.15,21 This prob¬ lem is exacerbated in patients with chronic hypertension whose lower limits of autoregulation are set at higher levels than normotensive patients. 3,8,9 Furthermore, the hema¬ toma impairs the responsiveness of autoregulation in the surrounding area of marginal ischemia.12 It is logical, there¬ fore, to reduce the intracranial pressure by medical and, if necessary, surgical means, rather than reduce the systemic BP directly. I recently observed a patient with chronic hypertension who developed a massive left frontal parietal hematoma with extension of blood into the ventricles.…”

Section: Commentmentioning

confidence: 99%