A Population-Based Study on Blood Pressure and Brain Atrophy in 85-Year-Olds

Skoog, Ingmar; Andreasson, Lars-Arne; Landahl, Sten; Lernfelt, Bodil

doi:10.1161/01.hyp.32.3.404

Cited by 99 publications

(82 citation statements)

References 46 publications

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“…Brain abnormalities related to dementia might contribute to neurovascular instability and blood pressure dysregulation. 32 There is a U-shaped association between blood pressure and cognitive performance among elderly subjects, 33,34 but in the present study cognitive dysfunction was not associated with the occurrence of hypertension per se.…”

Section: Discussioncontrasting

confidence: 63%

Association of cognitive dysfunction with neurocirculatory abnormalities in early Parkinson disease

et al. 2012

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Objective: Cognitive impairment and neurocirculatory abnormalities such as orthostatic hypotension (OH), supine hypertension (SH), and failure to decrease blood pressure at night (nondipping) occur relatively commonly in Parkinson disease (PD); however, whether cognitive dysfunction in early PD is related to neurocirculatory abnormalities has not been established. Cognitive dysfunction in PD is associated with white matter hyperintensities on MRI. We report results of an analysis of neuropsychological and hemodynamic parameters in patients with early PD.Methods: Among 87 patients, 25 had normal cognition, 48 had mild cognitive impairment, and 14 had dementia, based on comprehensive neuropsychological tests. Orthostatic vital signs and ambulatory 24-hour blood pressure monitoring were recorded, and brain magnetic resonance scans were obtained for all patients. Results:Cognitive impairment was associated with OH, SH, and white matter hyperintensities but not with nondipping. Dementia and white matter hyperintensities were common in SH. Of 13 patients with OH ϩ SH, every one had mild cognitive impairment or dementia. Conclusions:Cognitive dysfunction is related to neurocirculatory abnormalities, especially OH ϩ SH, in early PD, raising the possibility that early detection and effective treatment of those abnormalities might slow the rate of cognitive decline. Neurology It is increasingly being recognized that Parkinson disease (PD) involves prominent nonmotor manifestations such as dementia and autonomic failure.A variety of neurocirculatory abnormalities have been noted in PD, including orthostatic hypotension (OH), 1-4 supine hypertension (SH), 5-7 labile blood pressure, and the absence of a decrease in pressure during the night, a phenomenon called nondipping. 8 These abnormalities are related to each other. SH is found in a substantial proportion of patients with PD with OH.

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Section: Discussioncontrasting

confidence: 63%

Association of cognitive dysfunction with neurocirculatory abnormalities in early Parkinson disease

et al. 2012

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“…First, the brain regulates a number of functions important for survival, such as blood pressure, body temperature, appetite, energy balance, control of body fluids, electrolyte homeostasis, and cardiac function. 26,27 We have previously shown that larger bifrontal ratio and frontal atrophy were associated with lower blood pressure in 85-yearolds without dementia, 28 areas related to decreased survival in our study. Second, brain atrophy is related to midlife factors, such as obesity 21 and hypertension.…”

Section: Resultssupporting

confidence: 57%

A population-based study on the influence of brain atrophy on 20-year survival after age 85

Olesen¹,

Guo²,

Gustafson³

et al. 2011

Neurology

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“…The prefrontal cortex is known to exert an inhibitory control on brain activation in response to external and internal stimuli (28,29). While generally performing well on standard tests of memory and cognitive function, subjects with alterations of the prefrontal cortex suffer from inappropriate social behavior (28), altered cardiovascular homeostasis (30), and hyperphagia (16). We postulate that the activation (25), such that x is the distance in millimeters to the right (+) or left (-) of midline, y is the distance in millimeters anterior (+) or posterior (-) to the anterior commissure, and z is the distance in millimeters superior (+) or inferior (-) to a horizontal plane through the anterior and posterior commissures.…”

Section: Discussionmentioning

confidence: 99%

Differential brain responses to satiation in obese and lean men.

et al. 2000

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Knowledge of how the brain contributes to the regulation of food intake in humans is limited. We used positron emission tomography and measures of regional cerebral blood flow (rCBF) (a marker of neuronal activity) to describe the functional anatomy of satiation (i.e., the response to a liquid meal) in the context of extreme hunger (36-h fast) in 11 obese (BMI ≥35 kg/m 2 , age 27 ± 5 years, weight 115 ± 11 kg, 38 ± 7% body fat; mean ± SD) and 11 lean (BMI ≤25 kg/m 2 , age 35 ± 8 years, weight 73 ± 9 kg, 19 ± 6% body fat) men. As in lean men, satiation in obese men produced significant increases in rCBF in the vicinity of the ventromedial and dorsolateral prefrontal cortex and significant decreases in rCBF in the vicinity of the limbic/paralimbic areas (i.e., hippocampal formation, temporal pole), striatum (i.e., caudate, putamen), precuneus, and cerebellum. However, rCBF increases in the prefrontal cortex were significantly greater in obese men than in lean men (P < 0.005). rCBF decreases in limbic/paralimbic areas, temporal and occipital cortex, and cerebellum were also significantly greater in obese men than in lean men (P < 0.005), whereas rCBF decreases in the hypothalamus and thalamus were attenuated in obese men compared with lean men (P < 0.05). This study raises the possibility that the brain responses to a meal in the prefrontal areas (which may be involved in the inhibition of inappropriate response tendencies) and limbic/paralimbic areas (commonly associated with the regulation of emotion) may be different in obese and lean men. Additional studies are required to investigate how these differential responses are related to the pathophysiology of obesity. Diabetes 49:838-846, 2000 O besity is a chronic relapsing disease with a prevalence reaching epidemic proportions in most industrialized countries (1,2). Whereas the exact pathophysiology of this disease remains unclear, studies in animals (3,4) and numerous reports in humans (5-10) indicate that eating behavior disorders (i.e., hyperphagia) and the resulting excessive energy intake play a major role in the development of obesity.The role of the brain (especially the hypothalamus) in the regulation of body weight is well established in animals (11). In humans, substantial molecular (12) and neuropharmacologic evidence (13) attest to the importance of the central nervous system in maintaining energy balance. However, the neuroanatomical correlates of human feeding behavior are largely unknown. Some information comes from pathological conditions associated with hyperphagia and obesity such as hypothalamic tumors (14) and Prader-Willi syndrome, the most common type of inherited human hypothalamic disorder (15). In addition, patients with frontal lobe dementia with computerized tomography documented prefrontal atrophy frequently present with hyperphagia (16). Furthermore, seizures of the opercula (including the insular cortex) induce mastication, salivation, swallowing, and gustatory hallucinations (17). Finally, in 1 study, 50% of patients with eating epi...

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A Population-Based Study on Blood Pressure and Brain Atrophy in 85-Year-Olds

Cited by 99 publications

References 46 publications

Association of cognitive dysfunction with neurocirculatory abnormalities in early Parkinson disease

Association of cognitive dysfunction with neurocirculatory abnormalities in early Parkinson disease

A population-based study on the influence of brain atrophy on 20-year survival after age 85

Differential brain responses to satiation in obese and lean men.

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