Wiseman, R. M. et al. Hippocampal atrophy, whole brain volume, and white matter lesions in older hypertensive subjects. Neurology 63, 1892-1897
Institute for Aging and Health, University of Newcastle upon Tyne, UK. Neurology
(Impact Factor: 8.29).
11/2004; 63(10):1892-7. DOI: 10.1212/01.WNL.0000144280.59178.78
To determine the potential role of whole brain atrophy, hippocampal atrophy, or both, and small vessel disease/white matter lesions as mechanisms underlying the cognitive impairment associated with hypertension.
Using MRI scanning the authors determined hippocampal volumes, whole brain volumes, and location and severity of white matter lesions, using Scheltens scale, in 103 hypertensive (166 +/- 8/88 +/- 7 mm Hg, 54 female) and 51 normotensive (132 +/- 12/74 +/- 7 mm Hg, 21 female) subjects age > or = 70 years.
Compared to normotensive subjects, older hypertensive subjects had significantly smaller whole brain volumes (887 +/- 109 vs 930 +/- 97 cm3, p = 0.02) and nonsignificantly reduced hippocampal volumes (5.39 +/- 1.60 vs 5.67 +/- 1.80 cm3, p = 0.33). Hypertensive subjects had an increased burden of periventricular lesions: bands (p = 0.03), frontal caps (p = 0.08), occipital caps (p = 0.07), and total periventricular hyperintensities (p = 0.02). They also had higher scores in subcortical areas: frontal (p = 0.04), temporal (p = 0.03), and deep white matter areas (p = 0.05). A correlation was found between whole brain volumes and systolic blood pressure (r = -0.19, p = 0.02). No correlation was seen between whole brain volumes and white matter lesion burden.
Moderate hypertension in non-impaired older subjects is associated with smaller whole brain volume and an increased burden of subcortical and periventricular white matter lesions.
Available from: Caterina Rosano
- "Aging and Disease • Volume 3, Number 1, February 2012 20 hemodynamic dysregulation      "
[Show abstract] [Hide abstract]
ABSTRACT: Maintaining brain health promotes successful aging. The main determinants of brain health are the preservation of cognitive function and remaining free from structural and metabolic abnormalities, including loss of neuronal synapses, atrophy, small vessel disease and focal amyloid deposits visible by neuroimaging. Promising studies indicate that these determinants are to some extent modifiable, even among adults seventy years and older. Converging animal and human evidence further suggests that inflammation is a shared mechanism, contributing to both cognitive decline and abnormalities in brain structure and metabolism. Thus, inflammation may provide a target for intervention. Specifically, circulating inflammatory markers have been associated with declines in cognitive function and worsening of brain structural and metabolic characteristics. Additionally, it has been proposed that older brains are characterized by a sensitization to neuroinflammatory responses, even in the absence of overt disease. This increased propensity to central inflammation may contribute to poor brain health and premature brain aging. Still unknown is whether and how peripheral inflammatory factors directly contribute to decline of brain health. Human research is limited by the challenges of directly measuring neuroinflammation in vivo. This review assesses the role that inflammation may play in the brain changes that often accompany aging, focusing on relationships between peripheral inflammatory markers and brain health among well-functioning, community-dwelling adults seventy years and older. We propose that monitoring and maintaining lower levels of systemic and central inflammation among older adults could help preserve brain health and support successful aging. Hence, we also identify plausible ways and novel experimental study designs of maintaining brain health late in age through interventions that target the immune system.
Aging and Disease 02/2012; 3(1):16-33. · 3.07 Impact Factor
Available from: Egill Rostrup
- "In one study, hypertensive subjects had a higher load of periventricular WMH and fronto-temporal WMH in comparison to normotensive subjects (Wiseman et al., 2004). On the contrary, other investigators showed that hypertension is correlated with subcortical WMH (Murray et al., 2005) or found no difference in WMH pattern at all (Enzinger et al., 2006). "
[Show abstract] [Hide abstract]
ABSTRACT: White matter hyperintensities (WMH) are a frequent finding on brain MRI of elderly subjects, and have been associated with various risk factors, as well as with development of cognitive and functional impairment. While an overall association between WMH load and risk factors is well described, possible spatially restricted vulnerability remains to be established. The aim of this study was to investigate the spatial distribution of WMH in normally functioning elderly subjects. We introduce a voxel-based approach in which lesion probability is mapped as a function of clinical risk factors using logistic regression, and validate the method using simulated datasets. The method was then applied in a total of 605 participants of the LADIS study (age 74 ± 5 years, all with WMH), and the location of manually delineated WMH was investigated after spatial normalisation. Particularly strong and widespread associations were found for age, gender and hypertension. Different distribution patterns were found for men and women. Further, increased probability was found in association with self-reported alcohol and tobacco consumption, as well as in those with a history of migraine. It is concluded that the location of WMH is dependent on the risk factors involved pointing towards a regionally different pathogenesis and/or vulnerability of the white matter.
NeuroImage 01/2012; 60(3):1597-607. DOI:10.1016/j.neuroimage.2012.01.106 · 6.36 Impact Factor
Available from: David M Schnyer
- "However, despite evidence of seemingly widespread regional impact to brain structure, the predominant finding has been that high BP has at least an initial direct and selective impact on anterior brain regions , particularly in the absence of overt dementia or severe cognitive impairment. This impact includes damage to white matter connecting frontal and subcortical brain regions (Debette et al., 2007; Gouw et al., 2008; Jouvent et al., 2008; Gold et al., 2005; Wiseman et al., 2004) as well as anterior corpus callosum fibers (Chen et al., 2009; Delano-Wood et al., 2008). The vulnerability of anterior brain regions to high BP is supported by studies in patients with more advanced CVD, such as vascular dementia (Chen et al., 2009; Hallam et al., 2008; Zarei et al., 2009). "
[Show abstract] [Hide abstract]
ABSTRACT: We examined how wide ranges in levels of risk factors for cerebrovascular disease are associated with thickness of the human cerebral cortex in 115 individuals ages 43-83 with no cerebrovascular or neurologic history. Cerebrovascular risk factors included blood pressure, cholesterol, body mass index, creatinine, and diabetes-related factors. Variables were submitted into a principal components analysis that confirmed four orthogonal factors (blood pressure, cholesterol, cholesterol/metabolic and glucose). T1-weighted MRI was used to create models of the cortex for calculation of regional cortical thickness. Increasing blood pressure factor scores were associated with numerous regions of reduced thickness. Increasing glucose scores were modestly associated with areas of regionally decreased thickness. Increasing cholesterol scores, in contrast, were associated with thicker cortex across the whole brain. All findings were primarily independent of age. These results provide evidence that normal and moderately abnormal levels of parameters used to assess cerebrovascular health may impact brain structure, even in the absence of cerebrovascular disease. Our data have important implications for the clinical management of vascular health, as well as for what is currently conceptualized as "normal aging" as they suggest that subclinical levels of risk may impact cortical gray matter before a disease process is evident.
NeuroImage 10/2010; 54(4):2659-71. DOI:10.1016/j.neuroimage.2010.10.050 · 6.36 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.