Diabetic Brain Damage in Hypertension

Kario, Kazuomi; Ishikawa, Joji; Hoshide, Satoshi; Matsui, Yoshio; Morinari, Masato; Eguchi, Kazuo; Ishikawa, Shizukiyo; Shimada, Kazuyuki

doi:10.1161/01.hyp.0000163460.07639.3f

Cited by 49 publications

(27 citation statements)

References 36 publications

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“…These cascades activate proapoptotic pathways and ultimately cause neuronal cell damage and death. The finding that N-acetyl aspartate (an indicator of functional neuronal mass) was reduced in hypertensive diabetic patients in the areas affected by WMHs supports the notion that neuronal loss in frontal and temporal associative areas may contribute to functional decline in type 2 diabetes (25). In our study, WMHs were associated with regional differences in white matter volume, vasoreactivity, and higher A1C.…”

Section: Regional Perfusion and Brain Volumes In Diabetessupporting

confidence: 87%

Global and Regional Effects of Type 2 Diabetes on Brain Tissue Volumes and Cerebral Vasoreactivity

et al. 2007

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OBJECTIVE -The aim of this study was to evaluate the regional effects of type 2 diabetes and associated conditions on cerebral tissue volumes and cerebral blood flow (CBF) regulation.RESEARCH DESIGN AND METHODS -CBF was examined in 26 diabetic (aged 61.6 Ϯ 6.6 years) and 25 control (aged 60.4 Ϯ 8.6 years) subjects using continuous arterial spin labeling (CASL) imaging during baseline, hyperventilation, and CO 2 rebreathing. Regional gray and white matter, cerebrospinal fluid (CSF), and white matter hyperintensity (WMH) volumes were measured on a T1-weighted inversion recovery fast-gradient echo and a fluid attenuation inversion recovery magnetic resonance imaging at 3 Tesla.RESULTS -The diabetic group had smaller global white (P ϭ 0.006) and gray (P ϭ 0.001) matter and larger CSF (36.3%, P Ͻ 0.0001) volumes than the control group. Regional differences were observed for white matter (Ϫ13.1%, P ϭ 0.0008) and CSF (36.3%, P Ͻ 0.0001) in the frontal region, for CSF (20.9%, P ϭ 0.0002) in the temporal region, and for gray matter (Ϫ3.0%, P ϭ 0.04) and CSF (17.6%, P ϭ 0.01) in the parieto-occipital region. Baseline regional CBF (P ϭ 0.006) and CO 2 reactivity (P ϭ 0.005) were reduced in the diabetic group. Hypoperfusion in the frontal region was associated with gray matter atrophy (P Ͻ 0.0001). Higher A1C was associated with lower CBF (P Ͻ 0.0001) and greater CSF (P ϭ 0.002) within the temporal region.CONCLUSIONS -Type 2 diabetes is associated with cortical and subcortical atrophy involving several brain regions and with diminished regional cerebral perfusion and vasoreactivity. Uncontrolled diabetes may further contribute to hypoperfusion and atrophy. Diabetic metabolic disturbance and blood flow dysregulation that affects preferentially frontal and temporal regions may have implications for cognition and balance in elderly subjects with diabetes. Diabetes Care 30:1193-1199, 2007D iabetes is a prevalent condition associated with substantial morbidity attributed to vascular complications (1). Diabetes alters endothelial function (2) and permeability of the bloodbrain barrier, thus affecting microcirculation and regional metabolism (3).Studies in type 1 diabetes have shown that the fronto-temporal cortex and periventricular white matter (3) are more affected by diabetic metabolic disturbance. Single proton emission computed tomography (SPECT) studies suggest that chronic hyperglycemia alters cerebral blood flow (CBF) in the frontal, temporal, parietal, occipital, and cerebellar regions of interest (ROIs) (4,5). Vasoreactivity to acetazolamide is not homogeneous, with a majority of hypoperfused and some hyperperfused ROIs (6). White matter hyperintensities (WMHs) on T2-weighted magnetic resonance imaging (MRI) (7) have been associated with arteriolosclerosis, arising as consequences of aging, diabetes, and other cardiovascular risk factors (8,9). Vascular and neurodegenerative changes in these structures have consequences for regional perfusion, cognitive impairment, and balance in elderly people with type 2 diabetes (10,...

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Section: Regional Perfusion and Brain Volumes In Diabetessupporting

confidence: 87%

Global and Regional Effects of Type 2 Diabetes on Brain Tissue Volumes and Cerebral Vasoreactivity

et al. 2007

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“…43 Furthermore, these classes of antihypertensive drugs have been shown to reduce arterial stiffness 44 and reserve cerebral blood flow, thus are thought to be suitable for patients with SVD. 45 These findings may suggest that the classes of antihypertensive drugs may influence on the development of SVD including MBs. In the preset study, ACE inhibitors were more frequently used in patients with MBs than those without MBs.…”

Section: Discussionmentioning

confidence: 95%

Silent cerebral microbleeds associated with arterial stiffness in an apparently healthy subject

et al. 2009

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Silent cerebral microbleeds (MBs) are a common finding in stroke patients, especially those with intracerebral hemorrhage, and are thought to be a marker of future cerebral hemorrhage. Clinically, two distinct forms of MBs have been documented, those observed with either or both stroke or small vessel disease (SVD) and those associated with cerebral amyloid angiopathy. We investigated a possible association between MBs and arterial stiffness in a general population. Subjects were 443 apparently healthy individuals with a mean age of 67.1 ± 8.1 years. The presence of MBs, lacunar infarcts and periventricular hyperintensity (PVH) was determined by 3-tesla magnetic resonance imaging. Carotid intima-media thickness (IMT) was measured by ultrasonography. Arterial stiffness was evaluated by brachial-to-ankle pulse wave velocity (baPWV), and the Framingham stroke risk score (FSRS) was obtained as an integrated cerebrovascular risk factor. The prevalence of MBs was 5.0%. Both baPWV and FSRS were significantly higher in subjects with MBs (1820 ± 308 vs. 1645 ± 325 cm/s, P¼0.014 and 12.1 ± 8.6 vs. 8.9 ± 7.5%, P¼0.047, respectively). Odds ratio of a high baPWV, defined as X1500 cm/s, for the presence of MBs was 6.05 even after correction for confounding parameters, including age and hypertension. This association with high baPWV remained irrespective of MBs location, whether strictly located in the lobes or in the basal ganglia and infratentorial regions. These findings indicate an association between arterial stiffness and the presence of MBs. Assessment of arterial stiffness may be useful in identifying subjects at high risk for the presence of MBs.

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“…Such elevations are strongly associated with neurocognitive impairments [10] and cortical atrophy [22], and appear to have a synergistic effect insofar as individuals with both diabetes and elevated blood pressure tend to have the poorest neurocognitive outcomes [22][23][24]. Similarly, cerebral blood flow, especially in the frontal and frontotemporal brain regions, is reduced in diabetic patients [25,26] as is cerebrovascular reactivity, with this latter effect being most pronounced in those with retinopathy [27] or hypertension [28]. Cerebral metabolism, as measured by proton magnetic resonance spectroscopy, has also been found to be significantly affected in diabetic patients and again, this is linked to the presence of hypertension [28] and retinopathy [29], with abnormalities being greatest among those with the poorest long-term metabolic control.…”

Section: Is Diabetes-related Brain Dysfunction a 'Vasocognopathy'?mentioning

confidence: 99%

Diabetes and brain damage: more (or less) than meets the eye?

Ryan

2006

Diabetologia

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Brain damage is now a well-established complication of diabetes, but its pathophysiological basis remains controversial. Until very recently, most research on this topic was devoted to demonstrating that hypoglycaemic events are the primary cause of neurocognitive dysfunction. This was a plausible hypothesis because the central nervous system (CNS) has very limited stores of glucose and other substrates, but neurons have a very high rate of glucose utilisation; any reduction in glucose availability would probably induce neuroglycopenia, ultimately leading to significant neuronal damage. Support for this view came from research demonstrating that profound hypoglycaemia could produce neuronal necrosis [1] and induce distinctive patterns of neuropathological [2] and neurocognitive [3] impairment in humans who had experienced very low blood glucose levels over an extended period of time. Fortunately, most diabetic patients never experience profound hypoglycaemia. Although some writers have speculated that recurrent episodes of moderately severe hypoglycaemia could induce a less severe degree of neurocognitive dysfunction [4,5], most recent studies of children [6] and adults [7,8] have failed to find compelling evidence for that possibility. Taken together, these findings suggest that there is not a linear relationship between falling blood glucose levels and permanent brain dysfunction. Rather, necrotising neuronal damage occurs only after the threshold for cerebral energy failure is reached-most typically when blood glucose values fall below 1.5 mmol, and the electroencephalogram has reached an isoelectric (flat) state [9]. Retinopathy predicts neurocognitive dysfunctionIf moderately low blood glucose levels are not sufficient to induce detectable brain damage, and if profound hypoglycaemia is a rare event, to what can we attribute the modest, but consistently reported, brain dysfunction found in many diabetic patients? A growing literature now suggests that functional and structural CNS changes may have a vascular basis, and reflect the occurrence of cerebral microangiopathy that is secondary to chronic hyperglycaemia and indicated by the presence of retinopathy. For example, when adults with type 1 diabetes were followed for 7 years, a significant decline in mental efficiency was found over time, but this was limited to those who either had clinically significant diabetic proliferative retinopathy when they entered the study or who subsequently developed diabetic proliferative retinopathy during the follow-up period; those without retinopathy showed no cognitive changes. The magnitude of cognitive decline was further, and independently, influenced by elevated systolic blood pressure and by duration of diabetes [10]. The presence of retinopathy-even relatively early retinopathy-has also been associated with cerebral white matter lesions [11] in otherwise healthy diabetic adults, and a recent exploratory analysis has suggested that increasing severity of retinopathy is related to reductions in cortical grey matter ...

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Diabetic Brain Damage in Hypertension

Cited by 49 publications

References 36 publications

Global and Regional Effects of Type 2 Diabetes on Brain Tissue Volumes and Cerebral Vasoreactivity

Global and Regional Effects of Type 2 Diabetes on Brain Tissue Volumes and Cerebral Vasoreactivity

Silent cerebral microbleeds associated with arterial stiffness in an apparently healthy subject

Diabetes and brain damage: more (or less) than meets the eye?

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