Reduced Vasomotor Reactivity in Cerebral Microangiopathy

Small-vessel disease or cerebral microangiopathy (CMA) is a common finding in elderly people. It is related to a variety of vascular risk factors and may finally lead to subcortical ischemic vascular dementia. Because vessel stiffness is increased, we hypothesized that slow spontaneous oscillations are reduced in cerebral hemodynamics. Accordingly, we examined spontaneous oscillations in the visual cortex of 13 patients suffering from CMA, and compared them with 14 agematched controls. As an imaging method we applied functional near-infrared spectroscopy, because it is particularly sensitive to the microvasculature. Spontaneous low-frequency oscillations (LFOs) (0.07 to 0.12 Hz) were specifically impaired in CMA in contrast to spontaneous very-lowfrequency oscillations (0.01 to 0.05 Hz), which remained unaltered. Vascular reagibility was reduced during visual stimulation. Interestingly, changes were tightly related to neuropsychological deficits, namely executive dysfunction. Vascular alterations had to be attributed mainly to the vascular risk factor arterial hypertension. Further, results suggest that the impairments might be, at least partly, reversed by medical treatment such as angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers. Results indicate that functional near-infrared spectroscopy may detect changes in the microvasculature due to CMA, namely an impairment of spontaneous LFOs, and of vascular reagibility. Hence, CMA accelerates microvascular changes due to aging, leading to impairments of autoregulation.

Section: Discussionsupporting

confidence: 85%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Spontaneous Slow Hemodynamic Oscillations are Impaired in Cerebral Microangiopathy

Schroeter

Bücheler

Preul

et al. 2005

“…These changes may contribute to the attenuation of vasomotor reactivity in response to hypercapnia or acetazolamide seen in cSVD, 43 and consequently lead to an impairment of neurovascular coupling. Such impairment of neurovascular coupling appears to be specific for cSVD.…”

Section: Blood-brain Barrier Dysfunctionmentioning

confidence: 99%

Late-Onset Epilepsy and Occult Cerebrovascular Disease

Gibson

Hanby

Al–Bachari

et al. 2014

The interface between cerebrovascular disease (CVD) and epilepsy is complex and multifaceted. Late-onset epilepsy (LOE) is increasingly common and is often attributed to CVD, and is indeed associated with an increased risk of stroke. This relationship is easily recognizable where there is a history of stroke, particularly involving the cerebral cortex. However, the relationship with otherwise occult, subcortical CVD is currently less well established yet causality is often invoked. In this review, we consider the diagnosis of LOE in clinical practice-including its behaviour as a potential mimic of acute ischemic stroke and transient ischemic attack; evidence for an association between occult CVD and LOE; and potential mechanisms of epileptogenesis in occult CVD, including potential interrelationships between disordered cerebral metabolism and perfusion, disrupted neurovascular unit integrity, blood-brain barrier dysfunction, and inflammation. We also discuss recently recognized issues concerning antiepileptic drug treatment and vascular risk and consider a variety of less common CVD entities associated with seizures.

“…Moreover, we did not measure PaCO 2 during investigation in this study. The pCBF may change with changes in CO 2 , and this reactivity may be influenced by atherosclerosis or may indicate cerebral small vessel disease (Terborg et al, 2000). However, although our patients were included in the SMART study after referral to the University Medical Center Utrecht with coronary artery disease, cerebrovascular disease, peripheral disease, or abdominal aortic aneurysm, they are all treated in an outpatient setting and were generally in good condition.…”

Section: Discussionmentioning

confidence: 99%

Total Cerebral Blood Flow and Hippocampal Volume in Patients with Arterial Disease. the SMART-MR Study

Knoops

Graaf

Appelman

et al. 2009

It has been suggested that compared with other brain tissues, the hippocampus in particular is vulnerable to chronic hypoperfusion. We investigated whether total parenchymal cerebral blood flow (pCBF) was associated with hippocampal atrophy, and also whether this relationship was modified by white matter lesions (WMLs). In a cross-sectional analysis within the SMART-MR (Second Manifestations of ARTerial disease-magnetic resonance) study, which is a cohort study among patients with arterial disease, total CBF (tCBF) and hippocampal volume were assessed in 392 patients (mean age: 62 ± 9 years, 84% men). Total CBF was expressed in per 100 mL brain volume for obtaining pCBF. Manual volumetric measurements of the hippocampus were carried out on a three-dimensional fast field-echo T1-weighted magnetic resonance imaging scan with isotropic voxels. Automated brain segmentation was used to quantify volumes of the WML and the total brain. A linear regression analysis showed that reduced pCBF was not associated with smaller hippocampal volume after adjustments were made for age and sex. The association attenuated further after additional adjustments were made for vascular risk factors, lacunar infarcts, and WMLs (b = 0.01 mL per s.d. decrease in pCBF; 95% confidence interval: À0.06 to 0.08). The association was not modified by WML (P-value for interaction term pCBF * WML = 0.84). We found no evidence of the fact that lower parenchymal blood flow contributes to the neurodegeneration of the hippocampus in a population of patients with arterial disease.