Association of late-life blood pressure change with cerebral small vessel disease in the MIND-China study.

OBJECTIVES: This study aimed to investigate the associations between changes in blood pressure (BP) and cerebral small vessel disease (CSVD). METHODS: This study included 401 participants in the magnetic resonance imaging (MRI) sub-study conducted between 2018 and 2020 as a part of the Multidomain Interventions to Delay Dementia and Disability in Rural China project. MRI markers of CSVD were assessed based on international criteria. Individualized linear regression models evaluated changes in BP by estimating the trend of blood pressure changes over time and fitting a straight line from 2014 to 2018. The data were analyzed using logistic and general linear regression models. RESULT: The mean age of the participants was 64.48 ± 2.69 years, with 237 (59.1%) being females. Increases in systolic BP in later life were significantly associated with larger volumes of periventricular white matter hyperintensity (WMH), greater perivascular spaces in the basal ganglia (BG-PVS) burden, and the presence of deep lacunes and cerebral microbleeds. Additionally, increases in diastolic BP in later life were significantly associated with the presence of infratentorial and deep lacunes. CONCLUSIONS: CSVDs are associated with increased exposure to elevated BP later in life.

Towards an explanation for 'unexplained' dizziness in older people.

BACKGROUND: Subjective unsteadiness or dizziness, usually without increase in body sway, is common in older people. The absence of mechanistic understanding of such symptoms renders clinical management difficult. Here, we explore the mechanisms behind such idiopathic dizziness (ID), focusing on postural control abnormalities. METHODS: Thirty patients with ID and 30 age-matched controls stood on a moving platform. Platform oscillations were randomly delivered at different velocities (from 0 to 0.2 m/s). Markers of postural control, including objective sway (trunk sway path, recorded via a sensor attached to vertebrae C7), stepping responses, subjective instability and anxiety ratings were obtained. MRI scans were available for correlations with levels of cerebral small vessel disease in 28 patients and 24 controls. RESULTS: We observed a significant relationship between objective and subjective instability in all groups. The slope of this fit was significantly steeper for patients than controls, indicating greater perceived instability for the same body sway. Stepwise linear regression showed that the slopes of this objective-subjective instability relationship were best explained by concerns about falling (Falls Efficacy Scale-International), clinical physical functioning (Short Physical Performance Battery) and, to some degree, by neuroimaging markers of cerebral small vessel disease. In addition, patients had a reduced stepping threshold, suggesting an overly cautious postural response. CONCLUSION: The distorted perception of instability and subtle impairments in balance control, including abnormal and overly cautious stepping responses, underlies the emergence of ID. It appears to relate to changes in postural performance, psychological functioning and disruption of postural brain networks associated with cerebral small vessel disease.

The Spectrum of Cerebral Small Vessel Disease: Emerging Pathophysiologic Constructs and Management Strategies.

Cerebral small vessel disease (CSVD) is a spectrum of disorders that affect small arterioles, venules, cortical and leptomeningeal vessels, perivascular spaces, and the integrity of neurovascular unit, blood brain barrier, and surrounding glia and neurons. CSVD is an important cause of lacunar ischemic stroke and sporadic hemorrhagic stroke, as well as dementia-which will constitute some of the most substantive population and public health challenges over the next century. This article provides an overview of updated pathophysiologic frameworks of CSVD; discusses common and underappreciated clinical and neuroimaging manifestations of CSVD; and reviews emerging genetic risk factors linked to sporadic CSVD.

Cerebrovascular Effects of Sildenafil in Small Vessel Disease: The OxHARP Trial.

BACKGROUND: Vascular cognitive impairment due to cerebral small vessel disease is associated with cerebral pulsatility, white matter hypoperfusion, and reduced cerebrovascular reactivity (CVR), and is potentially improved by endothelium-targeted drugs such as cilostazol. Whether sildenafil, a phosphodiesterase-5 inhibitor, improves cerebrovascular dysfunction is unknown. METHODS: OxHARP trial (Oxford Haemodynamic Adaptation to Reduce Pulsatility) was a double-blind, randomized, placebo-controlled, 3-way crossover trial after nonembolic cerebrovascular events with mild-moderate white matter hyperintensities (WMH), the most prevalent manifestation of cerebral small vessel disease. The primary outcome assessed the superiority of 3 weeks of sildenafil 50 mg thrice daily versus placebo (mixed-effect linear models) on middle cerebral artery pulsatility, derived from peak systolic and end-diastolic velocities (transcranial ultrasound), with noninferiority to cilostazol 100 mg twice daily. Secondary end points included the following: cerebrovascular reactivity during inhalation of air, 4% and 6% CO2 on transcranial ultrasound (transcranial ultrasound-CVR); blood oxygen-level dependent-magnetic resonance imaging within WMH (CVR-WMH) and normal-appearing white matter (CVR-normal-appearing white matter); cerebral perfusion by arterial spin labeling (magnetic resonance imaging pseudocontinuous arterial spin labeling); and resistance by cerebrovascular conductance. Adverse effects were compared by Cochran Q. RESULTS: In 65/75 (87%) patients (median, 70 years;79% male) with valid primary outcome data, cerebral pulsatility was unchanged on sildenafil versus placebo (0.02, -0.01 to 0.05; P=0.18), or versus cilostazol (-0.01, -0.04 to 0.02; P=0.36), despite increased blood flow (∆ peak systolic velocity, 6.3 cm/s, 3.5-9.07; P<0.001; ∆ end-diastolic velocity, 1.98, 0.66-3.29; P=0.004). Secondary outcomes improved on sildenafil versus placebo for CVR-transcranial ultrasound (0.83 cm/s per mm Hg, 0.23-1.42; P=0.007), CVR-WMH (0.07, 0-0.14; P=0.043), CVR-normal-appearing white matter (0.06, 0.00-0.12; P=0.048), perfusion (WMH: 1.82 mL/100 g per minute, 0.5-3.15; P=0.008; and normal-appearing white matter, 2.12, 0.66-3.6; P=0.006) and cerebrovascular resistance (sildenafil-placebo: 0.08, 0.05-0.10; P=4.9×10-8; cilostazol-placebo, 0.06, 0.03-0.09; P=5.1×10-5). Both drugs increased headaches (P=1.1×10-4), while cilostazol increased moderate-severe diarrhea (P=0.013). CONCLUSIONS: Sildenafil did not reduce pulsatility but increased cerebrovascular reactivity and perfusion. Sildenafil merits further study to determine whether it prevents the clinical sequelae of small vessel disease. REGISTRATION: URL: https://www.clinicaltrials.gov/study/NCT03855332; Unique identifier: NCT03855332.

Pathophysiology of cerebral small vessel disease: a journey through recent discoveries.

Cerebral small vessel disease (cSVD) encompasses a heterogeneous group of age-related small vessel pathologies that affect multiple regions. Disease manifestations range from lesions incidentally detected on neuroimaging (white matter hyperintensities, small deep infarcts, microbleeds, or enlarged perivascular spaces) to severe disability and cognitive impairment. cSVD accounts for approximately 25% of ischemic strokes and the vast majority of spontaneous intracerebral hemorrhage and is also the most important vascular contributor to dementia. Despite its high prevalence and potentially long therapeutic window, there are still no mechanism-based treatments. Here, we provide an overview of the recent advances in this field. We summarize recent data highlighting the remarkable continuum between monogenic and multifactorial cSVDs involving NOTCH3, HTRA1, and COL4A1/A2 genes. Taking a vessel-centric view, we discuss possible cause-and-effect relationships between risk factors, structural and functional vessel changes, and disease manifestations, underscoring some major knowledge gaps. Although endothelial dysfunction is rightly considered a central feature of cSVD, the contributions of smooth muscle cells, pericytes, and other perivascular cells warrant continued investigation.

Association of pulsatility index with total burden of cerebral small vessel disease and cognitive impairment.

OBJECTIVE: This study investigated the correlation between the pulsatility index (PI) of the middle cerebral artery with the total burden of cerebral small vessel disease and cognitive impairment. METHOD: Information on patients hospitalized in the Department of Neurology was collected retrospectively. These patients had complete clinical and laboratory data. The middle cerebral artery PI was measured using transcranial Doppler, a Mini-Mental State Examination (MMSE) was used to assess cognitive function, and the total cerebral small vessel disease burden was assessed using magnetic resonance imaging. Patients were grouped according to their scores for total imaging burden of cerebral small vessel disease and cognitive function. Logistic regression analysis assessed the association between the PI, total imaging burden, and cognitive impairment. Spearman analysis was used to evaluate the correlation between the PI and total imaging burden and cognitive impairment, and receiver operating characteristic (ROC) curves were used to determine the predictive value of the PI for cognitive function. RESULTS: The PI was higher in the cognitive impairment (CI) group than in the no-CI group. Binary logistic regression analysis showed that increased PI was an independent risk factor for CI (OR = 1.582; 95% CI: 1.043-2.401; p = .031) and total imaging burden (OR = 1.842; 95% CI: 1.274-2.663; p = .001). Spearman analysis found that the PI correlated negatively with the MMSE score (r = -.627, p < .001). ROC curve analysis showed the PI predicted CI with an area under the curve of 0.784. The PI combined with the total imaging burden predicted CI in cerebral small vessel disease with an area under the curve of 0.832. CONCLUSION: An increased PI was associated with CI and a high imaging burden in cerebral small vessel disease patients. The PI combined with the total burden score shows a high predictive value for CI.

Analysis of gait pattern related to high cerebral small vessel disease burden using quantitative gait data from wearable sensors.

BACKGROUND AND OBJECTIVES: Sensor-based wearable devices help to obtain a wide range of quantitative gait parameters, which provides sufficient data to investigate disease-specific gait patterns. Although cerebral small vessel disease (CSVD) plays a significant role in gait impairment, the specific gait pattern associated with a high burden of CSVD remains to be explored. METHODS: We analyzed the gait pattern related to high CSVD burden from 720 participants (aged 55-65 years, 42.5 % male) free of neurological disease in the Taizhou Imaging Study. All participants underwent detailed quantitative gait assessments (obtained from an insole-like wearable gait tracking device) and brain magnetic resonance imaging examinations. Thirty-three gait parameters were summarized into five gait domains. Sparse sliced inverse regression was developed to extract the gait pattern related to high CSVD burden. RESULTS: The specific gait pattern derived from several gait domains (i.e., angles, phases, variability, and spatio-temporal) was significantly associated with the CSVD burden (OR=1.250, 95 % CI: 1.011-1.546). The gait pattern indicates that people with a high CSVD burden were prone to have smaller gait angles, more stance time, more double support time, larger gait variability, and slower gait velocity. Furthermore, people with this gait pattern had a 25 % higher risk of a high CSVD burden. CONCLUSIONS: We established a more stable and disease-specific quantitative gait pattern related to high CSVD burden, which is prone to facilitate the identification of individuals with high CSVD burden among the community residents or the general population.

Gait Parameters can Reflect Cognitive Performance in Older Adults with Cerebral Small Vessel Disease: A Cross-sectional Research.

BACKGROUND: Cerebral small vessel disease (CSVD) is a common chronic progressive disease. It remains unclear whether high gait variability is a marker of cognitive cortical dysfunction. METHODS: This study included 285 subjects (aged from 60 to 85 years, 60.3% female) including 37 controls, 179 presented as Fazekas II, and 69 presented as Fazekas III. The severity of white matter hyperintensities was assessed by the Fazekas Rating Scale. Gait parameters were assessed using a vision-based artificial intelligent gait analyzer. Cognitive function was tested by MMSE, MoCA, DST, and VFT. RESULTS: Three gait parameters including gait speed, gait length, and swing time were associated with cognitive performance in patients with CSVD. Gait speed was associated with cognitive performance, including MMSE (ß 0.200; 95%CI 1.706-6.018; p <.001), MoCA (ß 0.183; 95%CI 2.047-7.046; p <.001), DST (order) (ß 0.204; 95%CI 0.563-2.093; p =.001) and VFT (ß 0.162; 95%CI 0.753-4.865; p =.008). Gait length was associated with cognitive performance, including MMSE (ß 0.193; 95%CI 3.475-12.845; p =.001), MoCA (ß 0.213; 95%CI 6.098-16.942; p <.001), DST (order) (ß 0.224; 95%CI 1.056-4.839; P <.001) and VFT (ß 0.149; 95%CI 1.088- 10.114; p =.015). Swing time was associated with cognitive performance, including MMSE (ß - 0.242; 95%CI -2.639 to -0.974; p<.001), MoCA (ß -0.211; 95%CI -2.989 to -1.034; p <.001) and DST (reverse order) (ß -0.140; 95%CI -0.568 to -0.049; p =.020). CONCLUSION: This study revealed that the relationship between gait parameters and cognitive performance in patients with CSVD and the deteriorated gait parameters can reflect cognitive impairment and even dementia in older people with CSVD.

The structural-functional-connectivity coupling of the aging brain.

Aging primarily affects memory and executive functions, a relationship that may be underpinned by the fact that almost all adults over 60 years old develop small vessel disease (SVD). The fact that a wide range of neuropathologies could only explain up to 43% of the variation in age-related cognitive impairment suggests that other factors, such as cognitive reserve, may play a role in the brain's resilience against aging-related cognitive decline. This study aims to examine the relationship between structural-functional-connectivity coupling (SFC), and aging, cognitive abilities and reserve, and SVD-related neuropathologies using a cohort of n = 176 healthy elders from the Harvard Aging Brain Study. The SFC is a recently proposed biomarker that reflects the extent to which anatomical brain connections can predict coordinated neural activity. After controlling for the effect of age, sex, and years of education, global SFC, as well as the intra-network SFC of the dorsolateral somatomotor and dorsal attention networks, and the inter-network SFC between dorsolateral somatomotor and frontoparietal networks decreased with age. The global SFC decreased with total cognitive score. There were significant interaction effects between years of education versus white matter hyperintensities and between years of education versus cerebral microbleeds on inter-network SFC. Enlarged perivascular space in basal ganglia was associated with higher inter-network SFC. Our results suggest that cognitive ability is associated with brain coupling at the global level and cognitive reserve with brain coupling at the inter-functional-brain-cluster level with interaction effect from white matter hyperintensities and cerebral microbleed in a cohort of healthy elderlies.

Exploring the neuroprotective role of physical activity in cerebral small vessel disease.

Cerebral small vessel disease (cSVD) is a common neurological finding characterized by abnormalities of the small blood vessels in the brain. Previous research has established a strong connection between cSVD and stroke, as well as neurodegenerative disorders, notably Alzheimer's disease (AD) and other dementias. As the search for effective interventions continues, physical activity (PA) has emerged as a potential preventative and therapeutic avenue. This review synthesizes the human and animal literature on the influence of PA on cSVD, highlighting the importance of determining optimal exercise protocols, considering aspects such as intensity, duration, timing, and exercise type. Furthermore, the necessity of widening the age bracket in research samples is discussed, ensuring a holistic understanding of the interventions across varying pathological stages of the disease. The review also suggests the potential of exploring diverse biomarkers and risk profiles associated with clinically significant outcomes. Moreover, we review findings demonstrating the beneficial effects of PA in various rodent models of cSVD, which have uncovered numerous mechanisms of neuroprotection, including increases in neuroplasticity and integrity of the vasculature and white matter; decreases in inflammation, oxidative stress, and mitochondrial dysfunction; and alterations in amyloid processing and neurotransmitter signaling. In conclusion, this review highlights the potential of physical activity as a preventive strategy for addressing cSVD, offering insights into the need for refining exercise parameters, diversifying research populations, and exploring novel biomarkers, while shedding light on the intricate mechanisms through which exercise confers neuroprotection in both humans and animal models.

Correlation between Carotid Blood Flow Velocity and Total Magnetic Resonance Imaging Burden of Cerebral Small Vessel Disease in Patients with Recent Small Subcortical Infarcts.

BACKGROUND: The common and internal carotid arteries are the upstream vessels of the small cerebral vessels. The relationship between hemodynamic changes in the significant cervical vessels and cerebral small vessel disease (CSVD) remains uncertain. This research sought to analyze the correlation between carotid blood flow velocity and the total magnetic resonance imaging (MRI) burden of CSVD in patients with recent small subcortical infarcts (RSSIs). METHODS: Data were gathered from individuals diagnosed with RSSIs admitted to Changzhou Second People's Hospital between January 2022 and June 2023. Brain MRI was performed on every patient to determine the overall MRI burden of CSVD, along with carotid duplex ultrasound to evaluate carotid blood flow velocity and pulsatility index (PI) of the common carotid (CCA) and internal carotid (ICA) arteries. The association between carotid blood flow velocity and the total MRI load of CSVD was examined using univariate and multivariate analyses. RESULTS: For our investigation, 272 individuals with RSSIs were screened. 82 individuals had a moderate to severe load of CSVD, while 190 participants showed a mild burden. Patients with moderate to severe burden of CSVD had lower end-diastolic velocity (EDV) and higher PI in CCA and ICA than those with mild load (P < 0.001). After adjusting for variables like age, hypertension, systolic blood pressure, and blood homocysteine levels, multivariate logistic regression analysis showed that EDV in CCA (OR, 0.894; P = 0.011), PI in CCA (OR, 5.869; P = 0.017), EDV in ICA (OR, 0.909; P = 0.008), and PI in ICA (OR, 5.324; P = 0.041) were independently related to moderate to severe CSVD burden. Spearman correlation analysis showed that EDV in CCA and ICA was negatively related to the total MRI load of CSVD in patients with RSSIs (P < 0.001). PI in CCA and ICA was positively associated with the whole MRI load of CSVD (P < 0.001). CONCLUSION: Low carotid blood flow velocity and high carotid pulsatility index are independently associated with moderate to severe burden of CSVD.

Effects of Cilostazol and Isosorbide Mononitrate on Cerebral Hemodynamics in the LACI-1 Randomized Controlled Trial.

BACKGROUND AND PURPOSE: Cerebral small vessel disease-a major cause of stroke and dementia-is associated with cerebrovascular dysfunction. We investigated whether short-term isosorbide mononitrate (ISMN) and cilostazol, alone or in combination, improved magnetic resonance imaging-measured cerebrovascular function in patients with lacunar ischemic stroke. METHODS: Participants were randomized to ISMN alone, cilostazol alone, both ISMN and cilostazol, or no medication. Participants underwent structural, cerebrovascular reactivity (to 6% carbon dioxide) and phase-contrast pulsatility magnetic resonance imaging at baseline and after 8 weeks of medication. RESULTS: Of 27 participants (mean age, 68±7.7; 44% female), 22 completed cerebrovascular reactivity and pulsatility imaging with complete datasets. White matter cerebrovascular reactivity increased in the ISMN (ß=0.021%/mm Hg [95% CI, 0.003-0.040]) and cilostazol (ß=0.035%/mm Hg [95% CI, 0.014-0.056]) monotherapy groups and in those taking any versus no medication (ß=0.021%/mm Hg [95% CI, 0.005-0.037]). CONCLUSIONS: While limited by small sample size, we demonstrate that measuring cerebrovascular function with magnetic resonance imaging is feasible in clinical trials and that ISMN and cilostazol may improve cerebrovascular function. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT02481323. URL: www.isrctn.com; Unique identifier: ISRCTN12580546. URL: www.clinicaltrialsregister.eu; Unique identifier: EudraCT 2015-001953-33.

Impaired dynamic cerebral autoregulation is associated with the severity of neuroimaging features of cerebral small vessel disease.

AIMS: Cerebral small vessel disease (CSVD) is characterized by functional and structural changes in small vessels. We aimed to elucidate the relationship between dynamic cerebral autoregulation (dCA) and neuroimaging characteristics of CSVD. METHODS: A case-control study was performed. Cerebral blood flow velocity (CBFV) of bilateral middle cerebral arteries and spontaneous arterial blood pressure were simultaneously recorded. Transfer function analysis was used to calculate dCA parameters (phase, gain, and the rate of recovery of CBFV [RoRc]). Neuroimaging characteristics of CSVD patients were evaluated, including lacunes, white matter hyperintensities (WMH), cerebral microbleeds (CMBs), perivascular spaces (PVS), and the total CSVD burden. RESULTS: Overall, 113 patients and 83 controls were enrolled. Compared with the control group, the phase at low frequency and the RoRc in CSVD patients were lower, and the gain at very low and low frequencies were higher, indicating bilaterally impaired dCA. Total CSVD burden, WMH (total, periventricular and deep), severe PVS, and lobar CMBs were independently correlated with the phase at low frequency. CONCLUSIONS: Our findings suggested that dCA was compromised in CSVD patients, and some specific neuroimaging characteristics (the total CSVD burden, WMH, severe PVS and lobar CMBs) might indicate more severe dCA impairment in CSVD patients.

Cerebral small vessel disease phenotype and 5-year mortality in asymptomatic middle-to-old aged individuals.

The present study aimed to determine whether a recently proposed cerebral small vessel disease (CSVD) classification scheme could differentiate the 5-year all-cause mortality in middle-to-old aged asymptomatic CSVD. Stroke-free and non-demented participants recruited from the community-based I-Lan Longitudinal Aging Study underwent baseline brain magnetic resonance imaging (MRI) between 2011 and 2014 and were followed-up between 2018 and 2019. The study population was classified into control (non-CSVD) and CSVD type 1-4 groups based on MRI markers. We determined the association with mortality using Cox regression models, adjusting for the age, sex, and vascular risk factors. A total of 735 participants were included. During a mean follow-up of 5.7 years, 62 (8.4%) died. There were 335 CSVD type 1 (57.9 ± 5.9 years), 249 type 2 (65.6 ± 8.1 years), 52 type 3 (67.8 ± 9.2 years), and 38 type 4 (64.3 ± 9.0 years). Among the four CSVD types, CSVD type 4 individuals had significantly higher all-cause mortality (adjusted hazard ratio = 5.0, 95% confidence interval 1.6-15.3) compared to controls. This novel MRI-based CSVD classification scheme was able to identify individuals at risk of mortality at an asymptomatic, early stage of disease and might be applied for future community-based health research and policy.

White Matter but not Gray Matter Volumes Are Associated with Cognition in Community-Dwelling Chinese Populations.

BACKGROUND: Few studies have investigated the association between cognition and brain volume associated with cerebral small vessel disease (CSVD). OBJECTIVE: We investigated the association between cognition and brain volume and neuroimaging markers of CSVD in a community-dwelling population. METHODS: Participants (n = 993, age≥35 years) from the community-based Shunyi Study were included to investigate the association between neuroimaging markers and cognition cross-sectionally. Magnetic resonance imaging markers included brain volume measurements of the total cerebrum, white matter, gray matter, and CSVD imaging markers. Cognitive performance was assessed using neuropsychological tests of the Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), Fuld Object Memory, digit span, Trail Making Test (TMT)-A, and TMT-B. RESULTS: For brain volume measurement, subcortical white matter fraction was positively associated with MMSE score (ß= 0.034, p = 0.0062) and MoCA score (ß= 0.034, p = 0.0174), and negatively associated with TMT-A and TMT-B completion time (ß= -2.319, p = 0.0002; ß= -2.827, p = 0.0073, respectively). For evaluation of CSVD imaging markers, the presence of lacunes was positively associated with TMT-B completion time (ß= 17.241, p = 0.0028). CONCLUSION: In community-dwelling populations, reduced white matter volumes, as a consequence of aging and vascular damage, are associated with worse global cognition and executive function. Our findings provide potential insights into the correlation between cognition and CSVD-associated subcortical white matter injury.

Altered Functional Connectivity Patterns of Parietal Subregions Contribute to Cognitive Dysfunction in Patients with White Matter Hyperintensities.

BACKGROUND: The white matter hyperintensities (WMHs) are considered as one of the core neuroimaging findings of cerebral small vessel disease and independently associated with cognitive deficit. The parietal lobe is a heterogeneous area containing many subregions and play an important role in the processes of neurocognition. OBJECTIVE: To explore the relationship between parietal subregions alterations and cognitive impairments in WHMs. METHODS: Resting-state functional connectivity (rs-FC) analyses of parietal subregions were performed in 104 right-handed WMHs patients divided into mild (n = 39), moderate (n = 37), and severe WMHs (n = 28) groups according to the Fazekas scale and 36 healthy controls. Parietal subregions were defined using tractographic Human Brainnetome Atlas and included five subregions for superior parietal lobe, six subregions for inferior parietal lobe (IPL), and three subregions for precuneus. All participants underwent a neuropsychological test battery to evaluate emotional and general cognitive functions. RESULTS: Differences existed between the rs-FC strength of IPL_R_6_2 with the left anterior cingulate gyrus, IPL_R_6_3 with the right dorsolateral superior frontal gyrus, and the IPL_R_6_5 with the left anterior cingulate gyrus. The connectivity strength between IPL_R_6_3 and the left anterior cingulate gyrus were correlated with AVLT-immediate and AVLT-recognition test in WMHs. CONCLUSION: We explored the roles of parietal subregions in WMHs using rs-FC. The functional connectivity of parietal subregions with the cortex regions showed significant differences between the patients with WMHs and healthy controls which may be associated with cognitive deficits in WMHs.

Small vessel disease disrupts EEG postural brain networks in 'unexplained dizziness in the elderly'.

OBJECTIVE: To examine the hypothesis that small vessel disease disrupts postural networks in older adults with unexplained dizziness in the elderly (UDE). METHODS: Simultaneous electroencephalography and postural sway measurements were undertaken in upright, eyes closed standing, and sitting postures (as baseline) in 19 younger adults, 33 older controls and 36 older patients with UDE. Older adults underwent magnetic resonance imaging to determine whole brain white matter hyperintensity volumes, a measure of small vessel disease. Linear regression was used to estimate the effect of instability on electroencephalographic power and connectivity. RESULTS: Ageing increased theta and alpha desynchronisation on standing. In older controls, delta and gamma power increased, and theta and alpha power reduced with instability. Dizzy older patients had higher white matter hyperintensity volumes and more theta desynchronisation during periods of instability. White matter hyperintensity volume and delta power during periods of instability were correlated, positively in controls but negatively in dizzy older patients. Delta power correlated with subjective dizziness and instability. CONCLUSIONS: Neural resource demands of postural control increase with age, particularly in patients with UDE, driven by small vessel disease. SIGNIFICANCE: EEG correlates of postural control saturate in older adults with UDE, offering a neuro-physiological basis to this common syndrome.