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Differences in retinal vessels support a distinct vasculopathy causing lacunar stroke.

ABSTRACT: Lacunar stroke is common, but the etiology of the small vessel abnormality is unknown. Retinal vessels share ontogeny, size, and physiologic characteristics with cerebral small vessels, and retinopathy is associated with stroke. We compared retinal microvessel appearance as a surrogate for cerebral small vessels in patients with lacunar and large artery cortical ischemic stroke.We prospectively recruited patients with lacunar ischemic stroke and cortical stroke controls. We took digital retinal photographs of each eye. We assessed central retinal artery equivalent (CRAE) and central retinal vein equivalent (CRVE) diameters and arteriovenous ratios (AVRs) using semiautomated computer software methods and quantified arteriovenous nicking and focal arteriolar narrowing.Among 212 patients (105 lacunar, 107 cortical strokes) of mean age 68 years (SD 12 years), AVR was decreased (0.76 vs 0.78, p = 0.03) and CRVE was increased (44.9 pixels/218 microm vs 42.8 pixels/208 microm, p = 0.01) in lacunar patients compared with cortical patients, but CRAE did not differ (33.2 pixels/161 microm vs 33.7 pixels/163 microm, p = 0.4). On multivariable analysis, increased CRVE was associated with lacunar stroke subtype (p = 0.03) and younger age (p < 0.001) after correcting for other vascular risk factors. Arteriovenous nicking and focal arteriolar narrowing did not differ between ischemic stroke subtypes.Retinal venules are wider and arteriovenous ratios are smaller in patients with lacunar strokes compared with those in patients with cortical strokes.

SUBMITTER: Doubal FN

PROVIDER: S-EPMC2827311 | biostudies-literature | 2009 May

REPOSITORIES: biostudies-literature

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Differences in retinal vessels support a distinct vasculopathy causing lacunar stroke.

Doubal F N FN MacGillivray T J TJ Hokke P E PE Dhillon B B Dennis M S MS Wardlaw J M JM

Neurology 20090501 20

<h4>Background</h4>Lacunar stroke is common, but the etiology of the small vessel abnormality is unknown. Retinal vessels share ontogeny, size, and physiologic characteristics with cerebral small vessels, and retinopathy is associated with stroke. We compared retinal microvessel appearance as a surrogate for cerebral small vessels in patients with lacunar and large artery cortical ischemic stroke.<h4>Methods</h4>We prospectively recruited patients with lacunar ischemic stroke and cortical stroke ...[more]

PMID: 19451533

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Project description:Lacunar strokes are a common type of ischemic stroke. They are associated with long-term disability, but the factors affecting the dynamic of the infarcted lesion and the brain imaging features associated with them, reflective of small vessel disease (SVD) severity, are still largely unknown. We investigated whether the distribution, volume and 1-year evolution of white matter hyperintensities (WMH), one of these SVD features, relate to the extent and location of these infarcts, accounting for vascular risk factors. We used imaging and clinical data from all patients [n = 118, mean age 64.9 (SD 11.75) years old] who presented to a regional hospital with a lacunar stroke syndrome within the years 2010 and 2013 and consented to participate in a study of stroke mechanisms. All patients had a brain MRI scan at presentation, and 88 had another scan 12 months after. Acute lesions (i.e., recent small subcortical infarcts, RSSI) were identified in 79 patients and lacunes in 77. Number of lacunes was associated with baseline WMH volume (B = 0.370, SE = 0.0939, P = 0.000174). RSSI volume was not associated with baseline WMH volume (B = 3.250, SE = 2.117, P = 0.129), but predicted WMH volume change (B = 2.944, SE = 0.913, P = 0.00184). RSSI location was associated with the spatial distribution of WMH and the pattern of 1-year WMH evolution. Patients with the RSSI in the centrum semiovale (n = 33) had significantly higher baseline volumes of WMH, recent and old infarcts, than patients with the RSSI located elsewhere [median 33.69, IQR (14.37 50.87) ml, 0.001 ≤ P ≤ 0.044]. But patients with the RSSI in the internal/external capsule/lentiform nucleus experienced higher increase of WMH volume after a year [n = 21, median (IQR) from 18 (11.70 31.54) ml to 27.41 (15.84 40.45) ml]. Voxel-wise analyses of WMH distribution in patients grouped per RSSI location revealed group differences increased in the presence of vascular risk factors, especially hypertension and recent or current smoking habit. In our sample of patients presenting to the clinic with lacunar strokes, lacunar strokes extent influenced WMH volume fate; and RSSI location and WMH spatial distribution and dynamics were intertwined, with differential patterns emerging in the presence of vascular risk factors. These results, if confirmed in wider samples, open potential avenues in stroke rehabilitation to be explored further.

Project description:Neuroinflammation is believed to be involved in the pathophysiological mechanisms of silent brain infarcts (SBI). However, the immunological profile of SBI has been scarcely investigated. In the context of a national research project named SILENCE, aimed at investigating clinical, biochemical and pathogenic features of SBI, we have measured the plasma profile of some inflammatory-related molecules in SBI patients (n?=?21), patients with recent lacunar infarcts (LI, n?=?28) and healthy controls (n?=?31), consecutively enrolled in four Italian centres. A panel of chemokines (MIG, CTACK, IL16, SDF1a, MCP1), growth factors (SCF, SCGFb, HGF, IL3), immunoglobulin-type adhesion molecules (ICAM1, VCAM1), proinflammatory cytokines (IL18, INFa2, MIF, IL12p40), cell surface receptors on T-cells (IL2Ra), and inductors of apoptosis (TRAIL) was assessed in plasma samples by Luminex xMAP™ technology. Immunological parameters were compared using non-parametric statistics and performance to distinguish SBI and LI was evaluated by receiver operating characteristic (ROC) analysis. Plasma levels of ICAM1 were significantly higher in both SBI and LI patients as compared to controls (SBI?LI>Ctrl). A different trend was observed for IL16 (SBI<LI>Ctrl), SCF (LI<SBI>Ctrl) and SCGFb (SBI>LI<Ctrl). SBI subjects had significantly increased levels of MIG when compared to controls (LI?SBI>Ctrl) and IL18 when compared to LI patients (Ctrl?SBI>LI). All the other immunological markers did not significantly differ among groups. According to ROC analysis, the best predictor for SBI condition was the chemokine MIG (AUC?=?0.84, sensitivity 86%, specificity 77%), while SCF had the best performance in distinguishing LI patients (AUC?=?0.84, sensitivity 86%, specificity 68%). These results confirm the involvement of inflammatory processes in cerebrovascular disorders, particularly in SBI, a very common age-related condition. The differences in plasma profile of inflammatory molecules may underlie different pathological mechanisms in SBI and LI patients.

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Differences in retinal vessels support a distinct vasculopathy causing lacunar stroke.

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Differences in retinal vessels support a distinct vasculopathy causing lacunar stroke.

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