Lacunar Stroke Subtypes Research Articles

Enlarged Perivascular Spaces and Cerebral Small Vessel Disease

Background and aimsEnlarged perivascular spaces (also known as Virchow–Robin spaces) on T2-weighted brain magnetic resonance imaging are common, but their etiology, and specificity to small vessel as opposed to general cerebrovascular disease or ageing, is unclear. We tested the association between enlarged perivascular spaces and ischemic stroke subtype, other markers of small vessel disease, and common vascular risk factors.MethodsWe prospectively recruited patients with acute stroke, diagnosed and subtyped by a stroke physician using clinical features and brain magnetic resonance imaging. A neuroradiologist rated basal ganglia and centrum semiovale enlarged perivascular spaces on a five-point scale, white matter lesions, recent and old infarcts, and cerebral atrophy. We assessed associations between basal ganglia-, centrum semiovale- and total (combined basal ganglia and centrum semiovale) enlarged perivascular spaces, stroke subtype, white matter lesions, atrophy, and vascular risk factors.ResultsAmong 298 patients (mean age 68 years), after adjusting for vascular risk factors and white matter lesions, basal ganglia–enlarged perivascular spaces were associated with increasing age (P = 0·001), centrum semiovale–enlarged perivascular spaces (P < 0·001), cerebral atrophy (P = 0·03), and lacunar stroke subtype (P = 0·04). Centrum semiovale–enlarged perivascular spaces were associated mainly with basal ganglia–enlarged perivascular spaces. Total enlarged perivascular spaces were associated with increasing age (P = 0·01), deep white matter lesions (P = 0·005), and previous stroke (P = 0·006).ConclusionsEnlarged perivascular spaces are associated with age, lacunar stroke subtype and white matter lesions and should be considered as another magnetic resonance imaging marker of cerebral small vessel disease. Further evaluation of enlarged perivascular spaces in studies of ageing, stroke, and dementia is needed to determine their pathophysiological importance.

Effect of Prestroke Use of Angiotensin-Converting Enzyme Inhibitors Alone Versus Combination With Antiplatelets and Statin on Ischemic Stroke Outcome

Angiotensin-converting enzyme inhibitors (ACEIs), antiplatelets (APs), and statin are increasingly being prescribed for ischemic stroke prevention. The objective of the study was to examine whether previous combination therapy of ACEI with AP and/or statin has additive effect compared with ACEI alone on functional outcome after ischemic stroke. Furthermore, factors associated with improving functional outcome were investigated. Ischemic stroke patients attending a Malaysian hospital in 2008 were categorized according to Barthel Index at discharge. Favorable outcome was defined as Barthel Index of 75 or greater. Data included demographic information, clinical characteristics, and previous medications with particular attention to ACEI, AP, and statin. Overall, 505 patients were included. Variables associated with good functional outcome were younger age (P = 0.002), first-ever attack (P = 0.016), lacunar (P = 0.015) or posterior circulation infarct stroke subtype (P = 0.034), minor Glasgow Coma Scale (P < 0.001), and previous use of ACEI alone or combined with AP and/or statin (P = 0.002). Using ACEI alone as the reference for ACEI + AP, ACEI + statin, or ACEI + AP + statin combinations, there was no significant difference among combinations on improving functional outcome (P = 0.852). Prestroke use of ACEI either alone or combined with AP and/or statin was associated with better functional outcome. Previous use of ACEI in combination with AP and/or statin did not significantly differ from ACEI alone in their effect on outcome. Our study provides a potential rationale for optimizing the use of ACEI among individuals at risk of developing ischemic stroke.

Infarctions in the vascular territory of the posterior cerebral artery: clinical features in 232 patients

BackgroundIschemic stroke caused by infarction in the territory of the posterior cerebral artery (PCA) has not been studied as extensively as infarctions in other vascular territories. This single centre, retrospective clinical study was conducted a) to describe salient characteristics of stroke patients with PCA infarction, b) to compare data of these patients with those with ischaemic stroke due to middle cerebral artery (MCA) and anterior cerebral artery (ACA) infarctions, and c) to identify predictors of PCA stroke.FindingsA total of 232 patients with PCA stroke were included in the "Sagrat Cor Hospital of Barcelona Stroke Registry" during a period of 19 years (1986-2004). Data from stroke patients are entered in the stroke registry following a standardized protocol with 161 items regarding demographics, risk factors, clinical features, laboratory and neuroimaging data, complications and outcome. The characteristics of these 232 patients with PCA stroke were compared with those of the 1355 patients with MCA infarctions and 51 patients with ACA infarctions included in the registry.Infarctions of the PCA accounted for 6.8% of all cases of stroke (n = 3808) and 9.6% of cerebral infarctions (n = 2704). Lacunar infarction was the most frequent stroke subtype (34.5%) followed by atherothrombotic infarction (29.3%) and cardioembolic infarction (21.6%). In-hospital mortality was 3.9% (n = 9). Forty-five patients (19.4%) were symptom-free at hospital discharge. Hemianopia (odds ratio [OR] = 6.43), lacunar stroke subtype (OR = 2.18), symptom-free at discharge (OR = 1.92), limb weakness (OR = 0.10), speech disorders (OR = 0.33) and cardioembolism (OR = 0.65) were independent variables of PCA stroke in comparison with MCA infarction, whereas sensory deficit (OR = 2.36), limb weakness (OR = 0.11) and cardioembolism as stroke mechanism (OR = 0.43) were independent variables associated with PCA stroke in comparison with ACA infarction.ConclusionsLacunar stroke is the main subtype of infarction occurring in the PCA territory. Several clinical features are more frequent in stroke patients with PCA infarction than in patients with ischaemic stroke due to infarction in the MCA and ACA territories. In-hospital mortality in patients with PCA territory is low.

Clopidogrel vs. Aspirin Treatment on Admission Improves 5-Year Survival After a First-ever Acute Ischemic Stroke. Data from the Athens Stroke Outcome Project

Background and Aims We undertook this study to compare the impact of aspirin vs. clopidogrel treatment on 5-year survival of patients experiencing a first-ever acute ischemic noncardioembolic stroke. Methods This was a retrospective study involving patients with an acute ischemic stroke who had an indication for antiplatelet therapy (atherothrombotic, lacunar and cryptogenic stroke subtype). A total of 1228 (383 women) hospitalized due to an acute first-ever stroke and receiving aspirin ( n = 880) or clopidogrel ( n = 348) were finally involved. To determine the factors that independently predict 5-year survival statistical analysis including the Kaplan-Meier survival curve and multifactorial analysis (Cox regression) was performed. Results Subjects treated with clopidogrel had improved 5-year survival compared with those receiving aspirin (log rank test: 16.4, p <0.0001). The difference in survival was evident as early as 6 months from index stroke: cumulative survival 93.8% for aspirin vs. 97% for clopidogrel (log rank test: 4.01, p = 0.045). The composite cardiovascular event (including stroke recurrence, myocardial infarction, unstable angina, coronary revascularization, aortic aneurysm rupture, peripheral atherosclerotic artery diseases, and sudden death) rates were lower in the clopidogrel group ( n = 60, 17.2%) compared with the aspirin ( n = 249, 28.3%) group (log rank test: 12.4, p <0.0001). This preferential effect of clopidogrel over aspirin was independent of age, gender, presence of cardiovascular disease other than stroke or cardiovascular risk factors as well as irrespective of the severity of stroke and days of hospitalization. Conclusions This study supports that clopidogrel is superior to aspirin in preventing death and cardiovascular events after an acute noncardioembolic ischemic stroke.

Family History of Stroke Is an Independent Risk Factor for Lacunar Stroke Subtype With Asymptomatic Lacunar Infarcts at Younger Ages

Results from case-control and case-case studies indicate that a positive family history of stroke (FHstroke) is an independent risk factor for lacunar stroke. Different lacunar stroke phenotypes can be distinguished on the basis of the presence of asymptomatic lacunar infarcts (aLACs), ischemic white-matter lesions, or brain microbleeds. The aim of the present study was to determine whether familial aggregation of stroke was different for lacunar stroke phenotypes. In 157 patients with a first-ever lacunar stroke, a complete first-degree FHstroke was obtained by a standardized questionnaire and additional interview. Lacunar stroke patients were categorized successively into groups, depending on the presence of aLACs, ischemic white-matter lesions, and brain microbleeds on magnetic resonance imaging. Fifty-two percent of patients reported a positive FHstroke in at least one of their first-degree relatives. In younger (<65 years) probands, a high frequency of parental FHstroke (59% versus 20%, P<0.01) in those with aLACs compared with probands without aLACs was found. In multivariate analysis, the strongest associations were found for parental FHstroke (odds ratio=6.46; 95% CI=1.96 to 21.33), maternal FHstroke (odds ratio=4.00; 95% CI=1.18 to 13.56), and paternal FHstroke (odds ratio=5.40; 95% CI=1.14 to 25.61). A family history of stroke might be an independent risk factor for the lacunar stroke phenotype with aLACs at younger ages, suggesting a role for genetic factors in this phenotype caused by diffuse vasculopathy.

Letter by Tsuda Regarding Article “Endothelial Activation in Lacunar Stroke Subtypes”

To the Editor: We read with great interest the recent article by Knottnerus et al1 dealing with the relationship between endothelial activation and lacunar stroke subtypes. The results of their study demonstrated that tissue plasmonogen activator activity, a circulating blood marker of endothelial function, was increased in patients with white matter lesions (WML); WML is a subtpe of lacunar stroke caused by a diffuse small vessel disease. In addition, it was demonstrated that plasmonogen activator inhibitor type 1 antigen levels were lowest in patients with WML. The authors propose that differences in the activity of components of the fibrinolytic system might contribute to WML development in lacunar stroke. Numerous studies have focused on …

Response to Letter Regarding Article “Endothelial Activation in Lacunar Stroke Subtypes”

Response: We thank Dr Tsuda for his comments on our article in the August 2010 issue of Stroke regarding the hemostasis-related endothelial markers in first-ever lacunar stroke patients.1 First, Dr Tsuda points to the relation between the endogenous nitric oxide inhibitor asymmetrical dimethylarginine and cerebral small vessel disease, in particular in relation with ischemic white matter lesions.2 In our study, we evaluated endothelial function by measuring levels of hemostasis-related proteins normally excreted by the endothelium, and …

Retinal Arteriolar Geometry is Associated with Cerebral White Matter Hyperintensities on Magnetic Resonance Imaging

BackgroundCerebral small vessel disease (lacunar stroke and cerebral white matter hyperintensities) is caused by vessel abnormalities of unknown aetiology. Retinal vessels show developmental and pathophysiological similarities to cerebral small vessels and microvessel geometry may influence vascular efficiency.HypothesisRetinal arteriolar branching angles or coefficients (the ratio of the sum of the cross-sectional areas of the two daughter vessels to the cross-sectional area of the parent vessel at an arteriolar bifurcation) may be associated with cerebral small vessel disease.MethodsWe performed a cross-sectional observational study in a UK tertiary referral hospital. An experienced stroke physician recruited consecutive patients presenting with lacunar ischaemic stroke with a control group consisting of patients with minor cortical ischaemic stroke. We performed brain magnetic resonance imaging to assess the recent infarct and periventricular and deep white matter hyperintensities. We subtyped stroke with clinical and radiological findings. We took digital retinal photographs to assess retinal arteriolar branching coefficients and branching angles using a semi-automated technique.ResultsTwo hundred and five patients were recruited (104 lacunar stroke, 101 cortical stroke), mean age 68-years (standard deviation 12). With multivariate analysis, increased branching coefficient was associated with periventricular white matter hyperintensities (P=0·006) and ischaemic heart disease (P<0·001), and decreased branching coefficient with deep white matter hyperintensities (P=0·003), but not with lacunar stroke subtype (P=0·96). We found no associations with retinal branching angles.ConclusionsRetinal arteriolar geometry differs between cerebral small vessel phenotypes. Further research is needed to ascertain the clinical significance of these findings.

Fractal analysis of retinal vessels suggests that a distinct vasculopathy causes lacunar stroke

Lacunar strokes account for 25% of all ischemic strokes and may represent the cerebral manifestation of a systemic small vessel vasculopathy of unknown etiology. Altered retinal vessel fractal dimensions may act as a surrogate marker for diseased cerebral vessels. We used a cross-sectional study to investigate fractal properties of retinal vessels in lacunar stroke. We recruited patients presenting with lacunar stroke and patients with minor cortical stroke as controls. All patients were examined by a stroke expert and had MRI at presentation. Digital retinal photographs were taken of both eyes. Monofractal and multifractal analyses were performed with custom-written semiautomated software. We recruited 183 patients. Seventeen were excluded owing to poor photographic quality, leaving 166 patients (86 with lacunar and 80 with cortical stroke). The mean age was 67.3 years (SD 11.5 years). The patients with lacunar stroke were younger but the prevalence of diabetes, hypertension, and white matter hyperintensities did not differ between the groups. The mean Dbox (monofractal dimension) was 1.42 (SD 0.02), the mean D0 (multifractal dimension) 1.67 (SD 0.03). With multivariate analysis, decreased Dbox and D0 (both representing decreased branching complexity) were associated with increasing age and lacunar stroke subtype after correcting for hypertension, diabetes, stroke severity, and white matter hyperintensity scores. Lacunar stroke subtype and increasing age are associated with decreased fractal dimensions, suggesting a loss of branching complexity. Further studies should concentrate on longitudinal associations with other manifestations of cerebral small vessel disease.

Differing Risk Factor Profiles of Ischemic Stroke Subtypes

Differences in risk factor profiles between lacunar and other ischemic stroke subtypes may provide evidence for a distinct lacunar arteriopathy, but existing studies have limitations. We overcame these by pooling individual data on 2875 patients with first-ever ischemic stroke from 5 collaborating prospective stroke registers that used similar, unbiased methods to define risk factors and classify stroke subtypes. We compared risk factors between lacunar and nonlacunar ischemic strokes, altering the comparison groups in sensitivity analyses, and incorporated these data into a meta-analysis of published studies. Unadjusted and adjusted analyses gave similar results. We found a lower prevalence of cardioembolic source (adjusted odds ratio, 0.33; 95% CI, 0.24 to 0.46), ipsilateral carotid stenosis (odds ratio, 0.21; 95% CI, 0.14 to 0.30), and ischemic heart disease (odds ratio, 0.75; 95% CI, 0.58 to 0.97) in lacunar compared with nonlacunar patients but no difference for hypertension, diabetes, or any other risk factor studied. Results were robust to sensitivity analyses and largely confirmed in our meta-analysis. Hypertension and diabetes appear equally common in lacunar and nonlacunar ischemic stroke, but lacunar stroke is less likely to be caused by embolism from the heart or proximal arteries, and the lower prevalence of ischemic heart disease in lacunar stroke provides additional support for a nonatherosclerotic arteriopathy causing many lacunar ischemic strokes. Our findings have implications for how clinicians classify ischemic stroke subtypes and highlight the need for additional research into the specific causes of and treatments for lacunar stroke.

Enlarged Perivascular Spaces on MRI Are a Feature of Cerebral Small Vessel Disease

Enlarged perivascular spaces in the brain are common but generally overlooked and of uncertain pathophysiology. They may reflect underlying cerebral small vessel disease. We determined whether enlarged perivascular spaces were associated with lacunar stroke subtype and white matter hyperintensities, markers of established small vessel disease. We prospectively recruited patients with acute ischemic lacunar or cortical stroke. Age-matched nonstroke control subjects were also recruited. We rated basal ganglia and centrum semiovale enlarged perivascular spaces 0 to 4 (0=none, 4=>40) on T2-weighted MRI and white matter hyperintensities. We compared enlarged perivascular spaces between stroke subtypes and control subjects and assessed associations with vascular risk factors and white matter hyperintensities. We recruited 350 patients; 129 lacunar, 124 cortical stroke, and 97 age-matched control subjects. Adjusting for vascular risk factors and white matter hyperintensities, total enlarged perivascular spaces were associated with lacunar stroke subtype (P=0.04) in the acute stroke group (n=253); basal ganglia enlarged perivascular spaces were associated with lacunar stroke subtype (P=0.003), deep (P=0.02) and periventricular white matter hyperintensities (P=0.01); in all 350 subjects, total enlarged perivascular spaces were associated with deep (P<0.001) and periventricular (P<0.001) white matter hyperintensities. Although prevalent in patients with vascular risk factors and stroke, enlarged perivascular spaces are specifically associated with lacunar ischemic stroke and white matter hyperintensities. Further studies should determine the mechanism of this association while including adequate controls to account for stroke and vascular risk factors. Enlarged perivascular spaces should not be overlooked in studies of small vessel disease.

Differences in retinal vessels support a distinct vasculopathy causing lacunar stroke

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.

Lupus anticoagulants and anti-phospholipid antibodies as risk factors for a first episode of ischemic stroke.

Antiphospholipid antibodies (aPLA) and lupus anticoagulant (LAC) were shown to precipitate thromboembolic events. Their association with ischemic stroke remains to be seen. We investigated the contribution of LAC, and antibodies directed against the phospholipids cardiolipin (aCL), phosphatidylserine (aPS), and the phospholipid-dependent cofactors beta2-glycoprotein I and annexin V, to the risk for ischemic stroke. LAC and antibody levels were measured in 208 stroke patients and 203 age- and gender-matched control subjects. Positive LAC resulted in an increased risk for stroke [OR (95% CI) = 8.1 (2.4-27.5)]. Significant elevation in aPS IgG, aCL IgM and aCL IgG titers, and increased prevalence of elevated aPS IgG, aCL IgM and aCL IgG (based on P95 cutoff values of healthy individuals) were seen in patients. aPS IgG was associated with cardioembolic, whereas aCL IgG and IgM were elevated in lacunar, atherosclerotic and cardioembolic, and LAC positivity was documented only in lacunar stroke subtypes. The co-presence of LAC with a positive aCL IgM/IgG or aPS IgG did not affect the overall risk for stroke. Multivariate analysis confirmed the association of positive LAC with stroke [aOR (95% CI) = 9.7 (1.8-52.5)], and demonstrated a clear gradation of increasing risk of stroke associated with the four categories of aCL IgG and aPS IgG, and identified aCL IgM P95 as independent predictors of stroke after adjusting for potentially confounding covariates. Our study demonstrates that the presence of LAC, and elevated aCL IgG and aPS IgG antibodies are risk factors for stroke.

A SELDI-TOF-MS Study in Lacunar Stroke with Subsequent Haptoglobin Phenotyping

Using Surface-Enhanced Laser Desorption / Ionization Time-of-Flight Mass Spectrometry (SELDI-TOF-MS), we aimed to detect differences in protein profile in serum samples of two lacunar stroke subtypes. SELDI-TOF-MS, followed by protein identification, was performed in samples of 8 first-ever lacunar stroke patients with MR imaging showing a single symptomatic lacunar lesion (type 1), and 8 with multiple additional "silent" lacunar lesions and extensive white matter lesions (type 2). A 16 kDa protein, identified as alpha-2-chain of haptoglobin (Hp), was found to be overrepresented in type 1 compared to type 2 (peak intensity 12.5 vs. 5.0; p=0.02). As a polymorphism with two alleles, Hp-1 and Hp 2, determines the presence of alpha-1 and/or alpha-2-chains in the Hp-molecule, Hp phenotypic analysis was performed. Hp 1 : Hp-2 allele frequency was 0.562 : 0.438 in type 1 and 0.812 : 0.188 in type 2 (population reference approximately 0.4 : 0.6). We conclude that the overrepresentation of the alpha-2-chain in lacunar stroke type 1 compared to type 2 relates to a higher Hp-2 allele frequency in the former. Yet, compared to population reference, the phenotype distribution in both patient groups deviates towards a high Hp-1 allele frequency. Our findings suggest a role for the Hp gene in the etiology of cerebral small vessel disease. Larger studies are now needed to explore this new candidate gene.

Changes in Background Blood–Brain Barrier Integrity Between Lacunar and Cortical Ischemic Stroke Subtypes

Lacunar stroke is associated with endothelial dysfunction and histologically with intrinsic cerebral microvascular disease of unknown cause. Endothelial dysfunction could impair blood-brain barrier integrity. We assessed background blood-brain barrier leakage in patients with lacunar ischemic stroke compared with cortical stroke controls. We recruited patients with lacunar or mild cortical ischemic stroke and assessed generalized cerebral blood-brain barrier leak with MRI and intravenous gadolinium at least 1 month after stroke. We used detailed image processing to compare signal change before and for 30 minutes postcontrast throughout gray matter, white matter, and cerebrospinal fluid with summary analyses and general linear modeling. Among 48 patients (29 lacunar, 19 cortical), postcontrast enhancement was significantly higher in cerebrospinal fluid (P=0.04, Mann-Whitney U), and nonsignificantly higher in white matter, in lacunar than in cortical strokes, with no difference in gray matter. General linear modeling confirmed significantly greater postcontrast enhancement in cerebrospinal fluid in lacunar patients than in cortical controls (t=3.37, P<0.0008). These preliminary data suggest that the blood-brain barrier may be dysfunctional throughout subcortical white matter (white matter drains via interstitial spaces to cerebrospinal fluid) in patients with lacunar stroke. Further studies are required to confirm these findings and determine whether abnormal blood-brain barrier might predate development of lacunar disease. Blood-brain barrier dysfunction may be an important mechanism for brain damage in cerebral microvascular disease.

Differences in Long-Term Survival in Two Lacunar Stroke Types: A 15-Year Follow-Up Study in 782 Cerebral Infarct Patients

Background: Mortality studies in lacunar (LAC) stroke are scarce and often characterized by short follow-up time, small patient groups and absence of a nonlacunar stroke group for comparison. Besides, there are no separate long-term prognostic data on LAC stroke subtypes. We performed a long-term mortality study in LAC stroke, subtyping two distinct phenotypes and including nonlacunar ischemic stroke for comparison. Methods: We performedcross-sectional follow-up, determining survival status, after a median of 15.0 years, in 333 first-ever atherothrombotic (AT), 184 cardioembolic (CE) and 265 LAC strokes, distinguishing LAC stroke with (type 2) or without (type 1) asymptomatic LAC lesions on CT. Results: End of follow-up mortality (in 30-day survivors) in LAC stroke (76.2%) was significantly lower than in CE (87.1%; OR 0.48, 95% CI 0.27–0.84), but not AT strokes (79.0%; OR 0.85, 95% CI 0.57–1.26), and was significantly lower in LAC type 1 than type 2 strokes (70.9 vs. 87.5%; OR 0.35, 95% CI 0.17–0.73). Kaplan-Meier analysis showed most favorable survival in LAC type 1 stroke. In the Cox regression analyses, LAC type 1 strokeappearedas an independent predictor of better survival versus LAC type 2, versus AT and versus CE strokes. Conclusions: LAC stroke in general cannot be considered a ‘benign’ stroke type: only long-term survival in patients without concomitant asymptomatic LAC lesions is better than in large-vessel stroke. This difference in long-term survival between the two LAC stroke subtypes should be taken into account in prognostic counselling of individual LAC stroke patients.

Trends in post-stroke functional independence over a 5-year period: A pilot study

The aim of this pilot study was to identify trends in functional independence over time in community-dwelling stroke survivors. This community-based, follow-up study examined 75 community-dwelling, ischaemic stroke survivors in Newcastle, Australia. Post-stroke functioning was assessed using the Modified Rankin Scale (MRS) in stroke sub-type categories using the Oxfordshire Community Stroke Project Classification. Ischaemic stroke survivors who were discharged with a dependent level of functioning after first-ever stroke were shown to have a 54% chance of achieving independence if they survived up to 5 years in the community. Survivors with lacunar infarction and posterior circulation infarction stroke sub-types were the most likely to achieve independence.

Diabetic and non-diabetic subjects with ischemic stroke: Differences, subtype distribution and outcome

Background and aim Diabetes mellitus increases the risk of stroke, and pathophysiological changes of diabetic cerebral vessels may differ in comparison with non-diabetic ones; nonetheless, the clinical and prognostic profile of stroke in diabetic patients is not yet fully understood. On this basis, the aim of our study was to evaluate cerebrovascular risk factor prevalence in diabetic stroke patients in comparison with non-diabetics, to analyze whether diabetics have a different prevalence of stroke subtypes as classified by the TOAST classification, and determine whether diabetics and non-diabetics have a different prognosis. Methods and results We enrolled 102 diabetics and 204 non-diabetic subjects with acute ischemic stroke, matched by sex and age (± 3 years). We used as outcome indicators the Scandinavian Stroke Scale (SSS) score at admission and the modified Rankin disability scale at discharge and at a 6-month follow-up. We classified ischemic stroke according to the TOAST classification. Diabetes was associated with lacunar ischemic stroke subtype, with a record of hypertension, and with a better SSS score at admission. The association of diabetes with lacunar stroke remained significant even after adjustment for hypertension or for large artery atherosclerotic and cardioembolic stroke subtypes. Conclusion Our study shows some significant differences in acute ischemic stroke among diabetics in comparison with non-diabetics (higher frequency of hypertension, higher prevalence of lacunar stroke subtype, lower neurological deficit at admission in diabetics).

Are Mood Disorders a Stroke Risk Factor?

See related article, pages 16–21 A growing body of evidence suggests that biological mechanisms underlie a bidirectional link between depression and many neurological illnesses, and that mood disorders can affect the course of the diseases.1 Depression commonly occurs after a stroke, with an estimated prevalence as high as 30% in the first year after the event.2 It is well known that poststroke depression affects quality of life, functional recovery, cognitive function and health care use in stroke survivors.3 Inversely, does any association exist between a history of a previous affective disorder and future risk of cardiovascular events? Recent prospective studies have shown an association between depression and incidence of hypertension,4,5 coronary heart disease,6,7 and cardiovascular mortality.8–11 In the Multiple Risk Factor Intervention Trial, 12 866 men were followed for 18 years; those with greater depressive symptoms, as measured by the Center for Epidemiologic Studies Depression Scale (CES-D), were associated with a significant higher risk of cardiovascular mortality (hazard ratio=1.21; 95% CI, 1.03 to 1.41; P <0.05) and stroke mortality (hazard ratio= 2.03; 95% CI, 1.20 to 3.44; P <0.01).12 The NHANES I Epidemiologic Study13 showed that individuals reporting 5 or more symptoms of depression at baseline were 50% more likely to die of a stroke-related cause during a 29-year follow-up. The Baltimore Epidemiologic Catchment Area Study showed that individuals with a history of depressive disorder, measured with the diagnostic interview schedule, were 2.6 times more likely to report stroke.14 Depressive symptoms, measured by the Zung Self-rating Depression Scale, were also associated with an increased incidence of ischemic stroke in a Japanese 10-year follow study.15 Self-reported depression scores significantly predicted stroke in an Australian cohort of people …

Cerebral Microbleeds Are Associated With Lacunar Stroke Defined Clinically and Radiologically, Independently of White Matter Lesions

Associations among microbleeds, white matter lesions (WMLs), and small deep infarcts on imaging have been reported. Because many of these imaging infarcts were asymptomatic, the relationship of microbleeds to clinical lacunar stroke is unclear. An association between microbleeds and clinically defined lacunar stroke might suggest a common causal microangiopathy. Patients with lacunar, partial anterior circulation or posterior circulation stroke syndromes and older healthy subjects underwent MRI. Microhemorrhages, infarcts, hemorrhages, and WMLs were coded blind to clinical details. A final clinicoradiologic stroke subtype diagnosis was assigned. Among 308 subjects (67 older healthy and 241 with stroke), 54 patients had microbleeds (17%). Microbleeds were twice as frequent in lacunar than cortical strokes (26% versus 13%, P=0.03) or healthy older subjects (9%) and associated with increasing WML scores (P<0.0001). Lacunar and cortical stroke subtypes and healthy older subjects had similar WML scores. Microbleeds are associated with lacunar stroke defined clinicoradiologically more than other stroke subtypes but not simply by association with WMLs. This suggests that microbleeds and lacunar stroke have a similar microvascular abnormality.