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Lacunar infarcts represent a stroke subgroup with controversial risk factors. Lacunar syndromes may be divided into two groups: the classic group (pure motor hemiplegia, pure sensory stroke, ataxic hemiparesis, dysarthria-clumsy hand syndrome, sensorimotor stroke) and the miscellaneous group including all other lacunar syndromes. We studied risk factors of 200 consecutive patients with symptomatic lacunar infarcts diagnosed by magnetic resonance imaging. This study tested whether lacunar infarcts represent a homogeneous subgroup of strokes or not. Using descriptive and bivariate statistics, we found that the prevalences of arterial hypertension and cigarette smoking are lower in the miscellaneous group. Analysis of variance shows a significant difference in age between subgroups without interaction of sex. Nevertheless, using multivariate analysis, we did not find a difference between subgroups. Thus, lacunar infarcts seem to be a homogeneous subgroup of strokes, and the miscellaneous group of lacunar infarcts may be included into the lacunar infarct group and not into the vertebrobasilar large-artery infarct group.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a hereditary form of small vessel disease in which the pons may show lacunar infarcts and leukoaraiosis. Acute pure vestibular syndrome may be due to caudal pontine lesions and is probably underestimated. We describe a case of CADASIL with acute vestibular syndrome mimicking peripheral vestibulopathy, and evidence of focal infarction in the ponto-medullary junction at gadolinium-enhanced MRI including diffusion-weighted imaging, involving the area of the right vestibular nucleus and root entry zone of the ipsilateral vestibular nerve bundle. In CADASIL, both focal brainstem lesions and leukoaraiosis may parallel supratentorial white matter changes and may be related to poor outcome. Their actual extent should be evaluated in longitudinal studies that might predict clinical outcome and progression of disability.

Ambulatory arterial stiffness index (AASI) is associated with microvascular damage in other organs, but the association with microvascular brain damage is unknown. The association of AASI with magnetic resonance imaging (MRI) markers of cerebral small vessel disease in 143 patients with lacunar stroke was investigated. We performed 24‐hour ambulatory blood pressure monitoring and scored the presence of lacunes, white matter hyperintensities, perivascular spaces, and cerebral microbleeds on brain MRI. In logistic regression analyses, AASI was associated with white matter hyperintensities, but, after adjustment for age and sex, this association lost significance. AASI was not associated with lacunes, microbleeds, or perivascular spaces. Systolic and diastolic 24‐hour blood pressure values were associated with lacunes, perivascular spaces, and microbleeds independent of age and sex. Despite its significance and growing interest as a possible prognostic and therapeutic target in (micro)vascular diseases, AASI seems to have no added value over standard 24‐hour blood pressure in cerebral small vessel disease.

We studied 35 patients with lacunar infarcts, using diffusion-weighted echo-planar imaging (DW-EPI) at 1.5 T. The relative apparent diffusion coefficient ratio (ADCR) of each lesion was calculated and lesion conspicuity on DW-EPI was compared to that on images aquired with fast fluid-attenuated inversion recovery and T2-weighted fast spin-echo sequences. Acute small infarcts (within 3 days) were identified with DW-EPI as an area of decreased ADCR (range 0.33–0.87; mean 0.67) and high signal, subacute small infarcts (4–30 days) as a high-signal or isointense areas of decreased or nearly normal ADCR (0.54–0.98; 0.73), and chronic small infarcts (> 30 days) as low- or high-signal areas of nearly normal or increased ADCR (0.97–1.92; 1.32). In three patients, small infarcts of the brain stem in the hyperacute phase (within 6 h) were seen only with DW-EPI. In five patients, fresh small infarcts adjacent to multiple old infarcts could be distinguished only with DW-EPI.

The mirror sign is a delusional misidentification symptom (DMS) characterized by an inability to recognize one's own image in the mirror, often in the presence of an intact ability to recognize others in the mirror. The symptom has been only sparsely reported previously, and primarily within the Alzheimer's disease literature. A case is reported of an 82-year-old female with abrupt onset of mirror sign following a hypotensive crisis. Neuroradiographic studies revealed periventricular white matter change in the bifrontal and bilateral parietal occipital regions, right greater than left, as well as scattered lacunar infarcts. The patient was unable to recognize herself in the mirror and became progressively paranoid in response to the stranger in the mirror'. However, there was no evidence of prosopagnosia and she was able to recognize others in the mirror. Results from the neurobehavioral examinations replicated a previous report of mirror sign, and were consistent with those reported for other DM...

Background: The pathogenesis of lacunar infarcts is still incompletely established. Data from the literature suggest that vascular risk factors differ among patients with multiple (MLI) and single lacunar infarcts (SLI). We reexamined this hypothesis using stricter inclusion criteria and a less selected study population. Methods: We evaluated 136 patients consecutively admitted for first-ever minor stroke to a general hospital with the characteristics of a community hospital. Vascular risk factors were studied by univariate and multivariate statistical analyses among the following subgroups of patients, classified according to CT findings: (a) with lacunar infarct; (b) with nonlacunar infarct (NLI); (c) with SLI; (d) with MLI; (e) with single, either lacunar or nonlacunar, infarct. Results: No significant difference was observed between patients with lacunar infarcts and patients with NLI. Compared to patients with SLI or NLI, patients with MLI had significantly more often a family history of hypertension, cardiomegaly on the chest radiograph and CT leukoaraiosis as well as a higher systolic and diastolic blood pressure on admission. Logistic regression analysis selected CT leukoaraiosis, Rx cardiomegaly and admission diastolic blood pressure as independent, significant predictors of MLI. Conclusion: In patients with first-ever minor stroke, the risk factor profile differs according to the evidence of SLI or MLI on the CT scan. In terms of risk factors, patients with SLI seem more similar to those with NLI than those with MLI. Based on the predicting effect of variables linked with type and severity of arterial hypertension, the CT appearance of MLI might express a more univocal and specific cerebrovascular pathology (hypertensive arteriolosclerosis).

In this communication is reported a neonate with Yunis Varon syndrome, a rare autosomal recessive disorder, born to a consanguineously married couple who had microcephaly, wide cranial sutures, prominent eyes, hypertelorism, dysplastic ears, sparse hairs, cupid bow like upper lip with median pseudocleft and labio-gingival retraction. Bilateral hypoplasia of thumbs, absent great toes, short phalanges were other features. Additional features in this case included median pseudocleft unreported earlier and C.T. findings of underdeveloped gyri, ischemic changes in temperoparietal region and bilateral lacunar infarcts in middle cerebral artery territory.

Das Ausmaß des Gewebeschadens bei zerebraler Ischämie hängt unter anderem von der Ausprägung und Dauer der Blutflussminderung und den therapeutischen Maßnahmen ab, die durchgeführt wurden. Experimentelle Studien wiesen zum Teil auf unterschiedliche pathophysiologische Vorgänge nach Ischämie in der grauen und weißen Substanz des Gehirns hin. Die vorliegende Arbeit untersucht mit diffusionsgewichteter und T2-gewichteter Bildgebung (DWI, T2WI) die Frage, ob und wie der Gewebetyp die Entwicklung des Gewebeschadens bei der zerebralen Ischämie beeinflusst. Für diese Pilotstudie wurden aus 53 Patienten mit zerebraler Ischämie 10 Patienten mit lakunären subkortikalen Infarkten augewählt. Lacunäre subkortikale Infarkte ermöglichen die selektive Erfassung der ischämischen Läsionen und deren Entwicklung in der grauen und weißen Substanz. Die infarzierten Gefäßterritorien betrafen die Arteria choroidea anterior (N = 8) oder die Arteria thalamogeniculata (N = 2). Es wurden im Verlauf MRT-Messungen akut (2–13 h), subakut (22–55 h) und in der chronischen Phase (101–392 h) durchgeführt. Die MRT (1,5 T, Siemens Vision) umfasste die DWI (TR 4657 ms, TE 118 ms, Matrix 128 x 128, b-Werte 0 und 1000 s/mm2) für die Berechnung des Apparenten Diffusionskoeffizienten (ADC) und eine Turbo- Spin-Echo-Sequenz (TR 2900 ms, TE 75 ms, Matrix 256 x 256) für die T2WI. Es wurden jeweils 20 Schichten mit identischer Orientierung entlang der anterioren-posterioren Kommissur mit einem FOV von 240 mm und einer Schichtdicke von 6 mm durchgeführt. Es konnte festgestellt werden, dass ischämische Läsionen in der grauen Substanz ein Wachstum aufwiesen, das sowohl in der ADC-Map als auch in der T2WI von der Akut- zur Subakutphase beobachtet wurde. Während der chronischen Phase verkleinerte sich die Läsion wieder. Ein Teil der ADC-Läsion der Subakutphase ist demnach reversibel. Dagegen zeigten Läsionen in der weißen Substanz, sowohl in DWI- und T2WI von der Akut- über die Subakut- bis zur chronischen Phase eine Volumenzunahme. Die getrennte Beobachtung der grauen und weißen Substanz erbrachte im Rahmen dieser Pilotstudie Hinweise für den Einfluss des Gewebetypes auf die Läsionsentwicklung. Trotz geringer Fallzahl konnten Hinweise sowohl für Gemeinsamkeiten als auch Unterschiede in der Entwicklung des Gewebeschadens zwischen grauer und weißer Substanz gefunden werden. Als Ursachen hierfür kommen die Unterschiede in Anatomie, ischämischer Schadenskaskade und Ödementwicklung in Frage. Perspektivisch erscheinen Therapien sinnvoll, die auch den Gewebetyp berücksichtigen., The amount of tissue damage induced by cerebral ischemia depends on the extent and duration of reduced blood flow and therapeutic measures taken. Experimental studies have indicated that distinct pathophysiological processes occur in white and grey matter of the brain. The present study utilizes diffusion and T2-weighted imaging to analyze, whether, different tissue type affects the resulting damage from ischemia and gain insight into the underlying mechanisms. This pilot study was focused on 10 patients with subcortical lacunar infarcts. Studying lacunar infarcts enabled selective assessment of ischemic lesions in white and grey matter, relevant to their evolution over time. These patients were selected from 53 patients examined in acute (2-13 h), subacute (22-55 h), and chronic (101-392 h) stages of ischemia. These 10 patients displayed infarcts of either arteria choroidea anterior (n = 8) or arteria thalamogeniculata (n = 2). MRI (1,5 T, Siemens Vision) measurements comprised of DWI (TR 4657 ms, TE 118 ms, matrix 128 x 128, ß-values 0 und 1000 s/mm2) for calculation of apparent diffusion coefficients (ADC) and turbo spin echo sequences (TR 2900 ms, TE 75 ms, matrix 256 x 256) for T2-WI. Each acquisition consisted of 20 slices parallel to the anteroposterior commissure plane, with 240 mm FOV and 6 mm slice thickness. Measurements showed that ischemic lesions in grey matter progressed in size during acute and subacute phases of ischemia on both, ADC-maps and T2-WI. In chronic phases these lesions decreased. In conclusion ADC lesions depicted in subacute phase are partly reversible. In contrast, white matter lesions increased in volume over their evolution in time from acute over subacute to chronic phases both in DWI and T2-WI. This pilot study demonstrated by differential assessment of grey and white matter the impact of tissue type on lesion evolution. Although hindered by a relativelly small sample size, similarities and differences could be observed between grey and white matter in developing tissue damage. Potential explanations include differences in anatomy, damage cascades, and edema progression. Bridging to future therapies, tissue specific approaches may appear reasonable.

Objective Our study focused on acute lacunar infarct shapes to explore the risk factors and clinical significance of irregularly shaped lacunar infarctions. Methods Based on the shape of their acute lacunar infarct, patients (n=204) were classified into the “regular” group or “irregular” group. The characteristics of the lacunar infarction were compared between the regular and irregular groups, between patients with and without neurological deterioration, and between patients with different modified Rankin scale (mRS) scores. The risk factors for irregularly shaped lacunar infarctions, neurological deterioration, and high mRS scores were identified. Results Blood pressure variability (BPV) was an independent risk factor for irregularly shaped lacunar infarction. Infarction size, prevalence of advanced leukoaraiosis, and irregularly shaped lacunar infarcts were independent risk factors for higher mRS scores. Conclusions The irregularly shaped lacunar infarcts were correlated with BPV. Irregularly shaped lacunar infarctions and leukoaraiosis may be associated with unfavorable clinical outcomes.

The location of white matter lesions, especially in the anterior temporal poles (ATP), is helpful in the diagnosis of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). We report a 49-year-old man with CADASIL who developed migraine with atypical aura, silent lacunar infarcts, and leukoencephalopathy without involvement of the ATP. The prevalence of migraine with aura in subjects with CADASIL is several times greater than that in the general population. Particularly in patients with CADASIL, the aura is often atypical (hemiplegic, basilar, or prolonged). A diagnosis of CADASIL should be considered in patients with lacunar infarcts, leukoencephalopathy, and migraine with atypical aura, even in the absence of white matter lesion in the ATPs.

Background: Small deep infarcts (SDI), also called lacunar infarcts, resulting from the occlusion of deep branch arteries, account for 25% of ischemic strokes. The physiopathology of the disease remains largely unknown. However, evidence about the role of endothelial dysfunction has emerged. Whereas chronic platelet activation is of major importance in acute thrombosis of large atherosclerotic arteries, its role in SDI remains unclear. Frequently associated risk factors are hypertension and diabetes mellitus. The aim of this study was to determine platelet and endothelial activation in patients with recent SDI in comparison to population-based control subjects matched for age, sex and vascular risk factors. Methods: Platelet activation markers (activated glycoprotein IIb/IIIa, P-selectin and platelet microparticles), shear-induced platelet aggregation (SIPA) studied in the SIPAgreg device at 4,000 s-1, endothelial activation markers [including von Willebrand factor (vWF) antigen and homocysteine] and high-sensitivity C-reactive protein (hsCRP) were measured in 74 consecutive patients with recent SDI, in whom detectable large artery atherosclerosis or cardiac embolism had been ruled out. Blood samples were collected 1 and 3 months after symptom onset. These factors were also measured in 74 population-based controls with no stroke history and matched for age, sex, hypertension and diabetes. Results: One month after symptom onset, the patients had similar levels of platelet activation to matched controls (p > 0.40 for all comparisons). In contrast, endothelial activation parameters were increased in patients in comparison to controls (vWF: p = 0.002 and homocysteinemia/creatinemia: p = 0.025). The level of hsCRP was slightly increased in patients compared to controls (p = 0.059). At 3 months, we observed a significant decrease in vWF and hsCRP levels in patients (median change in vWF = 10%, p = 0.004; median change in hsCRP = 0.4 mg/l, p = 0.02). Homocysteine levels and all platelet parameters remained unchanged at this time compared to at 1 month. Conclusions: Our results confirm that chronic platelet activation, when compared to controls matched for age, sex and vascular risk factors, did not seem to play a central role in the pathophysiology of lacunar stroke. In contrast, we found markers of endothelial dysfunction, the role of which in the occurrence of lacunar infarction has still to be clarified in further studies.

The association of the presence of cerebral microbleeds with antiplatelet use remains controversial. Long durations of antiplatelet use and vascular risk factors may have a greater effect on the development of microbleeds than short durations. Our aim in the present study was to determine whether the durations of antiplatelet use and vascular risk factors are associated with cerebral microbleeds. Two hundred twenty outpatients with cerebrovascular disease detected by MRI were examined. Cerebral microbleeds were observed in 71 (32.3%) patients, and deep or infratentorial microbleeds and strictly lobar microbleeds in 53 (24.1%) patients and 18 (8.2%) patients, respectively. To determine the association the between durations of vascular risk factors and antiplatelet use, radiological findings regarding the presence and location of cerebral microbleeds were assessed by multivariate logistic regression analysis adjusted for age, sex, and relevant confounders. The duration of hypertension, the presence of lacunar infarcts and the severity of periventricular hyperintensity were associated with microbleeds in a deep or infratentorial region. Antiplatelet use and its duration of were not associated with the presence or location of microbleeds. Our results suggest that deep or infratentorial microbleeds reflect the severity of hypertensive vasculopathy. Thus, antiplatelet use may not be associated with the presence of cerebral microbleeds.

The purpose of this study was to determine the spectrum of neuroradiologic findings in patients with antiphospholipid antibodies (APA) and to compare findings in systemic lupus erythematosus (SLE) and non-SLE patients.We identified 110 patients with APA who underwent CT or MR imaging, of whom 59 (54%) had abnormal studies. Of these 59 patients, abnormalities were categorized as large infarcts, cortical infarcts, lacunar infarcts, hyperintense white matter foci on T2-weighted images, or dural sinus thrombosis. White matter foci were designated as small (5mm) or large (5 mm).Large infarcts were the most common abnormality, seen in 24 of 110 (22%) patients, followed in frequency by hyperintense white matter foci, seen in 19 of 110 (17%) patients. Ninety-five percent of patients with hyperintense white matter foci had at least one large lesion, and 76% had five or more small foci, three or more large foci, or both. Small cortical infarcts and lacunar infarcts were seen in 11 of 110 (10%) and 10 of 110 (9%) patients, respectively. Dural sinus thrombosis was seen in five patients. The frequency of abnormalities was high in both the SLE (57%) and the non-SLE (41%) groups. Large infarcts were more common in the non-SLE group (26%) than in the SLE group (5%). Although hyperintense white matter foci and cortical infarcts were more common in SLE patients, the differences were not statistically significant.Infarcts of various sizes and hyperintense white matter foci are the most common abnormalities seen on CT and MR imaging in patients with APA. We found no significant differences in frequencies of abnormalities seen between non-SLE and SLE patients.

Depression in the elderly is associated with increased mortality, persistence of symptoms and progression to dementia in a substantial number of cases. Minor cerebrovascular lesions such as deep white matter changes, lacunar infarcts and silent cerebral infarction can be demonstrated in some late-onset depressives and may be relevant to the development of depression, or associated with the persistence of symptoms and the emergence of treatment resistance. Increased morbidity and mortality may occur through subsequent cerebrovascular events, and progression to dementia might result from multiple cerebral infarcts. Treatment strategies that address underlying vascular risk factors could decrease the likelihood of fatal strokes or stepwise progression to (multi-infarct) dementia, thereby improving the long-term prognosis for a subgroup of late-onset depressives.

Of 73 patients with initial lacunar stroke subsequently treated with aspirin, 13 (18%) developed recurrent stroke (11 lacunar infarcts and 2 nonlacunar infarcts), and 4 (5%) died within 1 year. Of the aspirin-treated lacunar infarct patients, 58 received 325 mg or lower-dose aspirin, and 15 received 600-1,300 mg of aspirin. Thirteen aspirin-treated patients who developed recurrent ischemic stroke received 80 mg or 325 mg of aspirin, whereas recurrent stroke did not occur in 15 patients treated with 600-1,300 mg of aspirin daily. Of 25 patients with lacunar stroke who were subsequently treated with 250 mg of ticlopidine twice daily, 1 patient (4%) developed recurrent lacunar infarct, and none died within 1 year. Of 10 patients who had an initial lacunar stroke and subsequently received no antiplatelet medication, 4 (40%) developed recurrent lacunar stroke, and 1 (10%) died within 1 year.

Determination of the stroke type may be crucial to rational treatment and prediction of outcome. Patients with infarct in the anterior or posterior circulation, and patients with lacunar infarcts may

To the Editor: We read with great interest the article by Marielle et al1 that was recently published in Stroke . In their population-based study that included 1460 participants, increased arterial stiffness indicated by aortic pulse wave velocity (PWV), a conventional measurement of arterial stiffness, was associated with a larger volume of white matter lesions. Furthermore, lacunar infarcts and deep or infratentorial microbleeds were associated with a higher aortic PWV in persons with uncontrolled hypertension. We applaud their results, because we also showed an independent association between cerebral small vessel disease and increased arterial stiffness indicated by brachial-ankle …

Small-vessel disease is the accepted most frequent cause of lacunar stroke. The main clinical features seen with lacunar infarcts are motor and/or sensitive deficit, ataxic sign, without cortical involvement. A lacunar syndrome is generally the result of a small deep infarct within the territory of a single perforating artery with the maximum diameter on imaging of 15 mm. Recent studies have demonstrated alternative causes of lacunar stroke other than small-vessel disease (e.g. cardio embolism, atherosclerosis or other causes), especially in large lacunae, with a potential relevance on functional outcome. These findings suggest that lacunar stroke is not always a benign disease. Moreover, clinical features may be significant in terms of disability in lacunae in close proximity to crucial anatomical site. The following chapter reports the classical lacunar syndrome and discusses the debated etiology of lacunar stroke.

There are only a few reports on long-term prognosis and functional outcome after lacunar infarction, and little is known about the evolution of MRI abnormalities with time in this subtype of stroke. To address these issues, we performed a 1-year clinical and MRI follow-up study in 81 patients with presumed lacunar infarction. AT 1 year after stroke onset 1 patient had died, whereas 5 patients (6.2%) had had recurrent strokes. Based on the Oxford Handicap Scale, 63 (79%) of the surviving patients were functionally independent at the time of follow-up. MRI at 1 year revealed new, clinically silent infarcts in 8 patients (10%), and wallerian degeneration of the pyramidal tract in 8 (24%) of the 34 patients with posterior capsular or putamenal infarcts on initial MRI. Our data suggest that new, clinically silent infarcts may be at least as common as recurrent strokes in patients with lacunar infarctions.

Cerebral abnormalities such as white matter hyperintensity (WMH), cortical infarct (CI), and lacunar infarct (LI) are of clinical importance and frequently present in patients with stroke and dementia. Up to date, there are limited algorithms available to automatically delineate these cerebral abnormalities partially due to their complex appearance in MR images. In this paper, we describe an automated multi-stage segmentation approach for labeling the WMH, CI, and LI using multi-modal MR images. We first automatically segment brain tissues (white matter, gray matter, and CSF) based on the T1-weighted image and then identify hyperintense voxels based on the fluid attenuated inversion recovery (FLAIR) image. We finally label the WMH, CI, and LI based on the T1-weighted, T2-weighted, and FLAIR images. The segmentation accuracy is evaluated using a community-based sample of 272 old adults. Our results show that the automated segmentation of the WMH, CI, and LI is comparable with manual labeling in terms of spatial location, volume, and the number of lacunes. Additionally, the WMH volume is highly correlated with the visual grading score based on the Age-Related White Matter Changes (ARWMC) protocol. The evaluations against the manual labeling and ARWMC visual grading suggest that our algorithm provides reasonable segmentation accuracy for the WMH, CI, and LI.

The underlying pathology of lacunar infarcts, white matter lesions and also of microbleeds is poorly understood. We assessed whether the presence of lacunar infarcts, white matter lesions or microbleeds on MRI was associated with a decrease in cerebrovascular reactivity, and assessed whether this association was similar for lacunar infarcts, white matter lesions and microbleeds. BOLD-fMRI scan with breath-holding at 7 T and anatomical scans at 1.5 T were available in 49 patients with atherosclerotic disease from the Second Manifestations of ARTerial disease (SMART) study. Microbleeds and lacunar infarcts were scored visually and volumetric assessment of white matter lesions was performed on the 1.5 T scan. The percentage of voxels with a significant signal change on breath-holding and the whole brain signal change were calculated as measures of cerebrovascular reactivity. The mean percentage of voxels with a significant signal change was 25.1% (SD 6.6) and the mean percentage whole brain signal change was 1.20% (SD 0.51). Age, gender, and diastolic blood pressure were significantly associated with cerebrovascular reactivity. Cerebrovascular reactivity was lower with increasing age, lower in females compared to males and lower with lower diastolic blood pressure. ANCOVA showed that patients with microbleeds (n=18) had a significantly lower whole brain signal change than patients without microbleeds, with a mean difference of -0.36% (95% CI -0.64 to 0.07), independent of age, sex, systolic and diastolic blood pressure and non-lacunar infarcts. No significant associations were found for presence of lacunar infarcts or white matter lesion volume with whole brain signal change or percentage of voxels with a significant signal change. The results show that presence of microbleeds is associated with an impaired cerebrovascular reactivity in patients with atherosclerotic disease, whereas no significant association was found for the presence of lacunar infarcts or white matter lesions in our study.

Background and Purpose— Cerebral small vessel disease, including white matter lesions and lacunar infarcts, is related to cognitive impairment. Cerebral microbleeds (MBs) are increasingly being recognized as another manifestation of small vessel disease and are also related to cognitive function. However, it remains unclear whether this relation is independent of white matter lesions and lacunar infarcts and if location of MB plays a role. We investigated the relation between the presence, number, and location of MB and cognitive performance adjusted for white matter lesions and lacunar infarcts. Methods— Presence, number, and location of MB were rated on a gradient echo T2*-weighted MRI in 500 nondemented elderly patients with small vessel disease. Cognitive performance was assessed in different domains. Analyses were adjusted for age, sex, education, depressive symptoms, total brain volume, white matter lesion volume, and lacunar and territorial infarcts. Results— Mean age was 65.6 years (SD 8.8) and 57% were male. MBs were present in 10.4% of the participants. Subjects with MBs were significantly older, had a higher white matter lesion volume, and more lacunar infarcts ( P P =0.008; β−0.20, P =0.002), psychomotor speed (β−0.10, P =0.012; β−0.19, P =0.006), and attention (β−0.10, P =0.02; β−0.205, P =0.001). The relations with cognitive performance were mainly driven by frontal, temporal, and strictly deep located MB. Conclusions— Frontal and temporal located MBs correlate with cognitive performance in nondemented elderly patients independent of coexisting other small vessel disease-related lesions. MBs are clinically not silent and may help to understand the role of vascular disease in cognitive decline.

To determine the clinical usefulness of gadolinium-DPTA-enhanced MRI in identifying recent small, deep infarcts we prospectively studied 91 patients with first-ever stroke and presenting with a lacunar syndrome. In 78 patients (85.7%), plain MRI revealed possibly appropriate infarcts, classified as deep (n = 69), internal borderzone (n = 1), and cortical (n = 8 patients). Enhancement was seen in 38 (80.9%) of 47 patients with only one possibly relevant deep lesion on plain MRI, and in 14 (63.6%) out of 22 patients with multiple lesions. MRI with gadolinium-DPTA facilitates identification of the relevant lesion in patients with presumed lacunar infarcts.

In a prospective study, we compared the prognosis for survival, handicap, and recurrence of stroke in 103 patients with a first-ever lacunar infarct, presumably due to small-vessel obstruction, with that in 94 patients who had a first-ever superficial infarct associated with large-vessel disease. Patients with lacunar infarction had better survival, as shown by Kaplan-Meier analysis, and less disability than patients with superficial infarction, whereas the difference in risk of recurrent infarction was not statistically significant. Six of the 7 (86%) recipient infarcts in the lacunar infarction group were lacunar again, supporting the hypothesis that lacunar infarcts are usually caused by a local small-vessel obstruction.

Lacunar stroke in 100 black and 30 white patients with lacunar syndrome and computed tomography (CT) positive for lacunar infarct were compared. Of blacks, 88% were hypertensive, 77% had target-organ damage, and 86% were hypertensive for longer than 8 years. Of whites, 60% were hypertensive, 61% had target-organ damage, and 72% were hypertensive for longer than 8 years. Prior clinical stroke occurred in 7% of blacks and 50% of whites. Transient ischemic attacks (TIAs) were found in 33% of blacks and 53% of whites. In blacks, CT showed single lacunes in 57% and multiple lacunes in 43%. In whites, CT showed single lacunes in 64% and multiple lacunes in 36%. Angiography was abnormal in 22% of blacks and 54% of whites. In blacks, lacunar stroke was associated with hypertension in 88%, and lacunar stroke was the initial cerebrovascular manifestation in 80%; CT showed "silent" lacune(s) in 41% of hypertensive blacks. In whites, lacunar stroke was associated with hypertension in 60%, and 6% had "silent" lacunes. Based on CT findings, only hypertensive patients had "silent" lacunes.

Cerebral small vessel disease (CSVD) is considered to be caused by an increased permeability of the blood-brain barrier and results in enlargement of Virchow Robin spaces (VRs), white matter lesions, brain microbleeds, and lacunar infarcts. The increased permeability of the blood-brain barrier may relate to endothelial cell activation and activated monocytes/macrophages. Therefore, we hypothesized that plasma markers of endothelial activation (adhesion molecules) and monocyte/macrophage activation (neopterin) relate to CSVD manifestations. In 163 first-ever lacunar stroke patients and 183 essential hypertensive patients, we assessed CSVD manifestations on brain magnetic resonance imaging (MRI) and levels of C-reactive protein (CRP), neopterin, as well as circulating soluble adhesion molecules (sICAM-1, sVCAM-1, sE-selectin, sP-selectin). Neopterin, sICAM-1 and sVCAM-1 levels were higher in patients with extensive CSVD manifestations than in those without (p < 0.01). Neopterin levels independently related to higher numbers of enlarged Virchow Robin spaces (p < 0.001). An inflammatory process with activated monocytes/macrophages may play a role in the increased permeability of the blood brain barrier in patients with CSVD.

Carotid intervention in severe carotid stenosis after an anterior circulation ischemic event reduces the risk of further infarcts if the surgery is performed soon after the incident event. At present, there is no recommendation to differentiate among subtypes of anterior circulation infarcts or transient ischemic events. However, evidence is mounting that demonstrates a difference in pathophysiology of lacunar and nonlacunar (large artery) infarcts. The natural history of lacunar strokes is different from large artery infarcts for recurrence and mortality. Stroke is a heterogenous disease and consideration needs to be directed to manage different stroke subtypes differently. Lacunar infarcts mostly do not arise from large artery atheromatous disease or by cardioembolic phenomena, and there is a negative predictive value for severe carotid stenosis in lacunar strokes. Thus, current evidence suggests that lacunar strokes may not warrant investigation for carotid stenosis.

Memory function was studied in patients with Parkinson's disease (PD) or subcortical lacunar infarcts (SLI) using continuous visual recognition memory tasks and event-related potentials (ERPs). Response accuracy for new faces in PD patients, but not SLI patients, was significantly decreased compared to the normal control group. The ERP repetition effect for lag 0 was apparent in controls, but not in the PD or SLI patients. In addition, PD patients showed more positive ERP amplitude for new faces than control subjects and SLI patients. Our data suggest that recognition memory for visual stimuli declines in both PD and SLI patients. Recognition memory deficits in PD may result, at least in part, from impairment of the contex integration process, whereas contex integration may be relatively intact in SLI patients.

We report two cases of acute cerebral infarcts interpreted radiographically as "lacunes." Although the neurological deficits persisted, the "lacunes" seen on computed tomography and magnetic resonance imaging did not persist. These two cases suggest that the radiographic diagnosis of acute "lacunar infarcts" may not be a reliable predictor of lacune formation.

Background: No previous study has investigated the association of kidney dysfunction with silent lacunar infarcts and white-matter hyperintensity (WMH) independent of ambulatory blood pressure (BP). Methods: A cross-sectional study involving 1,008 participants (mean age 66 years) from a general population of Ohasama, Japan, was conducted. Calculated creatinine clearance (CCr) was estimated using the Cockcroft-Gault equation. In continuous and categorical analyses, the association between CCr and the prevalence of silent lacunar infarcts and WMH was investigated. Silent lacunar infarcts and WMH were detected on MRI. Multiple logistic regression analysis adjusted for 24-hour ambulatory BP, sex, age, body mass index, smoking and drinking status, antihypertensive medication, and histories of hypercholesterolemia, diabetes mellitus and heart disease was performed. Results: On univariate analysis, decreased CCr (continuous variable) and CCr 2 (categorical variable) were significantly associated with lacunar infarcts and WMH. After adjustment, each 1-standard-deviation decrease in CCr (odds ratio = 1.22; p = 0.036) and CCr 2 (odds ratio = 1.68; p = 0.007) was significantly associated with a high prevalence of lacunar infarcts. Even when 24-hour ambulatory BP was within the normal range (2 was associated with a high prevalence of lacunar infarcts (odds ratio = 1.62; p = 0.047). CCr 2 and 24-hour ambulatory BP had additive effects on lacunar infarcts. After the same adjustment, the association between CCr and WMH was not significant. Conclusions: CCr is closely associated with lacunar infarcts, suggesting that kidney dysfunction in the elderly is an independent risk factor or predictor for silent lacunar infarcts.

To determine whether the location of subcortical silent infarcts differs from that of symptomatic lacunar infarcts.32 silent infarcts and 59 acute lacunar infarcts located in the corona radiata were examined. The relative anterior-to-posterior locations of the silent infarcts in the corona radiata were compared with those of the symptomatic lacunes on T2-weighed MR imaging.The locations of the silent infarcts differed from those of the symptomatic lacunar lesions in the corona radiata (p0.001). Silent infarcts were distributed principally in the anterior half of the corona radiata, whereas most of the symptomatic lacunes were located in the posterior half of the corona radiata.The asymptomatic nature of subcortical silent infarcts may be attributable to their location in ineloquent portions of brain structures.

We report the case of a 66-year-old female who presented with dysarthria and dysphonia. Brain MRI abnormalities showed confluent white matter lesions and subcortical lacunar infarcts, suggesting cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL), confirmed by the presence of a heterozygous mutation in the Notch3 gene. Clinical signs and course were consistent with amyotrophic lateral sclerosis (ALS) as was the electromyographic pattern. The possible pathogenic role for a mutation in the Notch3 gene is discussed considering recent data on hypoxia in the pathophysiology of ALS.

Objective: To investigate the independent association of white matter lesions (WML) and lacunar infarcts (LI) with measures of global brain atrophy on MRI. Methods: Within the SMART-MR study, a cohort study among patients with manifest arterial disease, cross-sectional analyses were performed in 840 patients (mean age 58 ± 10 years, 80% male) without cortical, large subcortical or infratentorial infarcts. Brain segmentation was used to quantify volumes of brain tissue, cerebrospinal fluid and WML. Total brain volume, ventricular volume and cortical gray matter volume were divided by intracranial volume to obtain brain parenchymal fraction (BPF), ventricular fraction (VF) and cortical gray matter fraction (GMF). Location and number of infarcts were rated visually. Results: Mean ± SD BPF was 79.3 ± 2.8%, mean ± SD VF was 2.01 ± 0.95%, and mean ± SD GMF was 36.6 ± 3.3%. Linear regression analyses, adjusted for age, sex, vascular risk factors, intima media thickness and LI showed that in patients with moderate to severe WML (upper quartile) BPF was lower (–0.51%; 95% CI –0.93 to –0.08%), VF was higher (0.48%; 95% CI 0.31–0.65%) and GMF was lower (–1.48%; 95% CI –2.07 to –0.88%) than in patients with few WML (lower quartile). Presence of LI was associated with lower BPF (–0.52%; 95% CI –0.96 to –0.07%) and higher VF (0.25%; 95% CI 0.07–0.42%), but not with GMF, independent of WML and other potential confounders. Conclusion: WML are associated with total, subcortical and cortical brain atrophy, whereas LI are associated with total and subcortical atrophy, but not with cortical atrophy, suggesting an independent role for WML and LI in the pathogenesis of brain atrophy.

To the Editor: We read with great interest the article entitled ‘Retinopathy in ischemic stroke subtypes’1 appearing in Stroke , and would like to congratulate the authors for this novel effort. Doubal et al hypothesized that there would be higher rates of retinopathy in patients with acute lacunar infarcts but failed to demonstrate any significant correlation. We have reason to suggest that it may be due to the basis of their hypothesis. Doubal et al essentially believe that retinopathy and lacunar infarcts are both, by large, manifestations of disordered small vessel endothelium and an increased permeability in the blood-retinal or blood-brain barrier. Our knowledge …

Background: Cerebrovascular diseases (CVDs) are considered the second most common cause of cognitive decline in the elderly after neurodegeneration of the Alzheimer’s type. Despite impressive epidemiological data, the actual burden of CVDs in terms of cognitive decline is still incompletely appreciated by physicians and health regulators. Methods: In this brief position paper, we review some evidence related to the topic and its clinical relevance, and we present some concepts that we consider of crucial importance for the correct recognition of the problem. Results and Conclusions: We conclude that: (1) different approaches to the topic exist (clinical, neuroimaging-based, pathological) and the inconsistent use of one or another, together with lack of definitions, has limited the appreciation of the contribution of CVDs to cognitive decline; (2) cognitive impairment related to CVDs is very frequent and constitutes a topic with high epidemiological impact; (3) cognitive impairment associated with CVDs is heterogeneous in clinical and pathogenic terms; (4) vascular lesions often interact with other type lesions, the most important of which are today considered those of the Alzheimer’s type, in determining cognitive impairment; (5) for some vascular lesions, namely white matter lesions and lacunar infarcts, strong evidence suggests their role as determinants of cognitive decline; (6) cognitive impairment is only part of the consequences of CVDs as it is almost invariably accompanied by gait disturbances, depressive symptoms, and sphincteric control dysfunction, all factors contributing to loss of independence.

Background: Current clinical tools to identify lacunar infarct patients at risk of deterioration are inadequate, and imaging techniques to predict fluctuation and deterioration would be of value. We sought to determine the occurrence of MRI perfusion-weighted imaging (PWI) abnormalities in lacunes, and whether they help predict clinical and radiological outcome. Methods: Patients with lacunar stroke or TIA were selected from a prospective MR imaging study. MRI was performed within 24 h of the event and follow-up imaging completed at 30 or 90 days. Baseline perfusion maps were qualitatively assessed and infarct volumes measured. Early clinical deterioration (NIHSS worsening of ≥3 points within 72 h of event) and 90-day modified Rankin Scale score (mRS) were recorded. Results: Twenty-two patients were included. Fifteen (68.2%) had abnormal PWI at the site of the diffusion-weighted imaging lesion. Patients with abnormal PWI were more likely to have stroke than TIA as their index event (RR 2.2, 95% CI 0.9–5.2, p = 0.02). Early clinical deterioration occurred in 4 patients (18.2%), all of whom had abnormal PWI. PWI lesions were not associated with a higher 90-day NIHSS or mRS score, nor did they predict infarct volume growth. Conclusions: MR-PWI abnormalities are seen in two thirds of lacunar infarcts, and are associated with stroke rather than TIA. Normal PWI identifies patients at low risk of early clinical deterioration.

A longitudinal, clinical ethnography formed the basis of this study. Thirteen stroke survivors, all with lacunar infarcts of the internal capsule of the brain, participated. Survivors were interviewed within 72 hours of the infarct and during acute and rehabilitation phases of recovery. Each was followed for six months, providing a total of 120 interviews. The survivors experienced a paralyzed self secondary to bodily immobility, the shock of the stroke onset and fear of not knowing what might happen next. The terrifying loss of control over bodily movements led to an experiential breakdown. This article chronicles the shock of sudden immobility which left the individuals suspended in a passive, objectified body.

We evaluated clinical predictors of leukoaraiosis among 218 patients admitted to a neurogeriatric ward and submitted to cranial computed tomography. Leukoaraiosis was strongly correlated with increasing age, also when this effect was adjusted for the other risk factor variables. Since lacunar infarcts were positively and nonlacunar negatively associated with leukoaraiosis, a history of stroke significantly predicted leukoaraiosis only when its effect was corrected for the infarct type. A complaint of gait disturbance and an extensor plantar response were the only significant predictors of leukoaraiosis among neurologic symptoms and signs in a multivariate model including the age and infarct type as covariates. Based on age and on these clinical features, the probability of encountering leukoaraiosis on the computed tomography scan of elderly neurological patients can be determined.