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A 70-year-old right-handed housewife suffered an acute loss of taste, an unpleasant change in the taste of foods and liquids, and a strong aversion to all kinds of food due to a small lacune in the right dorsomedial pontine tegmentum. Eating became so unpleasant that she lost 7 kg in three weeks. Olfaction and the sensibility of the tongue were spared. The right medial longitudinal fascicle, the central tegmental tract, or both, were injured by the tegmental lesion. A discrete right-sided lesion in the upper pontine tegmentum may cause a reversible syndrome consisting of bilateral hypogeusia which is more severe ipsilaterally.

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BACKGROUND: An abnormal ankle-brachial index has been associated with overt stroke and coronary heart disease, but little is known about its relationship with silent cerebral small vessel disease. AIM: To assess the value of ankle-brachial index as a predictor of silent small vessel disease in an Ecuadorian geriatric population. METHODS: Stroke-free Atahualpa residents aged ≥60 years were identified during a door-to-door survey. Ankle-brachial index determinations and brain magnetic resonance imaging were performed in consented persons. Ankle-brachial index ≤0.9 and ≥1.4 were proxies of peripheral artery disease and noncompressible arteries, respectively. Using logistic regression models adjusted for age, gender, and cardiovascular health status, we evaluated the association between abnormal ankle-brachial index with silent lacunar infarcts, white matter hyperintensities, and cerebral microbleeds. RESULTS: Mean age of the 224 participants was 70 ± 8 years, 60% were women, and 80% had poor cardiovascular health status. Ankle-brachial index was ≤0.90 in 37 persons and ≥1.4 in 17. Magnetic resonance imaging showed lacunar infarcts in 27 cases, moderate-to-severe white matter hyperintensities in 47, and cerebral microbleeds in 26. Adjusted models showed association of lacunar infarcts with ankle-brachial index ≤ 0.90 (OR: 3.72, 95% CI: 1.35-10.27, P = 0.01) and with ankle-brachial index ≥ 1.4 (OR: 3·85, 95% CI: 1.06-14.03, P = 0.04). White matter hyperintensities were associated with ankle-brachial index ≤ 0.90 (P = 0.03) and ankle-brachial index ≥ 1.4 (P = 0.02) in univariate analyses. There was no association between ankle-brachial index groups and cerebral microbleeds. CONCLUSIONS: In this population-based study conducted in rural Ecuador, apparently healthy individuals aged ≥60 years with ankle-brachial index values ≤0.90 and ≥1.4 are almost four times more likely to have a silent lacunar infarct. Ankle-brachial index screening might allow recognition of asymptomatic people who need further investigation and preventive therapy.

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BACKGROUND: Studies looking for an association between incompleteness of the Circle of Willis (CoW) and small vessel disease (SVD) markers are scarce and conflicting. We aimed to evaluate this association in an unbiased population-based study conducted in Atahualpa (rural Ecuador). METHODS: Atahualpa residents 60 years of age or more were identified during a door-to-door survey and invited to undergo magnetic resonance imaging for identification of SVD markers, including white matter hyperintensities (WMHs), strokes, and deep microbleeds. Magnetic resonance imaging (MRA) was used for classifying the CoW according to the presence or absence of one A1 segment of the anterior cerebral artery or one or both P1 segments of posterior cerebral arteries. RESULTS: Of 311 eligible persons, 258 were enrolled. Mean age was 70 ± 8 years, 59% were women, and 74% had a poor cardiovascular health (CVH) status. Of these, 172 patients (67%) had WMH, 40 patients (16%) had SVD-related strokes, and 23 patients (9%) had deep microbleeds. MRA revealed a complete CoW in 157 persons (61%). Persons with SVD markers were older than those without markers (P < .0001). A poor CVH status was noted in 79% of persons with at least 1 SVD marker and in 65% of those with no markers (P = .02). Logistic regression models showed no association of incompleteness of the CoW with any marker of SVD-alone or in combination-after adjusting for age, sex, and CVH status. CONCLUSIONS: Lack of association between incompleteness of CoW and SVD markers suggest that genetically determined variants in the intracranial vasculature are not responsible for the high prevalence of SVD among native South American populations.

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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.

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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. .

Objetivo Estudar as diferentes formas dos infartos lacunares agudos, investigando os fatores de risco e o significado clinico daqueles com morfologia irregular. Métodos Os 204 pacientes com infartos lacunares agudos foram classificados em dois grupos: aqueles com morfologia regular e aqueles com morfologia irregular. Foram estudadas as características dos dois grupos e caracterizados os fatores de risco para infartos irregulares, deterioração neurológica e altos escores da escala de Rankin modificada. Resultados Variabilidade da pressão arterial é fator de risco independente para infartos lacunares irregulares. Tamanho do infarto, prevalência de leucoaraiose e formato irregular dos infartos lacunares são fatores de risco independentes para escores mais elevados na escala de Rankin modificada. Conclusões Variabilidade da pressão arterial está relacionada ao formato irregular dos infartos lacunares agudos. Este tipo de infarto e a leucoaraiose podem estar relacionado a desfechos clínicos desfavoráveis. .

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OBJECTIVE: Silent brain infarctions are the silent cerebrovascular events that are distinguished from symptomatic lacunar infarctions by their 'silence'; the origin of these infarctions is still unclear. This study analyzed the characteristics of silent and symptomatic lacunar infarctions and sought to explore the mechanism of this 'silence'. METHODS: In total, 156 patients with only silent brain infarctions, 90 with only symptomatic lacunar infarctions, 160 with both silent and symptomatic lacunar infarctions, and 115 without any infarctions were recruited. Vascular risk factors, leukoaraiosis, and vascular assessment results were compared. The National Institutes of Health Stroke Scale scores were compared between patients with only symptomatic lacunar infarctions and patients with two types of infarctions. The locations of all of the infarctions were evaluated. The evolution of the two types of infarctions was retrospectively studied by comparing the infarcts on the magnetic resonance images of 63 patients obtained at different times. RESULTS: The main risk factors for silent brain infarctions were hypertension, age, and advanced leukoaraiosis; the main factors for symptomatic lacunar infarctions were hypertension, atrial fibrillation, and atherosclerosis of relevant arteries. The neurological deficits of patients with only symptomatic lacunar infarctions were more severe than those of patients with both types of infarctions. More silent brain infarctions were located in the corona radiata and basal ganglia; these locations were different from those of the symptomatic lacunar infarctions. The initial sizes of the symptomatic lacunar infarctions were larger than the silent brain infarctions, whereas the final sizes were almost equal between the two groups. CONCLUSIONS: Chronic ischemic preconditioning and nonstrategic locations may be the main reasons for the 'silence' of silent brain infarctions.

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OBJECTIVE: Silent brain infarctions are the silent cerebrovascular events that are distinguished from symptomatic lacunar infarctions by their 'silence'; the origin of these infarctions is still unclear. This study analyzed the characteristics of silent and symptomatic lacunar infarctions and sought to explore the mechanism of this 'silence'. METHODS: In total, 156 patients with only silent brain infarctions, 90 with only symptomatic lacunar infarctions, 160 with both silent and symptomatic lacunar infarctions, and 115 without any infarctions were recruited. Vascular risk factors, leukoaraiosis, and vascular assessment results were compared. The National Institutes of Health Stroke Scale scores were compared between patients with only symptomatic lacunar infarctions and patients with two types of infarctions. The locations of all of the infarctions were evaluated. The evolution of the two types of infarctions was retrospectively studied by comparing the infarcts on the magnetic resonance images of 63 patients obtained at different times. RESULTS: The main risk factors for silent brain infarctions were hypertension, age, and advanced leukoaraiosis; the main factors for symptomatic lacunar infarctions were hypertension, atrial fibrillation, and atherosclerosis of relevant arteries. The neurological deficits of patients with only symptomatic lacunar infarctions were more severe than those of patients with both types of infarctions. More silent brain infarctions were located in the corona radiata and basal ganglia; these locations were different from those of the symptomatic lacunar infarctions. The initial sizes of the symptomatic lacunar infarctions were larger than the silent brain infarctions, whereas the final sizes were almost equal between the two groups. CONCLUSIONS: Chronic ischemic preconditioning and nonstrategic locations may be the main reasons for the 'silence' of silent brain infarctions.

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