Small Deep Infarcts Diagnosed on Computed Tomography

Review of 2,859 autopsy reports disclosed lacunar infarctions in 169 patients (6%). Review of the charts of 167 of these patients revealed hypertension in 64%, diabetes in 34%, smoking in 46%, and no known risk factor for cerebrovascular disease in 18%. As many as 81% of the patients with lacunes were asymptomatic. Symptomatic lacunes presented most commonly as pure motor hemiparesis (31%), aphasia plus right hemiparesis (20%), or sensorimotor dysfunction (11%); none presented as pure sensory stroke. These results suggest that the spectrum of lacunar infarction is more heterogeneous than previously thought. Most lacunes are asymptomatic, and the majority of symptomatic patients do not present with "classical" lacunar syndromes. Subjects and MethodsAutopsy records at The New York Hospital from 1975 to 1985 were reviewed for reports of lacunes or small subcortical infarcts sparing the overlying cortex. Infarcts that involved the cerebral cortex or extensive areas of the subcortical white matter or that were >2 cm in greatest diameter were excluded. At the time of autopsy, the brain and spinal cord were placed in formalin; after 2 weeks they were serially sectioned at 1-cm intervals. After being embedded in paraffin and stained with hematoxylin and eosin, routine microscopic sections of the cerebral cortex, basal ganglia, hippocampus, cerebellum, brainstem, and spinal cord were examined. Microscopic sections of a lacune were examined in nearly all patients in whom such infarction was suspected. The final autopsy report provided information about the cause of death, the size and location of lacunes if present, and atherosclerosis in the circle of Willis.Etiologic mechanisms underlying lacunes were evaluated by extensive pathologic investigation in a subset of consecutive patients with lacunar infarcts autopsied during the first 5 years of our study. The microscopic brain slides of the basal ganglia were reexamined for the presence of mild, moderate, or severe medial hypertrophy, hyalinization, and dilatation in the intraparenchymal arteries and arterioles. Lipohyalinosis and Charcot-Bouchard aneurysms were classified as severe changes. The final autopsy reports in this subset of patients were reviewed for diagnoses of hypertension, atherosclerotic cardiovascular disease (ASCVD) in the absence by guest on May 11, 2018 http://stroke.ahajournals.org/ Downloaded from

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“…Although this incidence is higher than in previous studies, which have estimated the incidence as roughly 30-33%, 8 …”

contrasting

confidence: 66%

Risk factors and clinical manifestations of pathologically verified lacunar infarctions.

Tuszynski

Petito

Levy

1989

Stroke

127

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“…Stroke subtypes were classified according to the TOAST as cardiac embolism, other or unknown cause of stroke. The subjects were divided into groups according to the size of infarction observed on CT (referent to Pullicino (13)): large infarction group (>10 cm 3 ), middle infarction group (4.1-10 cm 3 ) and small infarction group (! 4 cm 3 ).…”

Section: Methodsmentioning

confidence: 99%

The Prognostic Value of Combined NT-pro-BNP Levels and NIHSS Scores in Patients with Acute Ischemic Stroke

Chen

et al. 2012

Intern. Med.

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Objective Determining the prognoses of patients with acute ischemic stroke is difficult. Therefore, the aim of this study was to evaluate whether the combined assessment of plasma N-terminal pro-brain natriuretic peptide (NT-pro-BNP) and the National Institutes of Health Stroke Scale (NIHSS) variables is relevant to the prognosis of patients with acute cerebral ischemic infarction in-hospital. Methods We enrolled 122 patients who were within three days of onset of acute ischemic stroke. We measured the plasma NT-pro-BNP level of each patient within 72 hours and recorded the NIHSS score on admission. The factors associated with death were investigated using a multivariate logistic regression analysis. Results Twenty-three patients (18.85%) died during hospitalization. The frequency of atrial fibrillation (AF), the NIHSS score on admission (8.69±4.87 in the survival group vs. 14.48±2.54 in the deceased group, p<0.001) and the plasma NT-pro-BNP level (median: 926.30 pg/mL in the survival group vs. 3,280 pg/mL in the deceased group, p<0.001; Lg NT-pro-BNP 2.82±0.66 in the survival group vs. 3.46±0.52 in the deceased group, p<0.001) were each significantly higher in the deceased group than in the survival group. The optimal cut-off levels for the NT-pro-BNP level and NIHSS score to distinguish the deceased group from the survival group were 1,583.50 pg/mL and 12.5, respectively. Patients with both elevated NT-pro-BNP levels (>1,583.50 pg/mL) and NIHSS scores on admission (NIHSS >12.5) had a substantially higher mortality rate than those without elevated NT-pro-BNP levels and NIHSS scores (89.47% vs. 9.84%, p<0.001). A multivariate logistic regression analysis demonstrated that a NT-pro-BNP level >1,583.50 pg/mL (OR, 5.001; 95% CI, 1.233 to 20.287, p=0.024) and a NIHSS score >12.5 (OR, 1.465; 95% CI, 1.191 to 1.801, p<0.001) were each independent factors associated with in-hospital death. Conclusion The plasma NT-pro-BNP level and the NIHSS score added independent and incremental contributions to the prognostic stratification of patients with acute ischemic stroke.

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“…In most of these studies, carotid artery disease was found to be significantly less frequent in patients with lacunar strokes compared with nonlacunar strokes. [31][32][33][34][35][36] The frequency of carotid disease in lacunar strokes has been considerably variable in different studies, ranging from 3% to 39%, [31][32][33][34][35][36][37][38][39][40][41] although it must be noted that the methodology used to both classify lacunar infarcts as well as to detect carotid disease also varied widely. A study of 726 patients with anterior circulation transient ischemic events or infarcts, excluding total anterior circulation infarcts, revealed a negative association of severe carotid stenosis with lacunar events.…”

Section: Carotid Artery Disease and Lacunar Infarctsmentioning

confidence: 99%

Is Investigating for Carotid Artery Disease Warranted in Non-Cortical Lacunar Infarction?

Rajapakse

Rajapakse²,

Sharma³

2011

Stroke

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Abstract-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. (Stroke. 2011;42:217-220.)

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Small Deep Infarcts Diagnosed on Computed Tomography

Cited by 16 publications

References 0 publications

Risk factors and clinical manifestations of pathologically verified lacunar infarctions.

Risk factors and clinical manifestations of pathologically verified lacunar infarctions.

The Prognostic Value of Combined NT-pro-BNP Levels and NIHSS Scores in Patients with Acute Ischemic Stroke

Is Investigating for Carotid Artery Disease Warranted in Non-Cortical Lacunar Infarction?

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