Large Subcortical Hemispheric Infarctions

Levine, Ross L.; Lagrèze, H. L.; Dobkin, Jeffrey A.; Turski, Patrick A.

doi:10.1001/archneur.1988.00520340028006

Cited by 46 publications

(23 citation statements)

References 14 publications

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“…Although deep, these infarcts were larger, involved the territory of more than one lenticulostriate artery, and produced deficits of higher cortical functions in some patients. Others 28 have also suggested that larger subcortical infarcts may result from a carotid or cardiac embolism. A cardiac source of embolism was more common in our patients with larger lacunes, but the numbers are too small to draw any conclusions.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms in lacunar infarction.

Horowitz

Tuhrim

Weinberger

et al. 1992

Stroke

116

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Background and Purpose: Lacunes are thought to occur in patients with hypertension or diabetes mellitus as a result of small-vessel disease. This study evaluated the importance of other stroke mechanisms in a population of patients with lacunar infarction.Methods: We evaluated 108 consecutive patients with a lacune in the lenticulostriate distribution for other stroke risk factors such as carotid and cardiac disease.Results: Hypertension was present in 68% of the patients and diabetes mellitus in 37%; both occurred in 28% and neither occurred in 23%. Noninvasive carotid studies identified atherosclerotic plaque as a possible embolic source in 23%. By previously established criteria, 18% were at high risk for cardioembolism. Of those with hypertension or diabetes mellitus, 36% were at risk for a carotid or cardiac embolus. Of those without hypertension or diabetes mellitus, 32% had a possible carotid or cardiac etiology.Conclusions

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Section: Discussionmentioning

confidence: 99%

Mechanisms in lacunar infarction.

Horowitz

Tuhrim

Weinberger

et al. 1992

Stroke

116

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“…In contrast to the original concept that striatocapsular infarctions occur nearly exclusively because of embolic occlusion of the proximal middle cerebral artery (MCA) [1,2,3], a significant proportion of this type of infarction also occur as a result of in situ thrombosis of the MCA. According to the previous reports [4,5,6,7,8], the most frequent causes of striatocapsular infarcts are artery-to-artery embolism from the internal carotid artery (ICA; 38%) and cardiogenic embolism (37%), as well as atherosclerotic disease in the MCA at the origin of lenticulostriate arteries (32%). Furthermore, the MCA disease (MCAD) is a relatively common cause of stroke in patients with Asian ancestry [9, 10] and is expected to be a more important cause of striatocapsular infarctions.…”

Section: Introductionmentioning

confidence: 99%

Can We Discriminate Stroke Mechanisms by Analyzing the Infarct Patterns in the Striatocapsular Region?

Lee

Oh²,

Roh³

et al. 2008

Eur Neurol

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Background and Aims: The aims of our study were to elucidate the differences in the distribution of acute middle cerebral artery (MCA) infarctions involving the striatocapsular region and to compare those following embolic striatocapsular infarctions with those originating from MCA disease (MCAD). Methods: We prospectively enrolled patients with acute large infarcts located in the lenticulostriate artery territory. Brain coronal diffusion-weighted imaging (DWI) and magnetic resonance angiography were carried out in all patients. The types of infarct distribution were divided into 3 categories: (1) dominant in the distal territory (DD), (2) distributed equally between the distal and proximal territories (DE) and (3) dominant in the proximal territory. Stroke mechanisms were classified into stroke from proximal embolism, MCAD and stroke of undetermined etiology. Results: A total of 71 patients were recruited. Proximal embolic sources were significantly more prevalent in patients with a DE lesion, but symptomatic MCA stenoses were more common in patients with a DD lesion than in those with a DE lesion. Conclusion: These results suggest that the dominant area of striatocapsular infarctions on coronal DWI can be an important clue for stroke etiology.

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“…Patients with a large subcortical infarct can have signs of cortical involvement, such as aphasia or hemineglect, 6,7,10 but also signs of a small deep infarct, for example, a pure motor stroke. 7,8 The vascular risk factors of patients with large subcortical infarcts fail to show a distinctive profile. 6,7,10 -12 Our study shows that recurrence rates and clinical syndromes of recurrent strokes also show overlap with those of either small deep infarcts or cortical infarcts.…”

Section: Discussionmentioning

confidence: 99%

“…They are located in the carotid territory, like most symptomatic small deep infarcts, but are larger and supposedly not caused by small-vessel disease. [5][6][7][8] Clinical features, risk factors, and long-term outcome of these infarcts have been studied in small series, 6 -12 but without comparison with other types of infarction. In the present study we evaluated clinical features, risk factors, overall outcome, and type of recurrent infarction in a large series of patients with recent cerebral ischemia of presumed arterial origin who participated in a large clinical trial.…”

mentioning

confidence: 99%

Large Subcortical Infarcts

Halkes

Kappelle

Gijn

et al. 2006

Stroke

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Background and Purpose-In this study we compared risk factors, clinical features, and stroke recurrence in a large series of patients with large subcortical, cortical, or small deep infarcts. Methods-Patients with a transient or minor ischemic attack (modified Rankin Scale grade of Յ3) who had a single relevant supratentorial infarct of presumed noncardioembolic origin on CT were classified as suffering from a large subcortical (nϭ120), small deep (nϭ324), or cortical (nϭ211)

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Large Subcortical Hemispheric Infarctions

Cited by 46 publications

References 14 publications

Mechanisms in lacunar infarction.

Mechanisms in lacunar infarction.

Can We Discriminate Stroke Mechanisms by Analyzing the Infarct Patterns in the Striatocapsular Region?

Large Subcortical Infarcts

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