Are multiple acute small subcortical infarctions caused by embolic mechanisms?

Chowdhury, Debashish; Wardlaw, Joanna M.; Dennis, Martin

doi:10.1136/jnnp.2004.038653

Cited by 46 publications

(36 citation statements)

References 26 publications

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“…Large artery stenosis (%) 9 (12) 4 (9) 1 (7) 4 (29) Other embolic source (%) 2 (3) 0 1 (7) 1 (7) Stroke 22 In a number of studies, different rates for the detection of embolic sources in patients with multiple DWI lesions were identified. 9,19,21 Symptomatic extracranial arteriosclerosis or major cardioembolic sources were found in patients with lacunar infarctions, but 2 to 3ϫ less frequently than among patients with cortical infarctions.…”

Section: Imaging Characteristics and Clinical Findingsmentioning

confidence: 99%

Identification of Embolic Stroke Patterns by Diffusion-Weighted MRI in Clinically Defined Lacunar Stroke Syndromes

Wessels

Röttger

Jauß

et al. 2005

Stroke

105

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Background-A number of clinical syndromes describing the presentation of deep brain infarcts are called lacunar syndromes resulting from small vessel occlusion (SVO). To verify the reliability of the clinical diagnosis "lacunar syndrome," the value was investigated with diffusion-weighted MRI (DWI). Methods and Results-A total of 73 patients (mean age 66 years; range 35 to 83 years) with sudden onset of a classical lacunar syndrome were enrolled. On the basis of the DWI findings, patients were divided into 3 groups: group 1, single subcortical lesion (Ͻ15-mm lesion; 43 patients; 59%); group 2, large (Ն15 mm) or scattered lesions in 1 vascular territory (16 patients; 22%); and group 3, multiple lesions in multiple vascular territories (14 patients; 19%). A stroke mechanism other than SVO could be identified in 17 (23%) patients. Cardiac work-up revealed a cardiac embolic source in 8 patients (11%). Duplex sonography revealed symptomatic stenosis in 9 patients (12%). Based on the work-up information, 29 patients (40%) were found to have a potential cause of stroke other than SVO. A significant correlation with Ͼ1 single lesion on DWI-MRI and a clinical proven embolic source was observed (Pϭ0.002). In 9 patients with MRI suspicious for a pathomechanism other than SVO, no embolic source was found. Conclusions-The

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Section: Imaging Characteristics and Clinical Findingsmentioning

confidence: 99%

Identification of Embolic Stroke Patterns by Diffusion-Weighted MRI in Clinically Defined Lacunar Stroke Syndromes

Wessels

Röttger

Jauß

et al. 2005

Stroke

105

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“…MCA disease could also cause pure lacunar infarctions via the mechanism of branch atheromatous disease [6,16]. Lacunar infarction and white matter hyperintensities (WMHs) may share a common mechanism of small vessel disease [12,17]. We hypothesized that perforator territory infarcts in the LSA territory (pLSAIs) may have heterogeneous lesion patterns and stroke mechanisms.…”

Section: Introductionmentioning

confidence: 99%

“…Infarctions involving the vascular territory of the LSA, such as classic lacunar infarctions in the basal ganglia [3,4], lacunar or striatocapsular infarctions with middle cerebral artery (MCA) disease [5,6,7,8], embolism [9,10] or deep subcortical infarctions [11,12,13,14,15], have been studied in diverse ways. Lacunar infarcts with pial or border-zone infarcts are a probable lesion pattern for LSA territorial infarctions with MCA disease [7,14].…”

Section: Introductionmentioning

confidence: 99%

Perforator Territory Infarction in the Lenticulostriate Arterial Territory: Mechanisms and Lesion Patterns Based on the Axial Location

Cho¹,

Roh²,

Moon³

et al. 2010

Eur Neurol

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Background: We hypothesized that perforator territory infarcts in the lenticulostriate territory (pLSAIs) may have heterogeneous lesion patterns and stroke mechanisms. Methods: We reviewed prospectively collected patients who developed pLSAIs within 72 h after stroke onset. Lesion patterns were analyzed based on the six axial levels. Based on MR angiography, stenosis of the middle cerebral artery (MCA) was classified into 3 groups. White matter hyperintensities were assessed by Fazeka’s scale of periventricular hyperintensity (PVH) and deep white matter hyperintensity (DWMH). Results: Of 221 patients, 159 were normal, 44 had mild stenosis, and 18 had severe stenosis of the MCA. Larger infarct volume was correlated with the severity of MCA disease (r = 0.289, p < 0.001). Lower lesion patterns were correlated with the severity of MCA disease (r = –0.294, p < 0.001). A higher lesion pattern was correlated with the severity of DWMH or PVH scores (r = 0.205, p = 0.002 in DWMH, and r = 0.137, p = 0.042 in PVH). Conclusions: Patients with MCA disease have larger and lower lesion patterns beginning from the proximal territory of the lenticulostriate artery (LSA). Patients with severe white matter changes have smaller and higher lesion patterns in the distal territory of the LSA.

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“…Data on blood pressure at the time of stroke onset was not provided in any of these studies [14][15][16][17][18][19][20][21][22]. Only one previous study [24] which reported multiple, small, deep subcortical infarcts in most patients found no embolic source in 9 of 10 patients. In contrast to our study, MRI scans were done an average of 17 days after onset and the authors suggested that infarcts had occurred over several weeks.…”

Section: Discussionmentioning

confidence: 99%

Can Transient Drop in Blood Pressure in High-Risk Hypertensive Patients Cause Small Cerebral Infarcts?

Bhagavati

Choi

2013

ISRN Stroke

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Background. Multiple, simultaneous, acute cerebral infarcts in different arterial territories are usually secondary to embolic occlusion of multiple cerebral arteries. We observed, however, that no cardiac or aortic source could be found in many of these patients. We therefore undertook this study to attempt to identify other factors that may be important in the causation of these infarcts. Materials and Methods. We performed a five-year retrospective review of all patients with multiple, near simultaneous, acute cerebral infarcts detected on diffusion-weighted MRI scans. Results. We identified 78 patients with acute infarcts, in different cerebral arterial territories. We found a cardiac embolic source in 15 (19 percent) patients. Forty-one patients (53%) had no obvious cause for their infarcts after detailed cardiovascular and hematological evaluation. In 16 of these patients (20% of all 78 patients), all with a history of chronic hypertension who had multiple, acute, small (<2 cms), deep subcortical or superficial cortical infarcts (and most, 93%, with extensive evidence of chronic small vessel disease on MRI FLAIR images), blood pressure was low or normal on initial presentation (mean arterial pressure, MAP: 85 ± 11.4 mm Hg). Analysis of the last prestroke blood pressure, within the previous 1 to 11 days available in 13 of 16 patients, revealed much higher BP (MAP: 113.6 ± 11.3 mm Hg), indicating a mean drop of 25.1 percent (range 11 to 44 percent). Two weeks after the stroke, blood pressure had risen again to greater than 160/100 mm Hg (MAP: 128.2 ± 14.3). Conclusion. Our study suggests that transient drop in blood pressure in high-risk hypertensive patients with severe, small vessel disease may sometimes result in small, cerebral infarcts. More research is needed to further clarify and confirm this possibility.

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Are multiple acute small subcortical infarctions caused by embolic mechanisms?

Cited by 46 publications

References 26 publications

Identification of Embolic Stroke Patterns by Diffusion-Weighted MRI in Clinically Defined Lacunar Stroke Syndromes

Identification of Embolic Stroke Patterns by Diffusion-Weighted MRI in Clinically Defined Lacunar Stroke Syndromes

Perforator Territory Infarction in the Lenticulostriate Arterial Territory: Mechanisms and Lesion Patterns Based on the Axial Location

Can Transient Drop in Blood Pressure in High-Risk Hypertensive Patients Cause Small Cerebral Infarcts?

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