Diffusion weighted imaging, apparent diffusion coefficient maps and stroke etiology

Bonati, Leo H.; Lyrer, Philippe; Wetzel, Stephan G.; Steck, A. J.; Engelter, Stefan T.

doi:10.1007/s00415-005-0881-1

Cited by 28 publications

(34 citation statements)

References 24 publications

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“…Clinical findings are provided in the Table. DWI was performed 5 (IQR, 2-7) days after stroke onset in patients with stenotic sICAD and after 2 (IQR, 0 -4) days in occlusive sICAD (Pϭ0.024). The number of DWI-lesions was higher in patients with stenotic sICAD (5 [IQR, [1][2][3][4][5][6][7][8][9][10] …”

Section: Resultsmentioning

confidence: 99%

“…4,5 We assessed number, size (largest axial diameter 4 ), and vascular territories 6 of all hyperintense DWI-lesions with hypo-/isointense appearance on apparent diffusion coefficient maps. The following 4 lesion patterns were distinguished, using a published classification system 7,8 with mild modifications: pattern 1 (territorial infarct involving cortical and subcortical structures); pattern 2 (subcortical infarct in the territory of deep perforating branches); pattern 3 (multiple, mainly cortical lesions in the distal territory of the MCA); pattern 4 (border-zone infarction with lesions predominantly involving the junction of cerebral vascular territories).…”

Section: Diffusion-weighted Imagingmentioning

confidence: 99%

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Diffusion-Weighted Imaging in Stroke Attributable to Internal Carotid Artery Dissection

Bonati

Wetzel

Gandjour

et al. 2008

Stroke

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Background and Purpose-In stroke attributable to spontaneous dissection of the internal carotid artery (sICAD), arterial patency may influence the pattern and extent of cerebral ischemia. Methods-In 40 consecutive patients with stroke caused by sICAD, we compared the number, size and pattern of cerebral diffusion-weighted imaging lesions between patients with stenotic sICAD (nϭ15) and occlusive sICAD (nϭ25). Results-Patients with stenotic sICAD had more ischemic lesions (median 5, interquartile range 1 to 10) than patients with occlusive sICAD (2, 1 to 3; Pϭ0.014). Lesion diameters were larger in occlusive sICAD (62, 50 to 99 mm) than in stenotic sICAD (25, 10 to 50 mm; Pϭ0.007). Border-zone infarction occurred only in stenotic sICAD (7/15, 47%

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Section: Resultsmentioning

confidence: 99%

Section: Diffusion-weighted Imagingmentioning

confidence: 99%

Diffusion-Weighted Imaging in Stroke Attributable to Internal Carotid Artery Dissection

Bonati

Wetzel

Gandjour

et al. 2008

Stroke

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“…Lesions were considered separate if there was no continuity between them on the same slice as well as on adjacent slices. 6 Age-related white matter changes were quantified on pretreatment fluid-attenuated inversion recovery sequences, using a published scale. 7 Subgroup analyses were performed comparing lesion count between CAS and CEA with regard to the following baseline characteristics dichotomizing continuous and ordinal scaled variables at the median values of the study population: age (<71 vs ≥71 years); sex; hypertension; systolic blood pressure at randomization (<158.5 vs ≥158.5 mm Hg); diabetes mellitus; hyperlipidemia; any smoking (current smoking or history of); coronary heart disease; type of qualifying event (defined as the most recent ipsilateral ischemic event before randomization: retinal ischemia or transient ischemic attack versus hemispheric stroke); interval between qualifying event and treatment (<14 days vs ≥14 days); degree of stenosis (70%-99% [severe], 50%-69% [moderate]); side of treated stenosis (left vs right); presence vs absence of hyperintense DWI lesions on pretreatment MRI; and age-related white matter changes (sum score, 0-4 vs ≥5).…”

Section: Imaging Outcome Measuresmentioning

confidence: 99%

Characteristics of Ischemic Brain Lesions After Stenting or Endarterectomy for Symptomatic Carotid Artery Stenosis

Gensicke

Zumbrunn

Jongen

et al. 2013

Stroke

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Background and Purpose-In a substudy of the International Carotid Stenting Study (ICSS), more patients had new ischemic brain lesions on diffusion-weighted magnetic resonance imaging (MRI) after stenting (CAS) than after endarterectomy (CEA). In the present analysis, we compared characteristics of diffusion-weighted MRI lesions. Methods-Number, individual and total volumes, and location of new diffusion-weighted MRI lesions were compared in patients with symptomatic carotid stenosis randomized to CAS (n=124) or CEA (n=107) in the ICSS-MRI substudy. Results-CAS patients had higher lesion numbers than CEA patients (1 lesion, 15% vs 8%; 2-5 lesions, 19% vs 5%; >5 lesions, 16% vs 4%). The overall risk ratio for the expected lesion count with CAS versus CEA was 8.8 (95% confidence interval, 4.4-17.5; P<0.0001) and significantly increased among patients with lower blood pressure at randomization, diabetes mellitus, stroke as the qualifying event, left-side stenosis, and if patients were treated at centers routinely using filter-type protection devices during CAS. Individual lesions were smaller in the CAS group than in the CEA group (P<0.0001). Total lesion volume per patient did not differ significantly. Lesions in the CAS group were more likely to occur in cortical areas and subjacent white matter supplied by leptomeningeal arteries than lesions in the CEA group (odds ratio, 4.2; 95% confidence interval, 1.7-10.2; P=0.002). Conclusions-Compared with patients undergoing CEA, patients treated with CAS had higher numbers of periprocedural ischemic brain lesions, and lesions were smaller and more likely to occur in cortical areas and subjacent white matter. These findings may reflect differences in underlying mechanisms of cerebral ischemia. Clinical Trial Registration-URL: http://www.isrctn.org. Unique identifier: ISRCTN25337470. (Stroke. 2013;44:80-86.)

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“…Previous studies focusing on multiple, acute brain infarcts [14][15][16][17][18][19][20][21][22] have reported widely variable results, attributing infarcts to an embolic source in 28 to 100 percent, with a cardiac or aortic source found in 18 to 52 percent of patients. In these studies, however, a large proportion (27 to 40 percent) of multiple infarcts have been linked speculatively, to emboli from proximal large artery stenotic lesions [14][15][16][17][18][19][20][21][22]. However, it is implausible that emboli could arise near simultaneously from different proximal arteries or traverse from one proximal artery to circulations in both hemispheres or from carotid to vertebrobasilar circulation.…”

Section: Discussionmentioning

confidence: 99%

“…Emboli are also unlikely, as has been shown by injecting microspheres into carotid arteries of monkeys, to selectively occlude deep penetrating arteries [23]. 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.…”

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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Diffusion weighted imaging, apparent diffusion coefficient maps and stroke etiology

Cited by 28 publications

References 24 publications

Diffusion-Weighted Imaging in Stroke Attributable to Internal Carotid Artery Dissection

Diffusion-Weighted Imaging in Stroke Attributable to Internal Carotid Artery Dissection

Characteristics of Ischemic Brain Lesions After Stenting or Endarterectomy for Symptomatic Carotid Artery Stenosis

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

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