Changes in Brain and Pial Vessels in Arterial Border Zones

Background and Purpose-The pathophysiology of borderzone infarcts is not well understood. We investigated whether combined diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) could identify pathophysiologically meaningful categories of borderzone infarcts. Methods-Seventeen patients with borderzone infarcts were identified from the Beth Israel Deaconess Medical Center Stroke Database. All patients had DWI and PWI, the majority of them within the first 24 hours of symptom onset.

Section: Discussionmentioning

confidence: 99%

Diffusion- and Perfusion-Weighted MRI Patterns in Borderzone Infarcts

Chaves¹,

Silver²,

Schlaug³

et al. 2000

“…The border-zone, or watershed, regions between major cerebral arteries are susceptible to ischemia and infarction. 23,24 Bilateral watershed infarction is common after profound systemic hypotension resulting from cardiac arrest or from other causes. 25 Unilateral infarction within borderzone regions occurs with atherosclerotic disease, 26 -28 of which ICA disease is most frequent.…”

Section: Discussionmentioning

confidence: 99%

Atherothrombotic Middle Cerebral Artery Territory Infarction

Min

Park

Kim

et al. 2000

Background and Purpose-MRI has superior capabilities for the detection of cerebral infarcts compared with CT. CT was used to locate infarcts in most previous studies of atherothrombotic middle cerebral artery (MCA) territory infarcts. Thus, there was a possibility of missing concomitant small infarcts. More accurate identification of topographic lesions in MCA territory with MRI may help to establish the pathogenesis of stroke. The present study determines topographic patterns, distribution of vascular lesions, and probable mechanisms. Methods-Forty-two patients with MCA territory infarcts on routine MRI and no major cause of cardioembolism were studied with conventional angiography or MR angiography. Results-The topographic patterns seen on MRI were subdivided into 4 groups: cortical border-zone infarcts (nϭ6), pial territory infarcts without insular infarct (nϭ3), pial territory infarcts with insular infarct (nϭ14), and large subcortical infarcts (nϭ19). Of 6 patients with cortical border-zone infarcts, 4 had concomitant small cortical or subcortical multiple lesions. Angiography showed intrinsic MCA disease in 4 patients. Of 3 patients with pial territory infarcts without insular infarct, 2 also had small multiple centrum ovale lesions. All had intrinsic MCA disease. Pial territory infarcts with partial or whole insular lesions were present in 10 and 4 patients, respectively. Five patients had additional multiple cortical or subcortical lesions. Ten patients had intrinsic MCA disease. Of the 19 patients with large subcortical infarcts, 12 had centrum ovale infarcts, and 4 had both basal ganglia and centrum ovale lesions. Ten had concomitant small cortical or subcortical lesions. Six patients had intrinsic MCA disease. Conclusions-Similar vascular lesions induce different topographic patterns in MCA territory infarction, which are related to individual vascular variability, degree of primary and secondary collateralization, and pathogenesis of infarcts. Our study indicates that concomitant small cortical or subcortical lesions are also commonly associated findings in diverse patterns of MCA territory infarction, which can mostly be explained by probable embolic mechanism. Key Words: angiography, magnetic resonance Ⅲ cerebral embolism Ⅲ magnetic resonance imaging Ⅲ middle cerebral artery M ost middle cerebral artery (MCA) territory infarcts have been attributed to embolism from the heart or internal carotid artery (ICA), poor perfusion due to ICA occlusion, intrinsic MCA occlusive disease, or intrinsic disease in the lenticulostriate penetrating vessels.Previous studies 1,2 indicated racial differences in atherothrombotic occlusive diseases of the anterior cerebral circulation. Specifically, extracranial atherosclerosis is more common in whites, whereas intracranial atherosclerosis is more frequent in blacks, Chinese, and Japanese. However, how the common intracranial atherosclerotic vascular lesions are associated with topographic patterns of infarcts has not been studied sufficiently.MRI of the brain has supe...

“…Anterior WS infarcts develop between the ACA and MCA territories, either or both as a thin fronto-parasagittal wedge extending from the anterior horn of the lateral ventricle to the frontal cortex, or superiorly as a linear strip on the superior convexity close to the interhemispheric fissure, whereas posterior WS infarcts develop between the ACA, MCA, and PCA territories and affect a parieto-temporooccipital wedge extending from the occipital horn of the lateral ventricle to the parieto-occipital cortex. 1,28 IWS infarcts can affect the corona radiata (CR), between the territories of supply of the deep and superficial (or medullary) perforators of the MCA, or the centrum semiovale (CSO), between the superficial perforators of the ACA and MCA. 1 However, in carotid disease, ie, the focus of this review, it is unlikely that hemodynamic insufficiency will affect equally the basal and the superficial MCA perforators, a situation that could, however, arise from eg, added MCA stem disease.…”

Section: Ws Infarcts: Anatomy Structural Imaging and Angiographymentioning

confidence: 99%

“…19,53 This in turn is consistent with a classic postmortem study of the border zones distal to ICA disease, where infarcts involved the CSO and the AWS. 28 This relative vulnerability of the AWS as compared with the PWS may be because the MCA and the ACA are both supplied only by the ICA, so critical stenosis or occlusion of the ICA will exert its maximum effect on the AWS. Any contralateral ICA disease and/or inefficient collateralization, particularly affecting the anterior portion of the circle of Willis, will add to this intrinsic vulnerability of the AWS.…”

Section: Cws Infarctsmentioning

confidence: 99%

The Pathophysiology of Watershed Infarction in Internal Carotid Artery Disease

Momjian-Mayor

Baron

2005

311

224

Background and Purpose-In carotid disease, infarcts can occur in the cortical as well as internal watershed (WS), or both.Better understanding the pathophysiology of WS infarcts would guide treatment. Two distinct hypotheses, namely low-flow and micro-embolism, are equally supported by neuropathological and physiological studies. Here we review the evidence regarding the mechanisms for WS stroke in carotid disease and whether they differ between cortical and internal WS infarcts. Summary of Review-After a brief account of the anatomy of the WS and the cerebrovascular physiology in circumstances of low perfusion pressure, the literature concerning the mechanisms of WS infarction in carotid disease is reviewed and discussed with emphasis on imaging and ultrasound studies of the cerebral hemodynamics. Conclusion-The evidence strongly favors a hemodynamic mechanism for internal WS infarction, especially regarding the so-called rosary-like pattern in the centrum semiovale. However, the relationships between cortical WS infarction and hemodynamic compromise appear more complicated. Thus, although severe hemodynamic compromise appears to underlie combined cortical and internal WS infarction, artery-to-artery embolism may play an important role in isolated cortical WS infarcts. Based on the high prevalence of microembolic signals documented by ultrasound in symptomatic carotid disease, a recent hypothesis postulates that embolism and hypoperfusion play a synergetic role, according to which small embolic material prone to lodge in distal field arterioles would be more likely to result in cortical micro-infarcts when chronic hypoperfusion prevails. Future studies combining imaging of brain perfusion, diffusion-weighted imaging, and ultrasound detection of microembolic signals should help resolve these issues. (Stroke. 2005;36:567-577.)