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(Stroke. 2000;31:631.)
© 2000 American Heart Association, Inc.

Original Contributions

Internal Borderzone Infarction

A Marker for Severe Stenosis in Patients With Symptomatic Internal Carotid Artery Disease

M. Del Sette, MD; M. Eliasziw, PhD; J. Y. Streifler, MD; V. C. Hachinski, MD; A. J. Fox, MD; H. J. M. Barnett, MD for the North American Symptomatic Carotid Endarterectomy (NASCET) Group

From the Department of Neuroscience and Neurorehabilitation, University of Genova, Genova, Italy (M.D.S.); The John P. Robarts Research Institute (M.E., V.C.H., H.J.M.B.) and the Departments of Clinical Neurological Sciences (M.E., V.C.H., A.J.F., H.J.M.B.) and Diagnostic Radiology (A.J.F.), University of Western Ontario, London, Ontario, Canada and the Neurology Unit, Rabin Medical Center, Campus Golda, Petach Tikva, and the Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel (J.Y.S.).

Correspondence to H.J.M. Barnett, MD, The John P. Robarts Research Institute,100 Perth Drive, PO Box 5015, London, Ontario N6A 5K8, Canada.

	Abstract

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Background and Purpose—Among subcortical infarctions, internal borderzone infarcts (IBI) are considered to be separate entities from perforating artery infarcts (PAI). The purpose of the present study is to examine the relationship between the presence of IBI and the degree of angiographically defined internal carotid artery (ICA) stenosis in symptomatic patients.

Methods—A review of 1253 brain CTs from patients recruited by the North American Symptomatic Carotid Endarterectomy Trial was performed, using templates for the identification of subcortical and cortical vascular territories.

Results—A total of 413 patients had visible ischemic lesions on the side ipsilateral to their symptomatic ICA. Of these, 138 had PAI, 108 had IBI, 122 had cortical infarcts, and 45 had a combination of different lesions. Mean (±SD) lesion diameter was larger for IBI (11.0±5.9 mm) than for PAI (7.1±4.7 mm) (P<0.001 for comparing 2 means). IBI was associated with higher degrees of ICA stenosis (P<0.001). Sixty-three percent of the patients with IBI had severe (70% to 99%) ICA stenosis compared with 42% of patients with PAI; 18% of the IBI patients had stenosis of 90% or more compared with 8% of the patients with PAI. Multiple logistic regression did not identify any patient characteristics as confounders.

Conclusions—Among subcortical infarctions, IBI are associated with higher degrees of ICA stenosis in symptomatic patients. Differentiating between internal borderzone and perforating artery infarcts is important, because each may arise from different mechanisms, namely, carotid disease and small-vessel disease, respectively.

Key Words: carotid stenosis • subcortical infarction • tomography, x-ray computed

	Introduction

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Arecently proposed classification system for subcortical infarctions, based on arterial territory, suggests that cerebral infarctions in the territory of deep and superficial perforating arteries be differentiated from infarctions in the vascular borderzone, located between the deep and superficial perforators.¹ The borderzone type of subcortical infarct is referred to in the literature as an "internal borderzone infarct" or a "subcortical junctional infarct."^{1 2} A few studies comparing patients with internal borderzone infarction to patients with other types of cerebral infarction observed that patients with internal borderzone infarcts had a higher frequency of severe carotid stenosis and occlusion,³ diabetes mellitus,³ and heart disease.^{3 4} Other studies, taking into account the variability among vascular supply areas, did not confirm the association between internal borderzone infarction and severe carotid stenosis or occlusion^{4 5} but found a new association between chronic obstructive pulmonary disease combined with diabetes mellitus.⁴

The aim of the present study was to evaluate the characteristics of subcortical infarctions, identified by CT scans, in patients with ischemic symptoms and angiographically defined internal carotid artery (ICA) stenosis.

	Subjects and Methods

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Subjects
Brain CT scans from 1253 patients, who were recruited between January 1, 1988, and August 16, 1991, into the North American Symptomatic Carotid Endarterectomy Trial (NASCET), formed the basis of the present study. Baseline characteristics of the patients have been described elsewhere.⁶ In brief, patients were entered into the trial if they were younger than 80 years, had transient ischemic attacks or nondisabling strokes in the carotid vascular territory within 120 days prior to randomization, and the participating center considered the degree of ICA stenosis to be 30% to 99% by angiography. Patients with ipsilateral internal carotid occlusion were not entered into the trial, nor were those with a possible cardiac source of emboli or with angiographic evidence of severe intracranial vascular disease.

Neuroimaging
Hard copies of all brain CT scans and angiographic images were sent by the participating centers to the Central Office and were reviewed initially by the trial’s principal neuroradiologist (A.J.F.). In the majority of cases, CT scans were performed with a third-generation scanner and with a distance of 10 mm between 2 slices. Biplane (anterior-posterior, lateral, and/or oblique) selective carotid angiography was used for the assessment of the degree of stenosis, using strict criteria. The degree of luminal linear carotid stenosis was derived as a ratio, gauging the diameter of the narrowest lumen as the numerator against the diameter of the normal artery well beyond the carotid bulb and disease distally as the denominator. Detailed examination of the state of the circle of Willis was not feasible from the NASCET database.

All brain CT scans were subsequently reread by one of the authors (M.D.S.), who was unaware of the clinical features and angiographic results, with templates (Figure 1) for the identification of vascular territories.^{2 7 8 9 10 11} The primary interest was in identifying all subcortical lesions and then classifying them into different vascular territories and borderzone areas. For each lesion identified, the mean of 2 measured perpendicular diameters was calculated.

View larger version (59K): [in this window] [in a new window]   Figure 1. Schematic CT templates showing the idealized standard of the vascular territories. The vascular borderzones are the areas between the cortical supply of the ACA, MCA, and PCA. The internal borderzones are the areas between the ACA, MCA, and PCA, and the area supplied by the Heubner, the lenticulostriate, and the anterior choroidal arteries. These areas are the locations of internal borderzone infarcts.

Definitions
The CT lesions were classified into 3 categories: perforating artery infarcts (PAI), internal borderzone infarcts (IBI), and cortical infarcts (either territorial or watershed). PAI were identified, according to the criteria of Ghika et al⁸ and Bogousslavsky and Regli,² as a hypodense area within the vascular territory of deep perforators (region of the basal ganglia, internal capsule, and thalamus) or superficial perforators (region of the centrum ovale and external capsule). Infarcts in the territory of the superficial perforators have been designated "white matter medullary infarcts."¹⁰ IBI were defined as a hypodense area in the vascular internal borderzone, where the border between the deep and superficial perforating arteries divide the infarct into 2 approximately equal sections.^{1 2 3 9 11 12 13} Examples of IBI are shown in Figures 2 and 3. Lesions more likely to be leukoaraiosis¹⁴ were excluded. Cortical territorial infarctions were defined as hypodense areas in the superficial vascular territory of a main cerebral artery. Cortical watershed infarctions were defined as hypodense areas in which the border between 2 main cerebral arteries divided the infarct into 2 approximately equal parts.^{8 13}

View larger version (59K): [in this window] [in a new window]   Figure 2. CT slices (A) through the lateral ventricles and (B) high convexity, in the same patient, show the location of 3 small zones of left hemisphere borderzone infarction.

View larger version (103K): [in this window] [in a new window]   Figure 3. High CT slice shows the location of 3 small left hemisphere borderzone infarctions, appearing as a chain.

Statistical Analysis
The ² test and t test were used to compare the lesion types with respect to patient characteristics when the variables were categorical and continuous, respectively. Multiple logistic regression analysis was used to assess the association between degree of ICA stenosis and type of lesion, while controlling for all patient characteristics. Sixty-seven CT scans were reread blindly by one of the authors (M.D.S.), and the reliability of being able to distinguish among no lesion, PAI, IBI, and cortical lesions was high (=0.94). The reliability with which the reader was able to measure the dimension of the lesion was also high (=0.85).

	Results

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Of the 1253 CT scans, 723 were bilaterally normal. Another 117 were normal, ipsilateral to the symptomatic carotid artery, but showed lesions on the contralateral side. Among the remaining patients with ipsilateral ischemic lesions, 138 had PAI, 108 had IBI, and 122 had cortical infarcts. There were 45 patients with a combination of different lesions. Because the primary interest was in comparing groups with single-type subcortical infarctions, the subsequent analyses were restricted to the 138 patients who had 162 PAI and the 108 who had 145 IBI. Eighty-three patients had only 1 IBI, 15 had 2 IBI, 8 had 3 IBI, and 2 had 4 IBI in the same hemisphere. All the patients with multiple lesions of the same type were counted only once in the analyses.

The patient characteristics in the 2 groups are shown in Table 1. Except for the degree of ipsilateral ICA stenosis, no statistically significant differences were observed between patients with PAI and IBI lesions, although the presence of contralateral ICA occlusion was slightly higher in the IBI group. The relationship between the degree of stenosis and type of subcortical lesion is detailed in Figure 4. Sixty-three (45+18) percent of the patients with IBI had severe (70% to 99%) carotid stenosis compared with 42% (34+8) of patients with PAI (OR 2.3); 18% of the IBI patients had stenosis of 90% or more compared with 8% of the patients with PAI (OR 2.5). Results from the multiple logistic regression analysis indicated that none of the patient characteristics were confounding factors, and therefore the degree of stenosis remained significantly different between the 2 groups.

View this table: [in this window] [in a new window]   Table 1. Characteristics of Patients With Subcortical Infarctions

View larger version (58K): [in this window] [in a new window]   Figure 4. Bar graph comparing the distribution of the degree of ICA stenosis in the PAI group with the IBI group.

The distribution of the lesions in the different vascular territories is shown in Table 2. The majority of the PAI were located in the middle cerebral artery territory. Comparing the diameter of the lesions shows that IBI are on average 3.9 mm larger than PAI (P<0.001 for comparing 2 means). In fact, more than twice as many (59.3% versus 23.5%) of the IBI were 10 mm or greater in comparison with the PAI.

View this table: [in this window] [in a new window]   Table 2. Characteristics of the Subcortical Lesions

	Discussion

Top Abstract Introduction Subjects and Methods Results Discussion References

 
This is a large study on symptomatic patients with varying degrees of angiographically defined carotid artery stenosis and subcortical infarctions. Among all subcortical lesions seen on brain CT scans, IBI are associated with higher degrees of carotid stenosis. Patients with IBI are 2.3 times more likely to have severe (70% to 99%) ICA stenosis than patients with PAI.

The present study shows that internal borderzone infarcts are larger than infarctions in the areas of perforating arteries, yet about 80% of them are smaller than 15 mm (Table 2b). Even if the territory supplied by perforators may vary widely in different subjects,^{8 9 11} the templates used in this study may be useful in differentiating IBI from PAI (Figure 1). Infarcts within the vascular territory of perforating arteries are usually smaller than IBI.^{7 15} In some cases of centrum ovale infarction, it may be difficult to recognize IBI from infarction of the superficial territory of middle cerebral,² because of anatomic variation. The presence of 2 or more lesions, appearing as a chain of round infarcts along the internal vascular borderzone, can be helpful in some cases (Figure 3). Several authors have previously reported patients with carotid stenosis and subcortical infarctions, although most of the lesions were PAI.^{15 16 17 18 19 20 21}

Lesions in the internal borderzone are attributed to the effects of severe stenosis and occlusion of the internal carotid or middle cerebral artery. Read et al¹⁰ reported a higher proportion of carotid stenosis or occlusion in 18 IBI compared with 22 white matter medullary infarcts (PAI in the territory of the superficial perforators). Angeloni et al¹² performed angiography in 36 patients within 6 hours of an acute embolic stroke and reported 7 cases of internal borderzone infarctions and acute middle cerebral artery occlusion. Bogousslavsky and Regli¹³ reported 26 cases of internal carotid occlusion with "watershed infarctions," 6 of which were in the internal borderzone. In a CT-angiographic study, Wodarz²² found watershed infarctions (either cortical or in the internal borderzone) in 40% of 55 patients with carotid stenosis or occlusion. In a study of 107 patients with internal carotid occlusion, Ringelstein et al²³ reported that 8 had watershed cortical infarctions and 36 had "subcortical terminal supply area infarctions." Waterston et al²⁴ reported 10 cases of "small deep infarcts" associated with severe carotid stenosis or occlusion, and most of the small lesions were located in the internal borderzone areas. In a study of 383 patients with cerebral infarction, Gandolfo et al²⁵ reported a significant role of carotid stenosis or occlusion in the formation of "pure" IBI. A recent study of 384 patients in the European Carotid Surgery Trial reported a tendency for borderzone infarction to occur more often distal to severe carotid disease, but the finding was not statistically significant.⁵

Previous reports have described IBI as the effect of hemodynamic impairment, due to severe carotid stenosis or occlusion, or to severe heart disease.^{3 4 26 27} The "hemodynamic theory" of IBI etiology is indirectly supported by some PET studies, which report a functional reduction of rCBF in the cortical watershed areas of patients with severe carotid disease.^{28 29} A recent study performed with SPECT showed a significantly lower perfusion reserve in patients with deep watershed infarction.³⁰ Nevertheless, other functional studies have not confirmed these findings,^{31 32} and other clinical and experimental studies appear to support an embolic mechanism for both superficial territorial and watershed or internal borderzone infarctions.^{12 33 34 35 36 37} The perforating medullary arteries originating from the pial branches and reaching the deep white matter of the cerebral hemispheres are end arteries, as are the deep perforators.^{2 38} A partial or transient embolic occlusion of one main cerebral artery (or branches) may allow adequate flow in the lenticulostriate arteries, and sufficient collateral flow from the anastomotic network may restrict the area of infarction to the "last field," which in the case of IBI is the border between the deep and superficial perforators. The end result might be the formation of IBI.^{12 36 37}

In conclusion, the present study, using a large sample size, demonstrates that for symptomatic patients with ICA disease and without severe cardiac disease, the presence of IBI is a marker for severe ICA stenosis. Therefore, IBI can be regarded as a separate entity from PAI, because of the higher likelihood of finding severe ICA stenosis in the presence of IBI.

	Acknowledgments

 
This study was supported by grant RO1-NS-24456 from the National Institute of Neurological Disorders and Stroke. The authors acknowledge the support of all participants in NASCET, and to SmithKline Beecham for providing Ecotrin for all NASCET patients. The authors would also like to thank Prof Domenico Inzitari for his helpful comments.

Received April 29, 1999; revision received December 28, 1999; accepted December 28, 1999.

	References

Top Abstract Introduction Subjects and Methods Results Discussion References

 

1. Donnan GA, Norrving B, Bamford JM, Bogousslavsky J. Subcortical infarctions: classification and terminology. Cerebrovasc Dis. 1993;3:248–251.
2. Bogousslavsky J, Regli F. Centrum ovale infarcts: subcortical infarction in the superficial territory of the middle cerebral artery. Neurology. 1992;42:1992–1998.[Abstract/Free Full Text]
3. Bladin CF, Chambers BR. Clinical features, pathogenesis and computed tomographic characteristics of internal watershed infarction. Stroke. 1993;24:1925–1932.[Abstract/Free Full Text]
4. Hupperts RMM, Lodder J, Heuts-van Raak EPM, Wilmink JT, Kessel AGH. Borderzone brain infarcts on CT taking into account the variability in vascular supply areas. Cerebrovasc Dis. 1996;6:294–300.
5. Hupperts RMM, Warlow CP, Slattery J, Rothwell PM. Severe stenosis of the internal carotid artery is not associated with borderzone infarcts in patients randomised in the European Carotid Surgery Trial. J Neurol. 1997;244:45–50.[Medline] [Order article via Infotrieve]
6. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med. 1991;325:445–453.[Abstract]
7. Damasio H. A computer tomographic guide to the identification of cerebral vascular territories. Arch Neurol. 1983;40:138–142.[Abstract]
8. Ghika JA, Bogousslavsky J, Regli F. Deep perforators from the carotid system. Arch Neurol. 1990;47:1097–1100.[Abstract]
9. van der Zwan A, Hilen B, Tulleken CAF, Dujovny M, Dragovic L. Variability of the territories of the major cerebral arteries. J Neurosurg. 1992;77:927–940.[Medline] [Order article via Infotrieve]
10. Read SJ, Pettigrew L, Schimmel L, Levi CR, Bladin CF, Chambers BR, Donnan GA. White matter medullary infarcts: acute subcortical infarction in the centrum ovale. Cerebrovasc Dis. 1998;8:289–295.[Medline] [Order article via Infotrieve]
11. Hennerici M, Daffertshofer M, Jakobs L. Failure to identify cerebral infarct mechanism from topography of vascular territory lesions. AJNR Am J Neuroradiol. 1998;19:1067–1074.[Abstract]
12. Angeloni U, Bozzao L, Fantozzi L, Bastianello S, Kushner M, Fieschi C. Internal borderzone infarction following acute middle cerebral artery occlusion. Neurology. 1990;40:1196–1198.[Abstract/Free Full Text]
13. Bogousslavsky J, Regli F. Borderzone infarctions distal to internal carotid artery occlusion: prognostic implications. Ann Neurol. 1986;20:346–350.[Medline] [Order article via Infotrieve]
14. Hachinski VC, Potter P, Merksey H. Leuko-araiosis. Arch Neurol. 1987;44:21–23.[Abstract]
15. Fisher CM. Lacunar strokes and infarcts: a review. Neurology. 1982;32:871–876.[Abstract/Free Full Text]
16. Weisberg LA. Lacunar infarcts: clinical and computed tomographic correlations. Arch Neurol. 1982;39:37–40.[Abstract]
17. Nelson RF, Pullicino P, Kendall BE, Marshall J. Computed tomography in patients presenting with lacunar syndromes. Stroke. 1980;11:256–261.[Abstract/Free Full Text]
18. Pullicino R, Nelson RF, Kendall BE, Marshall J. Small deep infarcts diagnosed on computed tomography. Neurology. 1980;30:1090–1096.[Abstract/Free Full Text]
19. Loeb C, Gandolfo C, Mancardi GL, Primavera A, Tassinari T. The lacunar syndromes: a review with personal contribution. In: Lechner H, Meyer JS, Ott E, eds. Cerebrovascular Disease: Research and Clinical Management. Vol. 1. Amsterdam, Netherlands; Elsevier. 1986;1:107–156.
20. Ghika J, Bogousslavsky J, Regli F. Infarcts in the territory of the deep perforators from the carotid system. Neurology. 1989;39:507–512.[Abstract/Free Full Text]
21. Kappelle LJ, Koudstaal PJ, Van Gihn J, Ramos LM, Keunen JE. Carotid angiography in patients with lacunar infarction: a prospective study. Stroke. 1988;19:1093–1096.[Abstract/Free Full Text]
22. Wodarz R. Watershed infarctions and computed tomography: a topographical study in cases with stenosis or occlusion of the carotid artery. Neuroradiology. 1980;19:245–248.[Medline] [Order article via Infotrieve]
23. Ringelstein EB, Zeumer H, Angelou D. The pathogenesis of strokes from internal carotid artery occlusion: diagnostic and therapeutical implications. Stroke. 1983;14:867–875.[Abstract]
24. Waterston JA, Brown MM, Butler P, Swash M. Small deep cerebral infarcts associated with occlusive internal carotid artery disease: a hemodynamic phenomenon? Arch Neurol. 1990;47:953–957.[Abstract]
25. Gandolfo C, Del Sette M, Finocchi C, Calautti C, Loeb C. Internal borderzone infarction in patients with ischemic stroke. Cerebrovasc Dis. 1998;8:255–258.[Medline] [Order article via Infotrieve]
26. Hupperts RMM, Lodder J, Wilmink J, Boiten J, Heuts-van Raak EPM. Haemodynamic mechanism in small subcortical borderzone infarcts? Cerebrovasc Dis. 1993;3:231–235.
27. Mounier-Vehier F, Leys D, Godefroy O, Rondepierre PH, Marchau M Jr, Pruvo JP. Borderzone infarct subtypes: preliminary study of the presumed mechanism. Eur Neurol. 1994;34:11–15.[Medline] [Order article via Infotrieve]
28. Leblanc R, Yamamoto YL, Tyler JL, Hakim A. Hemodynamic and metabolic effects of extracranial carotid disease. Can J Neurol Sci. 1989;16:51–57.[Medline] [Order article via Infotrieve]
29. Yamauchi H, Fukuyama H, Yamaguchi S, Miyoshi T, Kimura J, Konishi J. High-intensity area in the deep white matter indicating hemodynamic compromise in internal carotid artery occlusive disorders. Arch Neurol. 1991;48:1067–1071.[Abstract]
30. Moriwaki H, Matsumoto M, Hashikawa K, Oku N, Ishida M, Seike Y, Watanabe Y, Hougaku H, Handa N, Nishimura T. Hemodynamic aspect of cerebral watershed infarction: assessment of perfusion reserve using iodine-123-iodoamphetamine SPECT. J Nucl Med. 1997;38:1556–1562.[Abstract/Free Full Text]
31. Carpenter DA, Grubb RL Jr, Powers WJ. Borderzone hemodynamics in cerebrovascular disease. Neurology. 1990;40:1587–1592.[Abstract/Free Full Text]
32. Powers WJ. Cerebral hemodynamics in ischemic cerebrovascular disease. Ann Neurol. 1991;29:231–240.[Medline] [Order article via Infotrieve]
33. Pollanen MS, Deck JH. Directed embolization is an alternate cause of cerebral watershed infarction. Arch Pathol Lab Med. 1989;113:1139–1141.[Medline] [Order article via Infotrieve]
34. Pollanen MS, Deck JH. The mechanism of embolic watershed infarction: experimental studies. Can J Neurol Sci. 1990;17:395–398.[Medline] [Order article via Infotrieve]
35. Torvik A. The pathogenesis of watershed infarcts in the brain. Stroke. 1984;15:221–223.[Free Full Text]
36. Bozzao L, Fantozzi LM, Bastianello S, Bozzao A, Fieschi C. Early collateral blood supply and late parenchymal brain damage in patients with middle cerebral artery occlusion. Stroke. 1989;20:735–740.[Abstract/Free Full Text]
37. Graeber MC, Jordan JE, Mishra SK, Nadeau SE. Watershed infarction on computed tomographic scan: an unreliable sign of hemodynamic stroke. Arch Neurol. 1992;49:311–313.[Abstract]
38. Furuta A, Ishii N, Nishihara Y, Horie A. Medullary arteries in aging and dementia. Stroke. 1991;22:442–446.[Abstract/Free Full Text]

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Del Sette, M. Articles by Barnett, H. J. M. Search for Related Content PubMed PubMed Citation Articles by Del Sette, M. Articles by Barnett, H. J. M. Related Collections Carotid Stenosis Embolic stroke Computerized tomography and Magnetic Resonance Imaging Pathology of Stroke