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Contributors
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- By Pierre Amarenco, Adrià Arboix, Marcel Arnold, Robert W. Baloh, John Bamford, Jason J. S. Barton, Claudio L. Bassetti, Christopher F. Bladin, Julien Bogousslavsky, Julian Bösel, Marie-Germaine Bousser, Thomas Brandt, John C. M. Brust, Erica C. S. Camargo, Louis R. Caplan, Emmanuel Carrera, Carlo W. Cereda, Seemant Chaturvedi, Claudia Chaves, Chin-Sang Chung, Isabelle Crassard, Hans Christoph Diener, Marianne Dieterich, Ralf Dittrich, Geoffrey A. Donnan, Paul Eslinger, Conrado J. Estol, Edward Feldmann, José M. Ferro, Joseph Ghika, Daniel Hanley, Ahamad Hassan, Cathy Helgason, Argye E. Hillis, Marc Hommel, Carlos S. Kase, Julia Kejda-Scharler, Jong S. Kim, Rainer Kollmar, Joshua Kornbluth, Sandeep Kumar, Emre Kumral, Hyung Lee, Didier Leys, Eric Logigian, Mauro Manconi, Elisabeth B. Marsh, Randolph S. Marshall, Isabel P. Martins, Josep Lluís Martí-Vilalta, Heinrich P. Mattle, Jérome Mawet, Mikael Mazighi, Patrik Michel, Jay Preston Mohr, Thierry Moulin, Sandra Narayanan, Kwang-Yeol Park, Florence Pasquier, Charles Pierrot-Deseilligny, Nils Petersen, Raymond Reichwein, E. Bernd Ringelstein, Gabriel J. E. Rinkel, Elliott D. Ross, Arnaud Saj, Martin A. Samuels, Jeremy D. Schmahmann, Stefan Schwab, Florian Stögbauer, Mathias Sturzenegger, Laurent Tatu, Pariwat Thaisetthawatkul, Dagmar Timmann, Jan van Gijn, Ana Verdelho, Francois Vingerhoets, Patrik Vuilleumier, Fabrice Vuillier, Eelco F. M. Wijdicks, Shirley H. Wray, Wendy C. Ziai
- Edited by Louis R. Caplan, Jan van Gijn
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- Book:
- Stroke Syndromes, 3ed
- Published online:
- 05 August 2012
- Print publication:
- 12 July 2012, pp vii-x
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Chapter 42 - Borderzone infarcts
- from Section 2 - Vascular topographic syndromes
- Edited by Louis R. Caplan, Jan van Gijn
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- Book:
- Stroke Syndromes, 3ed
- Published online:
- 05 August 2012
- Print publication:
- 12 July 2012, pp 480-500
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Summary
The basal ganglia (BG) including the caudate nucleus are well known for their motor functions. The BG nuclei are anatomically and functionally associated with each of the frontal-striatal-thalamic-frontal circuits or loops. The caudate nucleus assumes the shape of a comet, curving along the lateral wall of the lateral ventricle. The caudate nucleus receives its blood supply mainly through the deep penetrators arising from the anterior cerebral arteries (ACAs) and middle cerebral arteries (MCAs) although there are individual differences. The major risk factors for caudate nucleus infarcts are: hypertension, hypercholesterolemia, diabetes mellitus, previous myocardial infarct, and cigarette smoking. As caudate nucleus infarcts can develop from any stroke mechanisms including lipohyalinosis, branch atheromatous disease, large artery atherothrombosis, or embolism, treatment of patients with caudate nucleus infarcts depends on the underlying stroke mechanism. Caudate nucleus hemorrhages account for approximately 7% of all intracerebral hemorrhages (ICH) and are caused by rupture of penetrating arteries.
44 - Border zone infarcts
- from PART II - VASCULAR TOPOGRAPHIC SYNDROMES
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- By E. Bernd Ringelstein, Florian Stögbauer, Neurology Clinic, Westfälische Wilhelms-University, Münster, Germany
- Edited by Julien Bogousslavsky, Université de Lausanne, Switzerland, Louis R. Caplan, Harvard Medical School
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- Book:
- Stroke Syndromes
- Published online:
- 17 May 2010
- Print publication:
- 24 May 2001, pp 564-582
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Summary
Historical background and terminology
Low-flow infarctions, also called ‘border zone infarctions’, are the result of a critically reduced cerebral perfusion pressure in far-downstream brain arteries that leads to a critically reduced cerebral blood flow and oxygen supply in certain vulnerable brain areas. These areas are defined by the specific angioarchitecture of the cerebrum. The term watershed infarction should be reserved for the cortical infarcts located in-between the territories of the major cerebral arteries, and should not be extended to the more common, subcortical type of low-flow infarction. The latter is located within the affected vascular distribution but in a zone of marginal irrigation (i.e. border zone) comparable to the ‘last field’ in a unidirectional (i.e. non-collateralized) agricultural watering system (Zülch & Behrend, 1961). The more general terms ‘low-flow infarction’, or ‘hemodynamically induced infarction’, are preferred, whereas terms like ‘deep watershed territory’-infarct (Angeloni et al., 1990) or ‘internal border zone territory’-infarct ((Angeloni et al., 1990) or ‘internal watershed infarctions’ (Bladin & Chambers, 1993) are misleading.
In a wider sense, all ischemic brain infarcts are the consequence of a critically reduced blood flow. The concept underlying low-flow infarctions, however, emphasizes a difference between them and thromboembolically caused infarcts. In the thromboembolically induced brain infarcts, the corresponding cerebral artery(ies) is(are) occluded (rarely stenosed) by embolisms of various origins or by in situ atherothrombosis. By contrast, in low-flow infarctions the local brain artery(ies) supplying the infarcted area is(are) not diseased.