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Published in: Journal of Neurology 12/2006

01-12-2006 | LETTER TO THE EDITORS

Extensive corpus callosum infarction

An uncommon pattern of watershed ischaemia?

Authors: Konstantinos Spengos, MD, FESC, Georgios Tsivgoulis, MD, Achilleas Chatziioannou, MD, Constantin Potagas, MD, Nikolaos Zakopoulos, MD, Vassilios Zis, MD

Published in: Journal of Neurology | Issue 12/2006

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Excerpt

Sirs: A 60-year old man, current heavy smoker with a history of poorly controlled diabetes mellitus, hypertension and hypercholesterolaemia, but no alcohol consumption, developed hemihypaesthesia and confusion shortly after receiving 20 mg nifedipine sublingually, due to a hypertensive episode (195/110 mmHg before; 150/85 mmHg after medication). Detailed neurological examination on hospital admission six hours later revealed additionally an impressive disconnection syndrome with left visual and tactile extinction, anomia, left hemianopic alexia, pronounced apraxia with the left or with both hands and intermanual conflict. Computed tomography excluded haemorrhage, while two days later magnetic resonance imaging (MRI) visualized on FLAIR- and T2-weighted sequences signal hyperintensities affecting the entire corpus callosum, the left temporal-occipital cortex and the underlying subcortical white matter, adjacent to the posterior watershed area. Diffusion weighted imaging (DWI) and corresponding restricted apparent diffusion coefficient (ADC) maps established the subacute ischaemic nature of the lesion (Fig. 1) [8]. Digital subtraction angiography (DSA) excluded extracranial lesions and demonstrated subtotal and moderate stenosis of the proximal intracranial cavernous portion of the left and right internal carotid artery (ICA) respectively (Fig. 2), with anterograde flow in both ICAs. The left ICA territory was supplied mainly with anterograde flow through the stenotic lesion and to a lesser degree through ophthalmic collaterals from the ispilateral external carotid artery. Both anterior cerebral arteries (ACA) were supplied by the left ICA. The right A1 was not seen and was probably hypoplastic. The combination of hypoplastic right A1 with near occlusion of the ICA cavernous portion seemed to be the underlying cause of infarction. Detailed cardiological studies including transoesophageal echocardiogram and repeated Holter-electrocardiogram recordings revealed no pathological findings suggestive of cardioembolism.
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Metadata
Title
Extensive corpus callosum infarction
An uncommon pattern of watershed ischaemia?
Authors
Konstantinos Spengos, MD, FESC
Georgios Tsivgoulis, MD
Achilleas Chatziioannou, MD
Constantin Potagas, MD
Nikolaos Zakopoulos, MD
Vassilios Zis, MD
Publication date
01-12-2006
Publisher
Steinkopff-Verlag
Published in
Journal of Neurology / Issue 12/2006
Print ISSN: 0340-5354
Electronic ISSN: 1432-1459
DOI
https://doi.org/10.1007/s00415-006-0256-2

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