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|Title:||Mechanisms and clinical features of internal watershed infarction.|
|Authors:||Baird, A E;Donnan, Geoffrey A;Saling, Michael M|
|Affiliation:||Department of Neurology, Austin Hospital, Heidelberg, Victoria.|
|Citation:||Clinical and Experimental Neurology; 28(): 50-5|
|Abstract:||The mechanism of internal carotid watershed cerebral infarction is not well understood, but the phenomenon has been described in association with carotid occlusive disease, and more recently with distal middle cerebral artery occlusion beyond the origin of the lenticulostriate branches. The clinical correlates of these changes have not yet been described. We present 5 patients in whom acute internal watershed infarction had occurred, and correlate the clinical, neuropsychological and 99mTc-HMPAO SPECT (Single Photon Emission Computed Tomography using 99mtechnetium-hexamethylpropylene amine oxime) cerebral perfusion findings. Four patients had distal middle cerebral artery occlusion demonstrated on angiography, and one showed profound hemispheric depression in cerebral perfusion with only a small area of infarction. We have concentrated on the mechanism of distal middle cerebral artery occlusion to describe the "arc" of the watershed zone created. We propose that internal watershed infarcts can further be subdivided into anterior and posterior subtypes, outline the vascular territories involved, and propose an overall classification of cerebral watershed infarction.|
|Internal ID Number:||1821839|
Tomography, Emission-Computed, Single-Photon
Tomography, X-Ray Computed
|Appears in Collections:||Journal articles|
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