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From the Departments of Neurology and Radiology, John Hunter Hospital, and Hunter Medical Research Institute, University of Newcastle, Australia.
Address correspondence and reprint requests to Dr. Mark W. Parsons, Department of Neurology, John Hunter Hospital, Locked Bag No. 1, Hunter Region Mail Centre, NSW, Australia 2310; e-mail: mark.parsons{at}hnehealth.nsw.gov.au
Objectives: To correlate the two types of early ischemic change on noncontrast CT (NCCT) (parenchymal hypoattenuation [PH] and isolated focal swelling [IFS]) with concurrent assessment of cerebral perfusion and to compare their rates of progression to infarction.
Methods: We assessed cortical regions on NCCT for early ischemic change. Quantitative perfusion values were calculated for cortical regions from acute CT perfusion (CTP) maps of cerebral blood volume (CBV), blood flow (CBF), and mean transit time (MTT). Reperfusion and presence of infarction were determined from follow-up MRI.
Results: We studied 40 patients with sub-6 hour anterior circulation ischemic stroke; 19 received IV recombinant tissue plasminogen activator. Of the 202 regions acutely hypoperfused on CTP, 123 were normal on NCCT, 58 had PH, and 21 had IFS. Acute CBV was low in PH regions, and elevated in IFS regions. Acute CBF was reduced in IFS regions, but more so in PH regions. Progression to infarction occurred in virtually all PH regions, but IFS regions had much lower rates of infarction with major reperfusion. Acute CBV in hypoperfused normal NCCT regions ranged from reduced to elevated, with substantially differing risk of infarction.
Conclusions: Isolated focal swelling identifies penumbral tissue and parenchymal hypoattenuation identifies infarct core. Although this has prognostic implications when assessing patient suitability for thrombolytic therapy, the majority of acutely hypoperfused regions appear normal on noncontrast CT. Perfusion CT can stratify the level of risk of subsequent infarction for normal-appearing regions on noncontrast CT.
Commentary, see page 717
Supported by a National Health and Medical Research Council of Australia Project Grant (ID 351155).
Disclosure: The authors report no conflicts of interest.
Received July 10, 2006. Accepted in final form November 13, 2006.
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Neurology 2007 68: 717.
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