The results suggest that in acute stroke the severity of the initial ischemic event as determined on time-to-peak maps indicates hemodynamic compromise in addition to internal carotid artery or middle cerebral artery occlusion, because of abnormalities in other cerebral arteries.
Purpose: To determine whether the perfusion deficit could predict brain infarction in patients with chronic cerebral ischemia who experienced recurring episodes of neurological symptoms and showed a perfusion-diffusion mismatch on magnetic resonance (MR) images. Materials and Methods:In 53 consecutive patients (38 males and 15 females, 62 Ϯ 13 years old) with ischemia in the middle cerebral artery (MCA) territory, lesion volumetry was performed on parametric maps of the time-to-peak, the cerebral blood volume, and diffusion-weighted (DW) images. The infarct lesions were assessed on follow-up T2-weighted (T2W) MR images after eight days. Cerebrovascular changes were determined by time-of-flight (TOF) MR angiography (MRA). Inferential and correlation statistics were used. Results:Patients with chronic ischemic brain disease (N ϭ 39) who presented with a severe perfusion-diffusion mismatch in the presence of a normal cerebral blood volume had no or small brain infarctions as found on follow-up T2W images. MRA revealed widespread abnormalities of the basal cerebral arteries compatible with brain perfusion abnormalities. In contrast, in acute stroke patients (N ϭ 14) the deficit of cerebral perfusion predicted the infarct lesion in the T2W images. Conclusion:Our results suggest that in chronic cerebral ischemia the normal blood volume was maintained despite the depression of cerebral perfusion and recurring minor insults.
Purpose:To investigate the evolution of the perfusion deficit area following systemic thrombolysis with recombinant tissue plasminogen activator (rtPA) in a clinical study on acute cerebral ischemia. Materials and Methods:We performed volumetric measurements of the acute ischemic lesions in MR images of perfusion (TTP, MTT, and rCBV) and in diffusion-weighted (DW) images, as well as the manifest stroke lesions in T2-weighted MR images on day 8. We compared the data of 29 patients who were subjected to systemic thrombolysis with those of 18 patients who were not eligible for thrombolysis. Results:In the treated patients there were prominent MTT/ DWI and TTP/DWI mismatches (P Ͻ 0.0006). The acute TTP volumes were smaller than the acute MTT volumes, but as large as the T2 lesions on day 8. The MTT/T2 lesion volume reduction was significant (P Ͻ 0.03) in patients who received the GPIIb/IIIa receptor antagonist tirofiban (N ϭ 13) in addition to the low-dose rtPA. This corresponded to a greater neurological improvement compared to patients who received rtPA alone (P Ͻ 0.05). In contrast, in the nontreated patients the initial MTT and TTP lesion volumes were of similar magnitude and predicted the T2 lesions on day 8. In the treated and nontreated patients the TTP lesion signified the viability threshold of acute ischemia, which corresponded to a rCBF of 25 Ϯ 11 mL/100 g/min. Conclusion:The perfusion deficit area comprises the ischemic core that is destined to undergo necrosis, and an ischemic rim that is salvageable by systemic thrombolysis.
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