Diffusion magnetic resonance imaging provides an early marker of acute cerebral ischemic injury. Thrombolytic reversal of diffusion abnormalities has not previously been demonstrated in humans. Serial diffusion and perfusion imaging studies were acquired in patients experiencing acute hemispheric cerebral ischemia treated with intra-arterial thrombolytic therapy within 6 hours of symptom onset. Seven patients met inclusion criteria of prethrombolysis and postthrombolysis magnetic resonance studies, presence of large artery anterior circulation occlusion at angiography, and achievement of vessel recanalization. Mean diffusion-weighted imaging lesion volume at baseline was 23 cm3 (95% confidence interval [95% CI], 8-38 cm3) and decreased to 10 cm3 (95% CI, 3-17 cm3) 2.5 to 9.5 hours after thrombolysis. Mean apparent diffusion coefficient lesion volume decreased from 9 cm3 (95% CI, 2-16 cm3) at baseline to 1 cm3 (95% CI, 0.4-2 cm3) early after thrombolysis. A secondary increase in diffusion volumes was seen in 3 of 6 patients at day 7. In all 4 patients in whom perfusion imaging was obtained before and after treatment, complete resolution of the perfusion deficit was shown. Diffusion magnetic resonance signatures of early tissue ischemic injury can be reversed in humans by prompt thrombolytic vessel recanalization. The ischemic penumbra includes not only the region of diffusion/perfusion mismatch, but also portions of the region of initial diffusion abnormality.
Background and Purpose —This study had 2 goals: (1) to assess interrater reliability of academic neuroradiologists when classifying acute infarction by CT scan as >1/3 middle cerebral artery (MCA) involvement, <1/3 MCA involvement, or no infarction and (2) to determine the sensitivity of physicians potentially involved in acute stroke treatment in detecting >1/3 MCA acute infarctions. Studies of tissue plasminogen activator show an association between early signs of major infarction and poor outcome. The American Academy of Neurology and the American Heart Association recommend avoiding thrombolysis if early signs of major infarction are present. Methods —We presented 25 scans (normals, acute infarctions, and old infarctions) to 3 academic neuroradiologists. A scoring sheet based on Alteplase Thrombolysis for Acute Noninterventional Therapy in Ischemic Stroke (ATLANTIS)/CT Summit criteria was used to determine >1/3 MCA territory involvement. Nine of the 25 scans were presented again to assess intrarater reliability. We recalculated results of our previous study in which physicians interpreted infarction scans, now designating the scans as >1/3 MCA, <1/3 MCA, or normal, as determined by the neuroradiologists. Results —All 3 neuroradiologists agreed on no infarction, <1/3 MCA, and >1/3 MCA on 64% of the scans. Neuroradiologist test-retest agreement was 96% for >1/3 MCA territory. Overall sensitivity for emergency physicians, neurologists, and general radiologists for detecting the presence of infarction in scans rated as >1/3 MCA was 78%. Conclusions —Neuroradiologists can achieve moderate agreement in detecting >1/3 MCA infarction. The emergency physicians, neurologists, and general radiologists tested were reasonably skilled at detecting >1/3 MCA acute infarction. However, their performance did not reliably identify all patients who have early CT infarct signs that place them at increased risk for cerebral hemorrhage after thrombolytic therapy.
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