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  • Title: [Early ischemic lesion demonstrated by ictal diffusion-weighted MRI during prior TIA in a patient with cerebral infarction].
    Author: Shimizu H, Yoneda Y, Tabuchi M, Yamasaki T, Moriwaki H, Mori E.
    Journal: No To Shinkei; 2002 Mar; 54(3):247-53. PubMed ID: 11968816.
    Abstract:
    We reported a patient with transient ischemic attack (TIA), subsequently evolving to a cerebral infarction, in whom ictal diffusion-weighted magnetic resonance imaging (MRI) detected early ischemic lesion in the left hemisphere. The patient was a 30-year-old right-handed male medical doctor, who had an in-hospital episode of TIA with obtundation and right hemiparesis, which lasted for 150 minutes. Ictal diffusion-weighted MRI obtained 110 minutes after symptom onset demonstrated an area of high signal intensity in the left striatum and corona radiata, whereas T 2-weighted and FLAIR images were entirely normal. Ictal magnetic resonance angiography (MRA) showed occlusive lesions in the M 2 branches of the left middle cerebral artery. The second MRA obtained 90 minutes after resolution of the symptoms showed nearly complete recanalization of the left middle cerebral artery, suggesting that the TIA was embolic mechanism. However the patient rapidly developed similar neurological symptoms again 58.5 hours after the TIA episode, evolving finally to a completed stroke. A brain CT obtained 1 hour after the second episode demonstrated diffuse hypodense lesions in the left basal ganglia and corona radiata, and in the left temporal lobe. MRIs 3 and 7 days later displayed completed infarcts, of which distribution was consistent with that of the hypodense lesions on the earlier CT. The left middle cerebral artery remained patent on the follow-up MRAs. The patient fairly recovered and returned to his premorbid position as medical doctor with a mild residual right hand clumsiness. In this patient, ictal and post-ictal MRAs documented an occlusion and a reopening of the middle cerebral artery. The embolic mechanism remains unknown despite detailed cardiac, vascular, and hematological examinations. In addition to recurrent embolism, we would like to point out that the reperfusion injury, secondary delayed neuronal death, and other factors may be involved in the second exacerbation evolving to the completed stroke.
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