Fig 1. Patient 7. A, ROIs for parenchymal hypoattenuation and DWI hyperintensity were placed manually on unenhanced CT and DWI (TR, 10,000 ms; TE, 71.7 ms). The 2 ROIs for CT lesion and DWI hyperintensity provide an ROI for the lesion with reversed discrepancy showing CT parenchymal hypoattenuation and no obvious DWI hyperintensity.

B, Initial unenhanced CT shows subtle hypoattenuation of lentiform nucleus, caudate, and insula in the left MCA territory (white arrows). A hyperattenuated artery sign of the left inferior M2 branch (black arrow) is also seen. Maximum intensity projection CT angiography (CTA) shows occlusion of the left inferior M2 (arrow). DWI shows hyperintense lesions in the left temporal lobe and posterior insula, but DWI hyperintensity seems very subtle and not obvious in basal ganglia and is not seen in most areas of insula. ADC map shows cytotoxic edema in the left temporal lobe. Perfusion maps show an increased TTP delay and decreased rCBF only in the left temporal lobe, and no obvious perfusion abnormality is seen in the left basal ganglia. Initial MRA shows occlusion of the left inferior M2 (arrow).

C, Follow-up MR images at day 1 show delayed DWI hyperintensity and decreased ADC in the left basal ganglia (arrow). Perfusion maps and MRA demonstrate reperfusion in the left MCA territory and recanalization of the left M2 occlusion.

D, Follow-up CT and fluid-attenuated inversion recovery (FLAIR) images (TR, 10,000 ms; TE 133 ms; TI, 2200 ms) 7 days later show infarction in the RD lesion of basal ganglia and insula, and DWI shows increased extent of DWI hyperintense lesion in the left basal ganglia. FLAIR and T2-weighted MR images (TR, 3683 ms; TE, 104 ms) obtained 9 months after the initial CT show atrophy of the left basal ganglia and insula. T1 hyperintensity is seen in the left striatum at long-term follow-up. In this patient, there was a spontaneous rapid improvement of aphasia and motor weakness within 1 hour after symptom onset.