(Stroke. 1999;30:1038-1042.)
© 1999 American Heart Association, Inc.
Original Contributions |
Delayed Ischemic Hyperintensity on T1-Weighted MRI in the Caudoputamen and Cerebral Cortex of Humans After Spectacular Shrinking Deficit
From the Departments of Neurosurgery (M.F., K.-I.H., T.S.) and Radiology (T.T., S.S.), Nara Medical University, Nara, Japan.
Correspondence to Masayuki Fujioka, MD, Center for the Study of Neurological Disease, The Queen's Medical Center, University Tower, 8th Floor, 1356 Lusitana St, Honolulu, Hawaii 96813. E-mail mfujioka{at}www.cns.queens.org
Background and Purpose—Transient internal carotid artery (ICA)–middle cerebral artery (MCA) occlusion caused by cardiogenic embolus can lead to spectacular shrinking deficit (SSD): sudden hemispheric stroke syndrome followed by rapid improvement. The aim of this study was to investigate sequential neuroradiological changes in the brains of patients after SSD compared with those after brief cardiac arrest and hypoglycemia, which we previously studied with the same methods.
Methods—We serially studied CT scans and MR images obtained at 1.5 T in 4 patients with SSD. All 4 patients suffered from transient neurological deficits due to cardiogenic embolus in ICA-MCA. The symptoms began to disappear from 25 to 50 minutes after onset.
Results—Repeated CT scans demonstrated no abnormal findings in the affected cerebral hemisphere in 3 of the 4 patients and a small cortical infarct in the remaining 1. In each patient, repeated MRI between day 7 and month 23 after stroke showed basal ganglionic and cortical lesions. These lesions were hyperintense on T1-weighted and relatively hypointense on T2-weighted imaging. These ischemic lesions of hyperintensity on T1-weighted MRI subsided with time.
Conclusions—Transient ICA-MCA occlusion leading to SSD produces a specific ischemic change with delayed onset in the basal ganglia and cerebral cortex in humans on MRI but not CT scans. We speculate that the lesions represent incomplete ischemic injury, including selective neuronal death, proliferation of glial cells, paramagnetic substance deposition, and/or lipid accumulation. Unlike brief cardiac arrest or hypoglycemia, the localized lesions on MRI of patients after SSD seem to be incomplete and to differ from infarction or hemorrhage.
Key Words: carotid arteries • cerebral ischemia, transient • magnetic resonance imaging • neuronal death
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