Delayed Ischemic Hyperintensity on T1-Weighted MRI in the Caudoputamen and Cerebral Cortex of Humans After Spectacular Shrinking Deficit

Abstract

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. (Stroke. 1999;30:1038 -1042.)Key Words: carotid arteries Ⅲ cerebral ischemia, transient Ⅲ magnetic resonance imaging Ⅲ neuronal death T ransient internal carotid artery (ICA)-middle cerebral artery (MCA) occlusion due to cardiogenic embolus can lead to spectacular shrinking deficit (SSD) in patients with various heart diseases. 1 SSD refers to a sudden major hemispheric stroke syndrome followed by rapid improvement within a few hours after stroke, leaving mild or no deficits. Experimentally, 2,3 brief MCA occlusion (MCAO) causes selective neuronal necrosis and apoptosis with intact glial cells and microvessels in the caudoputamen and cerebral cortex. In these ischemic lesions, the brain tissue framework is preserved and no cavitation develops. This ischemic lesion with selective neuronal death and gliosis has been termed "incomplete infarction." 4 -6 Nakano et al 7 reported that selective neuronal damage slowly progressed in the dorsolateral striatum of rats for 4 weeks after 15 minutes' MCAO and that microvacuolation never occurred in the ischemic area. However, very few reports are available on the serial changes in the human brain after transient hemispheric ischemia leading to SSD, which represent the clinical equivalent of the experimental conditions described above.In humans, we previously invest...

Spectacular Shrinking Deficit: Insights from Multimodal Magnetic Resonance Imaging after Embolic Middle Cerebral Artery Occlusion in Sprague—Dawley Rats

“…This seems to be of special interest given the contradicting significance attributed to brief cerebral ischemia. Whereas some studies found that transient cerebral ischemia may improve stroke outcome by serving as a preconditioning stimulus that triggers neuroprotective pathways in the brain (Castillo et al, 2003;Wegener et al, 2004), others demonstrated secondary deterioration on MRI (Fujioka et al, 1999a) or neurological function (Johnston et al, 2003;Smith et al, 2005) similar to the herein observed pathology. Hence, withholding treatment in these patients should be reconsidered and more aggressive interventions may be indicated in patients with rapidly improving symptoms, who currently are often treated with little urgency or concern (Johnston et al, 2003;Smith et al, 2005).…”

“…In conclusion, this study may provide clinicians with the important information that rapid resolution of ADC lesions after embolic MCAO with spontaneous reperfusion may not be permanent, arguing against the notion that SSD is a monophasic phenomenon (Baird et al, 1995;Kraemer et al, 2005;Minematsu et al, 1992) and for a more heterogeneous event with potentially delayed ischemic sequelae (Fujioka et al, 1999a). Secondly, fMRI is capable of identifying dysfunctional tissue after embolic stroke that eludes standard structural MRI techniques, and may be a sensitive and complementary parameter in the evaluation of stroke patients with rapidly improving symptoms.…”

Novel Brain Ischemic Change on MRI

“…[1][2][3] However, we suggested in our clinical study that a delayed change on MRI represented incomplete ischemic injury, including selective neuronal death and gliosis without infarct or hemorrhage. 4 This ischemic change exhibited persistent hyperintensity and hypointensity on repeated T1-weighted (T1W) and T2-weighted (T2W) MRI, respectively, with the hyperintensity on T1W imaging gradually subsiding with time. Brief cerebral hemispheric ischemia leading to spectacular shrinking deficit produced the specific ischemic change in the basal ganglia and cerebral cortex in humans on MRI but not CT scans.…”

lschémie cérébrale

“…Les implications de ces mécanismes dans le traitement des attaques céré-brales et les raisons de l'échec de l'utilisation des antagonistes des récepteurs NMDA dans les essais cliniques humains sont également discutées. < [4][5][6]. In vitro, après une hypoxie-aglycémie de quatre à six minutes, la mort des neurones vulnérables est constatée entre 24 et 72 h [7].…”