Ischemic Stroke and Incomplete Infarction

García, Julio Herrero; Lassen, Niels A.; Weiller, C.; Sperling, Bjørn; Nakagawara, Jyoji

doi:10.1161/01.str.27.4.761

Cited by 192 publications

(114 citation statements)

References 29 publications

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“…5,13,16,17 Therefore, the delayed ischemic change of hyperintensity/relative hypointensity on T1W/T2W MRI in our patients could involve biochemical changes that shorten the T1 and T2 relaxation times. These biochemical factors include paramagnetic compounds 18 such as iron and manganese ions, and free radicals produced by macrophages.…”

Section: Fujioka Et Al 1999 1039mentioning

confidence: 87%

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

Fujioka

Taoka

Hiramatsu

et al. 1999

Stroke

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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...

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Section: Fujioka Et Al 1999 1039mentioning

confidence: 87%

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

Fujioka

Taoka

Hiramatsu

et al. 1999

Stroke

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“…One possible explanation is cortical ischemia due to occlusions of microvessels or chronic hypo-perfusion (Garcia, Lassen, Weiller, Sperling, & Nakagawara, 1996), which is the underlying pathogenesis of cerebral small vessel disease. Long-term hypo-perfusion may lead to incomplete infarction or microinfarction in cortical region, which cannot be detected by conventional MRI or CT (Garcia et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

“…Long-term hypo-perfusion may lead to incomplete infarction or microinfarction in cortical region, which cannot be detected by conventional MRI or CT (Garcia et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Cerebral gray matter volume reduction in subcortical vascular mild cognitive impairment patients and subcortical vascular dementia patients, and its relation with cognitive deficits

Meng

Wang

et al. 2017

Brain and Behavior

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“…The necrotic cells have completely resolved 2 weeks later, with macrophages remaining in the tissue adjacent to the infarcted area (Clark et al, 1993). If ischemia is mild, selective destruction of neurons can be observed ('selective neuronal necrosis') (Garcia et al, 1996).…”

Section: Lesion Developmentmentioning

confidence: 99%

Temporal profile of T₂-Weighted MRI Distinguishes between Pannecrosis and Selective Neuronal Death after Transient Focal Cerebral Ischemia in the Rat

Wegener

Weber

Ramos‐Cabrer

et al. 2005

J Cereb Blood Flow Metab

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Transient middle cerebral artery occlusion (MCAO) by an intraluminal thread leads to primarily subcortical infarctions with little sensorimotor impairment in the Wistar rat strain. We investigated the course of infarct development in this lesion type for 10 weeks using magnetic resonance imaging (MRI) along with histological characterization. MCAO was induced in male Wistar rats (260 to 300 g) for 60 mins. Animals received follow-up T 1 -and T 2 -weighted MRI from day 1 until week 10. Separate groups of animals were analyzed histologically after 2, 6, and 10 weeks. Histology included immunohistochemistry for neuronal and astrocytic markers as well as hematoxylin eosin and luxol fast blue-cresyl violet staining. In contrast to lesions involving the cortex, exclusively subcortical infarctions were characterized by a complete resolution of initially increased T 1 and T 2 relaxation times by 10 weeks. Between 2 and 10 weeks, neuronal death and gliosis as well as a dense inflammatory infiltrate were evident in these lesions, without damage to fiber tracts or development of cystic cavities. Exclusively subcortical lesions in Wistar rats are characterized by normalization of T 1 and T 2 relaxation times, which might, however, not be mistaken for tissue recovery. Despite this MRI normalization, selective neuronal death and gliosis develop. Although MRI at individual time points might therefore be ambiguous, the temporal profile of relaxation time changes over the chronic time period allows discrimination of the lesion development into selective neuronal death or pannecrosis.

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Ischemic Stroke and Incomplete Infarction

Cited by 192 publications

References 29 publications

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

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

Cerebral gray matter volume reduction in subcortical vascular mild cognitive impairment patients and subcortical vascular dementia patients, and its relation with cognitive deficits

Temporal profile of T₂-Weighted MRI Distinguishes between Pannecrosis and Selective Neuronal Death after Transient Focal Cerebral Ischemia in the Rat

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Ischemic Stroke and Incomplete Infarction

Cited by 192 publications

References 29 publications

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

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

Cerebral gray matter volume reduction in subcortical vascular mild cognitive impairment patients and subcortical vascular dementia patients, and its relation with cognitive deficits

Temporal profile of T2-Weighted MRI Distinguishes between Pannecrosis and Selective Neuronal Death after Transient Focal Cerebral Ischemia in the Rat

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Temporal profile of T₂-Weighted MRI Distinguishes between Pannecrosis and Selective Neuronal Death after Transient Focal Cerebral Ischemia in the Rat