Incomplete Infarct and Delayed Neuronal Death After Transient Middle Cerebral Artery Occlusion in Rats

García, Julio Herrero; Liu, Kai-Feng; Ye, Zhu-Rong; Gutiérrez, Jorge

doi:10.1161/01.str.28.11.2303

Cited by 154 publications

(128 citation statements)

References 25 publications

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“…2,3,6,7,[13][14][15][16] In experimental animals, transient MCAO leads to selective neuronal death and various glial responses without pannecrosis of the brain tissue in the ischemic region when reperfusion is instituted within a short period of time. 2,3,6,7 This selective neuronal loss advances from the striatum to the cerebral cortex in parallel with the prolongation of MCAO. In humans, several studies [13][14][15][16] suggest the presence of incomplete brain infarction after ischemia of either short or moderate severity.…”

Section: Discussion Delayed Ischemic Hyperintensity On T1w Mri After Ssdmentioning

confidence: 99%

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: Discussion Delayed Ischemic Hyperintensity On T1w Mri After Ssdmentioning

confidence: 99%

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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“…However, cortical SNL was found not to affect every subject, being for instance observed in 40% of rats subjected to 10-to 25-minute tMCAo. 11 In addition, with proximal MCAo, the fraction of dead neurons in the cortex is typically smaller than in the striatum, for instance B10% as compared with 15%, respectively. 42 Of note, scattered cortical SNL has been observed in association with striatal infarction after up to a 1-hour MCAo in one study.…”

Section: Animal Modelsmentioning

confidence: 99%

Selective Neuronal Loss in Ischemic Stroke and Cerebrovascular Disease

Baron

Yamauchi

Fujioka

et al. 2013

J Cereb Blood Flow Metab

192

205

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As a sequel of brain ischemia, selective neuronal loss (SNL)-as opposed to pannecrosis (i.e. infarction)-is attracting growing interest, particularly because it is now detectable in vivo. In acute stroke, SNL may affect the salvaged penumbra and hamper functional recovery following reperfusion. Rodent occlusion models can generate SNL predominantly in the striatum or cortex, showing that it can affect behavior for weeks despite normal magnetic resonance imaging. In humans, SNL in the salvaged penumbra has been documented in vivo mainly using positron emission tomography and 11 C-flumazenil, a neuronal tracer validated against immunohistochemistry in rodent stroke models. Cortical SNL has also been documented using this approach in chronic carotid disease in association with misery perfusion and behavioral deficits, suggesting that it can result from chronic or unstable hemodynamic compromise. Given these consequences, SNL may constitute a novel therapeutic target. Selective neuronal loss may also develop at sites remote from infarcts, representing secondary 'exofocal' phenomena akin to degeneration, potentially related to poststroke behavioral or mood impairments again amenable to therapy. Further work should aim to better characterize the time course, behavioral consequences-including the impact on neurological recovery and contribution to vascular cognitive impairment-association with possible causal processes such as microglial activation, and preventability of SNL.

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“…Moreover, most of the patients in this series with cystic lesions also have signs of gliosis around the lesion and at distance, which means that these insults have ocurred in a period when gliosis repair was already well developed. In addition, the nature and magnitude of an insult as well as its capacity to create a communication with the CSF system can be more relevant than the time of its occurence in determining the formation of a cystic or an atrophic lesion [29][30][31][32][33] .…”

Section: Discussion Discussionmentioning

confidence: 99%

Congenital destructive hemispheric lesions and epilepsy: clinical features and relevance of associated hippocampal atrophy

Teixeira

Leone

Honorato

et al. 2000

Arq. Neuro-Psiquiatr.

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-We studied the clinical, EEG and MRI findings in 19 patients with epilepsy secondary to congenital destructive hemispheric insults. Patients were divided in two groups: 10 with cystic lesions (group 1), and 9 with atrophic lesions (group 2). Seizure and EEG features, as well as developmental sequelae were similar between the two groups, except for the finding that patients of group 2 more commonly presented seizures with more than one semiological type. MRI showed hyperintense T2 signal extending beyond the lesion in almost all patients of both groups, and it was more diffuse in group 2. Associated hippocampal atrophy (HA) was observed in 70% of group 1 patients and 77.7% of group 2, and it was not correlated with duration of epilepsy or seizure frequency. There was a good concordance between HA and electroclinical localization. The high prevalence of associated HA in both groups suggests a common pathogenesis with the more obvious lesion. Our findings indicate that in some of these patients with extensive destructive lesions, there may be a more circumscribed epileptogenic area, particularly in those with cystic lesions and HA, leading to a potential rationale for effective surgical treatment.KEY WORDS: epilepsy, magnetic resonance image, hippocampal atrophy.Epilepsia secundária a lesões destrutivas hemisféricas congênitas: achados clínicos e relevância de atrofia hipocampal associada RESUMO -Analisamos os achados clínicos, de EEG e RM de 19 pacientes com epilepsia secundária a insultos destrutivos hemisféricos congênitos. Os pacientes foram divididos em dois grupos: 10 com lesões císticas (grupo 1), e 9 com lesões atróficas (grupo 2). As características das crises e achados de EEG foram similares entre os dois grupos exceto pelo fato dos pacientes do grupo 2 terem apresentado mais comumente crises com mais de um padrão semiológico. A RM mostrou sinal T2 hiperintenso estendendo-se ao redor da lesão e à distância em quase todos os pacientes de ambos os grupos, de modo mais extenso no grupo 2. Observou-se atrofia hipocampal (AH) associada em 70% dos pacientes do grupo 1 e 77,7% do grupo 2 e não houve correlação com a duração da epilepsia ou freqüência das crises. Houve boa correlação entre a AH e localização eletroclínica. A alta prevalência de AH associada em ambos os grupos sugere uma patogenia comum com a lesão mais óbvia. Estes achados indicam que alguns destes pacientes com extensas lesões destrutivas, particularmente aqueles com lesões císticas e AH, a zona epileptogênica pode ser mais circunscrita possibilitando a indicação de uma ressecção restrita para o controle das crises. PALAVRAS-CHAVE: epilepsia, ressonância magnética, atrofia hipocampal.

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Incomplete Infarct and Delayed Neuronal Death After Transient Middle Cerebral Artery Occlusion in Rats

Cited by 154 publications

References 25 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

Selective Neuronal Loss in Ischemic Stroke and Cerebrovascular Disease

Congenital destructive hemispheric lesions and epilepsy: clinical features and relevance of associated hippocampal atrophy

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