Developmental Neuropathology

Friede, Reinhard L.

doi:10.1007/978-3-7091-3338-5

Cited by 263 publications

(149 citation statements)

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“…, 1973) defects. Identical le sions develop in human fetuses exposed to severe intrauterine asphyxia (Hallervorden, 1944;Friede, 1975) or that suffer cerebral circulatory distur bances (Friede, 1975). Studies in our laboratory by Ting et al (1983) demonstrated that mid-gestational sheep fetuses subjected to 2 h of marked hypoxia develop damage to their brains only in those instances when MABP is reduced to values of <30 mm Hg.…”

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confidence: 91%

“…Also, periventricular white matter necrosis com monly has been described as resulting from peri natal asphyxia (Banker and Larroche, 1962). Other patterns of hypoxic-ischemic injury include focal brain necroses that encompass multicystic en cephalomalacia, porencephaly, and hydranenceph aly (Friede, 1975;Volpe, 1981). These latter pat terns of injury reflect asphyctic episodes taking place early during gestation in humans.…”

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Brain Metabolic Correlates of Hypoxic-Ischemic Cerebral Necrosis in Mid-Gestational Sheep Fetuses: Significance of Hypotension

Wagner

Ting

Westfall

et al. 1986

J Cereb Blood Flow Metab

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Summary: Midgestational sheep fetuses exposed to marked hypoxia for 2 h remain brain intact if MABP is maintained above 30 mm Hg. On the other hand, simi larly hypoxic fetuses, if they experience reductions in MABP below 30 mm Hg, develop foci of necrosis that predominantly affect hemispheric white matter and neo striatum. Cortex damage is more restricted and is usually associated with more massive underlying white matter damage. The present study examines the brain metabolic basis for the important role of hypotension in brain injury development in marked hypoxia. Sheep fetuses rendered hypoxic by respiring their ewes with 11 % oxygen (fetal PaOZ = 8-12 mm Hg) in which MABP was maintained above 30 mm Hg showed increases in brain lactic acid concentrations to 7 -13 f,Lmollg but unaltered energy charge. In contrast, fetuses that sustained MABP reduc tions below 30 mm Hg showed increases in lactic acid Fetal or neonatal hypoxic-ischemic encephalo pathy is commonly thought to result from an im paired oxygen supply to brain due to a decreased oxygen content of arterial blood and/or a decrease in CBF. Such asphyxia in utero, in contrast to various postnatal insults, is the predominant cause of "cerebral palsy," a syndrome that encompasses a variety of motor deficits and in which mental re tardation and epilepsy may or may not be present (Volpe, 1981).The neuropathology of perinatal hypoxic-isch emic encephalopathy includes selective neuronal Received July 8, 1985; accepted March 25, 1986. Address correspondence and reprint requests to Dr. K. R. Wagner at Veterans Administration Medical Center, Medical Research Service/15I , 3200 Vine Street, Cincinnati, OH 45220, U. S. A. 425concentrations in vulnerable structures to 16-24 f,Lmol/g accompanied by marked decreases in energy charge. The vulnerable structures also showed reductions in fructose concentrations but a variable behavior of other brain me tabolites including phosphocreatine, glycogen, and glu cose. Thus, the present findings suggest a relation be tween hypotension during marked hypoxia, low energy charge, lactic acid accumulation in brain at high concen trations, and fetal brain injury. The ewes of hypoxic hy potensive fetuses received pentobarbital at lower doses than did those of fetuses that maintained blood pressure. This suggests that pentobarbital plays an important role in protecting the fetal brain from asphyxia by extending the hypoxic fetus's ability to maintain blood pressure in addition to reducing its brain metabolism.

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confidence: 91%

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confidence: 99%

Brain Metabolic Correlates of Hypoxic-Ischemic Cerebral Necrosis in Mid-Gestational Sheep Fetuses: Significance of Hypotension

Wagner

Ting

Westfall

et al. 1986

J Cereb Blood Flow Metab

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“…Clinical features of them were also different between the patients. Some classifications of cortical dysplasia were proposed as based on the findings of neuroimaging and/or histological characteristics [1,2,3,6,11,16]. However, it may be difficult to classify into one of subtypes in these patients.…”

Section: Discussionmentioning

confidence: 99%

“…However, it may be difficult to classify into one of subtypes in these patients. Etiologically, it has been known that cortical dysplasia is caused by disorder of neuronal proliferation and/or migration [3,4,6,10,14,15,17], whereas polymicrogyria can occur from cortical damage such as cerebral ischemia in early postnatal period [16]. As microdysgenesis, which is identified only as microscopically abnormal structures of cortex, can not find in MR images, it seems to be better that cortical dysplasia is classified histopathologically.…”

Section: Discussionmentioning

confidence: 99%

Correlation of EEG, neuroimaging and histopathology in an epilepsy patient with diffuse cortical dysplasia

et al. 2000

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The correlation between scalp EEG, intraoperative electrocorticogram, neuroimaging and histopathology was examined in a epilepsy child with diffuse cortical dysplasia. A 6-year-old girl with moderate mental retardation had suffered from intractable complex partial and generalized epilepsy since 2-year-old. MR images demonstrated unilateral large macrogyria/polymicrogyria and schizencephaly in the right occipital lobe. The epileptic focus was detected on the macrogyria by EEG and single-photon emission tomography. However, intraoperative electrocorticogram showed frequent spikes from the polymicrogyria and no paroxysmal activity in the macrogyria. The polymicrogyria was resected including the macrogyria using an image-guided system. The histological findings revealed that the macrogyria was covered and separated with glial bundles. It has been reported that epileptogenisity was produced from abnormal neurons and their arrangement in cortical dysplasia, however in this case, the major dysplastic lesion had no epileptogenisity, rather the focus might be in polymicrogyria around the lesion.(144 words)

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“…These lesions are the result of extense areas of necrosis of the cerebral tissue predominantly due to hypoxic-ischemic insults but it is well known that other kinds of insults can be involved such as congenital infections, maternal exposure to toxic substances and trauma 14,[17][18][19][20] . There are several lines of evidence indicating that the response of the brain to injury changes according to timing of in utero development 1,4,21,22 . Cystic lesions tend to occur in earlier periods of development, usually before the 30 th week of gestation, due to the high water content of a brain in myelination process and the deficient response of the astrocytes to the formation of a glial scar 1,4 .…”

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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Developmental Neuropathology

Cited by 263 publications

References 0 publications

Brain Metabolic Correlates of Hypoxic-Ischemic Cerebral Necrosis in Mid-Gestational Sheep Fetuses: Significance of Hypotension

Brain Metabolic Correlates of Hypoxic-Ischemic Cerebral Necrosis in Mid-Gestational Sheep Fetuses: Significance of Hypotension

Correlation of EEG, neuroimaging and histopathology in an epilepsy patient with diffuse cortical dysplasia

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

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