Microgyria

Crome, L.

doi:10.1002/path.1700640308

Cited by 83 publications

(29 citation statements)

References 11 publications

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“…In 4 of our 5 cases, heterotopias were found in the form of arrays of immature cells in a fan like pattern, from the ependymal zone out ward or as nodules or large strands in the white matter up to the microgyric cortical plate and molecular layer. Heterotopias were already noticed by Crome [29], who suggested that whatever the cause, the insult had oc curred before the lamination of the cortex is complete. Similar heterotopic strands or clus ters of neurons, associated with microgyria, have been reported in the recent literature .…”

Section: Discussionmentioning

confidence: 92%

“…Very few isolated cases of microgyria have been described in twins [29][30][31][32][33] and hemody namic disorders and pathogenesis of brain perfusion failure in the twin-to-twin transfu sion svndrome have been discussed elsewhere [34], Whether in singletons or in twins, the mor phological patterns of microgyria are similar but vary in severity from case to case. The convoluted four-layered cortex with a pauci cellular medial layer, described as 'pure' form by Bielschowsky [13,14] and the 'impure' forms, as in some of our cases, considered as variants, were discussed by Crome [29] in his classical paper on microgyria, but mecha nisms of formation of the abnormality and the time of occurrence remain in dispute.…”

Section: Discussionmentioning

confidence: 99%

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Abnormal Cortical Plate (Polymicrogyria), Heterotopias and Brain Damage in Monozygous Twins

et al. 1994

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We report 5 cases of abnormal cortical plate (polymicrogyria or microgyric-like pattern) and heterotopias associated with hypoxic-ischemic brain injuries in monochorionic diamniotic twin fetuses of respectively 22, 26, 28, 31, 32 weeks gestation. These fetuses belonged to a series of 5 pairs of patients (10 cases) presenting with the characteristic features of the twin-to-twin transfusion syndrome. Three of them (2 donors and 1 recipient) were macerated and the brains were not available for study. Two (most likely recipient twins) survived. In the remaining 5 fetuses (3 donors and 2 recipients) with neuropathological study there were cortical plate abnormalities. In 2 cases, the cortex was dysmorphic and consisted of focal nodular distribution or vertical stripes of neurons. True polymicrogyria was focal in 2 cases and involved almost the entire surface of the hemispheres in another one. Heterotopias of immature cells were found in 4 cases, either in the white matter or in the cortex or in both sites. There was a focal laminar necrosis only in 2 cases. The morphological pattern of the anomalies depends on the time of occurrence of the insult and on its severity. These abnormalities, although similar to those already described in singleton fetuses, illustrate the variety of cortical dysmorphia which may be associated with fetal hypoxic-ischemic injuries and emphasize the particular vulnerability of the brain in monozygotic twins, whether it belongs to the donor or the recipient.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Abnormal Cortical Plate (Polymicrogyria), Heterotopias and Brain Damage in Monozygous Twins

et al. 1994

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“…[13][14][15][16][17][18] Diagnostic criteria for PMG as defined by Friede in 1989 include abnormal arrangement of cell layers, an intracortical fibre plexus, extensive folding of all layers or of the upper layers only, and fusion of gyral surfaces. 16 Norman highlighted that cases of PMG are morphologically heterogeneous and that identical morphology does not necessarily imply similar aetiology.…”

Section: Discussionmentioning

confidence: 99%

The histopathology of polymicrogyria: a series of 71 brain autopsy studies

Jansen

Robitaille

Honavar

et al. 2015

Develop Med Child Neuro

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PMG PolymicrogyriaAIM Polymicrogyria (PMG) is one of the most common forms of cortical malformation yet the mechanism of its development remains unknown. This study describes the histopathological aspects of PMG in a large series including a significant proportion of fetal cases.METHOD We have reviewed the neuropathology and medical records of 44 fetuses and 27 children and adults in whom the cortical architecture was focally or diffusely replaced by one or more festooning bands of neurons. RESULTSThe pial surface of the brain overlying the polymicrogyric cortex was abnormal in almost 90% of cases irrespective of the aetiology. This accords with animal studies indicating the importance of the leptomeninges in cortical development. The aetiology of PMG was highly heterogeneous and there was no correlation between cortical layering patterns and aetiology. PMG was almost always associated with other brain malformations. INTERPRETATIONThe inclusion of many fetal cases has allowed us to examine the early developmental stages of PMG. The study indicates the significance of surface signals responsible for human corticogenesis and the complex interaction between genetic and environmental factors leading to this common endpoint of cortical maldevelopment.Polymicrogyria (PMG) is a common and highly heterogeneous malformation of cortical development with variable clinical phenotype, imaging, and histology. 1-3 PMG may cause a variety of symptoms including seizures, developmental delay, motor problems, isolated language delay, feeding problems, microcephaly, and multiple congenital anomalies, all to a variable degree of severity. It usually occurs in association with other brain malformations and/or multiple congenital anomalies or intellectual disability. 1 During life, diagnosis of PMG is based on neuroimaging. The magnetic resonance imaging (MRI) features of PMG consist of an irregular and bumpy appearance of the cortex, with apparent cortical thickening, and a stippled grey-white matter junction.2,4 PMG can be focal or diffuse, unilateral or bilateral. Different imaging patterns have been described including bilateral frontal, frontoparietal, perisylvian, lateral parietal, parasagittal parietooccipital, and generalized, as well as unilateral PMG. 2,[5][6][7][8][9][10][11] Although histology is regarded as the diagnostic criterion standard, post-mortem pathology is rarely obtained. The descriptions in the neuropathological literature are based on patients who died or required surgery for intractable epilepsy and likely represent the most severe end of the spectrum. Detailed examination of fetal brains reveal the cortical malformation in the early developmental stages.The architectonic features of PMG were first described by Bielschowsky in 1915 12 and since by others. [13][14][15][16][17][18] Diagnostic criteria for PMG as defined by Friede in 1989 include abnormal arrangement of cell layers, an intracortical fibre plexus, extensive folding of all layers or of the upper layers only, and fusion of gyral surfaces. 16 Norma...

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“…Genetic defects could cause behavioral problems through a variety of mechanisms, including effects on neuronal migration, axonal routing, and synapse formation early in development [Caviness and Rakic, 19781. Neuropathological studies suggest that such developmental defects ma!! cause abnormalities in gyral formation [Crome, 1952;Galaburda et al, 19851 that are visible at autopsy. Such evidence is not plentiful due to the nonlethal nature of many of these disorders.…”

Section: Introductionmentioning

confidence: 97%

Angelman and Prader‐Willi syndrome: A magnetic resonance imaging study of differences in cerebral structure

et al. 1993

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Recent improvements in magnetic resonance imaging techniques now allow the developing brain to be visualized in sufficient detail to perform "in vivo neuropathology." In this study we compared the cortical morphology in six children with Angelman and four with Prader-Willi syndrome. These two syndromes are of special interest because, although they are both caused by deletions in the same region of chromosome 15, Angelman children are far more severely affected, and do not speak. We measured the length of the banks of the Sylvian fissure in a gapless series of thin sagittal images. Angelman children had a significantly larger proportion (75%) of anomalous fissures than the Prader-Willi children (12%). Anomalous cortical growth could result from mistimed expression and recognition of macromolecules involved in axonal guidance, target recognition, and pruning. We hypothesize that misrouting of long projection axons may be related to the Sylvian fissure anomalies and the language disorder in Angelman syndrome.

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Microgyria

Cited by 83 publications

References 11 publications

Abnormal Cortical Plate (Polymicrogyria), Heterotopias and Brain Damage in Monozygous Twins

Abnormal Cortical Plate (Polymicrogyria), Heterotopias and Brain Damage in Monozygous Twins

The histopathology of polymicrogyria: a series of 71 brain autopsy studies

Angelman and Prader‐Willi syndrome: A magnetic resonance imaging study of differences in cerebral structure

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