Defects of neuronal migration and the pathogenesis of cortical malformations

Cortical morphology changes in women with borderline personality disorder: a multimodal approach

“…17 Studies have highlighted that cortical thickness is likely to reflect dendritic arborization or changing myelination at the gray-white matter interface. [20][21][22] On the other hand, surface area is influenced by the division of progenitor cells in the embryological periventricular area, and is associated with the number of minicolumns. [11][12][13]20 Finally, geometric differences (depth of sulcus, curvature, and metric distortion) are predominantly linked with the development of neuronal connections and cortical pattern of connectivity, and are thus a marker for cerebral development.…”

“…[20][21][22] On the other hand, surface area is influenced by the division of progenitor cells in the embryological periventricular area, and is associated with the number of minicolumns. [11][12][13]20 Finally, geometric differences (depth of sulcus, curvature, and metric distortion) are predominantly linked with the development of neuronal connections and cortical pattern of connectivity, and are thus a marker for cerebral development. 21,22 Therefore, it is likely that the maps produced by approaches based on cortical morphology reflect multiple genetic and/or neurobiological etiologies, which need further investigation.…”

“…21,22 Therefore, it is likely that the maps produced by approaches based on cortical morphology reflect multiple genetic and/or neurobiological etiologies, which need further investigation. [20][21][22] Evidence suggests that the components of the frontolimbic network, such as the ACC, orbitofrontal cortex (OFC), dorsolateral prefrontal cortex, and amygdalahippocampus complex, are potentially involved in BPD pathophysiology; these structures have been investigated in previous region-of-interest-and VBM-based studies. [4][5][6]23 In addition, there is mounting evidence that patients with BPD exhibit deficits in structure and function of the ACC, OFC, and amygdala-hippocampus complex.…”

The neuronal migration hypothesis of dyslexia: a critical evaluation thirty years on

“…There is complementarity in the level of granularity each approach can 5 take: while the former typically offers large-scale features such as gray matter volume, white- 6 matter tract density and so on, the latter interrogates much more fine-grained problems such as 7 molecular interactions, formation of synapses or physiological activity. The link between cortical 8 migration defects and neurological and cognitive conditions is well established (Rakic 1988; 9 Walsh and Goffinet 2000; Ayala et al 2007). Our review specifically examines the link for 10 dyslexia.…”

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

“…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.…”