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PubMed2000

The evolution of cortical development. An hypothesis based on the role of the Reelin signaling pathway.

Expression of the genes encoding Reelin and Dab1 during cortical development in turtle, lizard, chick and mammals correlates with architectonic patterns. In all species, Reelin is secreted by marginal zone cells, whereas Dab1, which mediates the response to Reelin, is synthesized by cortical plate neurons. This pattern was presumably present in stem amniotes. In mammals, the cortical plate is radially organized and develops from inside to outside, these features depend on amplification of reelin synthesis in the marginal zone. In lizards, the cortical plate develops from outside to inside, similar to other non-mammals, but is radially organized, with an additional layer of Reelin added in the subcortex. Thus, the Reelin pathway played a key role in cortical architectonic evolution in mammalian and squamate lineages.

Animals↗
PubMed1991

Molecular cloning of the mouse CCK gene: expression in different brain regions and during cortical development.

In this paper we describe experiments that address specific issues concerning the regulation of the mouse cholecystokinin gene in brain and intestine. The mouse cholecystokinin gene was cloned and sequenced. Extensive homology among the mouse, man and rat genes was noted particularly in the three exons and the regions upstream of the RNA start site. RNAse protection assays for each of the three exons were used to demonstrate that CCK is expressed in only a subset of tissues and that the same cap site and splice choices are used in brain, intestine as well as in cerebellum, cortex, midbrain, hypothalamus and hippocampus. CCK RNA was also noted to be detectable in kidney. Thus the same gene using the same promoter is expressed in subsets of cells that differ in their biochemical, morphologic and functional characteristics. The level of expression of CCK was also monitored during mouse cortical development and the appearance of CCK RNA was compared to glutamate decarboxylase (GAD), enkephalin and somatostatin. It was noted that each of these cortical markers was first expressed at different times during cortical development. The appearance of CCK RNA during intestinal development was also measured and found to precede appearance in cortex by several days.

Amino Acid Sequence↗
PubMed2003

[Microscopic disorders of cortical development of the brain and its etiopathogenic importance for detection in patients with temporal epilepsy associated with hippocampal sclerosis].

Hippocampal sclerosis represents a common structural basis of temporal lobe epilepsy. However, the etiological factors and mechanisms leading to its development still remain unexplained. In our study, we present neuropathological findings in the resected hippocampus and the pole of the temporal lobe in 15 patients with hippocampal sclerosis. "Initial precipitating injuries" that are thought to cause the development of hippocampal sclerosis (febrile seizures in early childhood, head injury or meningoencephalitis) were present in the history of 12 patients. In the remaining 3 cases, no predisposing factors were found. Attention was paid to the histopathological identification of disturbed neuronal migration and differentiation in the temporal lobe. These defects were observed in 7 cases; in three of these, no predisposing factors were stated in the patients' histories. We suggest that in these cases, hippocampal sclerosis arises due to previously undetected disorders of cortical development. A latent neocortical malformation may also contribute to the development of hippocampal sclerosis in patients with an initial precipitating injury in anamnensis. Histopathological examination of resected epileptic brain tissue can provide insights into the individual pathogenesis of epileptic disorders, especially by the detection of microscopic disorders of cortical development.

Adolescent↗
PubMed2005

Cortical development: the art of generating cell diversity.

The fascinating question of how the enormous diversity of neuronal and glial cells in the cerebral cortex is generated during development was recently discussed at a meeting on cortical development and stem cells in Greece. What emerged from this meeting is an equally fascinating answer, namely that precursor diversity at rather early stages of development anticipates later cell type diversity.

Animals↗
PubMed1999

Dopamine affects parvalbumin expression during cortical development in vitro.

This study was undertaken to determine how dopamine influences cortical development. It focused on morphogenesis of GABAergic neurons that contained the calcium-binding protein parvalbumin (PV). Organotypic slices of frontoparietal cortex were taken from neonatal rats, cultured with or without dopamine, harvested daily (4-30 d), and immunostained for parvalbumin. Expression of parvalbumin occurred in the same regional and laminar sequence as in vivo. Expression in cingulate and entorhinal preceded that in lateral frontoparietal cortices. Laminar expression progressed from layer V to VI and finally II-IV. Somal labeling preceded fiber labeling by 2 d. Dopamine accelerated PV expression. In treated slices, a dense band of PV-immunoreactive neurons appeared in layer V at 7 d in vitro (DIV), and in all layers of frontoparietal cortex at 14 DIV, whereas in control slices such labeling did not appear until 14 and 21 DIV, respectively. The laminar distribution and dendritic branching of PV-immunoreactive neurons were quantified. More labeled neurons were in the superficial layers, and their dendritic arborizations were significantly increased by dopamine. Treatment with a D1 receptor agonist had little effect, whereas a D2 agonist mimicked dopamine's effects. Likewise, the D2 but not the D1 antagonist blocked dopamine-induced changes, indicating that they were mediated primarily by D2 receptors. Parvalbumin expression was accelerated by dopaminergic reinnervation of cortical slices that were cocultured with mesencephalic slices. Coapplication of the glutamate NMDA receptor antagonist MK801 or AP5 blocked dopamine-induced increases in dendritic branching, suggesting that changes were mediated partly by interaction with glutamate to alter cortical excitability.

Aging↗
PubMed2001

Combined functional magnetic resonance imaging and diffusion tensor imaging demonstrate widespread modified organisation in malformation of cortical development.

A patient with a mild left hemiparesis and a malformation of cortical development in the right hemisphere was investigated with fMRI (functional magnetic resonance imaging) and DTI (diffusion tensor imaging). The motor cortex was studied using a finger tapping fMRI experiment. The fibre orientation was studied by displaying the principal eigenvector of the diffusion tensor in the spatially normalised brain of the patient and of control subjects. In addition, the anisotropy (directionality) of water diffusion of the patient was statistically compared with control subjects. The malformation was located in the right central region in the expected position of the motor cortex. fMRI showed activation anterior and posterior to the malformation. DTI disclosed that fibres with rostrocaudal orientation, presumably representing the pyramidal tract, were deviating from their normal orientation and passing around the malformation. There were widespread regions of reduced anisotropy affecting both hemispheres. In conclusion, fMRI and DTI provided concordant information showing widespread modified functional and structural organisation including regions which appeared normal on standard imaging.

Adult↗
PubMed1989

Morphometric analysis of prefrontal cortical development following neonatal lesioning of the dopaminergic mesocortical projection.

In this study the possibility that dopamine (DA) plays a trophic role in cortical development was studied by analysing cortical morphology and dendritic arborization of pyramidal cells after neonatal depletion of DA. The prefrontal cortex (PFC) was depleted of a DA innervation from postnatal day 1 onwards by thermal lesions of the DA cell group (A10) in the ventral tegmental area. Measurements of the cortical thickness and volume of the PFC subareas did not reveal any gross alterations. The DA-depleted animals, however, showed a 30% decrease in the total length of the basal dendrites of the pyramidal cells in layer V of the medial PFC. These cells constitute the primary target of the dopaminergic innervation in the prefrontal cortex. The decreased dendritic length was due mainly to a reduced branching frequency of the basal dendrites. The present results of the dendritic measurements support a trophic role for DA in neuronal differentiation.

Aging↗
PubMed2003

Localization of ApoER2, VLDLR and Dab1 in radial glia: groundwork for a new model of reelin action during cortical development.

The reelin signaling pathway regulates laminar positioning of radially migrating neurons during cortical development. It has been suggested that reelin secreted by Cajal-Retzius cells in the marginal zone could provide either a stop or an attractant signal for migratory neurons expressing reelin receptors, but the proposed models fail to explain recent experimental findings. Here we provide evidence that the reelin receptor machinery, including the lipoprotein receptors ApoER2 and VLDLR along with the cytoplasmic adaptor protein Dab1, is located in radial glia precursors whose processes span the entire cortical wall from the ventricular zone to the pial surface. Moreover, in reeler mice, defective in reelin, decreased levels of Dab1 in the ventricular zone correspond to an accumulation of the protein in radial end-feet beneath the pia matter. Our results support that neural stem cells receive a functional reelin signal. They are also consistent with a working model of reelin action, according to which reelin signaling on the newborn neuron-inherited radial process regulates perikaryal translocation and positioning.

Animals↗
PubMed2004

Dynamic mapping of human cortical development during childhood through early adulthood.

We report the dynamic anatomical sequence of human cortical gray matter development between the age of 4-21 years using quantitative four-dimensional maps and time-lapse sequences. Thirteen healthy children for whom anatomic brain MRI scans were obtained every 2 years, for 8-10 years, were studied. By using models of the cortical surface and sulcal landmarks and a statistical model for gray matter density, human cortical development could be visualized across the age range in a spatiotemporally detailed time-lapse sequence. The resulting time-lapse "movies" reveal that (i) higher-order association cortices mature only after lower-order somatosensory and visual cortices, the functions of which they integrate, are developed, and (ii) phylogenetically older brain areas mature earlier than newer ones. Direct comparison with normal cortical development may help understanding of some neurodevelopmental disorders such as childhood-onset schizophrenia or autism.

Adolescent↗
PubMedDate not supplied

[Malformations in cortical development in patients with epilepsy. Neuroimaging of 17 cases].

This article reviews Malformations of Cortical Development (MCD) diagnosed by Magnetic Resonance Imaging (MRI) in a series of patients with epilepsy. This study spans a five year period. The frequency of these malformations was 7.1%. Most of these were focal or multifocal and the most common ones were polymicrogyria (35.3% of the patients), heterotopia (29.4%), and focal cortical dysplasia (29.4%). The frontal lobes were the most frequently affected regions. The various MCD encountered reflect the wide spectrum of MCD leading to epilepsy.

Adolescent↗
PubMed1998

Preliminary evidence for aberrant cortical development in abused children: a quantitative EEG study.

The objectives of this study were to investigate cortical development and hemispheric asymmetry in abused children. Fifteen hospitalized children (mean age 10.7 +/- 2.5 years) with severe physical or sexual abuse and 15 normal children (10.1 +/- 3.1 years) were studied with quantitative EEG. Abused children had higher levels of left hemisphere coherence and a reversed asymmetry, with left hemisphere coherence significantly exceeding right hemisphere coherence. Left hemisphere coherence decreased more rapidly across electrode distance in normal subjects, suggesting that increased left coherence in abused patients stemmed from a deficit in left cortical differentiation. These findings support the hypothesis that early severe abuse may have a deleterious effect on brain development.

Adolescent↗
PubMed2004

Cortical reorganization in malformations of cortical development: a magnetoencephalographic study.

BACKGROUND: The evaluation for epilepsy surgery of patients with malformations of cortical development (MCDs) in areas of clinically important cerebral function is a challenge because of the unpredictable localization of critical sensory, motor, and cognitive function. Magnetoencephalography (MEG) source localization of evoked fields can address whether functional reorganization of primary sensory modalities exists in MCDs. METHODS: Consecutive patients with MRI-demonstrated rolandic and calcarine cortex MCDs were identified who had a 148-channel whole-head MEG study to identify the localization of primary somatosensory and visual cortices. Reorganization was considered when localization contrasted that expected upon general anatomic or homuncular rules and was defined against controls. RESULTS: Twelve patients (n = 12) were studied. Six had focal cortical dysplasia, two had polymicrogyria and schizencephaly, and four had isolated polymicrogyria. In the patients with cortical dysplasias, the somatosensory cortices were identified outside the rolandic area. In the two patients with polymicrogyria and schizencephaly, the somatosensory cortices remained in the rolandic areas as long as the anatomy was not distorted by the presence of the schizencephalic cleft. In the patients with isolated polymicrogyria, the somatosensory cortex was mapped without evidence of reorganization. CONCLUSION: In patients with epileptic MCDs involving rolandic and calcarine regions, cortical function may be reorganized if the MCDs are due to an abnormal neuronal or glial proliferation (i.e., cortical dysplasia) but may not be in MCDs caused by abnormal cortical organization (i.e., polymicrogyria).

Adult↗
PubMed2000

Cognitive outcome of children with epilepsy and malformations of cortical development.

OBJECTIVE: To assess intellectual functioning (IQ) in 54 children and adolescents with intractable epilepsy who later underwent cortical resection due to unilateral malformations of cortical development acquired in utero. METHODS: Lesion type was classified into circumscribed mass lesions and diffuse cortical dysplasia based on histopathologic analysis of surgical tissue. Cortical dysplastic lesions were further graded as mild, moderate, or severe according to specific microscopic features. Laterality of lesion was determined through neurologic examination and electrophysiologic and neuroradiologic procedures. Classification of lesion type was corroborated by its significant relationship with other disease-related variables known to be related to clinical severity (age at seizure onset, age at resection, and extent of lesion). RESULTS: Analyses of covariance revealed that circumscribed lesions had a less deleterious effect on nonverbal IQ than did diffuse cortical dysplasia, after controlling for age at seizure onset and extent of lesion. This effect was also found on verbal IQ measures, but only in subjects with right-sided lesions. Subjects with left-sided lesions performed significantly more poorly on verbal IQ measures than those with right-sided lesions. Additionally, younger age at onset and greater extent of lesion were associated with poorer cognitive outcome. CONCLUSIONS: Cortical dysplasia and early left hemisphere lesions have a significantly worse impact on cognitive functioning than circumscribed lesions or right hemisphere developmental lesions in children with epilepsy.

Adolescent↗
PubMed2005

Malformations of cortical development: high-resolution MR and diffusion tensor imaging of fiber tracts at 3T.

Patients with malformations of cortical development and epilepsy may have a variety of abnormal brain findings, including abnormal gyral patterns, cortical thickening, decreased volume of white matter, and increased diffusion of white matter. The status of individual white matter fiber tracts, however, is unknown. We present a case of bilateral frontal schizencephaly and subcortical heterotopia and illustrate alterations of white matter fascicles by combined structural and functional diffusion tensor imaging at 3 T.

Adult↗
PubMed2000

Seizure outcome after surgery for epilepsy due to malformation of cortical development.

PURPOSE: To explore seizure outcome after surgery for focal epilepsy due to malformation of cortical development (MCD), with focus on the role of MRI. METHODS: Thirty-five patients who had surgery for intractable focal epilepsy due to MCD identified by preoperative MRI and confirmed by histopathologic analysis of resected tissue were studied. Patients were aged 3 months to 47 years (median, 14 years) at the time of surgery. Duration of follow-up was 1 to 7.9 (mean, 3.4) years. RESULTS: At latest follow-up, 17 patients (49%) had Engel Class I outcome with no seizures or auras only; eight patients (23%) had Class II outcome, with rare disabling seizures; seven patients (20%) had worthwhile improvement; and three patients (9%) had no improvement. Seizure-free outcome tended to be more frequent among patients who had complete resection of unilateral MCD (excluding hemimegalencephaly) based on postoperative MRI (7/12; 58%), compared with patients with unilateral MCD who had incomplete resection (3/11; 27%), but the difference was not significant. The frequency of seizure-free outcome did not differ significantly between children (8/14; 57%), adolescents (7/15; 47%) or adults (2/6; 33%); between patients who had daily (12/24; 50%), weekly (4/9; 44%), or monthly (1/2; 50%) seizures preoperatively; between patients who had temporal (2/6; 33%) or extratemporal or multilobar resections (14/28; 50%); or between patients who were (9/16; 56%) or were not (8/19; 42%) studied with subdural electrodes. Results for all analyses were similar when analyzed at latest available follow-up or at 1 year after surgery. CONCLUSIONS: Surgery can offer seizure-free outcome for approximately one half of carefully selected patients with intractable focal epilepsy due to MCD. Complete resection of the MRI-apparent lesion may improve the likelihood for favorable outcome. MRI evidence of hemimegalencephaly or bilateral MCD suggests a low likelihood for postoperative freedom from seizures.

Adolescent↗
PubMed2001

Seizure outcome after functional hemispherectomy for malformations of cortical development.

MRI features were correlated with postsurgical seizure outcome in patients with hemispheric malformations of cortical development (MCD). After functional hemispherectomy, 5 of 6 patients (83%) with hemimegalencephaly had persistent, although markedly improved, seizures; 5 of 6 patients (83%) with relative preservation of part of one lobe or atrophy were seizure free. Hemimegalencephaly and other types of hemispheric MCD appear to differ in prognosis for freedom from seizures after functional hemispherectomy.

Brain↗
PubMed1998

A novel disruption of cortical development in p35(-/-) mice distinct from reeler.

The p35/cdk5 neuronal-specific kinase complex has been shown to play an important role in the laminar configuration of cortical neurons. Mice lacking either p35 or cdk5 exhibit a disrupted cortical lamination pattern. We showed previously that instead of the normal "inside-out" layering pattern of cortical neurons, cortical neurons are layered from "outside-in" in p35 mutant mice. To gain insight into the mechanisms that underlie these defects, we examined the organization of landmark structures formed during cortical development and the migratory behavior of p35(-/-) cortical neurons by using bromodeoxyuridine labeling. In the present study, we show that reelin localization in the marginal zone is normal in p35 mutant mice. Furthermore, the preplate splits into the marginal zone and subplate properly, a developmental event that fails to occur in reeler mice. Finally, the migration of the earliest born cortical plate neurons is normal in p35 mutant mice; cortical neurons subsequently generated remain underneath these neurons. These data suggest that the p35/cdk5 kinase is required for cortical plate neurons to migrate past preexisting neurons and take up superficial positions to constitute the inside-outside layering order of cortical lamination.

Animals↗
PubMed2000

Septo-optic dysplasia plus: a spectrum of malformations of cortical development.

The authors describe three children with septo-optic dysplasia (SOD)-plus: SOD and an associated malformation of cortical development. All three children had developmental delay, and two of the children had significant associated motor deficits. The associated cortical malformations with SOD include a spectrum of disorders of neuronal organization, not limited, as previously described, to schizencephaly. SOD-plus should be suspected in children with SOD and developmental delay.

Abnormalities, Multiple↗