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PubMed1996

Pathogenesis and pathology of focal malformations of cortical development and epilepsy.

This article reviews the pathogenesis and pathology of the most common focal malformations of cortical development in association with epilepsy. The classification of these disorders is reviewed in the context of new developments in the areas of diagnosis and genetics. The major pathological substrates and the possible mechanisms of these malformations are discussed. The possible mechanisms of epileptogenesis in the context of focal malformations are complex and poorly understood at present. Advances in this area promise to enhance our understanding of the basic mechanisms of epilepsy.

Adult↗
PubMed1997

Proton spectroscopic imaging at 4.1 tesla in patients with malformations of cortical development and epilepsy.

We used proton magnetic resonance spectroscopic imaging (MRSI) at 4.1 tesla in patients with malformations of cortical development (MCDs) and epilepsy. We compared the spectroscopic results with normative data using 2 SDs (95% confidence) above normal values for detection of significant abnormalities for creatine-N-acetylated compounds (Cr/NA) ratio and choline-N-acetylated compounds (Cho/NA). The results were correlated with clinical, EEG, and histologic findings. Patients with focal cortical dysplasia showed significant metabolic abnormalities in correspondence with the structural lesions, whereas patients with heterotopia and polymicrogyria demonstrated no subcortical MRSI abnormalities. Significant correlations were found between the metabolic abnormalities and the frequency of seizures but not with the degree of interictal EEG discharges. Quantitative neuronal and glial cell counts revealed no statistically significant correlation between cell loss and the abnormal metabolic ratios in those who underwent surgery. These preliminary findings suggest that MRSI-based metabolic abnormalities in patients with MCDs are variable and are likely to be associated with complex cellular mechanisms involving the regulation of NA, total Cr content, and Cho.

Acetylation↗
PubMedDate not supplied

[Malformations of cortical development and their clinical repercussions in a series of 144 cases].

OBJECTIVE: To show the disorders of the brain cortical development and the possible origin in base to a large series studied in a Pediatric Neurology service. PATIENTS AND METHODS: A series of 144 children with ages ranging between newborn and 12 years was studied from the clinic, image (MR, 3DMR) and evolutive point of views. RESULTS: The diagnosis was: polymicrogyria in 61 cases, lissencephaly in 22, eschizencephaly in 16, heterotopia in 16, cortical dysplasia in 9, hemimegalencephaly in 8, cobblestone in 7, sublobar dysplasia in 3, and 'double cortex' in 2. Mental retardation, motor disorders and epilepsy were the most important anomalies. CONCLUSIONS: Actually, the image is the most important study to make the diagnosis of every type of cerebral malformation. However, to know the specific gene that origin every disorder seems to be the most important thing to make the classification of every malformative type and the possible prevention of this pathology.

Brain Diseases↗
PubMed1998

Sublobar dysplasia: a new malformation of cortical development.

We investigated the clinical presentations and neuroimaging characteristics of five patients with sublobar dysplasia, an unusual malformation of cortical development. Records and teaching files of five unrelated patients with a localized dysplasia of the cerebral hemisphere separated from the remainder of the affected lobe or hemisphere by a deep infolding of cortex (sublobar dysplasia) were retrospectively reviewed with regard to age at clinical presentation, manner of clinical presentation, neurologic examination, location of dysplasia, imaging characteristics, and the presence and type of associated malformations. Four of five patients presented with seizures; the fifth presented with a calvarial anomaly. All were neurologically and developmentally normal. MRI showed that the areas of sublobar dysplasia were frontal in two patients and temporal, parietal, and occipital in one patient each. The cortex in the affected region of brain was thickened with shallow sulci and an abnormal sulcal pattern in all affected patients. In three patients, the cortical-white matter junction was irregular. The ipsilateral lateral ventricle was dysplastic in all patients. Associated anomalies included callosal anomalies (five patients), cerebellar vermian hypoplasia (three patients), and venous malformation (one patient). Sublobar dysplasia appears to be a distinct cortical malformation of unknown etiology that causes no neurologic deficits but ultimately results in epilepsy. Possible causes include abnormal stem cell proliferation and in utero injury.

Adolescent↗
PubMed2006

Heterogeneous epileptogenicity and cortical function within malformations of cortical development: a case report.

The authors report a 24-year-old patient with intractable partial epilepsy and massive malformations of cortical development (MCD). Subdural EEG recordings of habitual seizures showed heterogeneous epileptogenicity, and visual evoked potential was recorded within the MCD just adjacent to the most active epileptogenic focus. Resection of the small cortical area presumably with core epileptogenicity, while sparing the cortical functional area, improved seizure outcome without any postoperative functional deficits.

Adult↗
PubMed2003

Brain-derived neurotrophic factor stimulates energy metabolism in developing cortical neurons.

Brain-derived neurotrophic factor (BDNF) promotes the biochemical and morphological differentiation of selective populations of neurons during development. In this study we examined the energy requirements associated with the effects of BDNF on neuronal differentiation. Because glucose is the preferred energy substrate in the brain, the effect of BDNF on glucose utilization was investigated in developing cortical neurons via biochemical and imaging studies. Results revealed that BDNF increases glucose utilization and the expression of the neuronal glucose transporter GLUT3. Stimulation of glucose utilization by BDNF was shown to result from the activation of Na+/K+-ATPase via an increase in Na+ influx that is mediated, at least in part, by the stimulation of Na+-dependent amino acid transport. The increased Na+-dependent amino acid uptake by BDNF is followed by an enhancement of overall protein synthesis associated with the differentiation of cortical neurons. Together, these data demonstrate the ability of BDNF to stimulate glucose utilization in response to an enhanced energy demand resulting from increases in amino acid uptake and protein synthesis associated with the promotion of neuronal differentiation by BDNF.

Amino Acids↗
PubMed1993

Altered distribution of nicotinamide-adenine dinucleotide phosphate-diaphorase cells in frontal lobe of schizophrenics implies disturbances of cortical development.

Epidemiological and anatomical studies support the theory that disturbances of brain development may play a contributory role in the etiology of schizophrenia. Anatomical findings suggest that the normal pattern of neuronal migration during development of the cerebral cortex may be affected in the brains of schizophrenics, with the implication that cortical connectivity and associative function will be disrupted. In the present investigation in matched schizophrenic and control brains, we examined a particular population of neurons found in the prefrontal cortex and underlying white matter and characterized by histochemical staining for the enzyme nicotinamide-adenine dinucleotide phosphate-diaphorase. In normal brains, these neurons are found in highest numbers in the white matter immediately deep to layer VI of the cortex where they remain from the subplate, an early formed, but transitory structure that plays a key role in cortical development and connection formation. The dorsolateral prefrontal area of schizophrenics showed a significant decline in nicotinamide-adenine dinucleotide phosphate-diaphorase neurons in the superficial white matter and in the overlying cortex but a significant increase in these neurons in white matter deeper than 3 mm from the cortex. These findings are consistent with a disturbance of the subplate during development in which the normal pattern of programmed cell death is compromised and accompanied by a defect in the normal orderly migration of neurons toward the cortical plate. These are likely to have serious consequences for the establishment of a normal pattern of cortical connections leading to a potential breakdown of frontal lobe function in schizophrenics.

Adult↗
PubMed2003

Activation of mu-calpain in developing cortical neurons following methylmercury treatment.

In order to examine the possible involvement of mu-calpain in methylmercury (MeHg)-induced neurotoxicity in developing cortical neurons, we performed biochemical and immunohistochemical studies utilizing two antibodies which specifically recognize the 150-kDa mu-calpain-specific alpha-spectrin breakdown product (SBDP) and the active form of mu-calpain in rats on postnatal day 16. Soluble fractions of the cerebral cortex from control rats exhibited slight immunoreactivity for SBDP. Although the amount of SBDP in the cerebral cortex was only slightly increased the day after the final treatment of MeHg (10 mg/kg) for 3 or 7 consecutive days, there was a prominent accumulation of SBDP 3 days after the final treatment of MeHg for 7 consecutive days. On the other hand, the 76-kDa isoform of mu-calpain gradually increased after chronic treatment of MeHg, but markedly decreased 3 days after the final treatment of MeHg for 7 consecutive days. At this stage, many cortical neurons were densely stained with anti-SBDP antibody. The delayed increase in SBDP corresponded well with the delayed nature of the MeHg-induced neurotoxicity. When MK-801 (0.1 mg/kg), a non-competitive antagonist of N-methyl-D-aspartate (NMDA), was administered intraperitoneally with MeHg for 7 consecutive days, both neuronal damage and accumulation of SBDP were markedly depressed in the cerebral cortex 3 days after the final treatment. Our results indicate that mu-calpain activation and mu-calpain-mediated proteolysis of alpha-spectrin preceded neuronal damage in the developing cerebral cortex induced by chronic treatment of MeHg.

Animals↗
PubMed2006

Proteomic analysis of hypoxia/ischemia-induced alteration of cortical development and dopamine neurotransmission in neonatal rat.

Perinatal hypoxia/ischemia (HI) is a common cause of neurological deficits in children. Our goal was to elucidate the underlying mechanisms that contribute to the neurological sequelae of HI-induced brain injury. HI was induced by permanent ligation of the left carotid artery followed by 90 min of hypoxia (7.8% O2) in female P7 rats. A two-dimensional differential proteome analysis was used to assess changes in protein expression in cortex 2 h after HI. In total, 17 proteins reflecting a 2-fold or higher perturbation of expression after HI as compared to sham-treated pups were identified by mass spectrometry. Of the altered proteins, 14-3-3epsilon and TUC-2, both playing an important role in the development of the central nervous system, decrease after HI, consistent with an early disturbance of cortical development. Also affected, DARPP-32 and alpha-synuclein, two proteins important for dopamine neurotransmission, increased more than 2-fold 2 h after HI injury. The differential expression of these proteins was validated by individual Western blot assays. The expression of several metabolic enzymes and translational factors was also perturbed early after HI brain injury. These findings provide initial insights into the mechanisms underlying neurodegenerative events after HI and may allow for the rational design of therapeutic strategies that enhance neuronal adaptation and compensation after HI.

Animals↗
PubMed2006

Clinical and electroencephalographic features of infantile spasms associated with malformations of cortical development.

The aim of this study was to reveal the clinical and encephalographic (EEG) features of infantile spasms (IS) with malformations of cortical development (MCDs). The clinical features, EEG findings, neuroimaging studies and outcomes of various therapeutic modalities for 27 patients with IS and MCDs were reviewed. Background activities of EEG on the MCDs, i.e. asymmetric hypsarrhythmia, localized persistent polymorphic slowing, asymmetric slowing and diffuse fast activities, were shown in 22, 15, 9 and 2 patients, respectively. Partial epileptiform discharges such as localized paroxysmal fast activities, spindle-shaped fast activities and subclinical seizures were shown in 15, 8 and 10 patients, respectively, and the lateralized prominence of generalized paroxysmal fast activities and generalized sharp and wave discharges in 4 and 5 patients, respectively. MCDs were suspected in 5 patients, as revealed by EEG and/or functional neuroimagings without distinct magnetic resonance imaging lesions, and confirmed by pathologic findings. Of the 11 patients treated with surgical resection, 8 became seizure free. EEG features can be very useful in the identification of underlying cortical dysgenesis in patients with IS. However, in one patient who underwent epilepsy surgery in early infancy, we observed easy bleeding and difficult hemostasis from friable vascular and parenchymal tissues. Various EEG features can be very useful in screening underlying MCDs. In addition, epilepsy surgery can be an effective therapeutic modality in many patients with otherwise medically intractable IS with MCDs. However, surgical intervention in extremely young infants should be performed with caution.

Cerebral Cortex↗
PubMed2000

Cortical development in roots of the aquatic plant Pontederia cordata (Pontederiaceae).

Adventitious roots of marsh-grown Pontederia cordata were examined to determine cortical development and structure. The innermost layer of the ground meristem forms the endodermis and aerenchymatous cortex. The outermost layer of the early ground meristem undergoes a precise pattern of oblique and periclinal cell divisions to produce a single or double layer of prohypodermis with an anchor cell for each radial file of aerenchyma cells. At maturity, endodermal cell walls are modified only by narrow Casparian bands. The central regions of the ground meristem become proaerenchyma and exhibit asymmetric cell division and expansion. They produce an aerenchymatous zone with barrel-shaped large cells and irregularly shaped small cells traversing the aerenchyma horizontally along radii; some crystalliferous cells with raphides are present in the aerenchyma. The walls of the hypodermis are modified early by polyphenols. The outermost layer of the hypodermis later matures into an exodermis with Casparian bands that are impermeable to berberine, an apoplastic tracer dye. The nonexodermal layer(s) of the hypodermis has suberin-modified walls. Radial files of aerenchyma are usually connected by narrow protuberances near their midpoints, the aerenchyma lacunae having been produced by expansion of cells along walls lining intercellular spaces. We are terming this type of aerenchyma development, which is neither schizogenous nor lysigenous, "differential expansion."

Journal Article↗
PubMed1996

Extracellular matrix in early cortical development.

Studies of the distribution and production of ECM components during development of the cerebral cortex have suggested several hypotheses regarding their functional role. In the earliest stages of cortical development, fibronectin is produced by cells in the ventricular zone throughout the telencephalic vesicle, where it may serve as a part of the local environment that supports cell division and determines cell fate. Fibronectin is also distributed along radial glial processes. It is closely associated with preplate neurons, as are chondroitin sulfate proteoglycans and several other ECM components. This association continues as preplate cells are divided into the marginal zone and subplate by the invasion of cortical plate neurons, suggesting that ECM, preplate cells and radial glia serve as a scaffold for cortical plate formation. Fibronectin is also produced by migrating neurons, but only by those moving into specific cortical domains, suggesting that it may help neurons destined for specific targets discriminate between adjacent glial guides. A recently defined ECM-like protein, reelin, is absent or abnormal in the reeler mutant mouse in which cortical neurons are severely malpositioned. Reelin is produced by marginal zone cells and is therefore appropriately located to serve as a stop signal for migrating neurons. Axons leaving the cortical plate cross the CSPG-rich subplate, then turn to follow a path containing much less CSPG. In contrast, the cortical trajectory of thalamic axons is centered on the subplate, indicating that CSPGs in the subplate are not a barrier to axon outgrowth and may instead be serving as guidance cues that distinguish afferent from efferent pathways. Neurocan, a CNS-specific CSPG with many molecular features that indicate roles in cell-cell and cell-substrate interactions, is the only CSPG defined to date whose distribution supports a role in distinguishing afferent from efferent pathways.

Animals↗
PubMed2000

Intrinsic and extrinsic control of cortical development.

Recent advances in the study of cerebral cortical early development are described in this chapter. The role of the anterior neural ridge in regulating telencephalon induction in the neural plate is discussed, followed by a review of the evidence for the roles of ventral, rostral and dorsal patterning centres in regulating regionalization of the telencephalon. The patterning centres produce secreted molecules (SHH, FGF, BMP, WNT) that regulate the expression of transcription factors which control regional identity, cell type specification, proliferation and differentiation. These intrinsic patterning mechanisms appear to be sufficient to generate much of the regional organization of the cerebral cortex present in newborn mice. While intrinsic mechanisms have a major role in cortical regionalization and in the production of cortical projection neurons, many cortical interneurons are derived from the basal ganglia and then migrate into the cerebral cortex. Furthermore, thalamic afferents appear to have an important role in maturation of the postnatal rodent cortex. Thus, both intrinsic and extrinsic mechanisms control development of the cerebral cortex.

Animals↗
PubMed2003

Malformations of cortical development with balloon cells: clinical and radiologic correlates.

BACKGROUND: Balloon cells are a key feature of tuberous sclerosis (TS) but are also seen in focal cortical dysplasia (FCD). The authors compare the clinical and MRI characteristics in children with medically refractory localization-related epilepsy who were found to have balloon cells on histology after cortical resections. METHODS: A retrospective review of clinical and MRI data in cases ascertained from a search of pathology records from 1990 until 2000 for those with a diagnosis of FCD or TS. Seventeen patients were identified with malformations of cortical development with balloon cells on histology. Seven had clinical diagnosis of TS and the remaining 10, FCD with balloon cells (FCDBC). RESULTS: Seventy percent of patients with FCDBC (mean follow-up 3.3 years) and 33% of patients with TS (mean follow-up 5.1 years) are seizure free after surgery. There was agreement between the diagnosis based on preoperative MR imaging and on histology in 60% of patients with FCDBC and 71% of patients with TS. Myelin depletion and calcification were noted more frequently in patients with TS. CONCLUSIONS: No significant differences were noted between patients with refractory epilepsy caused by TS or FCDBC. There was a trend toward better postoperative seizure control in the FCDBC group. These two conditions are difficult to distinguish on the basis of MR and histologic appearances. The authors conclude that FCDBC likely represents a phenotypic variation of TS, and as such, all patients with balloon cell dysplasias should be carefully screened for other features of TS to enable appropriate genetic counseling.

Cerebral Cortex↗
PubMed2000

Cortical development: receiving reelin.

Recent genetic and biochemical studies indicate that lipoprotein receptors are components of the neuronal receptor for Reelin, mediating the glycoprotein's essential function in cortical development. At least eight cadherin-related neuronal receptors may also play a part in this signalling system.

Animals↗
PubMed2006

Intellectual ability and cortical development in children and adolescents.

Children who are adept at any one of the three academic 'R's (reading, writing and arithmetic) tend to be good at the others, and grow into adults who are similarly skilled at diverse intellectually demanding activities. Determining the neuroanatomical correlates of this relatively stable individual trait of general intelligence has proved difficult, particularly in the rapidly developing brains of children and adolescents. Here we demonstrate that the trajectory of change in the thickness of the cerebral cortex, rather than cortical thickness itself, is most closely related to level of intelligence. Using a longitudinal design, we find a marked developmental shift from a predominantly negative correlation between intelligence and cortical thickness in early childhood to a positive correlation in late childhood and beyond. Additionally, level of intelligence is associated with the trajectory of cortical development, primarily in frontal regions implicated in the maturation of intelligent activity. More intelligent children demonstrate a particularly plastic cortex, with an initial accelerated and prolonged phase of cortical increase, which yields to equally vigorous cortical thinning by early adolescence. This study indicates that the neuroanatomical expression of intelligence in children is dynamic.

Adolescent↗
PubMed1995

Cortical development and neuropathology in schizophrenia.

Epidemiological studies suggest that perturbations occurring during pregnancy can increase the incidence of schizophrenia among offspring. Examination of the neuropathology of the brains of some schizophrenics suggests that a defect in the later phases of cerebral cortical development, notably the last phases of neuronal migration and the establishment and refinement of patterns of cortical connections, may be involved. Most of these studies are conjectural, and the relationship between primary lesions and potential secondary retrograde and anterograde effects in the circuitry linking the prefrontal cortex, basal forebrain, mediodorsal thalamus and medial temporal cortex is unknown. Our hypothesis, based on neuromorphological and gene expression studies, is that a disturbance of migration or in the pattern of preprogrammed cell death in the subplate zone of the developing cerebral cortex causes a failure to establish normal patterns of connections in the overlying cortex. This compromised circuitry subsequently decompensates, leading to schizophrenic symptoms and activity-dependent manifestations of altered gene expression for neurotransmitter- and receptor-related molecules.

Cerebral Cortex↗