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PubMed2006

Comparative aspects of cerebral cortical development.

This review aims to provide examples of how both comparative and genetic analyses contribute to our understanding of the rules for cortical development and evolution. Genetic studies have helped us to realize the evolutionary rules of telencephalic organization in vertebrates. The control of the establishment of conserved telencephalic subdivisions and the formation of boundaries between these subdivisions has been examined and the very specific alterations at the striatocortical junction have been revealed. Comparative studies and genetic analyses both demonstrate the differential origin and migratory pattern of the two basic neuron types of the cerebral cortex. GABAergic interneurons are mostly generated in the subpallium and a common mechanism governs their migration to the dorsal cortex in both mammals and sauropsids. The pyramidal neurons are generated within the cortical germinal zone and migrate radially, the earliest generated cell layers comprising preplate cells. Reelin-positive Cajal-Retzius cells are a general feature of all vertebrates studied so far; however, there is a considerable amplification of the Reelin signalling with cortical complexity, which might have contributed to the establishment of the basic mammalian pattern of cortical development. Based on numerous recent observations we shall present the argument that specialization of the mitotic compartments may constitute a major drive behind the evolution of the mammalian cortex. Comparative developmental studies have revealed distinct features in the early compartments of the developing macaque brain, drawing our attention to the limitations of some of the current model systems for understanding human developmental abnormalities of the cortex. Comparative and genetic aspects of cortical development both reveal the workings of evolution.

Animals↗
PubMed2002

Classification issues in malformations caused by abnormalities of cortical development.

Malformations caused by abnormalities of cortical development (MCDs) as a group are now widely recognized as a key cause of medically refractory epilepsies, often leading to a consideration of surgical treatment. A practical classification scheme including histopathologic, imaging, and, if possible, clinical-electrographic features of the various different types of MCDs, will be important to the delineation of surgical strategies and anticipation of medical and surgical prognoses. A proposal of such a scheme with emphasis on the focal cortical dysplasias is given in the hopes that it will reopen the debate on the best way to classify these disorders.

Cerebral Cortex↗
PubMed2000

Aberrant neural circuits in malformations of cortical development and focal epilepsy.

Malformations of cortical development (MCD) account for a high proportion of medically resistant partial seizures in children and figure prominently in pediatric surgical series. In contrast to the results of epilepsy surgery for postnatally acquired lesions, seizure freedom in patients with MCD is less certain owing to difficulties in defining the epileptic zone, and fully excising the epileptogenic cortex. The authors present evidence that, compared with postnatally acquired lesions such as those due to tumors or trauma, focal epileptogenesis associated with MCD is best conceptualized as a disorder of widespread and patchy disturbance of cortical networks. This developmental perspective implies that the epileptogenic region in MCD is rarely discrete even in patients with focal anatomic lesions, and may include remote cortical or subcortical areas. Preoperative investigative protocols based on this model have improved surgical results, but outcome remains far from optimal and further progress in understanding the complex developmentally based features of MCD is required.

Cerebral Cortex↗
PubMed2006

Malformations of cortical development in children: clinical manifestation, neuroimaging and neuropathology in selected cases.

Cerebral cortical development can be divided into three steps: cellular proliferation, neuronal migration and organization. Based on known pathologic, genetic and neuroimaging features a classification for malformations of cortical development was proposed by Barkovich in 2001, and updated in 2005. Malformations of cerebral cortex development (MCCD) often demonstrate epileptic seizures and delay in psychomotor development. About 20-40% of children with epilepsy are drug-resistant and there is a large paediatric population requiring epilepsy surgery operations. In our work we performed clinical analysis of 68 children with MCCD treated in our hospital between 2000 and 2006. In our work to consider the type of MCCD we used the updated classification scheme proposed by Barkovich et al. We analyzed epilepsy, gestational and perinatal history, initial symptoms, time to establishing full diagnosis and neurodevelopmental/IQ status. In our results we found that despite similar clinical manifestation neuropathological basis could be significantly different, and vice versa: children with nearly identical neuropathological findings could have completely different neurological and radiological symptoms. Children with drug-resistant epilepsy are potential candidates for neurosurgical treatment; especially lesionectomies in such cases could be very promising in terms of epilepsy management and quality of life as well.

Anticonvulsants↗
PubMed2003

Effect of recurrent epileptiform discharges induced by magnesium-free treatment on developing cortical neurons in vitro.

As seizures in infants and children often originate from the neocortex, neocortical epilepsy models may be appropriate for studying epileptiform activity and seizure-induced injury in the developing nervous system. However, the characterization of epileptiform activity or seizure-induced injury in cultured developing cortical neurons has seldom been reported. Therefore, We attempted to establish a cultured developing cortical neuronal epilepsy model, and to study the subsequent effect on neurons. Cultures were exposed to Mg(2+)-free media for 3 h, and then returned to regular media. Using whole-cell patch-clamp intracellular recording techniques, we found that spontaneously recurrent epileptiform discharges for at least 72 h could be induced after transient Mg(2+)-free treatment. Neuron morphology following Mg(2+)-free treatment demonstrated no prominent alterations. At different time points (6, 24 and 72 h) after Mg(2+)-free treatment, neuronal viability, identified by trypan blue staining and LDH activity, and apoptosis, measured by flow cytometry, showed modest but non-significant (P>0.05) changes compared with the age-matched control group after various culture periods (6 and 17 days) in vitro. Mitochondrial metabolic activity, measured by MTT assay, significantly decreased by 15% at 6 h after Mg(2+)-free treatment (P<0.05) in neurons cultured for 6 days, and at 24 h showed a 29% decrease in neurons cultured for 17 days (P<0.05). In conclusion, brief Mg(2+)-free treatment constitutes a cultured developing cortical neuron 'seizure' model, and can induce transient mitochondrial dysfunction without cell loss.

Animals↗
PubMed2004

Hemispheric malformations of cortical development.

The term hemispheric malformations of cortical development (MCDs) is used in this article to represent congenital malformations that predominantly or exclusively involve complete or substantial portion of one cerebral hemisphere. Hemispheric MCDs usually present during early childhood with intractable epilepsy, cognitive delay, and contralateral hemiparesis. Early identification and selection of children who may be candidates for epilepsy surgery are important during diagnostic evaluation of hemispheric MCD. Surgical intervention at an appropriate time, whenever possible, offers the best chance for seizure freedom and improved cognitive outcome. In addition, making an accurate genetic diagnosis is imperative to offer genetic testing and counseling to the family. In this article, the authors discuss the developmental and genetic mechanisms, pathologic features, diagnosis, and treatment of hemispheric MCD that are substrates of catastrophic childhood epilepsy amenable to surgical treatment.

Brain Diseases↗
PubMed1987

Postnatal development of immunohistochemically localized spectrin-like protein (calspectin or fodrin) in the rat visual cortex: its excessive expression in developing cortical neurons.

Postnatal development of the expression and localization of a membrane-associated cytoskeletal protein, calspectin (fodrin or brain spectrin), in the visual cortex, was immunohistochemically studied in newborn to adult rats, by using an anti-calspectin antibody. At birth, calspectin-immunoreactivity was already present at the plasma membrane and in the cytoplasm of neurons which were mostly pyramidal cells located in the upper part of the cortical subplate. Immature neurons located in the cortical plate were not stained by the antibody, suggesting that calspectin is expressed only in neurons which have differentiated or are differentiating. At postnatal days 2 to 7, immunoreactive neurons were dramatically increased in layers V and VI and very intense labelling was seen in the apical dendrites of layer V pyramidal cells. Most of the stained processes of these and other neurons showed signs of rapid dendritic growth, i.e. non-terminal as well as terminal growth cones and filopodia. At days 10 to 17, dendrites of pyramidal cells in layers II and III became clearly detectable, although still slender. At days 24 to 34, the basal dendrites of pyramidal cells in layers II, III and V became intensely immunoreactive and dendritic spines were visualized by the antibody. In the adult, however, the calspectin immunoreactivity became very weak and spines were not recognizable. At all the ages, axons and neuroglia were unstained. Also, most of the neurons in layer IV of the cortex were not immunoreactive. These results suggest that calspectin is most abundantly expressed in growing parts of the dendrites and spines. A hypothesis that calspectin may play a role in synaptic plasticity in the developing visual cortex is discussed.

Aging↗
PubMed1994

Cortical development and topographic maps: patterns of cell dispersion in developing cerebral cortex.

Cortical neurons are organized into highly patterned ensembles of cells, each with a distinct physiological function. The precursors of these cells arise in the ventricular zone, itself a highly patterned mosaic of cells. To determine whether the ventricular pattern presages the adult, investigators examine the process of cell migration. Recent evidence suggests that both radial (pattern-preserving) and tangential (pattern-blurring) cell movements occur during development.

Animals↗
PubMed1996

Neuroimaging of focal malformations of cortical development.

Neuroimaging is playing an increasingly important role in the evaluation of patients with malformations of cerebral cortical development. In this review, the authors address optimal neuroimaging of cortical malformations using x-ray computed tomography, single-photon-emission computed tomography, positron emission tomography, magnetic resonance imaging, and magnetic resonance spectroscopy. Initially, the authors discuss the strengths and weaknesses of the various imaging techniques. This is followed by a discussion of the clinical and neuroimaging characteristics of several different imaging manifestations of focal malformations of cortical development, including polymicrogyria, focal subcortical heterotopia, schizencephaly, focally thickened gyri, focally irregular gyri, hemimegalencephaly, and transmural dysplasia. The authors intend that, after reading this review, the reader will have a better understanding of the optimal neuroimaging techniques for evaluating these malformations and their many neuroimaging appearances.

Cerebral Cortex↗
PubMed2003

Malformations of cortical development in neurofibromatosis type 1.

The authors report three patients with neurofibromatosis type 1 and different types of malformations of cortical development: Patient 1 had a possible transmantle cortical dysplasia involving the right temporoinsuloparieto-occipital areas; Patient 2 had a periventricular band of heterotopic gray matter with an overlying pachygyric cerebral cortex; and Patient 3 had a left perisylvian polymicrogyria. Because all of these lesions result from different pathogenetic mechanisms, neurofibromin may play a role during several stages of cortical development.

Adolescent↗
PubMed1998

Cholinergic regulation of cortical development and plasticity. New twists to an old story.

Cholinergic afferents innervate cerebral cortex during the most dynamic period of neuronal differentiation and synapse formation, suggesting they play a possible regulatory role in these events. A number of in vivo studies have shown over the last decade that alterations in cholinergic innervation during early postnatal development can change various features of cortical ontogeny. In particular, neonatal lesions to basal forebrain cholinergic afferents result in delayed cortical neuronal development and permanently altered cortical cytoarchitecture and cognitive behaviors. Likewise, cholinergic manipulations affect morphological plasticity in cat visual cortex as well as in the somatosensory cortex of rodents. Furthermore, augmentation of cholinergic function by means of perinatal choline treatment enhances cognitive performance in a sex specific manner. Additional indications for a sexual dimorphism in cortical cholinergic innervation and resulting function are gathered from a variety of paradigms. Recent information about effects of NGF, BDNF and NTB-4/5 on cortical morphogenesis and plasticity reveals complex interactions between the cholinergic basal forebrain afferents and this neurotrophin family. Detailed studies on the expression of cholinergic receptor proteins in cortical development and their associated signal transduction pathways strongly point towards a morphogenetic function of muscarinic receptors, in particular. Transient receptor localization in thalamocortical terminal fields and on a variety of other non-cholinergic fiber bundles suggest a cholinergic role in target finding and/or synapse formation for cortical afferents and efferents. We propose a hypothesis regarding the mechanisms for cholinergic regulation of neuronal differentiation and synapse formation on the level of the individual growth cone and discuss possibilities for cholinergic interactions with differential gene expression. We conclude that understanding the precise role of the cholinergic system in cortical morphogenesis and its relationship to neurotrophin function will be of clinical relevance for a number of developmental brain disorders, including Down Syndrome and Rett Syndrome.

Acetylcholine↗
PubMed2003

Functional organization of the brain with malformations of cortical development.

We examined the localization of cerebral functions in 28 patients with focal epilepsy and malformations of cortical development (MCDs). Polymicrogyria occurred in nine, hemimegalencephaly in four, heterotopia in eight, and focal cortical dysplasia (FCD) in nine cases. We used simple (sensomotor, visual) or complex (language, memory) functional magnetic resonance imaging (fMRI) paradigms. Two thirds of MCDs were activated by simple fMRI paradigms, whereas they less frequently showed activity during complex cognitive fMRI paradigms. During simple paradigms, all disturbances of cortical organization (polymicrogyria, schizencephaly, and mild-type FCD) showed activity, whereas other MCDs (disturbances of earlier steps of cortical development: hemimegalencephaly, Taylor-type FCD, and heterotopia) showed activity in only 44% (p < 0.01). The association between the pathophysiology and morphology of MCDs confirms the recently proposed classification system. Both focal neurological signs (p < 0.05) and focal electroencephalogram slowing (p < 0.05) independently correlated with MCD inactivity, confirming that fMRI showed neuronal functions of MCDs. Conclusively, fMRI visualizes the MCD functions and their relationship to the eloquent cortex, providing useful information before epilepsy surgery. Surgery of cortical organization disturbances should be cautiously performed because these malformations may participate to some degree in brain functions.

Adolescent↗
PubMed2007

Prenatal diagnosis of malformations of cortical development by dedicated neurosonography.

OBJECTIVE: Malformations of cortical development (MCD) are rarely diagnosed in utero. We describe and compare the ultrasonographic and pathology findings in a cohort of fetuses with MCD. METHODS: Fetuses with MCD were identified among all fetuses evaluated for suspected brain anomalies at the Fetal Neurology Clinic, and the ultrasonographic findings were compared with the results of the pathology examination. RESULTS: We suspected the presence of MCD by ultrasonography in 23 fetuses. The mean gestational age at the time of ultrasound diagnosis was 26.2 (range, 18-40) weeks. The ultrasonographic findings leading to the diagnosis of MCD were abnormally overdeveloped gyri and sulci for gestational age (n = 7), delay in sulcation (n = 5), abnormally thin cortex (n = 5) abnormally wide and broad sulci (n = 3), bulging into the lateral ventricle (n = 1), cortical cleft (n = 1), and multiple intraparenchymal echogenic nodules (n = 1). All fetuses had associated central nervous system (CNS) and/or non-CNS anomalies. Pathology examination (performed in 17 fetuses) confirmed MCD in 16. CONCLUSIONS: Cortical malformations can be diagnosed in utero by ultrasonography based on the presence of specific deviations from the normal pattern of development. The identified cases may represent the more severe forms in the MCD spectrum. The pathology findings do not always conform to the current classification systems of MCD but help in differentiating between possible genetic and acquired etiologies and in some cases provide a definitive syndromic diagnosis.

Cerebral Cortex↗
PubMed2002

Disorders of cortical development and epilepsy.

There has been an impressive increase in our ability to identify and categorize patients with cortical development lesions over the past decade. The clinical features associated with disorders of cortical development (DCD) have been described, and epilepsy has been shown to be a frequent symptom. In this review, we categorize DCD based on their structure and discuss their underlying causes and clinical features. Just as the cause of each type of disorder is thought to be unique, each disorder also has distinct types of seizures, treatment strategies, and electroencephalographic features. Studies in human tissue and animal models of DCD have begun to shed light on why DCD are associated with epilepsy. Aberrant synaptic connections within the dysplastic tissue and between the dysplastic tissue and more normal-appearing adjacent tissue form an abnormal, hyperexcitable network that increases seizure susceptibility. In the future, strategies for blocking formation of the aberrant networks may prevent the development of epilepsy.

Animals↗
PubMed2001

Seckel's syndrome and malformations of cortical development: report of three new cases and review of the literature.

Seckel's syndrome is a rare form of primordial dwarfism, characterized by peculiar facial appearance. In the past, this condition was overdiagnosed, and most attention was given to the facial and skeletal features to define more precise diagnostic criteria. The presence of mental retardation and neurologic signs is one of the peculiar features of this syndrome, but only recently were rare cases of malformation of cortical development described, as documented by magnetic resonance imaging (MRI). Here, we present three new cases of Seckel's syndrome showing different malformations of cortical development (one gyral hypoplasia, one macrogyria and partial corpus callosum agenesis, and one bilateral opercular macrogyria). We hypothesize that the different types of clinical expression of our patients could be explained by different malformation of cortical development types. We think that MRI studies could be performed in malformative syndromes because of the possible correlations between type and extent of the lesion and the clinical picture of any individual case.

Abnormalities, Multiple↗
PubMed2005

Reflex seizures in patients with malformations of cortical development and refractory epilepsy.

PURPOSE: Malformations of cortical development (MCDs) are usually highly epileptogenic, and their hyperexcitability could facilitate the occurrence of reflex seizures. We sought to characterize reflex seizures in patients with MCDs and refractory epilepsy. METHODS: Clinical, electrographic, and neuroimaging data were reviewed in eight patients with MCDs who had reflex seizures reproduced during presurgical evaluation. RESULTS: All eight patients had both reflex and spontaneous seizures. In six, however, drop attacks or axial myoclonic seizures occurred only upon specific sensory stimulation. Reflex seizures were induced by more than one type of stimulus in most patients, but anatomofunctional correlations could usually be invoked. Six patients had significant intellectual impairment. Surgical resection controlled seizures in two patients. CONCLUSIONS: Reflex seizures in patients with MCDs may be medically refractory and may often manifest as drop attacks or axial myoclonus. Surgical resection of focal lesions can bring reflex seizures under control. Putative mechanisms related to the relatively low frequency of reflex seizures in MCDs are discussed.

Adolescent↗
PubMed2000

Disorders of cortical development.

It is only a decade since the realization (facilitated by magnetic resonance imaging) in early 1990s that disorders of cortical development occupy an important place in the aetiologic categorization of epilepsy. Since then research has demonstrated the intrinsic epileptogenicity of disorders of cortical development, their genetic bases and their functional properties. Some of the key points of this most exciting medical and scientific enterprise are reviewed here, with an emphasis in the advances seen within the past 2 years.

Animals↗
PubMed2004

Malformations of cortical development: molecular pathogenesis and experimental strategies.

Malformations of cortical development (MCD) are developmental brain lesions characterized by abnormal formation of the cerebral cortex and a high clinical association with epilepsy in infants, children, and adults. Despite multiple anti-epileptic drugs (AEDs), treatment of epilepsy associated with MCD may require cortical resection performed to remove the cytoarchitecturally abnormal region of cortex. Single genes responsible for distinct MCD including lissencephaly, subcortical band heterotopia, and tuberous sclerosis, have been identified and permit important mechanistic insights into how gene mutations result in abnormal cortical cytoarchitecture. The pathogenesis of MCD such as focal cortical dysplasia, hemimegalencephaly, and polymicrogyria, remains unknown. A variety of new techniques including cDNA array analysis now allow for analysis of gene expression within MCD.

Animals↗