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PubMed2006

Epilepsy surgery in patients with malformations of cortical development.

PURPOSE OF REVIEW: Patients with malformations of cortical development often suffer from intractable focal epilepsy. This review considers recent progress in the selection and seizure outcome of patients undergoing resective epilepsy surgery for this condition. RECENT FINDINGS: Patients with malformations of cortical development restricted to part or even a whole hemisphere may be candidates for epilepsy surgery even when, due to microscopic malformations, magnetic resonance imaging shows no detectable lesion. Despite recent advances in structural and functional imaging, the majority of patients with this condition undergo invasive evaluation. Patients with focal cortical dysplasia, with and without a detectable lesion on magnetic resonance imaging, often have a favorable outcome with epilepsy surgery. The underlying pathological substrate seems to be a better predictor for surgical outcome in patients with focal cortical dysplasia than the presence of a lesion on magnetic resonance imaging. Epilepsy surgery can be offered in a highly selected subgroup of patients with unilateral nodular heterotopia. Seizures in hemimegalencephaly may respond favorably to hemispherectomy, although most children will continue to have seizures and significant functional impairments. SUMMARY: Patients with focal epilepsy due to malformations of cortical development are often intractable to medical management. Resective epilepsy surgery can be beneficial, particularly for patients with focal cortical dysplasia and unilateral hemispheric malformations.

Brain Diseases↗
PubMed2007

Adolescent cortical development: a critical period of vulnerability for addiction.

Cortical growth and remodeling continues from birth through youth and adolescence to stable adult levels changing slowly into senescence. There are critical periods of cortical development when specific experiences drive major synaptic rearrangements and learning that only occur during the critical period. For example, visual cortex is characterized by a critical period of plasticity involved in establishing visual acuity. Adolescence is defined by characteristic behaviors that include high levels of risk taking, exploration, novelty and sensation seeking, social interaction and play behaviors. In addition, adolescence is the final period of development of the adult during which talents, reasoning and complex adult behaviors mature. This maturation of behaviors corresponds with periods of marked changes in neurogenesis, cortical synaptic remodeling, neurotransmitter receptors and transporters, as well as major changes in hormones. Frontal cortical development is later in adolescence and likely contributes to refinement of reasoning, goal and priority setting, impulse control and evaluating long and short term rewards. Adolescent humans have high levels of binge drinking and experimentation with other drugs. This review presents findings supporting adolescence as a critical period of cortical development important for establishing life long adult characteristics that are disrupted by alcohol and drug use.

Adolescent↗
PubMed2001

Radiologic classification of malformations of cortical development.

Malformations of cerebral cortical development are common birth defects that can cause delayed development, epilepsy, focal neurologic deficits, and mental retardation. Rational classification of these disorders is essential for proper prognosis, genetic testing and counseling, and investigation of the underlying molecular causes. A rational approach to this classification is a framework based on whether these disorders are the result of abnormal cell proliferation or apoptosis, abnormal migration of immature neurons, or abnormal horizontal and radial orientation in the cortex. Superimposed on this framework are subclassifications that are based on topology of the malformation, associated central nervous system (CNS) or extra-CNS malformations, and results of molecular genetic testing. Characteristics that correlate with and enforce this system of classification can be identified by modern neuroimaging studies.

Animals↗
PubMed2001

Involvement of enhanced sensitivity of N-methyl-D-aspartate receptors in vulnerability of developing cortical neurons to methylmercury neurotoxicity.

The developing cortical neurons have been well documented to be extremely vulnerable to the toxic effect of methylmercury (MeHg). In the present study, a possible involvement of N-methyl-D-aspartate (NMDA) receptors in MeHg neurotoxicity was examined because the sensitivity of cortical neurons to NMDA neurotoxicity has a similar developmental profile. Rats on postnatal day 2 (P2), P16, and P60 were orally administered MeHg (10 mg/kg) for 7 consecutive days. The most severe neuronal damage was observed in the occipital cortex of P16 rats. When MK-801 (0.1 mg/kg), a non-competitive antagonist of NMDA, was administered intraperitoneally with MeHg, MeHg-induced neurodegeneration was markedly ameliorated. Furthermore, there was a marked accumulation of nitrotyrosine, a reaction product of peroxynitrite and L-tyrosine, after chronic treatment of MeHg in the occipital cortex of P16 rats. The accumulation of nitrotyrosine was also significantly suppressed by MK-801. In the present electrophysiological study, the amplitude of synaptic responses mediated by NMDA receptors recorded in cortical neurons of P16 rats was significantly larger than those from P2 and P60 rats. These observations strongly suggest that a generation of peroxynitrite through activation of NMDA receptors is a major causal factor for MeHg neurotoxicity in the developing cortical neurons. Furthermore, enhanced sensitivity of NMDA receptors may make the cortical neurons of P16 rats most susceptible to MeHg neurotoxicity.

Age Factors↗
PubMed2000

Progressive restriction in fate potential by neural progenitors during cerebral cortical development.

During early stages of cerebral cortical development, progenitor cells in the ventricular zone are multipotent, producing neurons of many layers over successive cell divisions. The laminar fate of their progeny depends on environmental cues to which the cells respond prior to mitosis. By the end of neurogenesis, however, progenitors are lineally committed to producing upper-layer neurons. Here we assess the laminar fate potential of progenitors at a middle stage of cortical development. The progenitors of layer 4 neurons were first transplanted into older brains in which layer 2/3 was being generated. The transplanted neurons adopted a laminar fate appropriate for the new environment (layer 2/3), revealing that layer 4 progenitors are multipotent. Mid-stage progenitors were then transplanted into a younger environment, in which layer 6 neurons were being generated. The transplanted neurons bypassed layer 6, revealing that layer 4 progenitors have a restricted fate potential and are incompetent to respond to environmental cues that trigger layer 6 production. Instead, the transplanted cells migrated to layer 4, the position typical of their origin, and also to layer 5, a position appropriate for neither the host nor the donor environment. Because layer 5 neurogenesis is complete by the stage that progenitors were removed for transplantation, restrictions in laminar fate potential must lag behind the final production of a cortical layer. These results suggest that a combination of intrinsic and environmental cues controls the competence of cortical progenitor cells to produce neurons of different layers.

Animals↗
PubMed2006

Histopathologic findings of malformations of cortical development in an epilepsy surgery cohort.

CONTEXT: Malformations of cortical development (MCDs) are an important cause of pharmacoresistent epilepsy and are frequently diagnosed in surgical pathology. The lack of uniform tissue processing and standard histopathologic nomenclature to describe MCDs has resulted in diagnostic ambiguity. OBJECTIVE: To describe the immunohistochemical findings of MCDs from a relatively large surgical epilepsy cohort and incorporate terminology that more adequately reflects the histopathologic findings into a contemporary classification of MCD. DESIGN: Utilizing the Mayo Clinic Rochester Surgical Pathology Database and patient records, 53 patients with previous intractable epilepsy and a known malformation of cortical development were identified. All of the cohort's paraffin embedded surgical specimens were resectioned and stained with hematoxylin-eosin, Luxol fast blue/cresyl violet, neurofilament protein, and glial fibrillary acidic protein. Each specimen was reviewed histologically and categorized according to a proposed focal MCD classification scheme that substitutes cytoarchitectural dysmorphism for cortical dysplasia and architectural disorganization for microdysgenesis. RESULTS: An MCD was recognized in 49 patients and grouped into 1 of the following 4 categories: (1) cytoarchitectural dysmorphism with balloon cells (n = 19), (2) cytoarchitectural dysmorphism without balloon cells (n = 12), (3) architectural disorganization (n = 8), or (4) polymicrogyria (n = 9). CONCLUSIONS: The histopathologic features of focal MCD in a large epilepsy surgical cohort by using practical immunohistochemistry and a contemporary MCD classification scheme are described. It is proposed that the term focal cortical dysplasia be renamed as focal malformations of cortical development.

Adolescent↗
PubMed2001

Classification system for malformations of cortical development: update 2001.

The many recent discoveries concerning the molecular biologic bases of malformations of cortical development and the discovery of new such malformations have rendered previous classifications out of date. A revised classification of malformations of cortical development is proposed, based on the stage of development (cell proliferation, neuronal migration, cortical organization) at which cortical development was first affected. The categories have been created based on known developmental steps, known pathologic features, known genetics (when possible), and, when necessary, neuroimaging features. In many cases, the precise developmental and genetic features are uncertain, so classification was made based on known relationships among the genetics, pathologic features, and neuroimaging features. A major change since the prior classification has been the elimination of the separation between diffuse and focal/multifocal malformations, based on the recognition that the processes involved in these processes are not fundamentally different; the difference may merely reflect mosaicism, X inactivation, the influence of modifying genes, or suboptimal imaging. Another change is the listing of fewer specific disorders to reduce the need for revisions; more detail is added in other smaller tables that list specific malformations and malformation syndromes. This classification is useful to the practicing physician in that its framework allows a better conceptual understanding of the disorders, while the component of neuroimaging characteristics allows it to be applied to all patients without necessitating brain biopsy, as in pathology-based classifications.

Brain↗
PubMed2003

Malformation of cortical development in adult patients.

Few studies have focused on the clinical, neurophysiological and prognostic features of adult epileptic patients with malformation of cortical development. We reviewed the clinical data of a series of sixty adult epileptic patients with different types of malformation of cortical development, who had been followed at the Epilepsy Centre of the Department of Neurological Sciences of the University of Bologna, with particular attention to age at seizure onset, mental retardation, response to therapy, and EEG features. The heterogeneity of our population, especially when divided into the different groups of malformation of cortical development, precluded any general conclusions, but we stress the following aspects: 1). epilepsy due to malformation of cortical development may begin in adolescents and young adults; 2). epileptic seizures with clinical and polygraphic features of infantile spasms may persist into adulthood; 3). complex cortical malformation is not necessarily associated with severe epileptic encephalopathy. In periventricular nodular heterotopias, the largest in our series (nine patients), age at onset of seizures, response to therapy and mental deterioration differed according to the presence of nodules confined to the ventricular wall ('pure' form) or periventricular nodules associated with other cerebral cortical malformations ('plus' form).

Adolescent↗
PubMed2000

Surgery for malformations of cortical development causing epilepsy.

Malformations of cortical development (MCD) are responsible for many cases of refractory epilepsy in adults and children. The results of surgical treatment are difficult to assess from the published literature. Judging from the limited number of adequately reported cases, approximately 40% of all cases of MCD treated surgically may be rendered seizure-free over a minimum 2-year follow-up period. This figure is the same for focal cortical dysplasia (FCD), the most common variety of MCD in surgical reports. In comparison with outcome for epilepsy associated with hippocampal sclerosis, this figure is low. Part of the difference may be artificial and related to limited reporting. Much of the difference is likely to relate to the complex underlying biology of MCD. Analysis of epileptogenesis in MCD has been undertaken. Different types of MCD have different sequelae. Some varieties are intrinsically epileptogenic; these include FCD and heterotopia. Although in most cases, the visualized MCD lies within the region of brain responsible for generating seizures (the epileptogenic zone), it may not constitute the entire epileptogenic zone in all cases. For polymicrogyria and schizencephaly in particular, the visualized abnormalities are probably not the most important component of the epileptogenic zone. There is evidence that the epileptogenic zone is spatially distributed and also, in some cases, temporally distributed. These findings may explain poor surgical outcome and the inadequacy of current presurgical evaluative methods. New preoperative techniques offer the opportunity of improved presurgical planning and selection of cases more likely to be rendered seizure-free by current surgical techniques. Of paramount importance is improved reporting. The establishment of a central registry may facilitate this aim. Specific recommendations are made for surgical strategies based on current experience and understanding.

Adult↗
PubMed1991

Cortical development and visual function.

Hypotheses are advanced regarding some of the processes underlying the development of an accurate retinotopic map in striate cortex, and the development of cortical magnification. In the first case it is suggested that competitive pruning of afferent synapses may be important in the increase in grating acuity seen in infancy, and that this process may be disrupted in anisometropic amblyopia. In the second it is argued that the development of vernier acuity in infancy may reflect changes in cortical magnification, and that this may be due to increasing functional independence of the columnar units in striate cortex.

Humans↗
PubMed2002

Surgery for hemispheric malformations of cortical development.

The treatment of patients with hemispheric malformations of cortical development presents a challenging clinical problem that often requires surgical intervention. The development of a safe and effective treatment strategy for these patients requires an extensive work-up with a great deal of attention to a variety of multidisciplinary testing methods. In this article, the authors describe the presurgical evaluation of patients with hemispheric malformations of cortical development and epilepsy and review the surgical techniques currently available. They also detail some of the controversial issues regarding surgical treatment of these patients.

Cerebral Cortex↗
PubMed2001

Malformations of cortical development and epilepsy.

Although once thought to be rare, malformations of cortical development are being increasingly recognized as the underlying cause of developmental delay in children and of epilepsy in children and young adults. Advances in neuroimaging and developmental neurobiology have created the tools by which these important malformations have been investigated. Through a symbiotic type of relationship, these investigations, and the search for a better understanding of these malformations, have led to advances in neuroimaging techniques and better understanding of both normal and abnormal brain development. In this review, the most common malformations or cortical development associated with epilepsy are discussed in regard to their clinical manifestations, classification, imaging appearance and basic neurobiology.

Cell Movement↗
PubMed2006

Abnormal cortical development after premature birth shown by altered allometric scaling of brain growth.

BACKGROUND: We postulated that during ontogenesis cortical surface area and cerebral volume are related by a scaling law whose exponent gives a quantitative measure of cortical development. We used this approach to investigate the hypothesis that premature termination of the intrauterine environment by preterm birth reduces cortical development in a dose-dependent manner, providing a neural substrate for functional impairment. METHODS AND FINDINGS: We analyzed 274 magnetic resonance images that recorded brain growth from 23 to 48 wk of gestation in 113 extremely preterm infants born at 22 to 29 wk of gestation, 63 of whom underwent neurodevelopmental assessment at a median age of 2 y. Cortical surface area was related to cerebral volume by a scaling law with an exponent of 1.29 (95% confidence interval, 1.25-1.33), which was proportional to later neurodevelopmental impairment. Increasing prematurity and male gender were associated with a lower scaling exponent (p < 0.0001) independent of intrauterine or postnatal somatic growth. CONCLUSIONS: Human brain growth obeys an allometric scaling relation that is disrupted by preterm birth in a dose-dependent, sexually dimorphic fashion that directly parallels the incidence of neurodevelopmental impairments in preterm infants. This result focuses attention on brain growth and cortical development during the weeks following preterm delivery as a neural substrate for neurodevelopmental impairment after premature delivery.

Biometry↗
PubMed2004

A focused and efficient genetic screening strategy in the mouse: identification of mutations that disrupt cortical development.

Although the mechanisms that regulate development of the cerebral cortex have begun to emerge, in large part through the analysis of mutant mice (Boncinelli et al. 2000; Molnar and Hannan 2000; Walsh and Goffinet 2000), many questions remain unanswered. To provide resources for further dissecting cortical development, we have carried out a focused screen for recessive mutations that disrupt cortical development. One aim of the screen was to identify mutants that disrupt the tangential migration of interneurons into the cortex. At the same time, we also screened for mutations that altered the growth or morphology of the cerebral cortex. We report here the identification of thirteen mutants with defects in aspects of cortical development ranging from the establishment of epithelial polarity to the invasion of thalamocortical axons. Among the collection are three novel alleles of genes for which mutant alleles had already been used to explore forebrain development, and four mutants with defects in interneuron migration. The mutants that we describe here will aid in deciphering the molecules and mechanisms that regulate cortical development. Our results also highlight the utility of focused screens in the mouse, in addition to the large-scale and broadly targeted screens that are being carried out at mutagenesis centers.

Alleles↗
PubMed2005

A distinct asymmetrical pattern of cortical malformation: large unilateral malformation of cortical development with contralateral periventricular nodular heterotopia in three pediatric cases.

PURPOSE: To describe a distinct asymmetrical pattern of cortical malformation with large focal malformations of cortical development (MCDs) and contralateral periventricular nodular heterotopia (PNH). METHODS: We identified three patients with epilepsy and focal EEG abnormalities. Each patient underwent 1.5-Tesla magnetic resonance imaging (MRI) to obtain sagittal T1-weighted, axial fluid-attenuated inversion recovery (FLAIR), fast spin-echo (FSE) T2-weighted, and coronal fast spin-echo inversion recovery (FSEIR) T2-weighted images; coronal spoiled gradient recalled (SPGR) T1-weighted images were obtained in two cases. RESULTS: Patient 1, an 18-year-old right-handed man, had a 4-year history of intractable seizures. MRI revealed a right frontal subcortical heterotopia (SH) and a single left anterior PNH. Patient 2, a 10-year-old left-handed boy, had a 4-year history of epilepsy. MRI revealed a large region of SH in the left temporal, parietal, and occipital lobes and three right-sided PNH. Patient 3, a 16-month-old girl, had medically refractory infantile spasms. MRI revealed a large MCD in the left parietal lobe with contiguous underlying periventricular heterotopia as well as a small contralateral PNH. CONCLUSIONS: These cases together illustrate a distinct asymmetrical pattern of a large focal MCD with small contralateral PNH. The asymmetrical involvement of the two hemispheres suggests that the stage of maximal disruption of cortical development may differ between the two hemispheres. Further study into the mechanisms underlying such asymmetrical patterns of cortical malformation should enhance our understanding of cortical development as well as hemispheric lateralization.

Adolescent↗
PubMed1990

Interocular torsional disparity and visual cortical development in the cat.

1. The present experiments were designed to assess the effects of relatively large optically induced interocular torsional disparities on the developing kitten visual cortex. Kittens were reared with restricted visual experience. Three groups viewed a normal visual environment through goggles fitted with small prisms that introduced torsional disparities between the left and right eyes' visual fields, equal but opposite in the two eyes. Kittens in the +32 degrees goggle rearing condition experienced a 16 degrees counterclockwise rotation of the left visual field and a 16 degrees clockwise rotation of the right visual field; in the -32 degrees goggle condition the rotations were clockwise in the left eye and counterclockwise in the right. In the control (0 degree) goggle condition, the prisms did not rotate the visual fields. Three additional groups viewed high-contrast square-wave gratings through Polaroid filters arranged to provide a constant 32 degrees of interocular orientation disparity. 2. Recordings were made from neurons in visual cortex around the border of areas 17 and 18 in all kittens. Development of cortical ocular dominance columns was severely disrupted in all the experimental (rotated) rearing conditions. Most cells were classified in the extreme ocular dominance categories 1, 2, 6, and 7. Development of the system of orientation columns was also affected: among the relatively few cells with oriented receptive fields in both eyes, the distributions of interocular disparities in preferred stimulus orientation were centered near 0 degree but showed significantly larger variances than in the control condition.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Ocular↗
PubMed1988

Neonatal lesions of the basal forebrain cholinergic neurons result in abnormal cortical development.

The effect of electrolytic lesions of the neonatal forebrain on the morphogenesis of the mouse neocortex has been examined. Balb/C mice were lesioned unilaterally within 24 h of birth. The development of cortical cytoarchitecture was assessed in Nissl-stained sections, and the levels of presynaptic markers for cholinergic, noradrenergic and serotonergic afferents were measured in the fronto-parietal cortex ipsilateral and contralateral to the lesion at various postnatal ages and in adulthood. The basal forebrain (nBM) lesion resulted in a transient but severe reduction of cortical cholinergic markers and in abnormal cortical cytoarchitecture. Cytoarchitectural abnormalities were expressed as delay in the emergence of differentiated cell populations and affected sequentially more superficial layers with maturation following lesion. Furthermore, the location and extent of these morphologic abnormalities appeared to correlate with the degree of cholinergic denervation. Cortical monoamines were also temporarily reduced as a result of the lesion; however, pharmacologic lesions of the monoaminergic projections alone did not result in the abnormal cortical cytoarchitecture. Thus, the basal forebrain cholinergic projection appears to serve a role in regulating cortical differentiation.

5,7-Dihydroxytryptamine↗
PubMed1999

Recording and manipulating the in vivo correlational structure of neuronal activity during visual cortical development.

Many aspects of visual cortical functional architecture, such as orientation and ocular dominance columns, are present before animals have had any visual experience, indicating that the initial formation of cortical circuitry takes place without the influence of environmental cues. For this reason, it has been proposed that spontaneous activity within the developing visual pathway carries instructive information to guide the early establishment of cortical circuits. Recently developed recording and stimulation techniques are revealing new information about the in vivo organization of this spontaneous activity and its contribution to cortical development. Multielectrode recordings in the developing lateral geniculate nucleus (LGN) of ferrets demonstrate that retinal spontaneous activity is not simply relayed to the visual cortex, but is reshaped and transformed by a variety of mechanisms including cortical feedback and endogenous oscillatory activity. The resulting patterns are consistent with many of the predictions of correlation-based models of cortical development. In addition, the introduction of artificially correlated activity into the visual pathway disrupts some but not all aspects of orientation tuning development. Thus, while these results support an instructive role of spontaneous activity in shaping cortical development, there still appears to be a number of aspects of this process that cannot be accounted for by activity alone.

Animals↗