Cerebral activation in malformations of cortical development

Richardson, Mark P.; Koepp, MJ; Brooks, David J.; Coull, Jennifer T.; Grasby, Paul M.; Fish, D. R.; Duncan, John S.

doi:10.1093/brain/121.7.1295

Cited by 76 publications

(51 citation statements)

References 27 publications

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“…It might therefore be of therapeutic value to resect normotopic tissue in the vicinity of a heterotopia, and spare the heterotopic tissue, as an alternative surgical approach. With this approach, heterotopic cortical tissue, which has been shown to be functionally activated in clinical studies using motor and cognitive tasks (71), would be spared while a primary epileptogenic site would be removed. The tish rat should prove useful for evaluating this paradoxical concept.…”

Section: Discussionmentioning

confidence: 99%

Distribution and Initiation of Seizure Activity in a Rat Brain with Subcortical Band Heterotopia

et al. 2000

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Summary:Purpose: Misplaced (heterotopic) cortical neurons are a common feature of developmental epilepsies. To better understand seizure disorders associated with cortical heterotopia, the sites of aberrant discharge activity were investigated in vivo and in vitro in a seizure-prone mutant rat (tish) exhibiting subcortical band heterotopia. Methods: Depth electrode recordings and postmortem assessment of regional cfos mRNA levels were used to characterize the distribution of aberrant discharge activity during spontaneous seizures in vivo. Electrophysiologic recordings of spontaneous and evoked activity also were performed by using in vitro brain slices from the tish rat treated with proconvulsant drugs (penicillin and 4-aminopyridine). Results: Depth electrode recordings demonstrate that seizure activity begins almost simultaneously in the normotopic and heterotopic areas of the tish neocortex. Spontaneous seizures induce c-fos mRNA in normotopic and heterotopic neocortical areas, and limbic regions. The threshold concentrations of proconvulsant drugs for inducing epileptiform spiking were similar in the normotopic and heterotopic areas of tish brain slices. Manipulations that blocked communication between the norniotopic and heterotopic areas of the cortex inhibited spiking in the heterotopic, but not the normotopic, area of the cortex. Conclusions: These findings indicate that aberrant discharge activity occurs in normotopic and heterotopic areas of the neocortex, and in certain limbic regions during spontaneous seizures in the tish rat. Normotopic neurons are more prone to exhibit epileptiform activity than are heterotopic neurons in the tish cortex, and heterotopic neurons are recruited into spiking by activity initiated in normotopic neurons. The findings indicate that seizures in the tish brain primarily involve telencephalic structures, and suggest that normotopic neurons are responsible for initiating seizures in the dysplastic neocortex.

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Section: Discussionmentioning

confidence: 99%

Distribution and Initiation of Seizure Activity in a Rat Brain with Subcortical Band Heterotopia

et al. 2000

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“…widespread metabolic disorders. For instance, the metabolic activation pattern in a visual-attention task in patients with malformations is atypical and involves cortical regions that appeared entirely normal on MRI (104,105). These final observations have important implications for the design and implementation of surgical resections for patients with epilepsy because it suggests that not 1.…”

Section: Several Lines Of Evidences Support the Idea Of An In-mentioning

confidence: 97%

Cortical Malformations and Epilepsy: New Insights from Animal Models

et al. 1999

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Summary:In the last decade, the recognition of the high frequency of cortical malformations among patients with epilepsy especially children, has led to a renewed interest in the study of the pathophysiology of cortical development. This field has also been spurred by the recent development of several experimental genetic and non-genetic, primarily rodent, models of cortical malformations. Epileptiform activity in these animals can appear as spontaneous seizure activity in vivo, in vitro hyperexcitability, or reduced seizure susceptibility in vitro and in vivo. In the neonatal freeze lesion model, that mimics human microgyria, hyperexcitability is caused by a reorganization of the network in the borders of the malformation. In the prenatal methylazoxymethanol model, that causes a diffuse cortical malformation, hyperexcitability is associated with alteration of firing properties of discrete neuronal subpopulations together with the formation of bridges between normally unconnected structures. In agreement with clinical evidence, these expenmental data suggest that cortical malformations can both form epileptogenic foci and alter brain development in a manner that causes a diffuse hyperexcitability of the cortical network. Key Words: Neocortex-Hippocampus-Development-Neuronal migration-Methylazoxymethanol.As early as the end of the nineteenth century, neuropathologists began to report an association between cortical malformations and epilepsy (1-3). Until recently, however, clinical and experimental research yielded few insights into the pathophysiology of this distinct class of epilepsies. In fact, the last decade has seen three major scientific advances that have directly contributed to the "rediscovery" and renewed interest in examining the cause of epilepsy in patients with cortical malformations: mation and epilepsy. Moreover, neuropathologic analysis of resected tissue has frequently demonstrated the presence of more subtle malformations that were not identified in vivo. 3. Recent progress in human molecular genetics has allowed the identification of several genes whose mutations lead to both malformations and epilepsy. In parallel, several genetic and nongenetic rodent models of cortical malformations were shown to be associated with either spontaneous seizures or hyperexcitability .Our goal is to review the contributions of these animal models to our understanding of the pathophysiology of cortical malformations and to discuss their possible link with epilepsy. CORTICAL MALFORMATIONS IN HUMANSHuman cortical malformations have been the subject of several reviews (4-8) and the histology of the major types of cortical malformations encountered is fairly well established (see Fig. 1). In addition, classification of cortical malformations (based on neuropathology, radiology, etiology, or a combination of these elements) has 811

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“…In fact, this overlapping of EZ and function has already been described. Several reports relate colocalization of function and malformation of cortical development [32] showing that even if some kind of compensatory reorganization occurs, FCD retains normal function. More specifically, Marusic et al [13] , when studying FCD in eloquent cortex, found that 75% of cases had overlapping and colocalization of function as well as dysplasia.…”

Section: Seeg Recordings and Electrical Mappingmentioning

confidence: 99%

Discrepancies between Preoperative Stereoencephalography Language Stimulation Mapping and Intraoperative Awake Mapping during Resection of Focal Cortical Dysplasia in Eloquent Areas

Robles

Gélisse

Vergani

et al. 2008

Stereotact Funct Neurosurg

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Background/Aims: To compare the reliability of preoperative stereoencephalography (SEEG) and intraoperative electrostimulation regarding functional mapping, and to select the indication for surgery for focal cortical dysplasia (FCD) in language areas. Methods: The authors present the case of a 21-year-old, right-handed female, suffering from chronic pharmacologically resistant epilepsy since the age of 8. MRI showed a subcortical hypersignal on FLAIR and T₂ sequences at the posterior end of the left superior temporal sulcus compatible with an FCD. SEEG invasive monitoring was performed to precisely identify the epileptogenic zone (EZ) and for functional language mapping. Results: The stimulation of the contacts implicated in the EZ through SEEG leads induced language disturbances, which were not reproducible. Surgery was performed under local anesthesia with awake corticosubcortical mapping. Direct intraoperative stimulation in the EZ, including FCD, did not induce language disturbances. Thus, EZ could be removed completely without any postoperative language deficit. Conclusions: The present case suggests that when language disturbances which occur during invasive SEEG functional mapping, in eloquent areas, are not reproducible, resection can be considered using intraoperative electrical mapping, without inducing permanent language impairment. This may be explained by a certain degree of plasticity and reshaping of functional areas associated with a congenital lesion and chronic epilepsy.

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Cerebral activation in malformations of cortical development

Cited by 76 publications

References 27 publications

Distribution and Initiation of Seizure Activity in a Rat Brain with Subcortical Band Heterotopia

Distribution and Initiation of Seizure Activity in a Rat Brain with Subcortical Band Heterotopia

Cortical Malformations and Epilepsy: New Insights from Animal Models

Discrepancies between Preoperative Stereoencephalography Language Stimulation Mapping and Intraoperative Awake Mapping during Resection of Focal Cortical Dysplasia in Eloquent Areas

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