Factors influencing surgical outcome in patients with focal cortical dysplasia

Fauser, Susanne; Bast, Thomas; Altenmüller, Dirk‐Matthias; Schulte‐Mönting, Jürgen; Strobl, Karl; Steinhoff, Bernhard J.; Zentner, Josef; Schulze‐Bonhage, Andreas

doi:10.1136/jnnp.2007.116038

Cited by 94 publications

(57 citation statements)

References 18 publications

(22 reference statements)

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“…Resting EEG was recorded for 5 to 20 minutes prior to scanning sessions, and resting state EEG-fMRI was recorded for two or three 20-minute sessions as tolerated. Sessions consisted of 404 T2*-weighted single-shot gradient-echo echo-planar images (EPIs; echo time/repetition time, 30/3000 milliseconds; flip angle, 90°; 43 2.5mm interleaved slices; FOV, 24 × 24cm2; matrix, 64 × 64) acquired continuously on a 3T Signa Excite HDX MRI scanner (General Electric, Milwaukee, WI). EPI time series were realigned and spatially smoothed with a cubic Gaussian Kernel of 8mm full width at half maximum.…”

Section: Methodsmentioning

confidence: 99%

Epileptic networks in focal cortical dysplasia revealed using electroencephalography–functional magnetic resonance imaging

Thornton

Vulliémoz

Rodionov

et al. 2011

Annals of Neurology

119

138

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ObjectiveSurgical treatment of focal epilepsy in patients with focal cortical dysplasia (FCD) is most successful if all epileptogenic tissue is resected. This may not be evident on structural magnetic resonance imaging (MRI), so intracranial electroencephalography (icEEG) is needed to delineate the seizure onset zone (SOZ). EEG-functional MRI (fMRI) can reveal interictal discharge (IED)-related hemodynamic changes in the irritative zone (IZ). We assessed the value of EEG-fMRI in patients with FCD-associated focal epilepsy by examining the relationship between IED-related hemodynamic changes, icEEG findings, and postoperative outcome.MethodsTwenty-three patients with FCD-associated focal epilepsy undergoing presurgical evaluation including icEEG underwent simultaneous EEG-fMRI at 3T. IED-related hemodynamic changes were modeled, and results were overlaid on coregistered T1-weighted MRI scans fused with computed tomography scans showing the intracranial electrodes. IED-related hemodynamic changes were compared with the SOZ on icEEG and postoperative outcome at 1 year.ResultsTwelve of 23 patients had IEDs during recording, and 11 of 12 had significant IED-related hemodynamic changes. The fMRI results were concordant with the SOZ in 5 of 11 patients, all of whom had a solitary SOZ on icEEG. Four of 5 had >50% reduction in seizure frequency following resective surgery. The remaining 6 of 11 patients had widespread or discordant regions of IED-related fMRI signal change. Five of 6 had either a poor surgical outcome (<50% reduction in seizure frequency) or widespread SOZ precluding surgery.InterpretationComparison of EEG-fMRI with icEEG suggests that EEG-fMRI may provide useful additional information about the SOZ in FCD. Widely distributed discordant regions of IED-related hemodynamic change appear to be associated with a widespread SOZ and poor postsurgical outcome. ANN NEUROL 2011

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Section: Methodsmentioning

confidence: 99%

Epileptic networks in focal cortical dysplasia revealed using electroencephalography–functional magnetic resonance imaging

Thornton

Vulliémoz

Rodionov

et al. 2011

Annals of Neurology

119

138

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“…There was no significant difference in the postsurgical seizure outcome between patients with Palmini type I and type II cortical dysplasia in UCLA cohort 70 and in other epilepsy center. 71 However, some studies reported less favorable outcome in patients with Palmini type I cortical dysplasia, 72,73 and other studies reported opposite results, 74 although a significant proportion of these patients also had HS. Such inconsistent results among various studies also appear to be a major problem in elucidating the clinicopathological correlation of cortical dysplasia as being discussed in HS, and may be due, at least in part, to the difference in inclusion and exclusion criteria.…”

Section: Focal Cortical Dysplasiamentioning

confidence: 99%

Surgical pathology of epilepsy‐associated non‐neoplastic cerebral lesions: A brief introduction with special reference to hippocampal sclerosis and focal cortical dysplasia

2013

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Among epilepsy-associated non-neoplastic lesions, mesial temporal lobe epilepsy with hippocampal sclerosis (mTLE-HS) and malformation of cortical development (MCD) including focal cortical dysplasia (FCD), are the two most frequent causes of drug-resistant focal epilepsies constituting about 50% of all surgical pathology of epilepsy. Several distinct histological patterns have been historically recognized in both HS and FCD, and several studies have tried to perform clinicopathological correlation; results, however, have been controversial, particularly in terms of postsurgical seizure outcome. Recently, the International League Against Epilepsy constituted a Task Forces of Neuropathology and FCD within the Commission on Diagnostic Methods, to establish an international consensus of histological classification of HS and FCD, respectively, based on agreement with the recognition of the importance of defining a histopathological classification system that reliably has some clinicopathological correlation. Such consensus classifications are likely to facilitate future clinicopathological study. Meanwhile, we reviewed neuropathology of 41 surgical cases of mTLE, and confirmed three type/patterns of HS along with no HS, based on the qualitative evaluation of the distribution and severity of neuronal loss and gliosis within hippocampal formation; i.e., HS type 1 (61%) equivalent to ‘classical’ Ammon’s horn sclerosis, HS type 2 (2%) representing CA1 sclerosis, HS type 3 (17%) equivalent to end folium sclerosis, and no HS (19%). Furthermore we performed a neuropathological comparative study on mTLE-HS and dementia associated HS (d-HS) in elderly, and confirmed that neuropathological features differ between mTLE-HS and d-HS in the distribution of hippocampal neuronal loss and gliosis, morphology of reactive astrocytes and their protein expression, and presence of concomitant neurodegenerative changes particularly Alzheimer type and TDP-43 pathologies. These differences may account, at least in part, for the difference in pathogenesis and epileptogenicity of HS in mTLE and senile dementia. However, the etiology and pathogenesis of most epileptogenic lesions are yet to be elucidated.

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“…Until recently, FCDs were mainly distinguished by the presence or absence of Balloon cells. Although the histological abnormalities in FCD with Balloon cells are more prominent than in FCD without Balloon cells, there is no difference regarding the severity of epilepsy [11,13-15]. In both patient groups a high seizure frequency and a pharmaco-resistant course of the disease is common [16-18].…”

Section: Introductionmentioning

confidence: 99%

Disorganization of neocortical lamination in focal cortical dysplasia is brain-region dependent: evidence from layer-specific marker expression

Fauser

Häussler

Donkels

et al. 2013

acta neuropathol commun

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BackgroundFocal cortical dysplasias (FCD) are local disturbances of neocortical architecture and a common cause of pharmaco-resistant focal epilepsy. Little is known about the pathomechanisms leading to architectural abnormalities associated with FCD.ResultsIn the present study we compared 52 FCD cases originating from the frontal or temporal lobe with or without Ammon’s horn sclerosis (AHS) with regard to structural and molecular differences. We applied layer-specific (ER81, RORß, SMI32, TLE4) and interneuron (calbindin, parvalbumin) markers by means of immunohistochemistry, in situ hybridization (ISH), and real time RT-PCR and correlated our findings with clinical parameters. We found that: (1) Structural abnormalities were most prominent in layers III-VI including changed morphology of individual neurons or dispersion, blurring and thinning of layers. These alterations were most pronounced in isolated frontal FCD, whereas the most homogeneous group was FCD IIIa. (2) Numbers of calbindin- and parvalbumin-positive interneurons varied considerably within the different FCD groups, but were not generally reduced. A significant decrease was only found for calbindin-positive interneurons in frontal FCD, and for parvalbumin-positive interneurons in FCD IIIa. (3) Interestingly, FCD IIIa presented with significant changes in the numbers of calbindin- or TLE4-positive neurons when compared to isolated FCD or controls. (4) Correlations between clinical and cellular parameters strongly depended on FCD localisation and age of the patients.ConclusionsIn summary, our data suggest that late cortical development is disturbed in FCD, yet most likely by different causes depending on brain region, FCD type and FCD severity.

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Factors influencing surgical outcome in patients with focal cortical dysplasia

Cited by 94 publications

References 18 publications

Epileptic networks in focal cortical dysplasia revealed using electroencephalography–functional magnetic resonance imaging

Epileptic networks in focal cortical dysplasia revealed using electroencephalography–functional magnetic resonance imaging

Surgical pathology of epilepsy‐associated non‐neoplastic cerebral lesions: A brief introduction with special reference to hippocampal sclerosis and focal cortical dysplasia

Disorganization of neocortical lamination in focal cortical dysplasia is brain-region dependent: evidence from layer-specific marker expression

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