Neuroimaging methods to evaluate the etiology and consequences of epilepsy

Duncan, John S.

doi:10.1016/s0920-1211(02)00075-x

Cited by 44 publications

(48 citation statements)

References 55 publications

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“…More marked abnormality of the cerebral cortex on MRI was reported in case 2 (poor hippocampal formation), case 5 (patchy periventricular increased T1 signal and prominence of temporal horns of the lateral ventricles), and case 10 (frontotemporal hypoplasia with temporal dysplasia). These changes of temporal lobe hypoplasia/ dysplasia are similar to those described in some patients with temporal lobe epilepsies, and could be due to primary cerebral dysgenesis or acquired temporal lobe damage from resistant seizures [Salmenperä et al, 2001;Duncan, 2002]. However, two of our patients (case 2, case 10) did not have a history of seizures, so it seems likely that the findings represent cerebral dysgenesis rather than an acquired abnormality.…”

Section: Discussionsupporting

confidence: 85%

Further delineation of the phenotype associated with heterozygous mutations in ZFHX1B

Wilson

Mowat

Moal

et al. 2003

American J of Med Genetics Pt A

101

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Mutations or deletions involving ZFHX1B (previously SIP1) have recently been found to cause one form of syndromic Hirschsprung disease (HSCR), associated with microcephaly, mental retardation, and distinctive facial features. Patients with the characteristic facial phenotype and severe mental retardation, but without HSCR, have now also been shown to have mutations in this gene. Mutations of ZFHX1B are frequently associated with other congenital anomalies, including congenital heart disease, hypospadias, renal tract anomalies, and agenesis of the corpus callosum (ACC). We present the clinical data and mutation analysis results from a series of 23 patients with this clinical syndrome, of whom 21 have proven ZFHX1B mutations or deletions (15 previously unpublished). Two patients with the typical features (one with and one without HSCR) did not have detectable abnormalities of ZFHX1B. We emphasize that this syndrome can be recognized by the facial phenotype in the absence of either HSCR or other congenital anomalies, and needs to be considered in the differential diagnosis of dysmorphism with severe mental retardation +/- epilepsy.

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Section: Discussionsupporting

confidence: 85%

Further delineation of the phenotype associated with heterozygous mutations in ZFHX1B

Wilson

Mowat

Moal

et al. 2003

American J of Med Genetics Pt A

101

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“…In agreement with previous studies [34,35], 18 FDG-PET was not able to lateralize or localize the epileptogenic zone in all patients. In our study, 18 FDG-PET was effective in only in three patients; the remaining four subjects had normal glucose metabolism.…”

Section: Discussionsupporting

confidence: 92%

1H MR spectroscopic imaging in patients with MRI-negative extratemporal epilepsy: correlation with ictal onset zone and histopathology

et al. 2007

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Proton magnetic resonance spectroscopy ((1)H MRS) is beneficial in the lateralization of the epileptogenic zone in temporal lobe epilepsy; however, its role in extratemporal and, especially, MRI-negative epilepsy has not been established. This study seeks to verify how (1)H MRS could help in localizing the epileptogenic zone in patients with MRI-negative extratemporal epilepsy. Seven patients (8-23 years) with MRI-negative refractory focal epilepsy were studied using (1)H MRS on a 1.5T MR system. Chemical shift imaging sequence in the transversal plane was directed towards the suspected epileptogenic zone localized by seizure semiology, scalp video/EEG, ictal SPECT and (18)FDG-PET. Spectra were evaluated using the program CULICH, and the coefficient of asymmetry was used for quantitative lateralization. MRS detected lateralization in all patients and was able to localize pathology in five. The most frequent findings were decreased ratios of N-acetylaspartate to choline compounds characterized by increasing choline concentration. The localization of the (1)H MRS abnormality correlated well with ictal SPECT and subdural mapping. In all cases, histopathological analysis revealed MRI-undetected focal cortical dysplasias. (1)H MRS could be more sensitive for the detection of discrete malformations of cortical development than conventional MRI. It is valuable in the presurgical evaluation of patients without MRI-apparent lesions.

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“…4 Currently, these techniques are considered reliable and reproducible for the detection of hippocampal pathology. 11 However, hippocampal volumetry by manual segmentation is time-consuming and depends on the expertise of the examiner. These 2 features have limited its use in clinical practice.…”

mentioning

confidence: 99%

3T MRI Quantification of Hippocampal Volume and Signal in Mesial Temporal Lobe Epilepsy Improves Detection of Hippocampal Sclerosis

Coan

Kubota

Bergo

et al. 2013

AJNR Am J Neuroradiol

142

123

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BACKGROUND AND PURPOSE:In mesial temporal lobe epilepsy, MR imaging quantification of hippocampal volume and T2 signal can improve the sensitivity for detecting hippocampal sclerosis. However, the current contributions of these analyses for the diagnosis of hippocampal sclerosis in 3T MRI are not clear. Our aim was to compare visual analysis, volumetry, and signal quantification of the hippocampus for detecting hippocampal sclerosis in 3T MRI.

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Neuroimaging methods to evaluate the etiology and consequences of epilepsy

Cited by 44 publications

References 55 publications

Further delineation of the phenotype associated with heterozygous mutations in ZFHX1B

Further delineation of the phenotype associated with heterozygous mutations in ZFHX1B

1H MR spectroscopic imaging in patients with MRI-negative extratemporal epilepsy: correlation with ictal onset zone and histopathology

3T MRI Quantification of Hippocampal Volume and Signal in Mesial Temporal Lobe Epilepsy Improves Detection of Hippocampal Sclerosis

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