Medial temporal lobe atrophy in patients with refractory temporal lobe epilepsy

University of Nottingham, Nottigham, England, United Kingdom
Journal of Neurology Neurosurgery & Psychiatry (Impact Factor: 5.58). 12/2003; 74(12):1627-30. DOI: 10.1136/jnnp.74.12.1627
Source: PubMed

ABSTRACT The objective of this study was to assess the volumes of medial temporal lobe structures using high resolution magnetic resonance images from patients with chronic refractory medial temporal lobe epilepsy (MTLE).
We studied 30 healthy subjects, and 25 patients with drug refractory MTLE and unilateral hippocampal atrophy (HA). We used T1 magnetic resonance images with 1 mm isotropic voxels, and applied a field non-homogeneity correction and a linear stereotaxic transformation into a standard space. The structures of interest are the entorhinal cortex, perirhinal cortex, parahippocampal cortex, temporopolar cortex, hippocampus, and amygdala. Structures were identified by visual examination of the coronal, sagittal, and axial planes. The threshold of statistical significance was set to p<0.05.
Patients with right and left MTLE showed a reduction in volume of the entorhinal (p<0.001) and perirhinal (p<0.01) cortices ipsilateral to the HA, compared with normal controls. Patients with right MTLE exhibited a significant asymmetry of all studied structures; the right hemisphere structures had smaller volume than their left side counterparts. We did not observe linear correlations between the volumes of different structures of the medial temporal lobe in patients with MTLE.
Patients with refractory MTLE have damage in the temporal lobe that extends beyond the hippocampus, and affects the regions with close anatomical and functional connections to the hippocampus.

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    • "In general, the closer the structure is anatomically to the hippocampus, the higher the degree of atrophy. Hence, the entorhinal and the perirhinal cortices tend to display a high degree of atrophy (Bonilha et al., 2003). Postoperative imaging studies have suggested that the extent of the resection of the parahippocampal area, which usually comprises the entorhinal and perirhinal cortex in its most anterior portion (Insausti et al., 1998), leads to better outcomes when associated with complete hippocampal resection (Siegel et al., 1990; Bonilha et al., 2007b). "
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    ABSTRACT: Surgical resection of the hippocampus is the most successful treatment for medication-refractory medial temporal lobe epilepsy (MTLE) due to hippocampal sclerosis. Unfortunately, at least one of four operated patients continue to have disabling seizures after surgery, and there is no existing method to predict individual surgical outcome. Prior to surgery, patients who become seizure free appear identical to those who continue to have seizures after surgery. Interestingly, newly converging presurgical data from magnetic resonance imaging (MRI) and intracranial electroencephalography (EEG) suggest that the entorhinal and perirhinal cortices may play an important role in seizure generation. These areas are not consistently resected with surgery and it is possible that they continue to generate seizures after surgery in some patients. Therefore, subtypes of MTLE patients can be considered according to the degree of extrahippocampal damage and epileptogenicity of the medial temporal cortex. The identification of these subtypes has the potential to drastically improve surgical results via optimized presurgical planning. In this review, we discuss the current data that suggests neural network damage in MTLE, focusing on the medial temporal cortex. We explore how this evidence may be applied to presurgical planning and suggest approaches for future investigation.
    Epilepsia 11/2011; 53(1):1-6. DOI:10.1111/j.1528-1167.2011.03298.x
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    • "These studies have consistently demonstrated that MTLE is associated with a large degree of brain atrophy that extends further into the temporal lobes and limbic areas. As a group, patients with MTLE display a network of brain atrophy that involves predominantly the limbic system, with more intense atrophy in regions that are functionally and anatomically connected to the hippocampus (Bonilha et al., 2003, 2004; Mueller et al., 2006). "
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    ABSTRACT: It is unclear whether extrahippocampal brain damage in patients with medial temporal lobe epilepsy (MTLE) is a homogeneous phenomenon, as most data relates to the average volume reduction in groups of patients. This study aimed to evaluate where and how much atrophy is to be expected in an individual patient with MTLE. High-resolution T(1) magnetic resonance imaging (MRI) was obtained from 23 consecutive patients with unilateral MTLE and from a matched control group. Parametric tests of voxel-based gray matter volume evaluated mean regional atrophy in MTLE compared with controls. Gray matter images were then submitted to a voxel by voxel calculation of the fitted receiver operating characteristic (ROC) curve area, plotting the sensitivity versus 1-specificity for a binary classifier (MTLE vs. controls). The area under the curve (AUC) was calculated for each voxel and a resulting three-dimensional map of gray matter voxel-wise AUCs was obtained. On average, patients with MTLE showed atrophy in the ipsilateral hippocampus and on a limbic network. Elevated AUC was demonstrated in the ipsilateral hippocampus and medial temporal lobe, the ipsilateral thalamus and occipitotemporal cortex, the ipsilateral cerebellum, the cingulate, the contralateral insula, and the occipitoparietal and dorsolateral prefrontal cortex. This study suggests that the medial temporal lobe, occipitotemporal areas, the cerebellum, the cingulate cortex, the ipsilateral insula, and thalamus are more likely to be atrophied in randomly selected patients with MTLE. Structures such as the orbitofrontal cortex, the contralateral medial temporal areas and insula, the putamen, and the caudate may be atrophied, but not as consistently.
    Epilepsia 04/2010; 51(9):1774-9. DOI:10.1111/j.1528-1167.2010.02576.x
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    • "Extrahippocampal gray matter atrophy in patients with MTLE was first observed via manual morphometry studies employing high-resolution MRI and anatomical protocols for segmentation of the medial temporal lobe (Andermann, 2003; Bernasconi et al., 2003; Bonilha et al., 2003). Those studies demonstrated that medial temporal structures such as the entorhinal and perirhinal cortices exhibit significant atrophy in patients with MTLE. "
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    ABSTRACT: Medial temporal epilepsy (MTLE) is associated with extrahippocampal brain atrophy. The mechanisms underlying brain damage in MTLE are unknown. Seizures may lead to neuronal damage, but another possible explanation is deafferentation from loss of hippocampal connections. This study aimed to investigate the relationship between hippocampal deafferentation and brain atrophy in MTLE. Three different MRI studies were performed involving 23 patients with unilateral MTLE (8 left and 15 right) and 34 healthy controls: (1) voxel-based morphometry (VBM), (2) diffusion tensor imaging (DTI) and (3) probabilistic tractography (PT). VBM was employed to define differences in regional gray matter volume (GMV) between controls and patients. Voxel-wise analyses of DTI evaluated differences in fractional anisotropy (FA), mean diffusivity (MD) and hippocampal PT. Z-scores were computed for regions-of-interest (ROI) GMV and peri-hippocampal FA and MD (to quantify hippocampal fiber integrity). The relationship between hippocampal deafferentation and regional GMV was investigated through the association between ROI Z scores and hippocampal fiber integrity. Patients with MTLE exhibited a significant reduction in GMV and FA in perihippocampal and limbic areas. There was a decrease in hippocampal PT in patients with MTLE in limbic areas. A significant relationship between loss of hippocampal connections and regional GMV atrophy was found involving the putamen, pallidum, middle and inferior temporal areas, amygdala and ceberellar hemisphere. There is a relationship between hippocampal disconnection and regional brain atrophy in MTLE. These results indicate that hippocampal deafferentation plays a contributory role in extrahippocampal brain damage in MTLE.
    Epilepsia 02/2010; 51(4):519-28. DOI:10.1111/j.1528-1167.2009.02506.x
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