Anterior temporal abnormality in temporal lobe epilepsy

Mitchell, L. Anne; Jackson, Graeme D.; Kalnins, Renate M; Saling, Michael M.; Fitt, Gregory J; Ashpole, Richard; Berkovic, Samuel F.

doi:10.1212/wnl.52.2.327

Cited by 140 publications

(179 citation statements)

References 21 publications

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“…These alterations are the most frequent pathological findings presented by these patients 1 . In addition ipsilateral temporal pole signal and volume abnormalities are described as part of the spectrum of MRI features in cases of MTS 2 . The hippocampal sclerosis (HS) is also known as Ammon's horn sclerosis and includes selective hippocampal cell loss, gliosis and synaptic reorganization as the mossy fibers sprouting 3,4 .…”

Section: Flair: Temporal Epilepsy Varella Et Almentioning

confidence: 99%

Relationship between fluid-attenuated inversion-recovery (FLAIR) signal intensity and inflammatory mediator's levels in the hippocampus of patients with temporal lobe epilepsy and mesial temporal sclerosis

Varella

Santiago

Carrete

et al. 2011

Arq. Neuro-Psiquiatr.

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We investigated a relationship between the FLAIR signal found in mesial temporal sclerosis (MTS) and inflammation. Twenty nine patients were selected through clinical and MRI analysis and submitted to cortico-amygdalo-hippocampectomy to seizure control. Glutamate, TNFα, IL1, nitric oxide (NO) levels and immunostaining against IL1β and CD45 was performed. Control tissues (n=10) were obtained after autopsy of patients without neurological disorders. The glutamate was decreased in the temporal lobe epilepsy (TLE) -MTS group (p<0.001), suggesting increased release of this neurotransmitter. The IL1β and TNFα were increased in the hippocampus (p<0.05) demonstrating an active inflammatory process. A positive linear correlation between FLAIR signal and NO and IL1β levels and a negative linear correlation between FLAIR signal and glutamate concentration was found. Lymphocytes infiltrates were present in hippocampi of TLE patients. These data showed an association between hippocampal signal alteration and increased inflammatory markers in TLE-MTS.

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Section: Flair: Temporal Epilepsy Varella Et Almentioning

confidence: 99%

Relationship between fluid-attenuated inversion-recovery (FLAIR) signal intensity and inflammatory mediator's levels in the hippocampus of patients with temporal lobe epilepsy and mesial temporal sclerosis

Varella

Santiago

Carrete

et al. 2011

Arq. Neuro-Psiquiatr.

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“…Emerging work also demonstrates dysregulation of water and K 1 homeostasis in patients with mesial TLE. First, imaging studies demonstrate abnormal T2 prolongation by magnetic resonance imaging in the epileptic hippocampus, possibly partially due to increased water content (Mitchell et al, 1999). This is accompanied by alterations in apparent diffusion coefficient with diffusion-weighted magnetic resonance imaging (Hugg et al, 1999).…”

Section: Human Tissue Studiesmentioning

confidence: 99%

Aquaporin‐4 and epilepsy

Binder

Nagelhus

Ottersen

2012

Glia

148

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Recent studies have implicated glial cells in modulation of synaptic transmission, so it is plausible that glial cells may have a functional role in the hyperexcitability characteristic of epilepsy. Indeed, alterations in distinct astrocyte membrane channels, receptors, and transporters have all been associated with the epileptic state. This review focuses on the potential roles of the glial water channel aquaporin-4 (AQP4) in modulation of brain excitability and in epilepsy. We will review studies of mice lacking AQP4 (Aqp4 2/2 mice) or a-syntrophin (an AQP4 anchoring protein) and discuss the available human studies demonstrating alterations of AQP4 in human epilepsy tissue specimens. We will conclude with new studies of AQP4 regulation and discuss the potential role of AQP4 in the development of epilepsy (epileptogenesis). While many questions remain unanswered, the available data indicate that AQP4 and its molecular partners may represent important new therapeutic targets. V

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“…Neuroimaging studies revealed that abnormalities in the temporal lobe may coexist with MTS 50,51 . The temporal pole in TLE with MTS patients may present signal abnormalities in up to 75% of the cases 52 .…”

Section: Temporal Lobe Epilepsy: Surgical Pathologymentioning

confidence: 99%

“…Signal abnormalities and atrophy of the temporal pole are ipsilateral to MTS in the majority of patients 53 . Despite the alterations observed in neuroimaging studies, neuropathological studies in patients with such alterations have been inconclusive 51 . Depth EEG studies revealed that the temporal pole cortex may play a pivotal role in originating seizures in TLE patients, with ictal discharges preceding or occurring simultaneously with discharges originated from the ipsilateral hippocampus 50 .…”

Section: Temporal Lobe Epilepsy: Surgical Pathologymentioning

confidence: 99%

Surgical and postmortem pathology studies: contribution for the investigation of temporal lobe epilepsy

Caboclo

Neves

Jardim

et al. 2012

Arq. Neuro-Psiquiatr.

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Pathology studies in epilepsy patients bring useful information for comprehending the physiopathology of various forms of epilepsy, as well as aspects related to response to treatment and long-term prognosis. These studies are usually restricted to surgical specimens obtained from patients with refractory focal epilepsies. Therefore, most of them pertain to temporal lobe epilepsy (TLE) with mesial temporal sclerosis (MTS) and malformations of cortical development (MCD), thus providing information of a selected group of patients and restricted regions of the brain. Postmortem whole brain studies are rarely performed in epilepsy patients, however they may provide extensive information on brain pathology, allowing the analysis of areas beyond the putative epileptogenic zone. In this article, we reviewed pathology studies performed in epilepsy patients with emphasis on neuropathological findings in TLE with MTS and MCD. Furthermore, we reviewed data from postmortem studies and discussed the importance of performing these studies in epilepsy populations.

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Anterior temporal abnormality in temporal lobe epilepsy

Abstract: These frequently seen ipsilateral changes are not caused by gliosis and may reflect a nonspecific increase in water content in the temporal lobe. This may be due to myelin abnormalities or some other as yet unidentified pathologic factor.

Cited by 140 publications

References 21 publications

Relationship between fluid-attenuated inversion-recovery (FLAIR) signal intensity and inflammatory mediator's levels in the hippocampus of patients with temporal lobe epilepsy and mesial temporal sclerosis

Relationship between fluid-attenuated inversion-recovery (FLAIR) signal intensity and inflammatory mediator's levels in the hippocampus of patients with temporal lobe epilepsy and mesial temporal sclerosis

Aquaporin‐4 and epilepsy

Surgical and postmortem pathology studies: contribution for the investigation of temporal lobe epilepsy

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