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A–H Histopathologic features found in anterior temporal lobe specimens. A A microscopic aggregate of neurons (arrows) in layers II–III of the epileptogenic cerebral cortex. Klüver- Barrera stain, ×180. B A polygonal neuron with satellite oligodendrocytes is found in the white matter of a nonepileptogenic temporal lobe. HE stain, ×300. C Many neurons are present in the white matter of an epileptogenic temporal lobe. HE stain, ×240. D Perivascular accumulation of small round cells resembling oligodendrocytes and sporadic heterotopic white matter neurons (arrows) are shown. HE stain, ×150. E Many GFAP-positive astrocytes are present in an epileptogenic temporal lobe neocortex. GFAP, ×200. F Many GFAP-positive astrocytes are present in the white matter of a nonepileptogenic temporal lobe. GFAP stain, ×200. G Corpora amylacea are present in the temporal white matter of a 32-year- old man with medial onset seizures. HE stain, ×330. H Marked dilataton of the perivascular spaces are noted in a 34-year-old man with medial onset seizures. HE stain, ×50
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The number of patients undergoing surgical treatment for pharmacoresistant temporal lobe epilepsy is rapidly increasing. While there have been many clinicopathological studies concerning the medial structures of the temporal lobe in temporal lobe epilepsy, its lateral structures have received little attention. To examine the nature and frequency of...
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Purpose
Ictal kissing has been described in the literature. Five cases were reported and associated with temporal lobe epilepsy lateralizing to the nondominant hemisphere.
Methods
A case of ictal kissing was identified. The aim was to demonstrate the clinical, clinical and electrophysiological features (as recorded by subdural electrodes). The sur...
Citations
... The most typical alteration observed in patients with TLE is hippocampal or Ammon's horn sclerosis, characterized by neuronal loss and gliosis in the hippocampus (e.g., Margerison and Corsellis, 1966;Falconer, 1974;Babb and Brown, 1987;Meldrum and Bruton, 1992;Babb and Pretorius, 1993;Wieser et al., 1993;Honavar and Meldrum, 1997; for a recent review see Blumcke et al., 2017). However, extrahippocampal pathologies in the temporal lobe are also found in up to 30% of cases with hippocampal sclerosis ("dual pathology"), focal cortical dysplasias being the most common alterations (Lévesque et al., 1991;Babb and Pretorius, 1993;Wieser et al., 1993;Cendes et al., 1995;Arai and Oda, 1997;Honavar and Meldrum, 1997;Nishio et al., 2000;Tassi et al., 2002;Salanova et al., 2004;Blümcke et al., 2011;Harroud et al., 2012). Although the lateral temporal cortex removed from patients with TLE may show a normal appearance in standard histopathological preparations, the use of more specific immunohistochemical staining techiques may reveal alterations of cortical circuits that could be overlooked with standard histological methods. ...
Temporal lobe epilepsy (TLE) is the most common form of focal epilepsy and is associated with a variety of structural and psychological alterations. Recently, there has been renewed interest in using brain tissue resected during epilepsy surgery, in particular ‘non-epileptic’ brain samples with normal histology that can be found alongside epileptic tissue in the same epileptic patients — with the aim being to study the normal human brain organization using a variety of methods. An important limitation is that different medical characteristics of the patients may modify the brain tissue. Thus, to better determine how ‘normal’ the resected tissue is, it is fundamental to know certain clinical, anatomical and psychological characteristics of the patients. Unfortunately, this information is frequently not fully available for the patient from which the resected tissue has been obtained — or is not fully appreciated by the neuroscientists analyzing the brain samples, who are not necessarily experts in epilepsy. In order to present the full picture of TLE in a way that would be accessible to multiple communities (e.g., basic researchers in neuroscience, neurologists, neurosurgeons and psychologists), we have reviewed 34 TLE patients, who were selected due to the availability of detailed clinical, anatomical, and psychological information for each of the patients. Our aim was to convey the full complexity of the disorder, its putative anatomical substrates, and the wide range of individual variability, with a view toward: (1) emphasizing the importance of considering critical patient information when using brain samples for basic research and (2) gaining a better understanding of normal and abnormal brain functioning. In agreement with a large number of previous reports, this study (1) reinforces the notion of substantial individual variability among epileptic patients, and (2) highlights the common but overlooked psychopathological alterations that occur even in patients who become “seizure-free” after surgery. The first point is based on pre- and post-surgical comparisons of patients with hippocampal sclerosis and patients with normal-looking hippocampus in neuropsychological evaluations. The second emerges from our extensive battery of personality and projective tests, in a two-way comparison of these two types of patients with regard to pre- and post-surgical performance.
... PTEN mutations have been associated with poorer prognosis in GBM and are also known to play a role in epilepsy syndromes. Targeted conditional deletion of PTEN in mice results in spontaneous seizures with post-mortem brains displaying the hallmark pathologies of temporal lobe epilepsy (Nishio et al., 2000;Backman et al., 2001;Luikart et al., 2011;Pun et al., 2012;Williams et al., 2015). NF1, and its protein neurofibromin 1, are known to negatively regulate Ras signaling through GTPase activity (Pearson and Regad, 2017;Soomro et al., 2017). ...
Glioblastoma (GBM) is the most common and advanced form of primary malignant tumor occurring in the adult central nervous system, and it is frequently associated with epilepsy, a debilitating comorbidity. Seizures are observed both pre- and post-surgical resection, indicating that several pathophysiological mechanisms are shared but also prompting questions about how the process of epileptogenesis evolves throughout GBM progression. Molecular mutations commonly seen in primary GBM, i.e., in PTEN and p53, and their associated downstream effects are known to influence seizure likelihood. Similarly, various intratumoral mechanisms, such as GBM-induced blood-brain barrier breakdown and glioma-immune cell interactions within the tumor microenvironment are also cited as contributing to network hyperexcitability. Substantial alterations to peri-tumoral glutamate and chloride transporter expressions, as well as widespread dysregulation of GABAergic signaling are known to confer increased epileptogenicity and excitotoxicity. The abnormal characteristics of GBM alter neuronal network function to result in metabolically vulnerable and hyperexcitable peri-tumoral tissue, properties the tumor then exploits to favor its own growth even post-resection. It is evident that there is a complex, dynamic interplay between GBM and epilepsy that promotes the progression of both pathologies. This interaction is only more complicated by the concomitant presence of spreading depolarization (SD). The spontaneous, high-frequency nature of GBM-associated epileptiform activity and SD-associated direct current (DC) shifts require technologies capable of recording brain signals over a wide bandwidth, presenting major challenges for comprehensive electrophysiological investigations. This review will initially provide a detailed examination of the underlying mechanisms that promote network hyperexcitability in GBM. We will then discuss how an investigation of these pathologies from a network level, and utilization of novel electrophysiological tools, will yield a more-effective, clinically-relevant understanding of GBM-related epileptogenesis. Further to this, we will evaluate the clinical relevance of current preclinical research and consider how future therapeutic advancements may impact the bidirectional relationship between GBM, SDs, and seizures.
... Temporal lobe epilepsy (TLE) is one of the most frequent drug-resistant epilepsies, commonly associated with hippocampal sclerosis, a surgically-amenable lesion (1). Histopathological studies have also identified widespread neuronal loss and gliosis (2)(3)(4)(5) and altered myelination of temporal neocortex (6)(7)(8)(9). In line with these observations, imaging studies have shown extensive neocortical (10)(11)(12)(13)(14)(15) and subcortical atrophy (10,(16)(17)(18)(19)) indicative of a system-level disorder (20,21)( (15,22). ...
... The FOV was 220x220x163 mm (APxISxRL) with an acquisition matrix of 128x128x96 corresponding to a voxel size of 1.72x1.72x1.7 mm. SPGR data was acquired with 8 flip angles (3,4,5,6,7,9,13,18 ...
... Neuronal loss and gliosis in TLE extends into parahippocampal and fusiform gyri and lateral temporal neocortex (2)(3)(4)(5) and post-mortem studies show similar changes in frontal and occipital cortices (62). ...
Purpose
: Previous imaging studies in patients with refractory temporal lobe epilepsy (TLE) have examined the spatial distribution of changes in imaging parameters such as diffusion tensor imaging (DTI) metrics and cortical thickness. Multi-compartment models offer greater specificity with parameters more directly related to known changes in TLE such as altered neuronal density and myelination. We studied the spatial distribution of conventional and novel metrics including neurite density derived from NODDI (Neurite Orientation Dispersion and Density Imaging) and myelin water fraction (MWF) derived from mcDESPOT (Multi-Compartment Driven Equilibrium Single Pulse Observation of T1/T2)] to infer the underlying neurobiology of changes in conventional metrics.
Methods
: 20 patients with TLE and 20 matched controls underwent magnetic resonance imaging including a volumetric T1-weighted sequence, multi-shell diffusion from which DTI and NODDI metrics were derived and a protocol suitable for mcDESPOT fitting. Models of the grey matter-white matter and grey matter-CSF surfaces were automatically generated from the T1-weighted MRI. Conventional diffusion and novel metrics of neurite density and MWF were sampled from intracortical grey matter and subcortical white matter surfaces and cortical thickness was measured.
Results
: In intracortical grey matter, diffusivity was increased in the ipsilateral temporal and frontopolar cortices with more restricted areas of reduced neurite density. Diffusivity increases were largely related to reductions in neurite density, and to a lesser extent CSF partial volume effects, but not MWF. In subcortical white matter, widespread bilateral reductions in fractional anisotropy and increases in radial diffusivity were seen. These were primarily related to reduced neurite density, with an additional relationship to reduced MWF in the temporal pole and anterolateral temporal neocortex. Changes were greater with increasing epilepsy duration. Bilaterally reduced cortical thickness in the mesial temporal lobe and centroparietal cortices was unrelated to neurite density and MWF.
Conclusions
: Diffusivity changes in grey and white matter are primarily related to reduced neurite density with an additional relationship to reduced MWF in the temporal pole. Neurite density may represent a more sensitive and specific biomarker of progressive neuronal damage in refractory TLE that deserves further study.
... Therefore, down-regulation of caspase-9 may contribute to the inhibition of cell apoptosis in the hippocampus of TLE rats. GFAP is a protoplasmic astrocyte marker that is up-regulated in patients with TLE [41]. GFAP levels reflect reactive gliosis, a prominent manifestation of TLE that involves structural and metabolic changes in astrocytes and microglia [42,43]. ...
This study aimed to evaluate the specific regulatory roles of microRNA-146a (miRNA-146a) in temporal lobe epilepsy (TLE) and explore the related regulatory mechanisms. A rat model of TLE was established by intraperitoneal injection of lithium chloride-pilocarpine. These model rats were injected intracerebroventricularly with an miRNA-146a inhibitor and Notch-1 siRNA. Then, neuronal damage and cell apoptosis in the cornu ammonis (CA) 1 and 3 regions of the hippocampus were assessed. SOD and MDA levels in the hippocampus were detected by chromatometry, and IL-1β, IL-6, and IL-18 levels were detected by ELISA. Then, we evaluated the expression levels of caspase-9, GFAP, Notch-1, and Hes-1 in the hippocampus. The interaction between Notch-1 and miRNA-146a was assessed by a dual luciferase reporter gene assay. A rat model of TLE was successfully established, which exhibited significantly increased miRNA-146a expression in the hippocampus. Silencing of miRNA-146a significantly alleviated the neuronal damage and cell apoptosis in the CA1 and CA3 regions of the hippocampus in TLE rats and decreased MDA, IL-1β, IL-6, and IL-18 levels and increased SOD levels in the hippocampus of TLE rats. In addition, silencing of miRNA-146a significantly decreased the expression levels of caspase-9, GFAP, Notch-1, and Hes-1 in the hippocampus of TLE rats. Notch-1 was identified as a target of miRNA-146a and silencing of Notch-1 aggravated the neuronal damage in the CA1 and CA3 regions. Silencing of miRNA-146a alleviated the neuronal damage in the hippocampus of TLE rats by down-regulating Notch-1.
... Gliosis is observed in most FCD, but it is also a common finding in the white matter of TLE patients (91)(92)(93) although it has no apparent relation to the severity of the disorder (94). Astrocytic gliosis, traditionally assessed by the expression of glial fibrillary acidic protein (GFAP), has been found in 18% to 100% of specimens of TLE patients, with severity ranging from mild to marked gliosis (79,94,95) and associated with enlarged glial cell nuclear volume (96,97). ...
... Even though gliosis is often seen in TLE specimens, it does not seem to be related to T2 signal changes or diffusion metrics of the temporal lobe white matter (98). Nevertheless it was proposed that the diffuse gliosis found in the temporal lobe white matter of patients with TLE could be an extension of temporal lobe dysplasia in patients with MTS (99), or an adaptive compensatory reaction to frequent seizures (92,94). ...
... Oligodendrogliosis in white matter is often found as clusters of cells (90,91,(100)(101)(102)(103), and they appear to be slightly more common in patients with gray/white matter blurring and related to reduced myelin content (91). Further, oligodendrocytes (OL) can be observed as groups or rows of small round cells along white matter vessels (perivascular clusters) and around a single neuron (perineural OL) (92,(100)(101)(102)104). Even though the main function of OL in the central nervous system is myelination, their increased © Quantitative Imaging in Medicine and Surgery. ...
Using magnetic resonance imaging, it is possible to measure the behavior of diffusing water molecules, and the metrics derived can be used as indirect markers of tissue micro-architectural properties. Numerous reports have demonstrated that patients with temporal lobe epilepsy (TLE) have water diffusion abnormalities in several white matter structures located within and beyond the epileptogenic temporal lobe, showing that TLE is not a focal disorder, but rather a brain network disease. Differences in severity and spatial extent between patients with or without mesial temporal sclerosis (MTS), as well as differences related to hemispheric seizure onset, are suggestive of different pathophysiological mechanisms behind different forms of TLE, which in turn result in specific cognitive disabilities. The biological interpretation of diffusion abnormalities is based on a wealth of information from animal models of white matter damage, and is supported by recent reports that directly correlate diffusion metrics with histological characteristics of surgical specimens of TLE patients. Thus, there is now more evidence showing that the increased mean diffusivity (MD) and concomitant reductions of diffusion anisotropy that are frequently observed in several white matter bundles in TLE patients reflect reduced axonal density (increased extra-axonal space) due to smaller-caliber axons, and abnormalities in the myelin sheaths of the remaining axons. Whether these histological and diffusion features are a predisposing factor for epilepsy or secondary to seizures is still uncertain; some reports suggest the latter. This article summarizes recent findings in this field and provides a synopsis of the histological features seen most frequently in post-surgical specimens of TLE patients in an effort to aid the interpretation of white matter diffusion abnormalities.
... Similarly, temporal lobe neocortex can be histopathologically examined in patients who undergo anterior temporal lobectomy (ATL). Results have indicated a wider range of lateral temporal lobe neocortical pathology, including gliosis and the presence of heterotopic white matter neurons in some patients with presumed mesial TLE (84). A recent post-mortem study reported significantly reduced neuronal density in the mediodorsal thalamic nucleus in patients with TLE ipsilateral to the side of HS (85), which is consistent with the VBM metaanalysis discussed above (62). ...
Medically intractable temporal lobe epilepsy (TLE) remains a serious health problem. Across treatment centers, up to 40% of patients with TLE will continue to experience persistent postoperative seizures at 2-year follow-up. It is unknown why such a large number of patients continue to experience seizures despite being suitable candidates for resective surgery. Preoperative quantitative MRI techniques may provide useful information on why some patients continue to experience disabling seizures, and may have the potential to develop prognostic markers of surgical outcome. In this article, we provide an overview of how quantitative MRI morphometric and diffusion tensor imaging (DTI) data have improved the understanding of brain structural alterations in patients with refractory TLE. We subsequently review the studies that have applied quantitative structural imaging techniques to identify the neuroanatomical factors that are most strongly related to a poor postoperative prognosis. In summary, quantitative imaging studies strongly suggest that TLE is a disorder affecting a network of neurobiological systems, characterized by multiple and inter-related limbic and extra-limbic network abnormalities. The relationship between brain alterations and postoperative outcome are less consistent, but there is emerging evidence suggesting that seizures are less likely to remit with surgery when presurgical abnormalities are observed in the connectivity supporting brain regions serving as network nodes located outside the resected temporal lobe. Future work, possibly harnessing the potential from multimodal imaging approaches, may further elucidate the etiology of persistent postoperative seizures in patients with refractory TLE. Furthermore, quantitative imaging techniques may be explored to provide individualized measures of postoperative seizure freedom outcome.
... However, there are few published studies describing them at either of these locations. [9][10][11] In light of the above, our study aims to assess the presence, distribution, and density of CoA in the lateral temporal lobes of surgically treated patients with DRTLE and FCD, as well as to determine the connection between CoA density and demographic and clinical variables (age at seizure onset, epilepsy duration, and post-operative results). ...
... Two of these studies 11,17 are case reports, and the rest of them also address associated microscopic alterations, including neuronal abnormalities, perivascular glial satellitosis, reactive gliosis, and FCD. 9,18,19 Keller proposes that accumulation of CoA is associated with ageing. 6 However, this premise is not applicable to our patients for two reasons: mean age at surgery was 41.11, and no correlations were identified between CoA density in the different studied locations and age at surgery. ...
... 20 None of our patients presented any of these conditions, and only two of them had experienced perinatal insult. Previous studies 10,11,17 and case series 8,9,15,18,19,[21][22][23][24][25][26] have described abundant CoA in the neocortex and hippocampus of patients with DRTLE and HS. CoA have been documented in the following regions of resected hippocampi: CA1, CA3, CA4, end folium and dentate gyrus, and to a lesser extent, the parahippocampal cortex. ...
Corpora amylacea (CoA) are present in about 60% of atrophic hippocampi resected from patients with drug resistant temporal lobe epilepsy (DRTLE). They have also been described in the lateral temporal neocortex, although less frequently.
The objective is to measure the presence, distribution and density of CoA in the lateral temporal lobes of patients with DRTLE and focal cortical dysplasia (FCD), also examining how CoA density may be linked to demographic and clinical traits.
Resected tissue from 35 patients was analysed. CoA density was assessed with a semi-quantitative scale according to the criteria established by Cherian et al.
Presence of CoA in the neocortex of 9 patients was associated with hippocampal sclerosis (FCD type iiia, 7 cases), disembryoplastic neuroepithelial tumour (FCD type iiib, 1 case), and cavernous angioma (FCD type iiic, 1 case). The meningeal surface (MS) was involved in all cases, and 8 cases displayed CoA in the cerebral parenchyma (white matter) and around blood vessels. CoA density on the MS showed a negative correlation with age at seizure onset (r=-0.828, P<.05) and a positive correlation with disease duration (r=0.678, P<.05) but not with postoperative clinical outcome.
Patients with DRTLE and a primary lesion (hippocampal sclerosis, tumour, vascular malformation) associated with mild FCD were shown to have CoA deposits in the neocortex. No association was found between presence of CoA and clinical outcome one year after surgery.
Copyright © 2013 Sociedad Española de Neurología. Published by Elsevier Espana. All rights reserved.
... The classically defined syndrome of mesial temporal lobe epilepsy (MTLE) has been restricted to the patients with typical seizure semiology, presence of MTS on MRI, and typical anterotemporal interictal and ictal EEG findings [12]. Although the pathophysiological basis of seizures in MRI negative TLE patients with no focal abnormality remains unclear, these patients have most of the same features as patients with traditional MTLE. ...
... The finding of no significant difference in the frequency of secondary generalization and duration of seizures is interesting, particularly in light of speculation that recurrent convulsions may contribute to hippocampal neuronal loss. In concordance with the prior studies, analysis of the ictal semiology of the groups in our study showed that most of the patients had signs and symptoms similar to that of mesial rather than lateral TLE [5][6][7][8]12]. ...
Introduction:
We studied the contribution of interictal FDG-PET ([18 F] fluorodeoxyglucose-positron emission tomography) in epileptic focus identification in temporal lobe epilepsy patients with positive, equivocal and negative magnetic resonance imaging (MRI).
Methods:
Ninety-eight patients who underwent surgical treatment for drug resistant temporal lobe epilepsy after neuropsychological evaluation, scalp video EEG monitoring, FDG-PET, MRI and/or long-term intracranial EEG and with >12 months clinical follow-up were included in this study. FDG-PET findings were compared to MRI, histopathology, scalp video EEG and long-term intracranial EEG monitoring.
Results:
FDG-PET lateralized the seizure focus in 95 % of MRI positive, 69 % of MRI equivocal and 84 % of MRI negative patients. There was no statistically significant difference between the surgical outcomes among the groups with Engel class I and II outcomes achieved in 86 %, 86 %, 84 % of MRI positive, equivocal and negative temporal lobe epilepsy patients, respectively. The patients with positive unilateral FDG-PET demonstrated excellent postsurgical outcomes, with 96 % Engel class I and II. Histopathology revealed focal lesions in 75 % of MRI equivocal, 84 % of MRI positive, and 23 % of MRI negative temporal lobe epilepsy cases.
Conclusion:
FDG-PET is an accurate noninvasive method in lateralizing the epileptogenic focus in temporal lobe epilepsy, especially in patients with normal or equivocal MRIs, or non-lateralized EEG monitoring. Very subtle findings in MRI are often associated with histopathological lesions and should be described in MRI reports. The patients with negative or equivocal MRI temporal lobe epilepsy are good surgical candidates with comparable postsurgical outcomes to patients with MRI positive temporal lobe epilepsy.
... Neuropathologic abnormalities predominantly involving the frontotemporal cortex (i.e., mesiotemporal sclerosis, neuronal loss, and gliosis) have been described in HS patients without (Cavanagh & Meyer, 1956;Falconer et al., 1964;Margerison & Corsellis, 1966;Kuzniecky et al., 1987;Nishio et al., 2000) and with psychosis (Taylor, 1975;Roberts et al., 1990;Bruton et al., 1994;Suckling et al., 2000). Microdysgenesis, local excitotoxic effects of seizures, and deafferentation of synaptically connected areas are possible mechanisms for these abnormalities that may be progressive in some patients (Bernhardt et al., 2009;Dabbs et al., 2009). ...
To determine whether cortical abnormalities are more severe and widespread in patients with temporal lobe epilepsy (TLE) and interictal psychosis (IP) compared to those with TLE only (NIP) and healthy controls (HC), and to explore the associations between cortical parameters (area, thickness and volume), psychotic symptoms, and cognitive performance.
Twenty-two patients with IP (9 male; 10 hippocampal sclerosis, HS), 23 TLE nonpsychotic (NIP) patients (11 male; 13 HS) matched for duration of epilepsy and 20 HC participated. Surface-based morphometry (SBM) was used to measure cortical parameters. Cognition was examined in IP and NIP patients. Associations between cortical parameters and cognition were examined using linear mixed models adjusted by age, gender, and brain volume.
IP patients had an earlier onset of epilepsy, more status epilepticus, and worse cognitive performance than NIP patients. In IP patients, cortical thickness was reduced in the inferior frontal gyrus (IFG), and their current IQ was associated with decreases in area, but not thickness, in regions of the frontotemporal cortex.
IP likely reflects the interplay of psychosis-related genetic factors and the cumulative effects of seizure activity on the brain. Cortical thinning in the IFG, a region implicated in schizophrenia, is likely to be related to seizure activity, whereas changes in IQ, associated with reductions in area of frontotemporal cortex, may be related to the presence of psychosis.
... The classically defined syndrome of mesial temporal lobe epilepsy (MTLE) has been restricted to the patients with typical seizure semiology, presence of MTS on MRI, and typical anterotemporal interictal and ictal EEG findings [12]. Although the pathophysiological basis of seizures in MRI negative TLE patients with no focal abnormality remains unclear, these patients have most of the same features as patients with traditional MTLE. ...
... The finding of no significant difference in the frequency of secondary generalization and duration of seizures is interesting, particularly in light of speculation that recurrent convulsions may contribute to hippocampal neuronal loss. In concordance with the prior studies, analysis of the ictal semiology of the groups in our study showed that most of the patients had signs and symptoms similar to that of mesial rather than lateral TLE [5][6][7][8]12]. ...
PURPOSE
Approximately 30 % of patients with temporal lobe epilepsy (TLE) have normal MRI scans. The presurgical evaluation of MRI-negative TLE patients has remained controversial due to ill-defined epileptogenic zone. We studied the contribution of FDG PET/CT to the localization of the epileptic focus in patients with TLE and normal MRI.
METHOD AND MATERIALS
A total of 234 patients with drug resistant TLE, underwent evaluation for possible surgical treatment with scalp EEG video monitoring, PET/CT, high resolution MRI and/or long-term intracranial electroencephalography between 2000-2009. 38 patients out of 98 patients surgically treated patients with normal MRI and > 12 months follow up were included in this study. For patients with good surgical outcome ( Engel 1 and Engel 2), the epileptogenic focus was assumed to be located in the area of surgical resection, and compared to the results of PET/CT, scalp EEG video monitoring, long-term intracranial electroencephalography, and pathology.
RESULTS
At the latest follow-up (mean 20.9 months ), 32 of 38 surgically treated patients with normal MRI, demonstrated good surgical outcome. 28 patients (72 %) were free of disabling seizures (Engel class I), 21 patients (53 %) were seizure free (Engel 1a) and 4 patients (13 %) were Engel class II. Six patients (15 %) who demonstrated either noncongruent PET/CT or extratemporal hypometabolism on PET/CT had poor outcomes (Engel class III-IV). The sensitivity and specificity of FDG PET/CT and scalp EEG video monitoring were 100 % – 83 %, and 61 % - 17 %, respectively. PET/CT demonstrated 100 % concordance with long-term intracranial electroencephalography in the 16 patients so assessed. Histopathology failed to reveal any focal pathology in 77 % of MR-negative cases.
CONCLUSION
FDG PET/CT increases the sensitivity and specificity, and is helpful in characterization of the epileptic focus in patient referred for surgical treatment of TLE with negative MRI. FDG PET imaging may be especially informative for targeting and narrowing the extension of invasive long-term intracranial electroencephalography.
CLINICAL RELEVANCE/APPLICATION
FDG PET/CT increases the sensitivity and specificity of presurgical characterization of the epileptic focus in patient referred for surgical treatment of TLE with negative MRI.
