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Results for “Epilepsy, Temporal Lobe”

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PubMed1990

Altered distribution of excitatory amino acid receptors in temporal lobe epilepsy.

In temporal lobe epilepsy, excitatory amino acid receptors in the hippocampus and temporal lobe may contribute to both increased excitability and vulnerability to excitotoxic damage. We used receptor autoradiography to examine the density of N-methyl-D-aspartate (NMDA) and kainic acid (KA) receptors in the hippocampus and parahippocampal gyrus obtained from five patients who had undergone anterior temporal lobectomy for the treatment of intractable seizures and from six control individuals, in which the hippocampus was obtained postmortem. Within the hippocampal formation, loss of [3H]KA and NMDA-sensitive L-[3H]glutamate binding was apparent in the sclerotic regions CA3, hilus, and CA1. In the subiculum and molecular layer of the denate gyrus, binding densities were maintained or even increased in some of the epileptic patients. A two-fold increase in L-[3H]glutamate binding, along with an increase in [3H]KA binding, was observed in the parahippocampal gyrus obtained from the epileptic patients. The results suggest that the vulnerability of the hippocampus in temporal lobe epilepsy may result, at least in part, from the presence of aberrant excitatory circuits in the parahippocampal gyrus.

Adult↗

PubMed2004

A dissociation between implicit and explicit verbal memory in left temporal lobe epilepsy.

PURPOSE: Temporal lobe epilepsy patients are well known to present deficits on explicit verbal memory procedures (e.g., recall, recognition). The integrity of implicit memory procedures in these patients is not established. Previous studies in this area used implicit memory measures contaminated by the effects of explicit memory. METHODS: We examined the integrity of verbal implicit and explicit memory in left temporal lobe epilepsy (LTLE) patients and hypothesized that a clear dissociation in performance would be found with a relative preservation of implicit memory. TLE patients (n = 15) and age- and education-matched healthy normal patients (n = 15) were shown a 40-word study list, followed by a test phase requiring completion of word stems based on the study words or new/unseen words. Experimental conditions involved instructions to provide either the old (study) words or novel/nonlist words when completing the stem. Measures of automaticity and recollection provided uncontaminated indices of implicit and explicit memory, respectively. RESULTS: The data showed a significant difference (p < 0.001) between the patients (Recollection, 0.12; SD, 0.18) and controls (0.50, SD, 0.15) on the measure of explicit memory. In contrast, the patients (Automaticity, 0.51; SD, 0.11) and controls (0.45, SD, 0.18) performed similarly on the implicit memory measure, with patient scores clearly at normative levels based on other Process Dissociation Procedure data. CONCLUSIONS: The data demonstrate the integrity of implicit memory in LTLE patients. Finding a dissociation between the two forms of verbal memory in LTLE patients provides evidence that they rely on different neuroanatomic systems.

Adolescent↗

PubMed1999

Neuroimaging evidence of progressive neuronal loss and dysfunction in temporal lobe epilepsy.

Whether temporal lobe epilepsy is the result of an isolated, early injury or whether there is ongoing neuronal dysfunction or loss due to seizures is often debated. We attempt to address this issue by using magnetic resonance techniques. Proton magnetic resonance spectroscopic imaging can detect and quantify focal neuronal dysfunction or loss based on reduced signals from the neuronal marker N-acetylaspartate (NAA), and magnetic resonance imaging (MRI)-based measurements of hippocampal volumes (MRIvol) can quantify the amount of atrophy in this structure. We performed magnetic resonance spectroscopic imaging and MRIvol in 82 consecutive patients with medically intractable temporal lobe epilepsy to determine whether there was a correlation between seizure frequency, or type or duration of epilepsy, with NAA to creatine (Cr) values or hippocampal volumes. Volumes and spectroscopic resonance intensities were categorized as to whether they were measured from the temporal lobe ipsilateral or contralateral to the predominant electroencephalographic focus. Ipsilateral and contralateral NAA/Cr was negatively correlated with duration of epilepsy. Hippocampal volumes were negatively correlated with duration ipsilaterally but not contralaterally. Frequency of complex partial seizures was not correlated with any of the magnetic resonance measures. However, patients with frequent generalized tonic-clonic seizures had lower NAA/Cr bilaterally and smaller hippocampal volumes ipsilaterally than patients with none or rare generalized tonic-clonic seizures. The results suggest that although an early, fixed injury may cause asymmetric temporal lobe damage, generalized seizures may also cause progressive neuronal dysfunction or loss.

Adult↗

PubMed1975

Outcome of surgery in 40 children with temporal-lobe epilepsy.

Temporal-lobe epilepsy commonly has its origins in childhood, particularly when the lesion involved is mesial temporal (Ammon's horn) Sclerosis. Evidence suggests that this lesion is probably a common cause of chronic epilepsy in adults and that often it is probably the result of a severe febrile convulsion in infancy. 40 children, fifteen years of age and younger, who had an anterior temporal lobectomy were followed up for one to twenty-four years. The findings confirm those already established in adults, that the best results of surgery, not only in seizure relief but also in behaviour, are obtained when mesial temporal sclerosis is the lesion found at operation, and also indicate that a severe febrile convulsion in infancy is often the chief provocative factor in the development of epilepsy.

Adaptation, Psychological↗

PubMed2004

Ictal neocortical slowing in temporal lobe epilepsy.

BACKGROUND: Temporal lobe epilepsy (TLE) may affect brain regions outside the temporal lobe, causing impaired neocortical function during seizures. METHODS: The authors selected 11 consecutive patients with mesial TLE and hippocampal sclerosis who underwent intracranial EEG monitoring and had no seizures during a follow-up period of at least 1 year after temporal lobe resection. Secondarily generalized seizures were excluded, and up to three seizures were analyzed per patient (31 seizures total). Electrode contacts were assigned to one of nine cortical regions based on MRI surface reconstructions. EEG during seizures was analyzed for specific patterns including low-voltage fast (LVF), rhythmic polyspike, spike-wave, irregular slowing, and postictal suppression. RESULTS: Mesial and lateral temporal contacts on the side of seizure onset showed significant increases in ictal patterns such as LVF and polyspike activity, followed by postictal suppression. Bilateral frontal and ipsilateral parietal cortex exhibited large amplitude irregular slow waves during seizures. This frontoparietal slowing persisted into the postictal period. Perirolandic and occipital cortex were relatively spared. These EEG patterns were accompanied by bland staring, minor automatisms, and unresponsiveness or amnesia in the majority of patients studied. CONCLUSIONS: Prominent irregular slowing occurs in bilateral frontal and ipsilateral parietal association cortex during and after temporal lobe seizures. EEG slowing in the frontoparietal association cortex may signify physiologic impairment that contributes to widespread altered cerebral function during partial seizures.

Adolescent↗

PubMed1995

The pathophysiologic relationships between lesion pathology, intracranial ictal EEG onsets, and hippocampal neuron losses in temporal lobe epilepsy.

In temporal lobe epilepsy (TLE) lesion patients the pathology, location of intracranial ictal EEG onsets, and hippocampal neuron losses were compared. Patients (n = 63) were classified into: (1) Tumors (n = 26, e.g. astrocytomas, gangliogliomas); (2) vascular (n = 9, e.g. cavernous and venous angiomas); (3) developmental (n = 17, e.g. cortical dysplasia, heterotopias); or (4) atrophic (n = 11, e.g. cortical or white matter encephalomalacia). Other variables were; (1) the location of the temporal lesion in the mesial to lateral, and anterior to posterior plane, (2) a clinical history of an initial precipitating injury (IPI) prior to the onset of TLE (e.g. prolonged first seizure, head trauma), (3) hippocampal neuron densities, (4) focal or regional location by intracranial depth EEG of ictal onsets, and (5) seizure outcomes. Results showed that severe hippocampal neuron losses were associated with two statistically significant findings. First, patients with mesial lesions in or adjacent to the body of the hippocampus had greater neuron losses compared to mesial lesions anterior or posterior to the hippocampus (P = 0.04). Second, lesion patients with an IPI history had greater Ammon's horn (AH) neuron losses compared to those without IPI histories (P = 0.0005), and the profile of loss was similar to hippocampal sclerosis (HS). Granule cell losses correlated in a complex manner in that; 1) by regression analysis densities decreased with longer intervals of TLE (P = 0.006), (2) tumor patients with IPIs had less granule cell loss compared to those without IPIs intervals of TLE (P = 0.006), (2) tumor patients with IPIs had less granule cell loss compared to those without IPIs (P = 0.05), and (3) developmental patients with IPIs had greater granule cell loss than patients without IPIs (P = 0.009). Mesial-temporal depth EEG electrodes were the first areas of ictal activity in 15 of 16 patients (94%), and greater hippocampal neuron losses were not associated with focal mesial-temporal EEG onsets. Seizure outcomes were worse in tumor patients compared to HS patients (P = 0.01), and patients with post-resection seizures had incomplete resections of their lesions and/or hippocampi. These results indicate that in TLE lesion patients the amount and pattern of hippocampal neuron loss depends on the location of the lesion, the pathologic classification, and a history of an IPI. Further, despite variable neuron losses, in temporal lesion patients the hippocampus was nearly always involved in the genesis or propagation of the chronic seizures.

Case-Control Studies↗

PubMed2005

Correlations between granule cell physiology and bioenergetics in human temporal lobe epilepsy.

Human temporal lobe epilepsy (TLE) is associated with bioenergetic abnormalities including decreased phosphocreatine (PCr) normalized to ATP. The physiological consequences of these metabolic alterations have not been established. We hypothesized that impaired bioenergetics would correlate with alterations in physiological functions under conditions that strongly activate neural metabolism. We correlated several physiological variables obtained from epileptic human dentate granule cells studied in slices with hippocampal PCr/ATP measured using in vivo magnetic resonance spectroscopy. The physiological variables included: the ability to fire multiple action potentials in response to single stimuli, the inhibitory postsynaptic potential (IPSP) conductance and the responses to a 10 Hz, 10 s stimulus train. We noted a significant negative correlation between the ability to fire multiple spikes in response to single synaptic stimulation and PCr/ATP (P < 0.03) and a positive correlation between the IPSP conductance and PCr/ATP (P < 0.05). Finally, there was a strong correlation between PCr/ATP and the recovery of the membrane potential following a stimulus train (P < 0.01), with low PCr/ATP being associated with prolonged recovery times. These data suggest that the bioenergetic impairment seen in this tissue is associated with specific changes in excitatory and inhibitory neuronal responses to synchronized synaptic inputs.

Adenosine Triphosphate↗

PubMed2006

Aberrant expression of cytoskeleton proteins in hippocampus from patients with mesial temporal lobe epilepsy.

Mesial temporal lobe epilepsy (MTLE), the most common form of epilepsy, is characterised by cytoarchitectural abnormalities including neuronal cell loss and reactive gliosis in hippocampus. Determination of aberrant cytoskeleton protein expression by proteomics techniques may help to understand pathomechanism that is still elusive. We searched for differential expression of hippocampal proteins by an analytical method based on two-dimensional gel electrophoresis (2-DE) coupled with mass spectrometry unambiguously identifying 77 proteins analysed in eight control and eight MTLE hippocampi. Proteins were quantified and we observed 18 proteins that were altered in MTLE. Cytoskeleton proteins tubulin alpha-1 chain, beta-tubulin, profilin II, neuronal tropomodulin were significantly reduced and one actin spot was missing, whereas ezrin and vinculin were significantly increased in MTLE. Proteins of several classes as e.g. antioxidant proteins (peroxiredoxins 3 and 6), chaperons (T-complex protein 1-alpha, stress-induced-phosphoprotein 1), signaling protein MAP kinase kinase 1, synaptosomal proteins (synaptotagmin I, alpha-synuclein), NAD-dependent deacetylase sirtuin-2 and 26S protease regulatory subunit 7 protein, neuronal-specific septin 3 were altered in MTLE. Taken together, the findings may represent or lead to cytoskeletal impairment; aberrant antioxidant proteins, chaperons, MAP kinase kinase 1 and NAD-dependent deacetylase sirtuin-2 may have been involved in pathogenetic mechanisms and altered synaptosomal protein expression possibly reflects synaptic impairment in MTLE.

Adult↗

PubMed2004

Increased expression of Nogo-A in hippocampal neurons of patients with temporal lobe epilepsy.

Mesial temporal lobe epilepsy (TLE) is associated with pronounced anatomical and biochemical changes in the hippocampal formation including extensive neurodegeneration, reorganization of mossy fibres and sprouting of interneurons. Although the anatomical features and some of the physiological consequences of hippocampal remodeling have been well documented, the molecular mechanisms underlying the profound and orientated outgrowth of hippocampal neurons in TLE are not yet understood. The reticulon protein Nogo-A has been associated with an inhibitory action on axon growth and plasticity. Using immunohistochemistry and in situ hybridization, we investigated the expression of Nogo-A in specimens obtained at surgery from patients with TLE compared with those obtained from autopsy controls. In control specimens, Nogo-A immunoreactivity and mRNA were mainly confined to oligodendrocytes. Only approximately 40% of the specimens revealed low expression of Nogo-A mRNA in neurons. In contrast, in TLE patients with and without Ammon's horn sclerosis, Nogo-A mRNA and immunoreactivity were markedly up-regulated in most neurons (3.6- and 4.4-fold increases in Nogo-A mRNA in granule cells of sclerotic and nonsclerotic specimens) and their processes throughout the hippocampal formation. Similar elevations in Nogo-A mRNA and protein levels were determined by quantitative RT-PCR and Western blotting. Since Nogo-A expression was also up-regulated in specimens without hippocampal sclerosis, it may be induced by seizures prior to progressing neurodegeneration.

Adolescent↗

PubMed2004

Abnormalities of hippocampal signal intensity in patients with familial mesial temporal lobe epilepsy.

Mesial temporal lobe epilepsy (MTLE) is associated with hippocampal atrophy and hippocampal signal abnormalities. In our series of familial MTLE (FMTLE), we found a high proportion of hippocampal abnormalities. To quantify signal abnormalities in patients with FMTLE we studied 152 individuals (46 of them asymptomatic) with FMTLE. We used NIH-Image for volumetry and signal quantification in coronal T1 inversion recovery and T2 for all cross-sections of the hippocampus. Values diverging by 2 or more SD from the control mean were considered abnormal. T2 hippocampal signal abnormalities were found in 52% of all individuals: 54% of affected subjects and 48% of asymptomatic subjects. T1 hippocampal signal changes were found in 34% of all individuals: 42.5% of affected subjects and 15% of asymptomatic subjects. Analysis of the hippocampal head (first three slices) revealed T2 abnormalities in 73% of all individuals (74% of affected subjects and 72% of asymptomatic subjects) and T1 abnormalities in 59% (67% of affected subjects and 41% of asymptomatic subjects). Affected individuals had smaller volumes than controls (P < 0.0001). There was no difference in hippocampal volumes between asymptomatic subjects and controls, although 39% of asymptomatic patients had hippocampal atrophy. Patients with an abnormal hippocampal signal (133 individuals) had smaller ipsilateral volume, but no linear correlation could be determined. Hippocampal signal abnormalities in FMTLE were more frequently found in the hippocampal head in both affected and asymptomatic family members, including those with normal volumes. These results indicate that subtle abnormalities leading to an abnormal hippocampal signal in FMTLE are not necessarily related to seizures and may be determined by genetic factors.

Analysis of Variance↗

PubMed1999

GABAergic neurons and GABA(A)-receptors in temporal lobe epilepsy.

Mesial temporal lobe epilepsy (MTLE) is the most prevalent form of epilepsy, characterized by recurrent complex partial seizures and hippocampal sclerosis. The pathophysiology underlying this disorder remains unidentified. While a loss of benzodiazepine binding sites is a key diagnostic feature of MTLE, experimental studies have shown enhanced inhibitory transmission and increased expression of GABA(A)-receptors, suggesting that compensatory mechanisms are operative in epileptic hippocampus. In the present study, changes in the expression and cellular distribution of major GABA(A)-receptor subunits were investigated in the hippocampus of pilocarpine-treated rats during the phase of spontaneous recurrent seizures. A uniform decrease in GABA(A)-receptor subunit-immunoreactivity was observed in regions of extensive neuronal death (i.e. CA1, CA3, hilus). whereas a prominent increase occurred in the dentate gyrus (DG). Most strikingly, the increase was largest for the alpha3- and alpha5-subunits, which are expressed at very low levels in the DG of control rats, suggesting the formation of novel GABA(A)-receptor subtypes in epileptic tissue. Furthermore, an extensive loss of interneurons expressing the alpha1-subunit, representing presumptive basket cells, was seen in the DG. These changes were very similar to those reported in a novel mouse model of MTLE, based on the unilateral injection of kainic acid into the dorsal hippocampus (Bouilleret et al., 1999). This indicates that the regulation of GABA(A)-receptor expression is related to chronic recurrent seizures, and is not due to the extrahippocampal neuronal damage affecting pilocarpine-treated rats. These results allow causal relationships in the induction and maintenance of chronic recurrent seizures to be distinguished. The loss of a critical number of interneurons in the DG is a possible cause of seizure initiation, whereas the long-lasting upregulation of GABA(A)-receptors in granule cells represents a compensatory response to seizure activity.

Animals↗

PubMed2001

Vigabatrin protects against hippocampal damage but is not antiepileptogenic in the lithium-pilocarpine model of temporal lobe epilepsy.

In temporal lobe epilepsy (TLE), the nature of the structures involved in the development of the epileptogenic circuit is still not clearly identified. In the lithium-pilocarpine model, neuronal damage occurs both in the structures belonging to the circuit of initiation and maintenance of the seizures (forebrain limbic system) as well as in the propagation areas (cortex and thalamus) and in the circuit of remote control of seizures (substantia nigra pars reticulata). In order to determine whether protection of some brain areas could prevent the epileptogenesis induced by status epilepticus (SE) and to identify the cerebral structures involved in the genesis of TLE, we studied the effects of the chronic exposure to Vigabatrin (gamma-vinyl-GABA, GVG) on neuronal damage and epileptogenesis induced by lithium-pilocarpine SE. The animals were subjected to SE and GVG treatment (250 mg/kg) was initiated at 10 min after pilocarpine injection and maintained daily for 45 days. These pilo-GVG rats were compared with rats subjected to SE followed by a daily saline treatment (pilo-saline) and to control rats not subjected to SE (saline-saline). GVG treatment induced a marked, almost total neuroprotection in CA3, an efficient protection in CA1 and a moderate one in the hilus of the dentate gyrus while damage in the entorhinal cortex was slightly worsened by the treatment. All pilo-GVG and pilo-saline rats became epileptic after the same latency. Glutamic acid decarboxylase (GAD67) immunoreactivity was restored in pilo-GVG rats compared with pilo-saline rats in all areas of the hippocampus, while it was increased over control levels in the optical layer of the superior colliculus and the substantia nigra pars reticulata. Thus, the present data indicate that neuroprotection of principal cells in the Ammon's horn of the hippocampus is not sufficient to prevent epileptogenesis, suggesting that the hilus and extra-hippocampal structures, that were not protected in this study, may play a role in the genesis of spontaneous recurrent seizures in this model. Furthermore, the study performed in non-epileptic rats indicates that chronic treatment with a GABAmimetic drug upregulates the expression of the protein GAD67 in specific areas of the brain, independently from the seizures.

Animals↗

PubMed2005

Normal magnetic resonance imaging and medial temporal lobe epilepsy: the clinical syndrome of paradoxical temporal lobe epilepsy.

OBJECT: The syndrome of medial temporal lobe epilepsy (MTLE) may occur in patients in whom magnetic resonance (MR) images demonstrate normal findings. In these patients, there is no evidence of hippocampal sclerosis on neuroimaging, and histopathological examination of the resected hippocampus does not reveal significant neuron loss. In this paper the authors describe the distinct clinical features of this MTLE subtype, referred to as paradoxical temporal lobe epilepsy (PTLE). METHODS: The authors selected 12 consecutive patients with preoperative findings consistent with MTLE in whom MR imaging did not demonstrate any hippocampal abnormality. Onset of hippocampal seizure was confirmed by long-term intracranial monitoring. There were six female and six male patients with a mean age of 32 +/- 11 years, (mean +/- standard deviation [SD]) at presentation. These patients' seizure histories, available hippocampal volumetric measurements, and hippocampal cell densities in different subfields were reviewed. Sharp electrode recordings from dentate granule cells that had been maintained in hippocampal slices provided a measure of excitation and inhibition in the tissue. We compared these data with those of a cohort of 50 randomly selected patients who underwent anteromedial temporal resection for medial temporal sclerosis (MTS) during the same time period (1987-1999). The durations of follow up (means +/- SDs) for the PTLE and MTS groups were 51 +/- 59 months and 88 +/- 44 months, respectively. A history of febrile seizure was present less frequently in the PTLE group (8%) than in the MTS group (34%). Other risk factors for epilepsy such as trauma, meningoencephalitis, or perinatal injuries were present more frequently in the PTLE group (50%) than in the MTS cohort (36%). In patients in the PTLE group the first seizure occurred later in life (mean age at seizure onset 14 years in the PTLE group compared with 9 years in the MTS group, p = 0.09). Ten patients (83%) in the PTLE cohort and 23 patients (46%) in the MTLE cohort had secondary generalization of their seizures. Among patients with PTLE, volumetric measurements (five patients) and randomized blinded visual inspection (seven patients) of the bilateral hippocampi revealed no atrophy and no increased T2 signal change on preoperative MR images. All patients with PTLE underwent anteromedial temporal resection (amygdalohippocampectomy, in five patients on the left side and in seven on the right side). Electrophysiological studies of hippocampal slices demonstrated that dentate granule cells from patients with PTLE were significantly less excitable than those from patients with MTS. The mean pyramidal cell loss in the CAI subfield in patients in the PTLE group was 20% (range 0-59%) and that in patients in the MTS group was 75% (range 41-90%) (p < 0.001). Maximal neuron loss (mean loss 38%) occurred in the CA4 region in six patients with PTLE (end folium sclerosis). At the last follow-up examination, six patients (50%) in the PTLE group were seizure free compared with 38 patients (76%) in the MTS group. CONCLUSIONS: Clinical PTLE is a distinct syndrome with clinical features and surgical outcomes different from-those of MTS.

Adolescent↗

PubMed2002

Proton magnetic resonance spectroscopic imaging suggests progressive neuronal damage in human temporal lobe epilepsy.

Whether temporal lobe epilepsy (TLE) is the result of an isolated, early injury or whether there is ongoing neuronal damage due to seizures is often debated. We attempted to examine the long-term effect of seizures using proton magnetic resonance spectroscopic imaging (1H-MRSI), which can quantify neuronal loss or dysfunction based on reduced signals from the neuronal marker N-acetylaspartate (NAA). We performed 1H-MRSI in 82 consecutive patients with medically intractable, non-foreign-tissue TLE to determine whether there was a correlation between seizure frequency, type or duration of epilepsy and NAA to creatine ratios (NAA/Cr). Spectroscopic resonance intensities were categorized as to whether they were measured from the temporal lobe ipsilateral or contralateral to the predominant EEG focus. Ipsilateral and contralateral NAA/Cr was negatively correlated with duration of epilepsy. Furthermore, patients with frequent generalized tonic-clonic seizures had lower NAA/Cr than patients with no or rare generalized tonic-clonic seizures. The results suggest that although an early injury may cause asymmetric temporal lobe damage that is present at the onset of epilepsy, generalized seizures may induce additional neuronal damage that progresses over the course of the disease.

Cross-Sectional Studies↗

PubMed1993

Presurgical evaluation of temporal lobe epilepsy using interictal temporal spikes and positron emission tomography.

OBJECTIVE: Our goal was to determine the role of fludeoxyglucose F 18-positron emission tomography (18FDG-PET) and interictal temporal spikes in lateralizing the epileptogenic region in patients who (1) were diagnosed as having temporal lobe epilepsy based on clinical symptoms and exclusively temporal interictal spikes and (2) did not have a structural lesion on magnetic resonance imaging. DESIGN: This was a retrospective study of 40 consecutive patients fulfilling the above criteria who underwent 18FDG-PET scanning. A firm electrophysiologic diagnosis and 1 complete year of postsurgical follow-up, where applicable, were required. Outcome measures included surgical outcome and final electrophysiologic diagnosis. RESULTS: Unilateral, interictal temporal spikes (ITS) were present in 33 (82.5%) of 40 patients. Seven patients (17.5%) had bitemporal, independent spikes. Thirty-one (77.5%) of 40 patients had unilateral temporal hypometabolism (TH). Twenty-eight (70%) patients had concordant TH and ITS. One year after surgery, 31 of 33 patients with unilateral ITS were greatly improved; two of five who had bitemporal ITS showed similar improvement. In 28 patients, unilateral TH and unilateral ITS were concordant. The paired result always concurred with the final neurophysiologic assessment. Surgical outcome between patients with 18FDG-PET showing unilateral TH (26 of 30 greatly improved) and those not showing unilateral TH (six of eight greatly improved) was not significantly different. CONCLUSION: In temporal lobe epilepsy not associated with a mass lesion, unilateral ITS are reliable lateralizing features and suggest a good surgical outcome. Use of 18FDG-PET provides corroborative lateralizing information but 18FDG-PET that fails to show unilateral TH does not preclude a good surgical outcome.

Action Potentials↗

PubMed1996

MRI-guided flumazenil- and FDG-PET in temporal lobe epilepsy.

In temporal lobe epilepsy (TLE) patients without lesions, major hippocampal sclerosis, or atrophy on magnetic resonance imaging (MRI), the localizing power of [11C]flumazenil (FMZ) and 2-[18F]fluoro-2-deoxy-D-glucose (FDG) was compared using high-resolution positron emission tomography (PET) studies and individually coregistered MRI scans. Following complete clinical, neuropsychological, and electrophysiological evaluation, benzodiazepine receptor density was assessed using the FMZ equilibrium method. Thirty minutes later, interictal FDG-PET was performed under resting conditions. PET images were matched to three-dimensionally coregistered, T1-weighted MRI. Each temporal lobe (TL) was divided into 12 volumes of interest. The regional FMZ data were normalized with respect to average cortical values. For each patient the right-left asymmetries of rCMRGlc and normalized FMZ data were calculated. In 7 to 10 patients, mesial TL structures showed reduced FMZ binding, with a decrease by at least 10% in the affected TL. Reductions of 10% or more of rCMRGlc usually were more widespread than FMZ reductions and often involved lateral temporal cortex. The regions of most pronounced disturbances are not necessarily identical in both methods. Three patients had a complex correspondence of lateralization with PET, neuropsychological, and EEG data. In 4 patients, lateralization was less clear from EEG or neuropsychological results but was still consistent with lateralization by PET. In 3 of 10 patients, however, major discrepancies were found. These data suggest that the combination of neuropsychological testing, EEG, and MRI-guided FMZ- and FDG-PET will help to select patients with clearly defined epileptogenic foci especially in mesial TLE. Even in cases without MRI lesions, TL epileptic foci can be lateralized with consistency across the methods; FMZ-PET shows the pathologic focus more circumscribed than FDG-PET.

Adult↗

PubMed1992

MRI in the presurgical evaluation of patients with frontal lobe epilepsy and children with temporal lobe epilepsy: pathologic correlation and prognostic importance.

We performed magnetic resonance imaging (MRI) using a high-field strength magnet (1.5 T) in two series of 53 patients with intractable partial epilepsy of frontal lobe or temporal lobe origin who subsequently received ablative surgery for their seizure disorder. In the first series of patients the pathologic correlation and prognostic importance of an MRI-identified lesion in the frontal lobe were assessed. Twenty-five percent of the patients with negative MRI studies and 67% of patients with neuroimaging abnormalities restricted to the frontal lobe, were seizure-free at a minimum duration of follow-up of 1 year. None of the patients with a multilobar MRI-detected abnormality was seizure-free postoperatively. In the second study the sensitivity and specificity of MRI-based hippocampal volumetry was determined in pediatric patients with partial epilepsy of temporal lobe origin unrelated to foreign-tissue pathology. Hippocampal formation atrophy in the epileptic temporal lobe was identified in 63% of patients. The sensitivity and specificity of hippocampal volumetry was 100% in patients with mesial temporal sclerosis. The presence of an MRI-detected epileptogenic lesion in the frontal lobe and hippocampal formation atrophy in the temporal lobe may correlate with the underlying pathology and affect the identification of potential candidates for epilepsy surgery.

Adolescent↗

PubMedDate not supplied

[Defects in the visual field in resective surgery for temporal lobe epilepsy].

INTRODUCTION: Temporal lobe resection is the most used procedure in epilepsy surgery. Visual field defects after resection are frequent. AIM. We try to detect the frequency and severity of visual field defect after anterior temporal lobectomy (ATL) and to study the functional consequences. PATIENTS AND METHODS: We studied 30 patients with refractory temporal lobe epilepsy (15 men, 12 51 years, m= 32.9), in which ATL was performed (11 right, 19 left). The neocortical and hippocampal resection was variable. Visual field was studied with computerized campimetry type Humphrey. Our survey was filled to study the campimetric consequence, seizures incidence, quality of life and surgery satisfaction. RESULTS: Some campimetric disturb was found in 27 patients (90 %), superior or minor homonimus quadantapnosia in 18 (60 %), major one 8 and homonimus hemianopsia in one. Incongruent defects appeared in 19. The bigger neocortical and hippocampal resection was, the bigger defect, with exceptions. Only patient with a hemianopsia was conscious the deficit. 20 patients (66.6 %) were seizures free in the last year. 28 had better quality of life and 29 (96.6 %) would have chosen surgery again. CONCLUSION: Visual field defects after ATL, although frequent, have little functional consequences and in quality of life. The quality of life is better when seizures stopped. After ATL patients are very glad with their decision.

Adolescent↗