Hippocampal Atrophy Is Not a Major Determinant of Regional Hypometabolism in Temporal Lobe Epilepsy

Summary: Purpose : The pathophysiologic basis for the [¹⁸F]fluorodeoxyglucose positron-emission tomography (FDG-PET) temporal lobe hypometabolism in patients with hippocampal sclerosis (HS) is uncertain. We tested the hypothesis that hippocampal atrophy, which is strongly correlated with hippocampal cell loss, is largely responsible for the regional hypometabolism in HS.
Methods : Regions of interest (ROIs) on FDG-PET scanning were determined in the medial, lateral, and posterior temporal lobe, thalamus, and basal ganglia. A right/left asymmetry index for each ROI was calculated. These results were correlated with hippocampal magnetic resonance imaging (MRI) volume ratios.
Results : There was no correlation between the magnitudes of the FDG-PET asymmetry index and the MRI volume ratio for the mesial or lateral temporal regions (r =−0.09, r =−0.04). When the right/left asymmetry index was compared with the right/left hippocampal volume ratio, correlations for the mesial temporal ROI (r = 0.79, p < 0.0001) and lateral temporal ROI (r = 0.57, p < 0.0005) were found. These, however, simply indicated that both tests accurately reflect the side of the epileptogenic region. The concordance of the side of relative hypometabolism of the FDG-PET with the side of the hippocampal atrophy was higher for the mesial temporal region (100%) than for the lateral (77.5%).
Conclusions : The lack of correlation between the magnitudes of the ratios argues against hippocampal atrophy and cell loss having a central role in the FDG-PET temporal hypometabolism.     

FDG-PET and MRI in temporal lobe epilepsy: relationship to febrile seizures, hippocampal sclerosis and outcome

Objective – To correlate the volumetric head magnetic resonance imaging (MRI) and fluorodeoxyglucose-positron emission tomography (FDG-PET) scan findings with the history, intracarotid amobarbital procedure, pathology, and outcome in patients with medically refractory temporal lobe epilepsy. Material and methods – Thirty-eight patients with temporal lobe epilepsy treated surgically following a comprehensive presurgical evaluation. Follow-up ranged from 12 to 44 months. Results – Volumetric MRI showed ipsilateral hippocampal atrophy in 29 (76%), and PET scan showed ipsilateral temporal hypometabolism (PET-TH) in 31 (81.5%) of patients. Eighty-three percent of those patients with hippocampal sclerosis on MRI (MRI-HS) had ipsilateral PET-TH. Sixty-six percent of patients with MRI-HS had a history of prolonged febrile convulsions or a childhood febrile illness accompanied by convulsions, and 77% of patients with MRI-HS had pathologically proven hippocampal sclerosis (HS). Ninety percent became seizure free or had rare seizures. Conclusion – FDG-PET scans and head MRIs were complementary; 95% of patients had either MRI-HS or temporal hypometabolism. MRI-HS correlated with a history of febrile seizures and pathologically demonstrated hippocampal sclerosis. Ninety-three percent of patients had focal functional deficits on the epileptogenic side. Concordance between PET temporal hypometabolism and MRI-HS correlated with better outcome.     

Contralateral temporal hypometabolism on positron emission tomography in temporal lobe epilepsy

Introduction — No detailed case studies report lateralised hypometabolism on positron emission tomography (PET) contralateral to the epileptogenic focus in temporal lobe epilepsy (TLE). Material and methods — We performed ¹⁸F fluorodeoxyglucose (FDG) PET in two intractable TLE patients. Results — One had right temporal interictal spikes on electroencephalography (EEG) and a right medial temporal lobe lesion on magnetic resonance imaging (MRI). FDG-PET showed decreased uptake in the left temporal lobe. Right temporal ictal onset, with bilateral interictal epileptiform activity, occurred on intracranial EEG. He is seizure free after right temporal lobectomy and ganglioglioma resection. The second had right temporal lobe interictal and ictal EEG activity. MRI demonstrated right anteriomedial temporal increased T2 signal. Neuropsychology revealed bilateral cognitive dysfunction. FDG-PET showed left anterior temporal and lateral frontal hypometabolism. He is seizure free after right temporal lobectomy. Conclusion — These findings suggest that regional uptake asymmetry on FDG-PET may be give misleading lateralising information in TLE.     

Qualitative and quantitative imaging of the hippocampus in mesial temporal lobe epilepsy with hippocampal sclerosis

MR imaging allows the in vivo detection of hippocampal sclerosis (HS) and has been instrumental in the delineation of the syndrome of mesial temporal lobe epilepsy with HS (mTLE-HS). MR features of HS include hippocampal atrophy with an increased T2 signal. Quantitative MR imaging accurately reflects the degree of hippocampal damage.Ictal single photon emission computed tomography (SPECT) in mTLE-HS shows typical perfusion patterns of ipsilateral temporal lobe hyperperfusion, and ipsilateral frontoparietal and contralateral cerebellar hypoperfusion. Interictal 18fluoro-2-deoxyglucose positron emission tomography (PET) shows multiregional hypometabolism, involving predominantly the ipsilateral temporal lobe. 11C-flumazenil PET shows hippocampal decreases in central benzodiazepine receptor density. Future strategies to study the etiology and pathogenesis of HS should include longitudinal MR imaging studies,MR studies in families with epilepsy and febrile seizures, stratification for genetic background, coregistration with SPECT and PET, partial volume correction and statistical parametric mapping analysis of SPECT and PET images.     

Preoperative FDG-PET temporal lobe hypometabolism and verbal memory after temporal lobectomy

OBJECTIVE: To examine the relationship of preoperative fluorodeoxyglucose (FDG)-PET asymmetry in temporal lobe metabolism and memory outcome after anterior temporal lobectomy (ATL). METHODS: In a university-based epilepsy surgery center, 60 ATL patients (27 left, 33 right) were divided into two groups: no/mild (n = 21) or moderate/ severe (n = 39) asymmetry in temporal lobe hypometabolism as determined by FDG-PET. All patients were nonretarded, at least 18 years of age, left-hemisphere speech dominant, without MRI abnormalities other than hippocampal atrophy, and with unilateral temporal lobe origin of intractable complex partial seizures. Neuropsychological measures of intelligence and verbal and visual memory function were assessed preoperatively and 6 months postoperatively. RESULTS: Left ATL patients with no/mild asymmetry in FDG-PET temporal lobe metabolism exhibited significantly greater verbal memory decline compared with left ATL patients with moderate/severe hypometabolism. There was no significant relationship between PET asymmetry and pre- to postsurgical IQ change. No significant relationship was observed between extent of PET hypometabolism and memory outcome for right ATL patients. CONCLUSIONS: FDG-PET asymmetry can be added to the preoperative clinical markers that appear useful in predicting verbal memory decline after left ATL.     

Mesial temporal lobe epilepsy with lateral temporal lobe abnormalities in magnetoencephalography and glucose metabolism.

Magnetoencephalography (MEG) and positron emission tomography (PET) revealed abnormal findings in the lateral temporal lobe of a 22 year old female with mesial temporal lobe epilepsy. Electroencephalography identified the epileptogenic focus in the left mesial temporal lobe and standard anterior temporal lobectomy resulted in a good surgical outcome. These discrepancies can be explained by the presence of anatomical and functional pathways between the mesial and lateral temporal structures, or pathophysiological abnormalities in both the mesial and lateral temporal lobes. Careful evaluation is necessary for analysis of MEG and PET findings in patients with temporal lobe epilepsy.     

Dual pathology in a patient with temporal lobe epilepsy associated with neocortical glial scar after brain abscess and end folium sclerosis/hippocampal sclerosis type 3

End folium sclerosis or hippocampal sclerosis (HS) type 3 is often associated with another coexisting epileptogenic lesion (dual pathology); however, the pathogenesis of HS type 3 remains elusive. A 46‐year‐old man presented with medically intractable focal aware seizures and focal impaired awareness seizures (FIAS) with occasional focal to bilateral tonic–clonic seizures (FBTCS) two years after surgical treatment with extensive cranial reconstruction for a brain abscess in the right temporal lobe associated with intracranial extension of ipsilateral cholesteatoma. Head magnetic resonance imaging (MRI) at age 49 revealed atrophy of the right cerebral hemisphere including the hippocampus and amygdala. The patient's first epilepsy surgery was a lateral temporal lobectomy, in which the mesial temporal structures were preserved because no epileptiform discharge was detected on the intraoperative electrocorticogram. However, FIAS with FBTCS started 15 months after the operation. The second surgery, amygdalohippocampectomy, at age 52, resulted in the patient being seizure‐free again for one year before seizures of the right lateral temporal origin recurred. He underwent a third surgery, resection of the Heschl's and supramarginal gyri, at age 53, but he continued to have drug‐resistant epilepsy over two years after that. Histopathological examination revealed dual pathology consisting of glial scar in the lateral temporal lobe and ipsilateral HS type 3 with an unusually severe lesion in the subiculum. No significant inflammatory change was observed. The clinicopathological features in the present case indicate that HS developed secondarily in the context of neocortical epilepsy due to glial scar, suggesting a role of repetitive abnormal electrical input from neocortical epileptogenic lesions into the hippocampus finally via the perforant pathway in the pathogenesis of HS type 3. Severe hippocampal atrophy on preoperative MRI together with its silent electrocorticogram recording at initial epilepsy surgery may represent clinically pre‐epileptogenic HS in a seizure‐free “silent or latent period” before completion of hippocampal epileptogenesis to the extent that clinical epileptic seizures occur.     

Focal functional deficits in temporal lobe epilepsy on PET scans and the intracarotid amobarbital procedure: comparison of patients with unitemporal epilepsy with those requiring intracranial recordings

PURPOSE: To analyze the relationship between the intracarotid amobarbital procedure (IAP) and positron emission tomography (PET) and study the lateralizing value of these tests in patients with unitemporal epilepsy and those requiring intracranial recordings. METHODS: We compared 51 patients with unitemporal epilepsy (group1) with 26 patients in whom surface recordings failed to reveal a distinct unitemporal focus, necessitating invasive recordings (group 2). RESULTS: The brain magnetic resonance imaging (MRI) scans for group 1 showed mesial temporal sclerosis in 70.5% of the patients. PET showed unilateral temporal hypometabolism in 88%. In addition, 74.5% of the patients in group 1 had impaired memory on the epileptogenic side on the IAP, and 89.4% of those patients also had ipsilateral temporal hypometabolism on PET scans. All the group 1 patients underwent temporal resections. The pathologic examination showed hippocampal sclerosis in 72% of the patients. Eighty percent of group 1 patients became seizure free, and 16% had rare seizures (follow-up, 2-7 years). MRIs for group 2 showed mesial temporal sclerosis in 31% of the patients; PET scans showed temporal hypometabolism in 39%. The IAP was lateralized in 47.8%. Sixty-nine percent had temporal lobe resections. The pathologic examination showed hippocampal sclerosis in 44% of the patients. Forty-four percent of group 2 patients became seizure free, and 27.7% had rare seizures (follow-up, 2-8 years). CONCLUSIONS: Ninety-six percent of the patients with unitemporal foci had focal functional deficits on the epileptogenic side on 18-fluorodeoxyglucose-(FDG) PET scans, the IAP, or both. The results of the FDG-PET were predictive of impaired memory on the IAP. Memory impairment contralateral to the temporal hypometabolism found on the PET scans was never seen. These patients had an excellent outcome. In contrast, <50% of the patients requiring intracranial recordings had focal functional deficits, suggesting that more a diffuse pathology may account for their less favorable outcome.     

发作间期PET和MR海马像在难治性颞叶癫癇术前定侧中的应用

目的 探讨发作间期18FDG-PET和MR海马像在难治性颞叶癫(?)（TLE）致(?)源术前定侧中的价值。方法 对17例药物难治性TLE患者术前定侧资料及术后随诊情况进行分析。结果 本组患者中,有12例（71％）患者MR显示海马硬化（HS）,海马萎缩与信号改变常共存,T2加权像和FLAIR序列有利于显示信号的改变。HS侧多提示为致(?)源侧。PET检查均显示有至少一侧颞叶低代谢改变,并常多发或范围弥散。PET与MR的定侧准确率分别是100％（13/13）、77％（10/13）,经x2检验两者间无差异（P>0.05）。结论　18FDG-PET和MR海马像在致(?)源定侧中的作用是互补的,当颞叶低代谢侧与海马硬化侧相一致时手术效果较好。     

Correlation of hippocampal glucose oxidation capacity and interictal FDG-PET in temporal lobe epilepsy

PURPOSE: Interictal [18F]fluorodeoxyglucose (FDG) positron emission tomography (PET) demonstrates temporal hypometabolism in the epileptogenic zone of 60-90% of patients with temporal lobe epilepsy. The pathophysiology of this finding is still unknown. Several studies failed to show a correlation between hippocampal FDG-PET hypometabolism and neuronal cell loss. Because FDG is metabolized by hexokinase bound to the outer mitochondrial membrane, we correlated the glucose-oxidation capacity of hippocampal subfields obtained after surgical resection with the corresponding hippocampal presurgical FDG-PET activity. METHODS: In 16 patients with electrophysiologically confirmed temporal lobe epilepsy, we used high-resolution respirometry to determine the basal and maximal glucose-oxidation rates in 400-microm-thick hippocampal subfields obtained after dissection of human hippocampal slices into the CA1 and CA3 pyramidal subfields and the dentate gyrus. RESULTS: We observed a correlation of the FDG-PET activity with the maximal glucose-oxidation rate of the CA3 pyramidal subfields (rp = 0.7, p = 0.003) but not for the regions CA1 and dentate gyrus. In accordance with previous studies, no correlation of the FDG-PET to the neuronal cell density of CA1, CA3, and dentate gyrus was found. CONCLUSIONS: The interictal hippocampal FDG-PET hypometabolism in patients with temporal lobe epilepsy is correlated to the glucose-oxidation capacity of the CA3 hippocampal subfield as result of impaired oxidative metabolism.     

Correlation of Hippocampal Neuronal Density and FDG-PET in Mesial Temporal Lobe Epilepsy

Summary: Purpose: Interictal [¹⁸F]fluorodeoxyglucose (FDG) positron emission tomography (PET) reveals regional hypometabolism in 60–80% of patients with mesial temporal lobe epilepsy (MTLE). The extent of hypometabolism generally extends beyond the epileptogenic zone. The pathophysiology underlying this widespread change is unknown. This study evaluated the relation between hippocampal neuronal loss and hypometabolism in patients with MTLE.
Methods: Forty-three patients with MTLE after anterior temporal lobectomy were included. Pathology demonstrated mesial temporal sclerosis (n = 41) or endfolium sclerosis (n = 2). Interictal FDG-PET scans were graded by visual analysis on a scale ranging from normal (grade 1) to severe (grade 5) hypometabolism. Neuronal counting was performed in the subiculum, hippocampal subfields, and dentate granular cell layer (DG). Neuronal density of patients was compared with that of seven autopsy controls. Data were compared by using Student's t tests and Kruskal-Wallis one-way analysis of variance (ANOVA).
Results: Significant neuronal loss in CA1 through CA4 and DG was found in patients compared with controls. Neuronal density in the subiculum, CA1, CA4, and DG did not correlate with severity of hypometabolism. However, patients with abnormal FDG-PET had higher neuronal density in CA2 and CA3 versus patients with normal studies.
Conclusions: This study supports a previous observation that degree of FDG-PET hypometabolism does not parallel severity of hippocampal neuronal loss in MTLE.     

In vivo hippocampal glucose metabolism in mesial temporal lobe epilepsy

BACKGROUND: The appearance of decreased 2-[(18)F]fluoro-2-deoxy-D-glucose (FDG) uptake in the mesial temporal region in temporal lobe epilepsy may simply reflect loss of gray matter due to hippocampal atrophy. Increased partial volume effects due to atrophic hippocampi may further increase appearance of hypometabolism. METHODS: The authors used a combination of MRI-PET coregistration, with MRI-based gray matter segmentation, and partial volume correction to improve the examination of hippocampal specific glucose uptake in FDG PET. The goal was to determine 1) if relative mesial temporal hypometabolism is an artifact of gray matter (hippocampal) atrophy, 2) whether hippocampal metabolism correlates with atrophy evaluated on MRI, and 3) if MRI-based partial volume correction influences measurement of hippocampal metabolic-volume relationships, including epilepsy lateralization. RESULTS: Findings showed that ipsilateral hippocampi of mesial temporal lobe epilepsy (MTLE) are relatively hypometabolic per unit of gray matter volume, and that hippocampal metabolism directly correlates with hippocampal volume. Specifically, partial volume corrected hippocampal metabolism correlated strongly (r = 0.613, p < 0.001) with hippocampal volume. Without partial volume correction, a weaker, but still significant, correlation was present (r = 0.482, p < 0.001). Degree of asymmetry was consistently greater and provided higher sensitivity of lateralization with partial volume vs non-partial volume corrected metabolic measurements. CONCLUSIONS: Although, decreased metabolism may occur in the absence of neuronal cell loss, hippocampal atrophy and presumed degree of neuronal cell loss appears to be a primary factor involved in the cause of decreased metabolism in epileptogenic hippocampi. Partial volume correction is recommended for optimal interpretation of hippocampal structure and function relationships.     

Epilepsy duration impacts on brain glucose metabolism in temporal lobe epilepsy: Results of voxel-based mapping

Objective[¹⁸F]Fluorodeoxyglucose positron emission tomography ([¹⁸F]FDG-PET) is a valuable method for detecting focal brain dysfunction associated with epilepsy. Evidence suggests that a progressive decrease in [¹⁸F]FDG uptake occurs in the epileptogenic cortex with an increase in the duration of epilepsy. In this study, our aim was to use statistical parametric mapping (SPM) to test the validity of this relationship in a retrospective study of patients with temporal lobe epilepsy (TLE).Methods[¹⁸F]FDG-PET scans of 46 adult patients with pharmacoresistant unilateral TLE (25 RTLE and 21 LTLE) were subjected to SPM analysis.ResultsForty-six patients were diagnosed with nonlesional TLE, 16 of whom had hippocampal sclerosis (HS). The average duration of epilepsy was 17.4 ± 12.3 years (3–46 years), <5 years in 10 patients and ?10 years in 30 patients. Visual analysis of [¹⁸F]FDG-PET scans revealed hypometabolism in the epileptogenic temporal cortex in 31 (67%) patients. After SPM analysis of all [¹⁸F]FDG-PET images, hypometabolism was unilateral and reported in lateral and mesial structures of the epileptogenic temporal cortex in addition to the ipsilateral fusiform and middle occipital gyrus. Subsequent analysis revealed that temporal lobe hypometabolism was present only in patients with longer epilepsy duration (?10 years) in parahippocampal gyrus, uncus, and middle and superior temporal gyrus (P < 0.05 corrected). Epilepsy duration was inversely correlated with decreased glucose uptake in the inferior temporal gyrus, hippocampus, and parahippocampal gyrus of the epileptogenic temporal cortex (P < 0.05). Age at seizure onset did not affect the correlation between epilepsy duration and glucose uptake except in the inferior temporal gyrus (P < 0.05).ConclusionVoxel-based mapping supports the assertion that glucose hypometabolism of the epileptogenic temporal lobe cortex and other neighboring cortical regions increases with longer epilepsy duration in TLE.     

Decreased dopamine D2/D3-receptor binding in temporal lobe epilepsy: an [18F]fallypride PET study

PURPOSE: Although animal data are suggestive, evidence for an alteration of the extrastriatal dopaminergic system in human focal epilepsy is missing. METHODS: To quantify D2/D3-receptor density, we studied seven patients with temporal lobe epilepsy (TLE) and nine age-matched controls with positron emission tomography (PET) by using the high-affinity dopamine D2/D3-receptor ligand [18F]Fallypride ([18F]FP) suitable for imaging extrastriatal binding. TLE was defined by interictal and ictal video-EEG, magnetic resonance imaging (MRI), and [18F]fluorodeoxyglucose ([18F]FDG)-PET and was due to hippocampal sclerosis (HS), based on histology in all patients. Primary analysis was based on regions of interest (ROIs) defined on individual MRIs. For each patient, binding potential (BP) was calculated by using the simplified reference tissue model, and the epileptogenic was compared with the unaffected hemisphere in each ROI. To confirm the results, an additional voxel-based group analysis was performed by using statistical parametric mapping. RESULTS: Compared with controls, [18F]FP BP was significantly decreased in the epileptogenic temporal lobe in all patients. On ROI analysis, this reduction was evident in areas surrounding the seizure-onset zone at the pole (-34.2%) and lateral aspects (-32.9%) of the temporal lobe. Although the hippocampus [18F]FDG uptake (-8.1%) and hippocampal MR volume (-35.1%) were significantly reduced, no significant decrease of [18F]FP BP was found. Reduction of [18F]FP BP did not correlate with hippocampal atrophy. CONCLUSIONS: D2/D3-receptor binding is reduced at the pole and in lateral aspects of the epileptogenic temporal lobe in patients with mesial TLE and HS. This area might correspond to "the irritative zone," indicating that D2/D3 receptors might play a specific role in the pathophysiology of mesial TLE.     

Is Interictal Temporal Hypometabolism Related to Mesial Temporal Sclerosis? A Positron Emission Tomography/Magnetic Resonance Imaging Confrontation

Summary: The mechanism of interictal glucose hypometabolism remains unclear, but this abnormality occurs more frequently in temporal lobe epilepsy (TLE) than in other types of partial epilepsy. Therefore temporal hypometabolism has been suggested to reflect mesial temporal sclerosis (MTS). To investigate this, we selected 22 patients with refractory partial epilepsy of mesial temporal lobe origin (MTLE) who had hippocampal atrophy based on magnetic resonance imaging (MRI) volumetric analysis. We then analyzed the metabolic correlates of unilateral hippocampal atrophy. Thirteen temporal regions of interest (ROI) were defined on MRI scans for each individual and then applied to high-resolution FDG-positron emission tomography (PET) images obtained parallel to the long axis of the hippocampus. The most hypometabolic regions were the temporal pole and the hippocampal region. When we analyzed ensembles of temporal regions grouped into related networks, the temporolimbic network, which included the hippocampal region and the temporal pole, was abnormal in 95% of the patients at a 3-SD threshold. PET hypometabolism was highly correlated with the degree of hippocampal atrophy in this network, but not in other parts of the temporal lobe, which were less frequently hypometabolic. These data indicate that hypometabolism is a consequence of MTS in the temporolimbic region but not necessarily in the other parts of the temporal lobe. Our results also suggest that the combination of PET and MRI may facilitate the noninvasive diagnosis of MTLE.     

An operated case of medial temporal lobe epilepsy associated with schizencephaly]

A 24-year-old male of medial temporal lobe epilepsy associated with schizencephaly was presented. He developed complex partial seizure after head trauma at the age of a year and 7 months, which became intractable at the age of 13 year. MRI demonstrated a schizencephalic cleft in the right peri-Rolandic area, cortical dysplasia in the right medical parietal and occipital lobes, and right hippocampal atrophy. Scalp-recorded EEG failed to localize the ictal onset zone. Interictal FDG-PET and ECD-SPECT indicated hypometabolism and hypoperfusion of the right entire temporal lobe, and ictal ECD-SPECT increased perfusion of this area. Chronic subdural electrode recording clearly demonstrated that ictal onset zone was located not on the schizencephalic cleft or its surrounding cortex but on the right medial temporal lobe. Following right anterior temporal lobectomy with hipppocampectomy, seizure control became easy. For the identification of the epileptogenic zone in patients with schizencephaly, chronic subdural electrode recording is mandatory.     

Comparison of the intracarotid amobarbital procedure and interictal cerebral 18-fluorodeoxyglucose positron emission tomography scans in refractory temporal lobe epilepsy.

The relationship between interictal focal hypometabolism determined by 18-fluorodeoxyglucose positron emission tomography (FDG-PET) scans and memory function with the intracarotid amobarbital procedure (IAP) was evaluated in 23 patients with temporal lobe epilepsy. All patients underwent prolonged EEG/video monitoring. The epileptogenic focus was defined by interictal epileptiform discharges and ictal onsets. All 23 patients had recorded seizures arising exclusively from one temporal lobe. PET showed temporal lobe hypometabolism ipsilateral to the epileptogenic focus in 86% (20 of 23) of patients; IAP showed impaired memory of the hemisphere of seizure onset in 65% (15 of 23). Sixty-five percent (13 of 20) of patients with focal hypometabolism had ipsilateral memory impairment. Memory impairment contralateral to the hypometabolic zone was not observed. Ninety-five percent (22 of 23) of patients demonstrated functional impairment by either PET or IAP (or both) on the epileptogenic side.     

Metabolic evidence for episodic memory plasticity in the nonepileptic temporal lobe of patients with mesial temporal epilepsy

Purpose: Metabolic changes have been described in the nonepileptic temporal lobe of patients with unilateral mesiotemporal lobe epilepsy (MTLE) associated with hippocampal sclerosis (HS). To better understand the functional correlate of this metabolic finding, we have sought to characterize brain regions in patients with MTLE that show correlation between unilateral episodic memory performances, as assessed by intracarotid amobarbital test (IAT), and interictal regional cerebral metabolism measured by [¹⁸F]‐fluorodeoxyglucose positron emission tomography (FDG‐PET). Methods: Resting FDG‐PET was performed interictally in 26 patients with unilateral MTLE caused by HS (16 female, mean age: 36 years; 16 left HS). Using statistical parametric mapping (SPM8), we performed a group comparison analysis comparing brain metabolism in the patients and in 54 adult controls (27 female, mean age: 32 years), with FDG‐PET data of right HS patients being flipped. IAT scores of nonepileptic hemisphere functions (amobarbital injection ipsilateral to HS) were used as covariates of interest in a correlation analysis with regional brain metabolism. Key Findings: The group comparison analysis revealed significant hypometabolic areas in a widespread temporofrontal network ipsilateral to HS. In addition, a significant increase in metabolism was found in mesial and lateral temporal regions contralateral to HS. Significant positive correlations were found between IAT scores of nonepileptic hemisphere functions and mesial temporal metabolism in this hemisphere. Significance: This study demonstrates the existence of significant increase in relative regional cerebral glucose metabolism in mesial and lateral temporal regions contralateral to the epileptic focus in patients with unilateral MTLE associated with HS. The positive correlation in these brain regions between IAT scores and metabolism supports the role of disease‐induced plasticity mechanisms contralateral to HS in the preservation of episodic memory processes.     

The effects of mesial temporal and cerebellar hypometabolism on learning and memory.

The effects of mesial temporal (MT) and cerebellar hypometabolism were studied using measures of verbal, visual and motor skill learning. Twelve patients with refractory temporal lobe epilepsy who showed asymmetrical mesial temporal lobe hypometabolism on [18F] fluoro-2-deoxy-glucose positron emission tomography (FDG-PET) were given tests involving 4 consecutive learning trials and a 30-min delayed recall trial. Delayed recognition was also assessed for the words and designs, and skill transfer was evaluated for mirror drawing. Compared to 9 normal control participants, patients with more marked MT hypometabolism on the left had impaired delayed recall of words and patients with more marked MT hypometabolism on the right showed impaired learning of novel designs, but normal retention over delay. Patients were not impaired in their mirror-drawing performance. The findings for MT hypometabolism correspond well to those obtained in other studies where patients have been classified on the basis of side of hippocampal atrophy or temporal lobe excision.     

Structural abnormalities are similar in familial and nonfamilial mesial temporal lobe epilepsy

BACKGROUND/OBJECTIVE: Diffuse temporal lobe abnormalities can be observed on MRI of patients with mesial temporal lobe epilepsy (MTLE). Our objective was to perform qualitative and quantitative analyses of temporal lobe structures in patients with familial MTLE (FMTLE) and nonfamilial MTLE. METHODS: Two groups of patients were ascertained: 67 FMTLE patients (14 with refractory seizures) and 30 patients with nonfamilial refractory MTLE. We performed qualitative analyses of MRI (with multiplanar reconstruction) and volumes of hippocampi and anterior temporal lobes in all patients, and in a normal control group of 23 individuals. We used the Chi-square test and ANOVA for statistical analyses. RESULTS: We identified anterior temporal lobe abnormalities by visual analysis in only 4% of FMTLE patients and atrophy of the anterior temporal lobe by volumetric analysis in 19%. In the group of nonfamilial MTLE patients we found anterior temporal lobe abnormalities by visual analysis in 17% of patients and anterior temporal lobe atrophy in 13%. Hippocampal atrophy was present in 90% of FMTLE and in 83% of nonfamilial MTLE. No signs of cortical dysplasia were observed. CONCLUSION: Anterior temporal lobe atrophy and other abnormalities outside the mesial portion of temporal lobes were infrequent in both familial and nonfamilial MTLE patients. Despite the genetic basis, hippocampal atrophy in FMTLE is not associated with other abnormalities outside the mesial temporal regions.