Hippocampal cell density and subcortical metabolism in temporal lobe epilepsy

PURPOSE: Correlations between hippocampal cell density and subcortical metabolism in patients with temporal lobe epilepsy (TLE) were studied to explore possible links between subcortical function and the regulation of hippocampal excitability. METHODS: Resected hippocampal cell densities were correlated with cortical and subcortical regional cerebral metabolic rate for glucose (CMRglu), as measured by [18F]-fluorodeoxyglucose positron emission tomography (18-FDG-PET), in 39 patients with intractable TLE who underwent anterior temporal lobectomy (ATL). CMRglu was measured ipsilateral and contralateral to the resected temporal lobe. Linear regression techniques were used for statistical analysis. RESULTS: Hilar cell densities correlated positively and significantly with CMRglu in the bilateral thalamus, putamen and globus pallidus, and the ipsilateral caudate. Dentate granule cell densities correlated positively and significantly with CMRglu in the bilateral thalamus and putamen. There was no significant correlation between cell densities and CMRglu in any cortical region, including the hippocampus. CONCLUSIONS: We postulate that hippocampal cell loss results in decreased efferent synaptic activity to the thalamus and basal ganglia, causing decreased neuronal activity in these structures with consequent hypometabolism. This synaptic activity has a significant bilateral component. Subcortical hypometabolism in patients with TLE may reinforce the epileptogenic potential of mesial temporal lobe discharges.     

Subcortical metabolic alterations in partial epilepsy

The function of subcortical nuclei in partial epilepsy was investigated using positron emission tomography (PET) to measure metabolism in the basal ganglia and thalamus. Sixteen patients undergoing surgical evaluation were studied with 18F-fluorodeoxyglucose (FDG) interictally and had intensive extracranial and intracranial electrophysiologic evaluations. Eight patients had left temporal lobe seizure foci, six had right temporal lobe foci, and two had right posterotemporal or parietal foci. The PET data were analyzed visually and quantitatively, using a multivariate analysis of variance on the quantitative data. Hypometabolism of subcortical nuclei was present ipsilateral to the cortical seizure focus. Cortical hypometabolism was noted focally in the temporal lobe in patients with left temporal lobe seizure foci, whereas patients with right temporal lobe seizure foci had diffuse hemispheric hypometabolism. We postulate that the subcortical hypometabolism is secondary to decreased efferent activity from temporal lobe structures, in particular amygdala and hippocampus, to subcortical nuclei. Diminished subcortical activity may then lead to defective regulation of cortical excitability in the temporal lobe, increasing the likelihood of seizure development and spread.     

Hippocampal and thalamic diffusion abnormalities in children with temporal lobe epilepsy

PURPOSE: Previous studies using diffusion MRI in patients with temporal lobe epilepsy have shown abnormal water diffusion in the hippocampus. Because thalamus and lentiform nuclei are considered important for the regulation of cortical excitability and seizure propagation, we analyzed diffusion tensor imaging (DTI) abnormalities in these subcortical structures and in hippocampus of children with partial epilepsy with and without secondary generalization. METHODS: Fourteen children with partial epilepsy involving the temporal lobe underwent MRI including a DTI sequence. Fractional anisotropy (FA) and apparent diffusion coefficient (ADC) values were obtained in the hippocampus, thalamus, and lentiform nucleus, and compared with DTI data of 14 control children with no epilepsy, as well as glucose positron emission tomography (PET) findings. RESULTS: Decreased FA (p < 0.001) and increased ADC (p = 0.003) values were found in the hippocampi ipsilateral to the seizure focus. Significant FA decreases (p = 0.002) also were seen in the contralateral hippocampi, despite unilateral seizure onset and excellent surgical outcome in patients who underwent surgery. ADC values showed a trend for increase in the thalami ipsilateral to the epileptic focus in the seven children with secondarily generalized seizures (p = 0.09). No group differences of ADC or FA were found in the lentiform nuclei. The DTI variables did not correlate with regional glucose metabolism in any of the structures analyzed. CONCLUSIONS: Increased ADC values in hippocampus can assist in lateralizing the seizure focus, but decreased FA in the contralateral hippocampus suggests that it too may be dysfunctional despite unilateral seizure onset. Less-robust thalamic abnormalities of water diffusion in patients with secondarily generalized seizures suggest secondary involvement of the thalamus, perhaps due to recruitment of this structure into the epileptic network; however, this must be confirmed in a larger population. DTI appears to be a sensitive method for detection abnormalities in children with partial epilepsy, even in structures without apparent changes on conventional MRI.     

局灶性难治性颞叶癫痫全脑葡萄糖代谢特点

目的 探讨局灶性难治性颞叶癫痫全脑葡萄糖代谢特点。方法 回顾性分析2017年1~12月行发作间期18FDG-PET/CT检查的23例局灶性难治性颞叶癫痫的影像学资料。将PET图像导入MIM neuro软件,软件自动分析癫痫病人葡萄糖代谢水平与正常人群葡萄糖代谢的差异,各脑区差异结果以Z-Score值显示,分析颞叶癫痫病人全脑葡萄糖代谢特点。结果 术后病理为脑皮质发育不良22例,节细胞胶质瘤1例;病灶位于左侧颞叶16例,右侧颞叶7例。除颞叶呈葡萄糖低代谢改变外,还存在同侧海马、海马旁回、岛叶、杏仁核、颞叶岛盖以及双侧小脑半球葡萄糖代谢不同程度减低;对侧颞叶、额叶、顶叶、顶上小叶以及角回葡萄糖代谢不同程度增高。结论 颞叶癫痫具有一定葡萄糖代谢特点,其特定的葡萄糖代谢特点有助于更加精准的癫痫术前定位及其病理特征的分析。     

Regional brain glucose metabolism in patients with complex partial seizures investigated by intracranial EEG.

We performed interictal 18F-2-fluoro-2-deoxy-D-glucose positron emission tomography (18FDG-PET) studies in 57 patients with complex partial epilepsy (CPE), not controlled by medical treatment and considered for surgical resection of their epileptic focus. A precise localization of the epileptic focus was obtained in 37 of these patients with a combination of subdural and depth electrodes. We visually inspected the metabolic images; we also measured glucose consumption in a number of brain regions and compared the values with those obtained in 17 normal controls. Eighty-two percent of the 57 patients had an area of glucose hypometabolism on the 18FDG-PET images. Six patients had a frontal epileptic focus, 3 of them had a frontal lobe hypometabolism. Twenty-six patients had a unilateral temporal lobe focus and all of them displayed a temporal lobe hypometabolism. The asymmetry was more pronounced in the lateral temporal cortex (-20%) than in the mesial part of the temporal lobe (-9.6%). In each cortical brain region on the side of the epileptic focus (except the sensorimotor cortex), glucose consumption rate was lower than in the contralateral region or than in controls. No differences could be found between patients with a seizure onset restricted to the hippocampus and patients with a seizure onset involving the hippocampus and the adjacent neocortex. Divergent metabolic patterns were obtained in 5 patients with bilateral temporal seizure foci. Combined with other non invasive techniques (EEG, neuroradiology), PET contributes increasingly to the selection of patients with CPE who could benefit from surgical treatment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Bilateral medial prefrontal and temporal neocortical hypometabolism in children with epilepsy and aggression

PURPOSE: To identify brain regions with abnormal function in children with intractable partial epilepsy and aggressive behavior by using 2-deoxy-2-[18F]fluoro-D-glucose (FDG) positron emission tomography (PET). METHODS: Six children (mean age, 9.9 years) with intractable partial epilepsy and aggressive behavior underwent detailed psychodevelopmental assessment and FDG-PET scanning. The objective technique of statistical parametric mapping (SPM) was applied to define focal abnormalities of glucose metabolism, and compared those with those of a group of normal adult subjects (n = 17) as well as age-matched children with epilepsy with similar seizure characteristics but without aggression (n = 7). The findings were analyzed further by using a region-of-interest (ROI) approach. RESULTS: The aggressive children all showed developmental delay, and four of them also manifested autistic symptoms. SPM analysis demonstrated extensive glucose hypometabolism in the aggressive group bilaterally in the temporal and prefrontal cortex compared with that in normal adult controls. A focal area of medial prefrontal glucose hypometabolism was defined in the aggressive children as compared with the nonaggressive pediatric group with SPM, whereas ROI comparison of these groups confirmed prefrontal hypometabolism and also showed glucose hypometabolism of the temporal neocortex in the aggressive children. Severity of aggression correlated inversely with glucose metabolism of the left temporal as well as bilateral medial prefrontal cortex. CONCLUSIONS: Bilateral prefrontal and temporal neocortical brain glucose hypometabolism in children with epilepsy and aggressive behavior may indicate a widespread dysfunction of cortical regions, which normally exert an inhibitory effect on subcortical aggressive impulses. PET studies may be used to elucidate the neurobiologic basis of aggressive behavior in children.     

Volumetric measurements of subcortical nuclei in patients with temporal lobe epilepsy.

OBJECTIVE: To determine the volumes of subcortical nuclei in patients with chronic epilepsy. BACKGROUND: Animal and human data suggest a crucial role for subcortical structures in the modulation of seizure activity, mostly as seizure-suppressing relays. Although cortical epileptogenic foci can vary in localization and extent, it nevertheless appears that these structures subsequently influence seizure propagation in a universal fashion. There is, however, little knowledge about the size of implicated subcortical structures in patients with epilepsy. METHOD: Using high-resolution MRI, the volumes of selected subcortical nuclei, such as the thalamus, caudate nucleus, putamen, and pallidum, were measured in both hemispheres of 27 patients with temporal lobe epilepsy. Fourteen healthy volunteers served as controls. Statistical analysis was done for both normalized volumes (by total brain volume) and unnormalized volumes. RESULTS: Overall, the patient group had smaller thalamic and striatal volumes in both hemispheres, mostly ipsilateral to the epileptic focus. No significant correlations were noted between volume measurements and age, age at onset, duration of epilepsy, or total seizure frequency, including frequency of generalized seizures. The putamen and thalamus seemed to be affected predominantly in patients with a history of febrile convulsions, whereas patients without febrile convulsions had smaller caudate nuclei bilaterally. CONCLUSIONS: Volumetric measurements of subcortical nuclei reveal atrophy of distinct subcortical nuclei in the patient group, predominantly ipsilateral to the focus. This finding probably reflects persistent abnormalities and not secondary change. In addition, the structural differences between patients with and patients without previous febrile convulsions suggest that these conditions may have different causes.     

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.     

Interictal patterns of cerebral glucose metabolism,perfusion, and magnetic field in mesial temporal lobe epilepsy

PURPOSE: To characterize the epileptogenic condition of patients with mesial temporal lobe epilepsy, the interictal patterns of glucose metabolism, perfusion, and magnetic field in the temporal lobe were evaluated by using [18F]fluorodeoxyglucose-positron emission tomography, [99mTc]-ethylcysteinate dimer-single photon emission computed tomography, and magnetoencephalography (MEG). METHODS: Twenty-one patients with mesial temporal lobe epilepsy related to hippocampal sclerosis were studied. The ictal-onset area was located by continuous video-EEG monitoring. Quantitative analysis of glucose metabolism and perfusion in the temporal lobe was performed, and the cerebral magnetic field was evaluated to measure the equivalent current dipole (MEG-ECD). RESULTS: Although hypometabolism and hypoperfusion in the temporal lobe were lateralized with the ictal-onset area in 16 (76.2%) and in 11 (52.4%) respectively, they were localized in diverse ways without any coupling. MEG-ECD was distributed in diverse ways unrelated to the ictal-onset area: ipsilateral medial temporal origin in five (23.8%), ipsilateral lateral temporal origin in two (9.5%), ipsilateral mixed (medial and lateral) temporal origin in six (28.6%), bilateral temporal origin in four (19.0%), and contralateral temporal origin in two (9.5%). CONCLUSIONS: MEG-ECD was distributed in varied ways with the disorder and uncoupling of glucose metabolism and perfusion in the temporal lobe. These results may help resolve the clinical controversy over the possibility that the cortical irritative area generating the interictal epileptic discharge is distinct from the ictal-onset area, and also may have some functional implications in identifying different brain compartments in the generation of metabolic signals.     

Widespread epileptic networks in focal epilepsies: EEG-fMRI study

Purpose: To assess the extent of brain involvement during focal epileptic activity, we studied patterns of cortical and subcortical metabolic changes coinciding with interictal epileptic discharges (IEDs) using group analysis of simultaneous electroencephalography and functional magnetic resonance imaging (EEG‐fMRI) scans in patients with focal epilepsy. Methods: We selected patients with temporal lobe epilepsy (TLE, n = 32), frontal lobe epilepsy (FLE, n = 14), and posterior quadrant epilepsy (PQE, n = 20) from our 3 Tesla EEG‐fMRI database. We applied group analysis upon the blood oxygen–level dependent (BOLD) response associated with focal IEDs. Key Findings: Patients with TLE and FLE showed activations and deactivations, whereas in PQE only deactivations occurred. In TLE and FLE, the largest activation was in the mid–cingulate gyri bilaterally. In FLE, activations were also found in the ipsilateral frontal operculum, thalamus, and internal capsule, and in the contralateral cerebellum, whereas in TLE, we found additional activations in the ipsilateral mesial and neocortical temporal regions, insula, and cerebellar cortex. All three groups showed deactivations in default mode network regions, the most widespread being in the TLE group, and less in PQE and FLE. Significance: These results indicate that different epileptic syndromes result in unique and widespread networks related to focal IEDs. Default mode regions are deactivated in response to focal discharges in all three groups with syndrome specific pattern. We conclude that focal IEDs are associated with specific networks of widespread metabolic changes that may cause more substantial disturbance to brain function than might be appreciated from the focal nature of the scalp EEG discharges.     

Brain structure and aging in chronic temporal lobe epilepsy

Purpose: To characterize differences in brain structure and their patterns of age‐related change in individuals with chronic childhood/adolescent onset temporal lobe epilepsy compared with healthy controls. Methods: Subjects included participants with chronic temporal lobe epilepsy (n = 55) of mean childhood/adolescent onset and healthy controls (n = 53), age 14–60 years. Brain magnetic resonance imaging (MRI) studies (1.5 T) were processed using FreeSurfer to obtain measures of lobar thickness, area, and volume as well as volumes of diverse subcortical structures and cerebellum. Group differences were explored followed by cross‐sectional lifespan modeling as a function of age. Key Findings: Anatomic abnormalities were extensive in participants with chronic temporal lobe epilepsy including distributed subcortical structures (hippocampus, thalamus, caudate, and pallidum), cerebellar gray and white matter, total cerebral gray and white matter; and measures of cortical gray matter thickness, area, or volume in temporal (medial, lateral) and extratemporal lobes (frontal, parietal). Increasing chronologic age was associated with progressive changes in diverse cortical, subcortical, and cerebellar regions for both participants with epilepsy and controls. Age‐accelerated changes in epilepsy participants were seen in selected areas (third and lateral ventricles), with largely comparable patterns of age‐related change across other regions of interest. Significance: Extensive cortical, subcortical, and cerebellar abnormalities are present in participants with mean chronic childhood/adolescent onset temporal lobe epilepsy implicating a significant neurodevelopmental impact on brain structure. With increasing chronologic age, the brain changes occurring in epilepsy appear to proceed in a largely age‐appropriate fashion compared to healthy controls, the primary exception being age‐accelerated ventricular expansion (lateral and third ventricles). These cumulative structural abnormalities appear to represent a significant anatomic burden for persons with epilepsy, the consequences of which remain to be determined as they progress into elder years.     

Metabolic profiles and correlation with surgical outcomes in mesial versus neocortical temporal lobe epilepsy

Aims

Differentiating mesial temporal lobe epilepsy (MTLE) and neocortical temporal lobe epilepsy (NTLE) remains challenging. Our study characterized the metabolic profiles between MTLE and NTLE and their correlation with surgical prognosis using ¹⁸F-FDG-PET.

Methods

A total of 137 patients with intractable temporal lobe epilepsy (TLE) and 40 age-matched healthy controls were recruited. Patients were divided into the MTLE group (N = 91) and the NTLE group (N = 46). ¹⁸F-FDG-PET was used to measure the metabolism of regional cerebra, which was analyzed using statistical parametric mapping. The volume of abnormal metabolism in cerebral regions and their relationship with surgical prognosis were calculated for each surgical patient.

Results

The cerebral hypometabolism of MTLE was limited to the ipsilateral temporal and insular lobes (p < 0.001, uncorrected). The NTLE patients showed hypometabolism in the ipsilateral temporal, frontal, and parietal lobes (p < 0.001, uncorrected). The MTLE patients showed extensive hypermetabolism in cerebral regions (p < 0.001, uncorrected). Hypermetabolism in NTLE was limited to the contralateral temporal lobe and cerebellum, ipsilateral frontal lobe, occipital lobe, and bilateral thalamus (p < 0.001, uncorrected). Among patients who underwent resection of epileptic lesions, 51 (67.1%) patients in the MTLE group and 10 (43.5%) in the NTLE group achieved Engel class IA outcome (p = 0.041). The volumes of metabolic increase for the frontal lobe or thalamus in the MTLE group were larger in non-Engel class IA patients than Engel class IA patients (p < 0.05).

Conclusions

The spatial metabolic profile discriminated NTLE from MTLE. Hypermetabolism of the thalamus and frontal lobe in MTLE may facilitate preoperative counseling and surgical planning.     

颞叶癫痫放电在颅内外传播模式的研究

目的探索颞叶癫痫放电在颅内外的传播方式。方法对无法通过无创手段定侧、定位而高度怀疑为难治性颞叶癫痫的病人行双颞钻孔颅内电极植入术,同步记录10-20头皮脑电和双侧蝶骨电极。对最终确诊的颞叶癫痫病人,分析其同步记录脑电图,测量颅内癫痫起源传播到颅内外各个电极点的时间间隔。研究发作期放电的颅内外传播方式。结果颞下、海马、颞极和颞叶外侧各部位起源的癫痫在颅内外传播有各自的方式：①颞下→对侧海马或颞下→同侧蝶骨→对侧蝶骨→同侧前或中颞头皮→对侧前或中颞头皮;②海马→同侧蝶骨→对侧海马或颞下→对侧蝶骨→同侧前或中颞头皮→对侧前或中颞头皮;③颞极→对侧海马或颞下→同侧蝶骨→同侧前或中颞头皮→对侧蝶骨→对侧前或中颞头皮;④颞叶外侧→同侧中颞头皮→同侧蝶骨→对侧前颞或颞下→对侧蝶骨→对侧前或中颞头皮。结论了解各部位颞叶癫痫放电的颅内外传播顺序有助于癫痫灶的定侧、定位。     

Glucose and [11C]flumazenil positron emission tomography abnormalities of thalamic nuclei in temporal lobe epilepsy

OBJECTIVES: To analyze interictal patterns of thalamic nuclei glucose metabolism and benzodiazepine receptor binding in patients with medically intractable temporal lobe epilepsy (TLE) using high-resolution 2-deoxy-2-[18F]fluoro-D-glucose (FDG) and [11C]flumazenil (FMZ) PET. BACKGROUND: Structural and glucose metabolic abnormalities of the thalamus are considered important in the pathophysiology of TLE. The differential involvement of various thalamic nuclei in humans is not known. METHODS: Twelve patients with TLE underwent volumetric MRI, FDG and FMZ PET, and prolonged video-EEG monitoring. Normalized values and asymmetries of glucose metabolism and FMZ binding were obtained in three thalamic regions (dorsomedial nucleus [DMN], pulvinar, and lateral thalamus [LAT]) defined on MRI and copied to coregistered, partial-volume-corrected FDG and FMZ PET images. Hippocampal and amygdaloid FMZ binding asymmetries and thalamic volumes also were measured. RESULTS: The DMN showed significantly lower glucose metabolism and FMZ binding on the side of the epileptic focus. The LAT showed bilateral hypermetabolism and increased FMZ binding. There was a significant correlation between the FMZ binding asymmetries of the DMN and amygdala. The PET abnormalities were associated with a significant volume loss of the thalamus ipsilateral to the seizure focus. CONCLUSIONS: Decreased [11C]flumazenil (FMZ) binding and glucose metabolism of the dorsomedial nucleus (DMN) are common and have strong lateralization value for the seizure focus in human temporal lobe epilepsy. Decreased benzodiazepine receptor binding can be due to neuronal loss, as suggested by volume loss, but also may indicate impaired gamma-aminobutyric acid (GABA)ergic transmission in the DMN, which has strong reciprocal connections with other parts of the limbic system. Increased glucose metabolism and FMZ binding in the lateral thalamus could represent an upregulation of GABA-mediated inhibitory circuits.     

Identification of Frontal Lobe Epileptic Foci in Children Using Positron Emission Tomography

Summary: Purpose: Presurgical evaluation for intractable frontal lobe epilepsy (FLE) is difficult and invasive, partly because anatomic neuroimaging studies with computed tomography (CT) and magnetic resonance imaging (MRI) typically do not show a discrete lesion. In adult patients with FLE, functional neuroimaging of glucose metabolism with positron emission tomography (PET) is less sensitive in detecting focal metabolic abnormalities than in temporal lobe epilepsy (TLE). Comparable data on children with FLE are not available. Methods: We used high-resolution PET scanning of glucose metabolism to evaluate 13 children (age 17 months to 17 years; mean age 9.5 years) with intractable FLE being considered for surgical treatment. Only children with normal CT and MRI scans were included. Results: Hypometabolism including the frontal lobe was evident in 12 of the 13 children, was unilateral in 11 of 13, and was restricted to the frontal lobe in 8 of 13. One child showed bilateral frontal cortex hypometabolism and another had anictal PET scan demonstrating unilateral frontal cortex hyper-metabolism surrounded by hypometabolism. Additional hypo–metabolic areas outside the frontal cortex were observed in 5 children in parietal and/or temporal cortex. Localization of seizure onset on scalp EEG was available in 10 children and corresponded to the location of frontal lobe PET abnormality in 8. However, in 4 of the 10 children, the extent of hypometabolism exceeded the epileptogenic region indicated by ictal EEG. In 2 of the 13 children, the abnormality evident on EEG was more extensive than that evident on PET. In the remaining 3 children for whom only interictal EEG data were available, the PET foci did not correspond in location to the interictal EEG abnormalities. In 11 of the 13 children, the presumed region of seizure onset in the frontal lobe, as based on analysis of seizure semiology, corresponded to the locations of frontal lobe glucose metabolism abnormalities. Conclusions: Although high-resolution PET appears to be very sensitive in localizing frontal lobe glucose metabolic abnormalities in children with intractable FLE and normal CT/ MRI scans, the significance of extrafrontal metabolic disturbances requires further study; these may represent additional epileptogenic areas, effects of diaschisis, seizure propagation sites, or secondary epileptogenic foci.     

Depression in temporal lobe epilepsy surgery patients: an FDG-PET study

PURPOSE: Depression is common in temporal lobe epilepsy (TLE) and after temporal lobectomy, and its etiology is obscure. In nonepileptic depression (including depression associated with other neurologic disorders), a consistent PET imaging finding is frontal lobe hypometabolism. Many TLE patients have hypometabolism involving frontal regions. Thus in data available from routine clinical assessments in an epilepsy surgery unit, we tested the hypothesis that the pattern of hypometabolism, particularly in the frontal lobe, may be associated with the depression seen in patients with TLE and TLE surgery. METHODS: We studied 23 medically refractory TLE patients who underwent anterior temporal lobectomy and who had preoperative FDG-PET scanning. All patients had pre- and postoperative psychiatric assessment. By using statistical parametric mapping (SPM-99), patterns of hypometabolism were compared between patients who had a preoperative history of depression (n=9) versus those who did not (n=14) and between those in whom postoperative depression developed (n=13) versus those in whom it did not (n=10). A significant region of hypometabolism was set at p<0.001 for a cluster of >or=20 contiguous voxels. RESULTS: Patients with a history of depression at any time preoperatively showed focal hypometabolism in ipsilateral orbitofrontal cortex compared with those who did not (t=4.64; p<0.001). Patients in whom depression developed postoperatively also showed hypometabolism in the ipsilateral orbitofrontal region (t=5.10; p<0.001). CONCLUSIONS: Although this study is methodologically limited, and other explanations merit consideration, orbitofrontal cortex dysfunction, already implicated in the pathophysiology of nonepileptic depression, may also be relevant to the depression of TLE and temporal lobectomy.     

颞叶癫 的EEG和MR术前定位研究

目的：探讨 ＥＥＧ、ＭＲ对颞叶癫癎（ＴＬＥ）术前定位。方法：用 ＭＲ、ＥＥＧ对 ２０例 ＴＬＥ病例进行术前定位,与术中 ＥＥＧ和术后随访结果比较。结果：２０例病例中１７例依据ＭＲ及ＥＥＧ获得定位,主要在海马区域病变１２例,前颞叶５例．另３例ＭＲ检查正常,依据多次ＥＥＧ检查获得定位,随访疗效满意。结论：ＥＥＧ是诊断ＴＬＥ的重要手段,ＭＲ可对继发性ＴＬＥ作出正确诊断,ＭＲ对海马硬化检查可协助ＥＥＧ对ＴＬＥ定位诊断。     

Left thalamomegaly in a patient with partial epilepsy

Temporal lobe epilepsy (TLE) is associated with modification in thalamic structure and function. In particular, thalamic atrophy and hypometabolism can occur, affecting ipsilateral, contralateral thalami or both. We describe a 28-year-old epileptic woman, who presented peculiar neuroimaging findings, with enlargement of the thalamus contralateral to the epileptic focus. The patient was born from dystocic delivery, she presented partial motor seizures in the left side of the body, followed by generalisation, and the EEG showed a right temporal epileptic focus. Serial CT and MRI scan, performed along 11 years, showed a non-evolutive left thalamomegaly. 18-FDG PET showed reduced metabolic activity in the upper right temporal gyrus and in the ipsilateral thalamus. Thalamic asymmetry in our patient could be an occasional finding.     

Subcortical damage and cortical dysfunction in progressive supranuclear palsy demonstrated by positron emission tomography

Summary Regional cerebral glucose metabolism was studied in nine patients with progressive supranuclear palsy (PSP). (¹⁸F)-2-fluoro-2-deoxy-d-glucose (FDG) positron emission tomography (PET) revealed general cerebral hypometabolism in all PSP patients in comparison with an age-matched reference group. When comparing the degree of regional metabolic deterioration, a consistent pattern of the most affected brain regions became obvious: the strongest significant alteration of cerebral glucose metabolism was observed in subcortical regions, e.g. in caudate nucleus, lentiform nucleus and upper mid-brain, which showed nerve cell loss in previous pathological studies. Less severe, but still significant hypometabolism was observed in frontal cortex. This pattern of hypometabolism was distinctly different from that typically seen in dementias of Alzheimer's type. The present data show that PET findings agree with histopathological studies: PSP is a primarily subcortical disease with secondary inactivation of cortical, especially of frontal brain regions.     

Regional weight loss of the cerebral cortex and some subcortical nuclei in senile dementia of the Alzheimer type

Summary All the cerebral cortex and some subcortical nuclei from six examples of senile dementia of the Alzheimer type (SDAT) and six age- and sex-matched controls have been dissected and weighed. The weight of the parietal and temporal cortex are significantly reduced. The parietal lobe shows the largest weight loss and this is most obvious in the precuneus and the superior lobule. The posterior cingulate, the middle and superior temporal, the supramarginal and the superior frontal gyri also show significant weight reduction. Weight loss of the amygdala is more than that of the hippocampus, the caudate nucleus and the putamen, but the weights of all are reduced significantyl. These results are rather unexpected but are consistent with other data (e.g. the clinical parietal lobe syndrome and focus of glucose hypometabolism in Alzheimer's disease). They indicate that prominent changes occur in SDAT in the association areas of the parietal lobe as well as in the amygdala.Supported by The Brain Research Trust