Reduced variance in monozygous twins for multiple MR parameters: implications for disease studies and the genetic basis of brain structure.

Twin studies offer the opportunity to determine the relative contribution of genes versus environment in traits of interest. Here, we investigate the extent to which variance in brain structure is reduced in monozygous twins with identical genetic make-up. We investigate whether using twins as compared to a control population reduces variability in a number of common magnetic resonance (MR) structural measures, and we investigate the location of areas under major genetic influences. This is fundamental to understanding the benefit of using twins in studies where structure is the phenotype of interest. Twenty-three pairs of healthy MZ twins were compared to matched control pairs. Volume, T2 and diffusion MR imaging were performed as well as spectroscopy (MRS). Images were compared using (i) global measures of standard deviation and effect size, (ii) voxel-based analysis of similarity and (iii) intra-pair correlation. Global measures indicated a consistent increase in structural similarity in twins. The voxel-based and correlation analyses indicated a widespread pattern of increased similarity in twin pairs, particularly in frontal and temporal regions. The areas of increased similarity were most widespread for the diffusion trace and least widespread for T2. MRS showed consistent reduction in metabolite variation that was significant in the temporal lobe N-acetylaspartate (NAA). This study has shown the distribution and magnitude of reduced variability in brain volume, diffusion, T2 and metabolites in twins. The data suggest that evaluation of twins discordant for disease is indeed a valid way to attribute genetic or environmental influences to observed abnormalities in patients since evidence is provided for the underlying assumption of decreased variability in twins.

Temporal lobe epilepsy and GEFS+ phenotypes associated with SCN1B mutations.

SCN1B, the gene encoding the sodium channel beta 1 subunit, was the first gene identified for generalized epilepsy with febrile seizures plus (GEFS+). Only three families have been published with SCN1B mutations. Here, we present four new families with SCN1B mutations and characterize the associated phenotypes. Analysis of SCN1B was performed on 402 individuals with various epilepsy syndromes. Four probands with missense mutations were identified. Detailed electroclinical phenotyping was performed on all available affected family members including quantitative MR imaging in those with temporal lobe epilepsy (TLE). Two new families with the original C121W SCN1B mutation were identified; novel mutations R85C and R85H were each found in one family. The following phenotypes occurred in the six families with SCN1B missense mutations: 22 febrile seizures, 20 febrile seizures plus, five TLE, three other GEFS+ phenotypes, two unclassified and ten unaffected individuals. All individuals with confirmed TLE had the C121W mutation; two underwent temporal lobectomy (one with hippocampal sclerosis and one without) and both are seizure free. We confirm the role of SCN1B in GEFS+ and show that the GEFS+ spectrum may include TLE alone. TLE with an SCN1B mutation is not a contraindication to epilepsy surgery.

Major depression in temporal lobe epilepsy with hippocampal sclerosis: clinical and imaging correlates.

PURPOSE: Refractory temporal lobe epilepsy (TLE) is often associated with hippocampal sclerosis (HS). Patients with major depression (MD) may also show structural abnormalities in the limbic system. Co-occurrence of TLE with HS and MD is not uncommon. We have investigated the clinical and morphological characteristics of TLE patients in relation to MD. METHODS: 34 TLE patients with HS were assessed at a Comprehensive Epilepsy Programme. All relevant clinical data were obtained, including the history of antecedent events to epilepsy. MD was diagnosed based on detailed psychiatric investigation. MRI was used to measure the volume and tissue signal (T2 relaxometry) of the hippocampus and amygdala. The imaging data were expressed as a percentage of the values obtained in a series of 55 controls. RESULTS: A history of MD was present in 15 (44%) of 34 patients. Patients with MD had a longer duration of their epilepsy (p<0.05) and a lower frequency of antecedent events (13% with MD, 58% without MD, p<0.05). Both groups had a similar degree of ipsilateral HS (small hippocampal volume, increased hippocampal T2 relaxation time) and demonstrated bilateral amygdaloid atrophy. However, the contralateral amygdala showed lower signal in the presence of MD (97 (9) ms; no MD 103 (8) ms; ANCOVA, p = 0.02). CONCLUSION: The integrity of the amygdala may influence mood disturbances in TLE patients with HS, as depression was associated with a relative preservation of the contralateral amygdala. In contrast, hippocampal abnormalities were not related to the presence of depression.

Functional MRI of the pre-ictal state.

The mechanisms underlying the transition from interictal to ictal states are poorly understood. Non-linear mathematical analysis of EEG frequency components has confirmed the presence of a pre-ictal state in focal epilepsy. We report on functional MRI (fMRI) analysis of the pre-ictal state in three patients with intractable focal epilepsy. Each subject had a typical partial seizure in the scanner while continuous blood oxygen level dependent (BOLD) fMRI images were acquired. The pre-ictal BOLD changes were first analysed by statistically comparing BOLD signals of two one-minute blocks. Further examination of the full time course was then performed. Each patient showed highly significant, focal BOLD signal changes. In Patient 1, a striking pre-ictal BOLD signal increase was seen over the region of the seizure focus identified on complementary epilepsy investigations. No significant BOLD signal decreases were observed. Patient 2 showed widespread pre-ictal BOLD increase contralateral to the presumed seizure focus, as well as a focal BOLD decrease near the presumed seizure focus. In Patient 3, pre-ictal BOLD increase was co-localized with the site of hyperperfusion seen on ictal single photon emission computed tomography (SPECT). However, this was contralateral to the seizure focus localization based on seizure symptomatology. No significant BOLD decreases were seen. The time course data in each patient studied showed change of the BOLD signal several minutes before the onset of the seizure. Highly significant BOLD fMRI signal changes occur before the onset of seizures, supporting the presence of a pre-ictal state. These changes can be localized to the site of the presumed seizure focus, as well as to other brain regions, suggesting that the pre-ictal BOLD signal changes and their underlying mechanisms are complex.

Physiologic variability of single-voxel proton MR spectroscopic measurements at 3T.

BACKGROUND AND PURPOSE: Physiologic and scanner variability of proton MR spectroscopy (MRS) measurements can limit the detection of subtle metabolite fluctuations. We assessed the variability of such measurements at 3T and compared two methods to obtain absolute concentrations. METHODS: Variability over 14 days was assessed with short-echo, single-voxel proton MRS in 14 control subjects and in a phantom containing 50 mmol/L N-acetylaspartate (NAA). Spectra were analyzed by using LCModel, scaling factors determined with both the calibration phantom (CP), and water peak intensity (WP) methods. Relative (reflecting the systematic drift) and absolute variability (reflecting the magnitude of scanner variability) was determined. RESULTS: For the phantom, initial (49 +/- 1.7 mmol/L) and second measurements (50 +/- 1.6 mmol/L) showed similar results, with small variability (relative, -0.6 +/- 1.5 mmol/L; absolute, 1.1 +/- 1.1 mmol/L). Control subjects had no systematic difference between the two scans for any measurement. Absolute variabilities in the temporal lobe for total NAA (NAA+NAAG) were 13% (CP) and 11% (WP). The largest variability (29%) was found for glutamate-glutamine (29%) with the CP method, and for myo-inositol with the WP method (28%). Absolute variability was smaller for the frontal lobe measurements (total NAA 7% and overall 6-18% for CP; total NAA 6% and overall 5-19% for WP). No significant difference was observed between the two methods. CONCLUSION: Physiologic variability is the major source of measurement variability and accounts for 12% of the variability in temporal lobe total NAA. Therefore, total NAA variations must clearly exceed this before they can reliably be attributed to an effect of disease.

Temporal lobectomy: long-term seizure outcome, late recurrence and risks for seizure recurrence.

There is little information available relevant to long-term seizure outcome after anterior temporal lobectomy, particularly at extended postoperative periods. The aim of this study was an in-depth examination of patterns of longitudinal outcome and potential risk factors for seizure recurrence after lobectomy, utilizing a large patient sample with long follow-up. Included were 325 patients who underwent anterior temporal lobectomy between 1978 and 1998 (mean follow-up 9.6 +/- 4.2 years). Retrospective data were analysed using survival analysis and multivariate regression with Cox proportional hazard models. The probability of complete seizure freedom at 2 years post-surgery was 55.3% [95% confidence interval (CI) 50-61]; at 5 years, 47.7% (95% CI 42-53); and at 10 postoperative years it was 41% (95% CI 36-48). Patients with discrete abnormalities preoperatively (i.e. lesions and hippocampal sclerosis) had a significantly higher probability of seizure freedom than patients without obvious abnormality. The latter group had a pattern of recurrence similar to that in patients with lesions outside the area of excision. After adjustment for preoperative pathology, only the presence of preoperative secondarily generalized seizures had a significant association with recurrence [occasional preoperative generalized seizures, hazard ratio (HR) 1.6, 95% CI 1.1-2.3; frequent seizures, HR 2.0, 95% CI 1.4-2.9 compared with absence of preoperative generalized seizures]. Duration of preoperative epilepsy, age of seizure onset and age at surgery did not have an effect on outcome. Patients with two seizure-free postoperative years had a 74% (95% CI 66-81) probability of seizure freedom by 10 postoperative years. This late seizure recurrence was not associated with any identified risk factors. Specifically, patients with hippocampal sclerosis were not at higher risk. Surprisingly, complete discontinuation of anti-epileptic drugs (AEDs) after two postoperative years was not associated with an increased risk of recurrence (HR 1.03, 95% CI 0.5-2.1). This may be because selection of patients for AED discontinuation is biased towards those individuals perceived as 'low risk'. The results of this study indicate that the lack of an obvious abnormality or the presence of diffuse pathology, and preoperative secondarily generalized seizures are risk factors for recurrence after surgery. Late recurrence after initial seizure freedom is not a rare event; risk factors specific to this phenomenon are as yet unidentified.

Hippocampal pathology in refractory temporal lobe epilepsy: T2-weighted signal change reflects dentate gliosis.

BACKGROUND: The MR and pathologic features of hippocampal sclerosis (HS) are well described and include volume decrease and T2-weighted signal increase for MRI, and neuron cell loss and gliosis for pathology. OBJECTIVE: To confirm the established correlation between hippocampal volumes and neuron cell counts, and to study the still controversial association between signal change and gliosis. METHODS: The authors studied 44 patients (22 men and 22 women; mean age at surgery, 37 years) with refractory temporal lobe epilepsy. Quantitative assessment of hippocampal volumes and T2 relaxometry, and neuron and glial cell count in the region CA1 and molecular layer of the dentate gyrus was performed. The proportion of glial fibrillary acidic protein (GFAP)-positive glial cells (reactive astrocytes) was indicated. RESULTS: In a stepwise regression, the ipsilateral hippocampal volume was predicted best by the neuron cell count in the dentate gyrus (p = 0.005, r = 0.4). Hippocampal T2 time, however, was predicted best by the glial cell count in the dentate gyrus (p = 0.01, r = 0.4). None of the other cell counts contributed to either model. In the dentate, 31% of the glial cells were reactive astrocytes, whereas in CA1, 5% were reactive. CONCLUSION: The results confirmed the correlation between hippocampal volumes and neuron cell counts. T2-weighted signal increase in the hippocampus was mainly influenced by gliosis in the dentate gyrus, where a high proportion of glial cells show abnormal activity. This activity may reflect changes important in the development of hippocampal epileptogenicity.

Increased anterior temporal lobe T2 times in cases of hippocampal sclerosis: a multi-echo T2 relaxometry study at 3 T.

BACKGROUND AND PURPOSE: Increased T2 relaxation times in the ipsilateral hippocampus are present in patients with hippocampal sclerosis. Visual assessment of T2-weighted images of these patients suggests increased signal intensity in the anterior temporal lobe as well. Our aim was to assess hippocampal and anterior temporal T2 relaxation times in patients with partial epilepsy by using a new T2-relaxometry sequence implemented by using a 3-T General Electric imaging unit. METHODS: Coronal view T2 maps were generated by using an eight-echo Carr-Purcell-Meiboom-Gill sequence (TE, 28-231) with an acquisition time of 7 min on a 3-T General Electric Signa Horizon LX imaging unit. T2 relaxation times were measured in the hippocampus and anterior temporal lobe of 30 healthy control volunteers and 20 patients with partial epilepsy. RESULTS: For the 30 control volunteers, the mean hippocampal T2 relaxation time was 98 +/- 2.8 ms. In all measured areas, the asymmetry index was small (<0.01). For the 15 patients with independent evidence of hippocampal sclerosis established by visual, volumetric, and, when available, pathologic criteria, mean hippocampal T2 relaxation times were 118 +/- 7 ms (P <.0001) on the ipsilateral side and 101 +/- 4 ms (P =.005) on the contralateral side. The T2 values were also increased in the anterior temporal lobe (ipsilateral: 82 +/- 6 ms, P <.0001; contralateral: 79 +/- 6 ms, P =.01) as compared with the values for the control volunteers (75 +/- 3 ms). The five patients with focal cortical dysplasia had hippocampal T2 relaxation times that were not different from control values. CONCLUSION: T2 relaxometry at 3 T is feasible and useful and confirmed marked ipsilateral hippocampal signal intensity increase in patients with hippocampal sclerosis. Importantly, definite signal intensity change was also present in the anterior temporal lobe. T2 relaxometry is a sensitive means of identifying abnormalities in the hippocampus and other brain structures.

A high-field functional MRI study of quadri-lingual subjects.

We assessed six multilingual subjects by functional MRI using a Noun Verb Generation task in four different languages. We hypothesised that the degree of proficiency in each language would be related to the extent of functional activity measured in a region of interest analysis. Proficiency in each language was quantified using two neuropsychological tests. All four languages activated overlapping brain areas, corresponding to the major language regions. The number of activated voxels correlated with proficiency, so that the activated volume increased for languages in which a subject had poorer proficiency. Activation did not appear to be dependent on the age at which the language was learnt.

MR imaging of epilepsy: state of the art at 1.5 T and potential of 3 T.

Shortly after being introduced in the nineteen eighties, magnetic resonance imaging (MRI) became a key tool for the investigation of patients with epilepsy, due to its ability to acquire high quality images. The strength of the magnetic field of a scanner is measured in tesla (T). This review addresses the clinical and research potential in epilepsy of MR imaging at 1.5 T and 3 T. A typical clinical scanning protocol at 1.5 T for a patient with refractory epilepsy may include T1- and T2-weighted imaging, fluid-attenuated inversion recovery (FLAIR) imaging, and a 3D volume acquisition sequence. A research protocol may add quantification of structural imaging, such as volumetric assessment and T2-relaxometry, together with functional measures, such as MR-spectroscopy, functional MRI and diffusion weighted sequences. MR-spectroscopy assesses the metabolites of the seizure focus and other brain areas. Functional MRI allows localisation of cognitive and sensori-motor function and the ability to assess the spatial relationship of these functions to the seizure focus. Whereas these techniques can be performed at 1.5 T, particularly MR-spectroscopy and functional MRI benefit from increased magnetic field-strength. Higher magnetic field-strength is associated with a higher signal-to-noise ratio (SNR). The increased SNR can allow shorter imaging times for a given resolution, higher resolution for a given imaging time, or combination of both. The use of higher magnetic field-strengths is therefore indicated for the (fast) imaging of ill subjects, for long protocols, including structural, metabolic and functional imaging, and for novel applications, such as continuous EEG recording and functional MRI for the detection of the seizure focus. Disadvantages of MR imaging in epilepsy at a high field-strength of 3 T and above are, apart from engineering and technical challenges, the greater energy deposition into tissue and increased susceptibility to artefacts. So far, magnets of 3 T and above have been used mainly for research applications, however the benefits of high field-strength for MR spectroscopy and functional MRI, and the usefulness of these techniques for the investigation of epilepsy patients are obvious incentives for the use of 3 T systems in routine clinical investigations.

Temporal lobe dysembryoplastic neuroepithelial tumour: significance of discordant interictal spikes.

PURPOSE: Dysembryoplastic neuroepithelial tumours (DNET) are an important cause of refractory partial epilepsies. They usually occur within dysplastic cortex and tend to affect the temporal lobes. The EEG of these patients is characterised by slowing and/or epileptiform abnormalities with a multifocal distribution. We studied the EEG features of epilepsy patients with a temporal lobe DNET to assess the relationship of EEG abnormalities with the localisation of the tumour and the clinical features. METHODS: We retrospectively reviewed 16 patients with unilateral, temporal lobe DNET on MRI. The EEG abnormalities were classified as concordant to the lesion when the EEG discharges were confined to the ipsilateral temporal lobe or discordant when EEG discharges were found in other areas. Clinical and epilepsy characteristics were compared between patients with concordant and discordant EEG. RESULTS: Focal EEG abnormalities were found in 81% of the patients; 6/16 patients had concordant EEG abnormalities, and 7/16 patients had discordant EEG abnormalities. Epilepsy severity prior to the operation, antecedents and post-operative outcome were not different between patients with concordant or discordant EEG abnormalities. CONCLUSION: Patients with temporal lobe DNET often show EEG discharges discordant to the tumour. However, they do not appear to predict the clinical and epilepsy characteristics of these patients.

Composite voxel-based analysis of volume and T2 relaxometry in temporal lobe epilepsy.

Voxel-based analyses of tissue characteristics such as volume and T2 are usually carried out in isolation. However, as the images are analysed in a common voxel-based framework, it is possible to directly assess the spatial relationships of abnormalities detected by each technique. We utilize this approach in well-characterized patients with unilateral temporal lobe epilepsy (TLE) with hippocampal sclerosis (HS). TLE is associated with potentially widespread volume and T2 signal abnormalities in MRI images but the relationship between these two aspects of tissue abnormality is not well understood. Here we use a novel approach of combined univariate and multivariate voxel-wise analysis to investigate the spatial relationship of these abnormalities. We studied 19 TLE patients and compared them to 115 control subjects. Grey matter (GM) and white matter (WM) volume changes were assessed with voxel-based morphometry (VBM), and changes in T2 relaxation times were evaluated with voxel-based relaxometry (VBR). The volume and T2 changes obtained using the combined univariate approach were found in an extensive area, prominently in the ipsilateral hippocampus and amygdala (overlap of GM-VBM and VBR), and in the remaining temporal lobe (overlap of WM-VBR and VBR). Other cortical and subcortical areas showed isolated volume or T2 changes. The multivariate analysis based on the Hotelling T(2) statistic, indicated a similar pattern of distributed changes across the brain but with a greater degree of statistical significance in certain areas. The composite analyses appear to identify a network of affected areas not as easily appreciated by the individual analysis of volume or T2 changes.

Selection of the control group for VBM analysis: influence of covariates, matching and sample size.

Variability in the control group plays a crucial role in voxel-based morphometry (VBM) detection of structural abnormalities. Two common methods of minimising this variance are inclusion of covariates and matching of control and patient groups. We address two major questions: What are the optimal covariates in the VBM design? When a large pool of controls are available, is it better to choose a subset of matched control subjects at the expense of numbers, or include all available controls? We used regression analysis in a group of 176 controls to determine the contribution of gender, age, and total intracranial volume (TIV) to volume variation. We then used different matching and covariate strategies to determine the optimal design for VBM detection of abnormality in epilepsy patients with hippocampal sclerosis. In the regression analysis, focal gender effects disappeared with inclusion of TIV as an additional regressor. Age had a small but unique contribution to focal volume changes. In the VBM analysis of HS patients, detection of abnormalities was strongly influenced by choice of covariates. The optimal combination was different for grey and white matter (for grey matter: TIV; for temporal lobe white matter: TIV, age and gender). A control group size of 70-90 subjects allowed optimal detection of volume loss in the hippocampus and thalamus. At these group sizes, matched control groups did not consistently prove superior to deliberately "unmatched" groups of the same size. The optimal detection of volume loss was obtained with all available control subjects.

Differential contributions of the hippocampus and rhinal cortices to verbal memory in epilepsy.

The present study explored the left mesial temporal lobe correlates of verbal memory in patients with temporal lobe epilepsy (TLE). An index of structural integrity, T2 relaxation time, was measured bilaterally in three mesial temporal regions of interest, and correlated with measures of verbal memory. The acquisition of verbal arbitrary relational material was most strongly associated with left perirhinal T2 signal. In contrast, verbal memory consolidation was related to T2 signal in the left hippocampus. Our findings suggest a key role for the left perirhinal region in the uptake of arbitrary linkages that underlie new learning. The hippocampus, on the other hand, is important for protecting newly learned information from the effects of interference. This double dissociation provides a neurocognitive account of the left mesial temporal memory syndrome.

Hippocampal sclerosis: MR prediction of seizure intractability.

PURPOSE: Patients with refractory temporal lobe epilepsy (refractory TLE) often have hippocampal sclerosis (HS). However, some HS patients have less-severe, drug-responsive epilepsy (mild TLE). We investigated the pattern of MR changes in these two HS groups. METHODS: We acquired a 3D volumetric sequence, T(2) relaxation times (T2) and proton MR spectroscopy (MRS) in 41 HS patients (24 refractory TLE, 17 mild TLE) and 60 controls. Hippocampal volumes were measured bilaterally. T2 was measured in the hippocampus, amygdala, thalamus, in the white matter of the anterior temporal lobe (ATL), and in the frontal lobe. The temporal lobe MRS established concentrations of N-acetylaspartate (NAA), choline, creatine, myoinositol and glutamine/glutamate. RESULTS: The degree of hippocampal volume loss and hippocampal T2 increase was not different between the two HS groups. However, in refractory TLE, the T2 signal in the ipsilateral ATL was increased, and the ipsilateral NAA concentration was reduced (p < or = 0.05). CONCLUSIONS: In this group of HS patients, the degree of HS was not related to the clinical course, possibly reflecting the common cause of epilepsy. In contrast, refractory TLE patients had pronounced white matter changes and metabolite disturbance in the ipsilateral temporal lobe. These abnormalities may indicate the refractory nature of the epilepsy.

Functional connectivity networks are disrupted in left temporal lobe epilepsy.

OBJECTIVE: Functional connectivity maps the distributed network of brain regions fluctuating synchronously during a continuous brain state. This study sought to investigate whether patients with left temporal lobe epilepsy (TLE) differ from controls in their resting-state functional connectivity between typical language regions. METHODS: We studied 17 patients with left TLE, together with eight healthy controls, using seeded functional connectivity. Seed regions were defined using the regions of maximal activation and deactivation during a language functional magnetic resonance imaging (fMRI) task in a separate cohort of 30 controls. RESULTS: Language fMRI produced the expected activation pattern, which was not different between patients and controls. However, functional connectivity between language areas during rest was markedly different; whereas controls showed connectivity between each of the seed areas and the majority of the language areas, patients showed connectivity only with a few areas, particularly the seed area itself. This difference was significant in the direct comparison of patients and control connectivity maps. INTERPRETATION: We suggest that this reduced connectivity in left temporal lobe epilepsy may reflect a disturbance of the language network during resting state in patients and may be related to subtle language difficulties in this patient population.

Thalamic atrophy in childhood absence epilepsy.

PURPOSE: Patients with childhood absence epilepsy (CAE) have normal clinical magnetic resonance imaging (MRI) studies. The presence of abnormalities in corticothalamic networks has been suggested to be the functional basis of absence seizure generation. We assessed whether structural grey and white matter volume changes of these areas occurred in patients with absence seizures by using optimized voxel-based morphometry (VBM). METHODS: We recruited 13 patients with a clinical and EEG diagnosis of CAE (mean age at examination, 17 +/- 8 years) and compared them with a consecutive series of 109 controls (mean age, 29 +/- 9 years). The 3 tesla MRI examination included a 3D T(1)-weighted sequence, which was analyzed with an optimized VBM protocol using the SPM2 package. The threshold was set at p < 0.05, corrected for multiple comparisons. RESULTS: Compared with controls, CAE patients showed areas of grey matter decrease in both thalami and in the subcallosal gyrus. White matter decrease was found in the extranuclear subcortical area and in the white matter of the basal forebrain. Grey and white matter increase was restricted to small clusters of cortical and subcortical areas. CONCLUSIONS: Evidence exists of subcortical grey and white matter volume reduction in CAE patients. Bilateral thalamic atrophy may be either a result of damage from seizures (as in hippocampal sclerosis) or a reflection of a primary underlying pathology as the cause of absence seizures.

Optimized clinical T2 relaxometry with a standard CPMG sequence.

PURPOSE: To optimize the accuracy and precision of T2 measurements using the standard Carr-Purcell-Meiboom-Gill (CPMG) sequence. T2 values obtained with this technique are normally sensitive to imperfect refocusing due to the formation of unwanted stimulated echoes. MATERIALS AND METHODS: Modifications are made to the refocusing slice selection width and the interleaving scheme. A widened refocusing slice improves the uniformity of the refocusing flip angle across the slice. A slow spin echo acquisition provided "gold standard" T2 values. Repeated T2 measurements in phantom and human studies are used to compare the accuracy and precision of the optimized and non-optimized CPMG implementations. RESULTS: The required slice thickness ratio between refocusing and excitation slice widths is found to be 3:1 for typical optimized radiofrequency pulses. T2 values obtained using this optimized implementation more closely correspond to "gold standard" values. Repeated T2 measurements indicate significantly improved correspondence between data and model. A reduction in the fitting error of approximately 70% is demonstrated for phantoms. CONCLUSION: We demonstrate that a relatively simple change to the CPMG relaxometry sequence parameters from the default setup yields significant improvements in the accuracy and precision of T2 measurements.

Is language lateralization in temporal lobe epilepsy patients related to the nature of the epileptogenic lesion?

PURPOSE: Early acquired lesions are considered to be a risk factor for atypical language lateralization in epilepsy, whereas developmental lesions are not. Hippocampal sclerosis (HS) can be understood as an early, acquired lesion, whereas developmental tumors (DT) are thought to originate in utero. We assessed whether language lateralization differs between these groups of temporal lobe epilepsy patients. METHODS: We used 3-Tesla functional MRI (fMRI) to assess 41 patients (16 DT, 25 HS) and 50 controls, performing a noun-verb-generation task. fMRI data were processed by using SPM2. A laterality index (LI) was calculated based on the number of activated voxels in left- and right-sided frontal lobe language areas. Atypical lateralization was considered if the index was < or = 0.2. RESULTS: Patients had a lower LI (0.42 +/- 0.5) than controls (0.6 +/- 0.3; p < or = 0.05), but the LI was not different between DT (0.44 +/- 0.5) and HS patients (0.43 +/- 0.4; p = 0.9). The frequency of atypical lateralization was increased in patients (27%) compared with controls (8%) but was similar in both patient groups (DT, 31%; HS, 24%). HS patients had an earlier onset and longer duration of epilepsy and a higher frequency of significant antecedent events (p < or = 0.05). CONCLUSIONS: Patients with TLE demonstrate a deviation toward atypical language lateralization. However, language lateralization was not different between patients with presumably acquired lesions compared with patients with developmental pathology. This suggests that the nature of the temporal lobe lesion does not influence overall language lateralization.

Seizure-associated abnormalities in epilepsy: evidence from MR imaging.

Acute seizure-associated changes have been described in the animal and human literature. Controversy exists over whether seizures cause permanent damage to the brain, and whether a (prolonged) seizure can induce changes that lead to an epileptic lesion, resulting in habitual seizures and epilepsy. Current magnetic resonance imaging (MRI) offers a variety of imaging tools and is capable of detecting acute seizure-associated changes. In contrast to the histologic examination, serial MRI studies are possible and allow longitudinal observation of the fate of these changes. This report reviews the literature on acute seizure-associated effects emphasizing the MRI evidence.