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Aims\ud The causes of distinct patterns of reduced cortical thickness in the common human epilepsies, detectable on neuroimaging and with important clinical consequences, are unknown. We investigated the underlying mechanisms of cortical thinning using a systems-level analysis.\ud \ud Methods\ud Imaging-based cortical structural maps from a large-scale epilepsy neuroimaging study were overlaid with highly spatially resolved human brain gene expression data from the Allen Human Brain Atlas. Cell-type deconvolution, differential expression analysis and cell-type enrichment analyses were used to identify differences in cell-type distribution. These differences were followed up in post-mortem brain tissue from humans with epilepsy using Iba1 immunolabelling. Furthermore, to investigate a causal effect in cortical thinning, cell-type-specific depletion was used in a murine model of acquired epilepsy.\ud \ud Results\ud We identified elevated fractions of microglia and endothelial cells in regions of reduced cortical thickness. Differentially expressed genes showed enrichment for microglial markers and, in particular, activated microglial states. Analysis of post-mortem brain tissue from humans with epilepsy confirmed excess activated microglia. In the murine model, transient depletion of activated microglia during the early phase of the disease development prevented cortical thinning and neuronal cell loss in the temporal cortex. Although the development of chronic seizures was unaffected, the epileptic mice with early depletion of activated microglia did not develop deficits in a non-spatial memory test seen in epileptic mice not depleted of microglia.\ud \ud Conclusions\ud These convergent data strongly implicate activated microglia in cortical thinning, representing a new dimension for concern and disease modification in the epilepsies, potentially distinct from seizure control.

Summary Objective Although altered large-scale brain network organization in patients with temporal lobe epilepsy (TLE) has been shown using morphologic measurements such as cortical thickness, these studies, have not included critical subcortical structures (such as hippocampus and amygdala) and have had relatively small sample sizes. Here, we investigated differences in topological organization of the brain volumetric networks between patients with right TLE (RTLE) and left TLE (LTLE) with unilateral hippocampal atrophy. Methods We performed a cross-sectional analysis of 86 LTLE patients, 70 RTLE patients, and 116 controls. RTLE and LTLE groups were balanced for gender (p = 0.64), seizure frequency (Mann-Whitney U test, p = 0.94), age (p = 0.39), age of seizure onset (p = 0.21), and duration of disease (p = 0.69). Brain networks were constructed by thresholding correlation matrices of volumes from 80 cortical/subcortical regions (parcellated with Freesurfer v5.3 https://surfer.nmr.mgh.harvard.edu/) that were then analyzed using graph theoretical approaches. Results We identified reduced cortical/subcortical connectivity including bilateral hippocampus in both TLE groups, with the most significant interregional correlation increases occurring within the limbic system in LTLE and contralateral hemisphere in RTLE. Both TLE groups demonstrated less optimal topological organization, with decreased global efficiency and increased local efficiency and clustering coefficient. LTLE also displayed a more pronounced network disruption. Contrary to controls, hub nodes in both TLE groups were not distributed across whole brain, but rather found primarily in the paralimbic/limbic and temporal association cortices. Regions with increased centrality were concentrated in occipital lobes for LTLE and contralateral limbic/temporal areas for RTLE. Significance These findings provide first evidence of altered topological organization of the whole brain volumetric network in TLE, with disruption of the coordinated patterns of cortical/subcortical morphology.

We propose an automatic 3D medical image registration method that combines the watershed transform from greyscale marker, to effectively reduce the number of key points needed for registration, with a robust optimisation algorithm, called multi-scale parameter search (MSPS), to quickly estimate the mapping function. We evaluate it for rigid and intra-subject registration of pre- and post-surgery MR-T1 images of the brain. The visual analysis of its effectiveness is facilitated by a colour-coding scheme. Extensive experiments show that our approach is very accurate, robust to noise and provides 3D registration in less than 40 s, with no multi-resolution image schemes needed. We also evaluate MSPS on a testbed of 12 optimisation benchmark problems, in comparison with well-known optimisers, such as particle swarm optimiser, simulated annealing and differential evolution, showing that it can also be explored in other applications.

Objective Patients with mesial temporal lobe epilepsy (MTLE) may present unstable pattern of seizures. We aimed to evaluate the occurrence of relapse-remitting seizures in MTLE with (MTLE-HS) and without (MTLE-NL) hippocampal sclerosis. Method We evaluated 172 patients with MTLE-HS (122) or MTLE-NL (50). Relapse-remitting pattern was defined as periods longer than two years of seizure-freedom intercalated with seizure recurrence. “Infrequent seizures” was considered as up to three seizures per year and “frequent seizures” as any period of seizures higher than that. Results Thirty-seven (30%) MTLE-HS and 18 (36%) MTLE-NL patients had relapse-remitting pattern (X2, p = 0.470). This was more common in those with infrequent seizures (X2, p < 0.001). Twelve MTLE-HS and one MTLE-NL patients had prolonged seizure remission between the first and second decade of life (X2, p = 0.06). Conclusion Similar proportion of MTLE-HS or MTLE-NL patients present relapse-remitting seizures and this occurs more often in those with infrequent seizures. Objetivo Pacientes com epilepsia do lobo temporal mesial (ELTM) podem apresentar padrão instável de crises epilépticas. Nosso objetivo foi avaliar ocorrência de crises remitente-recorrentes em ELTM com (ELTM-EH) e sem (ELTM-NL) esclerose hipocampal. Método Avaliamos 172 pacientes com ELTM-EH (122) ou ELTM-NL (50). Padrão remitente-recorrente foi definido como períodos superiores a dois anos de remissão intercalados com recorrência de crises. Até três crises por ano foram consideradas como "infrequentes" e qualquer período com frequência maior como "frequentes". Resultados Trinta e sete (30%) pacientes com ELTM-EH e 18 (36%) com ELTM-NL apresentaram crises remitente-recorrentes (X2, p = 0,470), mais comum naqueles com crises infrequentes (X2, p < 0,001). Doze pacientes com ELTM-EH e um ELTM-NL apresentaram remissão prolongada de crises entre a primeira e a segunda década de vida (X2, p = 0,06). Conclusão Proporção semelhante de pacientes com ELTM-EH e ELTM-NL apresentam crises remitente-recorrentes e isso ocorre com maior frequência em pacientes com crises esporádicas.

Machado-Joseph disease (SCA3) is the most frequent spinocerebellar ataxia worldwide and characterized by remarkable phenotypic heterogeneity. MRI-based studies in SCA3 focused in the cerebellum and connections, but little is known about cord damage in the disease and its clinical relevance. To evaluate the spinal cord damage in SCA3 through quantitative analysis of MRI scans. A group of 48 patients with SCA3 and 48 age and gender-matched healthy controls underwent MRI on a 3T scanner. We used T1-weighted 3D images to estimate the cervical spinal cord area (CA) and eccentricity (CE) at three C2/C3 levels based on a semi-automatic image segmentation protocol. The scale for assessment and rating of ataxia (SARA) was employed to quantify disease severity. The two groups-SCA3 and controls-were significantly different regarding CA (49.5 ± 7.3 vs 67.2 ± 6.3 mm(2), p 0.001) and CE values (0.79 ± 0.06 vs 0.75 ± 0.05, p = 0.005). In addition, CA presented a significant correlation with SARA scores in the patient group (p = 0.010). CE was not associated with SARA scores (p = 0.857). In the multiple variable regression, we found that disease duration was the only variable associated with CA (coefficient = -0.629, p = 0.025). SCA3 is characterized by cervical cord atrophy and antero-posterior flattening. In addition, the spinal cord areas did correlate with disease severity. This suggests that quantitative analyses of the spinal cord MRI might be a useful biomarker in SCA3.

Summary Objective To investigate the effect of seizure frequency on memory, we performed a cross sectional study comparing mesial temporal lobe epilepsy (MTLE) patients with frequent and infrequent seizures. Methods We performed magnetic resonance imaging (MRI) hippocampal volume (HV) measurements and neuropsychological assessment in 22 patients with frequent seizures (at least one dyscognitive seizure [DS] per month) that were refractory to antiepileptic drugs and 20 patients with infrequent seizures (three or less DS per year and no event evolving to a bilateral convulsive seizure), all with MRI signs of hippocampal sclerosis (HS) on visual analysis. We also included 29 controls for comparison of volumetric data. Results There was no difference in memory performance between patients with frequent seizures and infrequent seizures. We observed a significant bilateral reduction of HV in patients with MTLE when compared to controls (p

Our objective was to investigate spinal cord (SC) atrophy in amyotrophic lateral sclerosis (ALS) patients, and to determine whether it correlates with clinical parameters. Forty-three patients with ALS (25 males) and 43 age- and gender-matched healthy controls underwent MRI on a 3T scanner. We used T1-weighted 3D images covering the whole brain and the cervical SC to estimate cervical SC area and eccentricity at C2/C3 level using validated software (SpineSeg). Disease severity was quantified with the ALSFRS-R and ALS Severity scores. SC areas of patients and controls were compared with a Mann-Whitney test. We used linear regression to investigate association between SC area and clinical parameters. Results showed that mean age of patients and disease duration were 53.1 ± 12.2 years and 34.0 ± 29.8 months, respectively. The two groups were significantly different regarding SC areas (67.8 ± 6.8 mm² vs. 59.5 ± 8.4 mm², p < 0.001). Eccentricity values were similar in both groups (p = 0.394). SC areas correlated with disease duration (r = - 0.585, p < 0.001), ALSFRS-R score (r = 0.309, p = 0.044) and ALS Severity scale (r = 0.347, p = 0.022). In conclusion, patients with ALS have SC atrophy, but no flattening. In addition, SC areas correlated with disease duration and functional status. These data suggest that quantitative MRI of the SC may be a useful biomarker in the disease.

Although white matter damage may play a major role in the pathogenesis of spinocerebellar ataxia 3 (SCA3), available data rely exclusively upon macrostructural analyses. In this setting we designed a study to investigate white matter integrity. We evaluated 38 genetically-confirmed SCA3 patients (mean age, 52.76 ± 12.70 years; 21 males) with clinical scales and brain magnetic resonance imaging (MRI) and 38 healthy subjects as a control group (mean age, 48.86 ± 12.07 years, 20 male). All individuals underwent the same protocol for high-resolution T1 and T2 images and diffusion tensor imaging acquisition (32 directions) in a 3-T scanner. We used Tract-Based Spatial Statistics (FSL 4.1.4) to analyze diffusion data and SPM8/DARTEL for voxel-based morphometry of infratentorial structures. T2-relaxometry of cerebellum was performed with in-house-developed software Aftervoxel and Interactive Volume Segmentation (IVS). Patients' mean age at onset was 40.02 ± 11.48 years and mean duration of disease was 9.3 ± 2.7 years. Mean International Cooperative Ataxia Rating Scale (ICARS) and Scale for Assessment and Rating of Ataxia (SARA) scores were 32.08 ± 4.01 and 14.65 ± 7.33, respectively. Voxel-based morphometry demonstrated a volumetric reduction of gray and white matter in cerebellum and brainstem (P

Naming difficulties are characteristic of Alzheimer’s disease (AD) and, to a lesser extent, of amnestic mild cognitive impairment (aMCI) patients. The association of naming impairment with anterior temporal lobe (ATL) atrophy in Semantic Dementia (SD) could be a tip of the iceberg effect, in which case the atrophy is a marker of more generalized temporal lobe pathology. Alternatively, it could reflect the existence of a functional gradient within the temporal lobes, wherein more anterior regions provide the basis for greater specificity of representation. We tested these two hypotheses in a study of 15 subjects with mild AD, 17 with aMCI, and 16 aged control subjects and showed that coordinate and circumlocutory semantic error production on the Boston Naming Test was weakly correlated with ATL gray matter density, as determined by voxel-based morphometry. Additionally, we investigated whether these errors were benefited by phonemic cues, and similarly to SD, our AD patients had small improvement. Because there is minimal gradient of temporal lobe atrophy in AD or MCI, and, therefore, no basis for a tip of the iceberg effect, these findings support the theory of a modest functional gradient in the temporal lobes, with the ATLs being involved in the naming of more specific objects. (JINS, 2010,16, 1099–1107.)

BACKGROUND AND PURPOSE: In mesial temporal lobe epilepsy, MR imaging quantification of hippocampal volume and T2 signal can improve the sensitivity for detecting hippocampal sclerosis. However, the current contributions of these analyses for the diagnosis of hippocampal sclerosis in 3T MRI are not clear. Our aim was to compare visual analysis, volumetry, and signal quantification of the hippocampus for detecting hippocampal sclerosis in 3T MRI. MATERIALS AND METHODS: Two hundred three patients with mesial temporal lobe epilepsy defined by clinical and electroencephalogram criteria had 3T MRI visually analyzed by imaging epilepsy experts. As a second step, we performed automatic quantification of hippocampal volumes with FreeSurfer and T2 relaxometry with an in-house software. MRI of 79 healthy controls was used for comparison. RESULTS: Visual analysis classified 125 patients (62%) as having signs of hippocampal sclerosis and 78 (38%) as having normal MRI findings. Automatic volumetry detected atrophy in 119 (95%) patients with visually detected hippocampal sclerosis and in 10 (13%) with visually normal MR imaging findings. Relaxometry analysis detected hyperintense T2 signal in 103 (82%) patients with visually detected hippocampal sclerosis and in 15 (19%) with visually normal MR imaging findings. Considered together, volumetry plus relaxometry detected signs of hippocampal sclerosis in all except 1 (99%) patient with visually detected hippocampal sclerosis and in 22 (28%) with visually normal MR imaging findings. CONCLUSIONS: In 3T MRI visually inspected by experts, quantification of hippocampal volume and signal can increase the detection of hippocampal sclerosis in 28% of patients with mesial temporal lobe epilepsy.

Agradecimentos: The Authors have no conflict of interest Abstract: Purpose: To investigate the degree of T2 relaxometry changes over time in groups of patients with familial mesial temporal lobe epilepsy (FMTLE) and asymptomatic relatives. Methods: We conducted both cross-sectional and longitudinal analyses of T2 relaxometry with Aftervoxel, an inhouse software for medical image visualization. The cross-sectional study included 35 subjects (26 with FMTLE and 9 asymptomatic relatives) and 40 controls; the longitudinal study was composed of 30 subjects (21 with FMTLE and 9 asymptomatic relatives; the mean time interval of MRIs was 4.4 +/- 1.5 years) and 16 controls. To increase the size of our groups of patients and relatives, we combined data acquired in 2 scanners (2T and 3T) and obtained z-scores using their respective controls. General linear model on SPSS21 (R) was used for statistical analysis. Results: In the cross-sectional analysis, elevated T2 relaxometry was identified for subjects with seizures and intermediate values for asymptomatic relatives compared to controls. Subjects with MRI signs of hippocampal sclerosis presented elevated T2 relaxometry in the ipsilateral hippocampus, while patients and asymptomatic relatives with normal MRI presented elevated T2 values in the right hippocampus. The longitudinal analysis revealed a significant increase in T2 relaxometry for the ipsilateral hippocampus exclusively in patients with seizures. Conclusions: The longitudinal increase of T2 signal in patients with seizures suggests the existence of an interaction between ongoing seizures and the underlying pathology, causing progressive damage to the hippocampus. The identification of elevated T2 relaxometry in asymptomatic relatives and in patients with normal MRI suggests that genetic factors may be involved in the development of some mild hippocampal abnormalities in FMTLE Fechado

Background and purpose In Friedreich's ataxia (FRDA), frataxin deficiency results in iron redistribution in the dentate nuclei (DNC). Clusters of iron cause inhomogeneities in a magnetic field and result in a reduction in T2 relaxation time (T2). Methods T2 was prospectively evaluated in DNC, putamen, substantia nigra (SN), cerebellar white matter (CWM) and caudate and the correlation with clinical parameters was investigated. Thirty-five patients (range 9–51 years) and 44 controls (12–49 years) underwent T2 multi-echo sequence in a 3T scanner. Twenty-three patients (12–50 years) and 19 controls (14–49 years) were reassessed after 1 year. T2 was evaluated using specialized software (Aftervoxel) and severity of disease was quantified with the Friedreich Ataxia Rating Scale (FARS). Results T2 of both DNC was significantly shorter in the FRDA group at baseline (right, 58.6 ± 8.3 ms vs. 63.7 ± 8.1 ms, P = 0.013; left, 56.7 ± 7.7 ms vs. 62.6 ± 6.8 ms, P = 0.001). No significant difference was found between groups regarding the SN, putamen, CWM and caudate T2. DNC T2 values correlated with age, FARS total score and FARS III subscore on both sides. Prospectively, there was a significant reduction of T2 in FRDA patients in right and left DNC (P = 0.001 and 0.009) but not in other structures. Amongst controls, none of the regions significantly changed after 1 year. DNC T2 change over time correlated with GAA expansions and clinical deterioration (expressed by a change in FARS scores). Conclusions DNC T2 values are abnormal in FRDA, progress over time and correlate with ataxia severity. These results strongly suggest that DNC relaxometry can be a useful neuroimaging marker in FRDA.

Background: Although aquaporin-4 (AQP4) is widely expressed in the human brain cortex, lesions are rare in neuromyelitis optica (NMO) spectrum disorders (NMOSD). Recently, however, several studies have demonstrated occult structural brain atrophy in NMO. Objective: This study aims to investigate magnetic resonance imaging (MRI) patterns of gray matter (GM) and white matter (WM) abnormalities in patients with NMOSD and to assess the visual pathway integrity during disease duration correlation of the retinal nerve fiber layer (RNFL) and pericalcarine cortex thickness. Methods: Twenty-one patients with NMOSD and 34 matched healthy controls underwent both high-field MRI (3T) high-resolution T1-weighted and diffusion-tensor MRI. Voxel-based morphometry, cortical analyses (Freesurfer) and diffusion-tensor imaging (DTI) analyses (TBSS-FSL) were used to investigate brain abnormalities. In addition, RNFL measurement by optic-coherence tomography (OCT) was performed. Results: We demonstrate that NMOSD is associated with GM and WM atrophy, encompassing more frequently the motor, sensory and visual pathways, and that the extent of GM atrophy correlates with disease duration. Furthermore, we demonstrate for the first time a correlation between RNFL and pericalcarine cortical thickness, with cortical atrophy evolving over the course of disease. Conclusions: Our findings indicate a role for retrograde and anterograde neurodegeneration in GM atrophy in NMOSD. However, the presence atrophy encompassing almost all lobes suggests that additional pathomechanisms might also be involved.

Mesial temporal lobe epilepsy (MTLE) associated with hippocampal sclerosis (HS) is considered an electroclinical syndrome, and there is a debate whether it is a unique disease or an entity with distinct subtypes. Together with other mesial temporal structures, the amygdala is important in the epileptogenic network of patients with MTLE with HS. During automatic volumetric analysis of mesial structures in a group of 102 patients with MTLE with MRI signs of HS, we observed significant amygdala enlargement in 14 (14%) individuals compared to a group of 79 healthy subjects. The increased amygdala volume was contralateral to the epileptogenic zone and MRI signs of HS in 93% of these patients. Patients with MTLE with HS and enlarged amygdala had significantly earlier epilepsy onset than those without an increase of amygdala volumes. Mesial temporal lobe epilepsy with HS and enlarged amygdala may be a part of the spectrum of this condition.

Although Friedreich's ataxia is characterized by spinal cord atrophy, it remains to be investigated the possible correlation of such atrophy with clinical disability and genetic parameters. Thirty-three patients with Friedreich's ataxia and 30 healthy controls underwent MRI on a 3 T scanner. We used T1-weighted 3D images to estimate spinal cord area and eccentricity at C2/C3 level based on a semi-automatic image segmentation protocol. We quantified severity of ataxia with the Friedreich ataxia rating scale (FARS). Mean cord area in Friedreich's ataxia was smaller than in controls (38 vs 67.9 mm(2), p < 0.001). In contrast, mean cord eccentricity was significantly higher in Friedreich's ataxia when compared to the controls (0.82 vs 0.76, p < 0.001). There was a significant correlation between cord areas and the FARS scores (r = -0.53, p = 0.002). Cord damage in Friedreich's ataxia results in atrophy combined with flattening. Cord area is associated to clinical disability and might be useful as a biomarker in the disease.

Although white matter damage may play a major role in the pathogenesis of spinocerebellar ataxia 3 (SCA3), available data rely exclusively upon macrostructural analyses. In this setting we designed a study to investigate white matter integrity. We evaluated 38 genetically-confirmed SCA3 patients (mean age, 52.76 ± 12.70 years; 21 males) with clinical scales and brain magnetic resonance imaging (MRI) and 38 healthy subjects as a control group (mean age, 48.86 ± 12.07 years, 20 male). All individuals underwent the same protocol for high-resolution T1 and T2 images and diffusion tensor imaging acquisition (32 directions) in a 3-T scanner. We used Tract-Based Spatial Statistics (FSL 4.1.4) to analyze diffusion data and SPM8/DARTEL for voxel-based morphometry of infratentorial structures. T2-relaxometry of cerebellum was performed with in-house-developed software Aftervoxel and Interactive Volume Segmentation (IVS). Patients' mean age at onset was 40.02 ± 11.48 years and mean duration of disease was 9.3 ± 2.7 years. Mean International Cooperative Ataxia Rating Scale (ICARS) and Scale for Assessment and Rating of Ataxia (SARA) scores were 32.08 ± 4.01 and 14.65 ± 7.33, respectively. Voxel-based morphometry demonstrated a volumetric reduction of gray and white matter in cerebellum and brainstem (P.001). We found reduced fractional anisotropy (P.05) in the cerebellum and brainstem. There were also areas of increased radial diffusivity (P.05) in the cerebellum, brainstem, thalamus, frontal lobes, and temporal lobes. In addition, we found decreased T2-relaxation values in the white matter of the right cerebellar hemisphere. Microstructural white matter dysfunction, not previously reported, occurs in the cerebellum and brainstem of SCA3 patients.

Extraction of the mid-sagittal plane (MSP) is a key step for brain image registration and asymmetry analysis. We present a fast MSP extraction method for 3D MR images, based on automatic segmentation of the brain and on heuristic maximization of the cerebro-spinal fluid within the MSP. The method is robust to severe anatomical asymmetries between the hemispheres, caused by surgical procedures and lesions. The method is also accurate with respect to MSP delineations done by a specialist. The method was evaluated on 64 MR images (36 pathological, 20 healthy, 8 synthetic), and it found a precise and accurate approximation of the MSP in all of them with a mean time of 60.0 seconds per image, mean angular variation within a same image (precision) of 1.26o and mean angular difference from specialist delineations (accuracy) of 1.64o.

Background Childhood-onset systemic lupus erythematosus (cSLE) is a chronic autoimune disease with fluctuating disease activity. Neurospichiatric manifestations are common and vary from common manifestations such as headache and anxiety to life threatening manifestations such as acute confusional syndrome. Ataxia has not been studied frequently in cSLE. Objectives To determine the prevalence of ataxia in cSLE and clinical, laboratory and treatment features associated with its occurrence. To determine neuroimaging features associated with ataxia, especially medullary area and cerebellar volume. Methods We included 62 cSLE patients followed at the State university of Campinas and 28 healthy controls with similar age and gender distribution. All patients and controls were evaluated for ataxia using Scale for the assessment and rating of ataxia (SARA), validated in portugues. All subjects realized magnetic resonance imaging using a 3 tesla scanner (Phillips). Sagittal T1 1mm thick slices were used for analysis. Medullary area and excentricity and cerebellar volume were analyzed using semiautomatic computer segemntation software (SpineSeg and Neuroline). Results We observed ataxia in 22 out of 62 (35.5%) patients and in none of the controls (p=0.002). Ataxia was associated with the presence of neuropsychiatric manifestations (p=0.003) and antifosfolipid antibodies (p=0.005). None of the other clinical, laboratory or treatment features were associated with ataxia. Medullary area was significant smaller in cSLE when compared to controls (p=0.002). Reduction of medullar area was associated with cumulative corticosteroid dose (r=-0.43; p=0.008) and the presence of ataxia (p=0.003). Cerebellar volume was significantly reduced in cSLE patients when compared to controls (p Conclusions Ataxia is frequently observed in cSLE and associated with neuropsychiatric manifestations and antiphospholipid antibodies. Neuroimaging features, especially medullary volume is associated with ataxia and cerebellar atrophy may be secondary. Disclosure of Interest None declared

Image segmentation using tree pruning (TP) and watershed (WS) has been presented in the framework of the image forest transform (IFT) - a method to reduce image processing problems related to connectivity into an optimum-path forest problem in a graph. Given that both algorithms use the IFT with similar parameters, they usually produce similar segmentation results. However, they rely on different properties of the IFT which make TP more robust than WS for automatic segmentation tasks. We propose and demonstrate an important improvement in the TP algorithm, clarify the differences between TP and WS, and provide their comparative analysis from the theoretical and practical points of view. The experiments involve automatic segmentation of license plates in a database with 990 images

The notion of "strength of connectedness" between pixels has been successfully used in image segmentation. We present an extension to these works, which can considerably increase the efficiency of object definition tasks. A set of pixels is said a e-connected component with respect to a seed pixel when the strength of connectedness of any pixel in that set with respect to the seed is higher than or equal to a threshold. While the previous approaches either assume no competition with a single threshold for all seeds or eliminate the threshold for seed competition, we found that seed competition with different thresholds can reduce the number of seeds and the need for user interaction during segmentation. We also propose automatic and user-friendly interactive methods for determining the thresholds. The improvements are demonstrated through several segmentation experiments involving medical images.

ObjectivePatients with temporal lobe epilepsy (TLE) with hippocampal sclerosis (HS) have diffuse subtle gray matter (GM) atrophy detectable by MRI quantification analyses. However, it is not clear whether the etiology and seizure frequency are associated with this atrophy. We aimed to evaluate the occurrence of GM atrophy and the influence of seizure frequency in patients with TLE and either normal MRI (TLE-NL) or MRI signs of HS (TLE-HS).MethodsWe evaluated a group of 172 consecutive patients with unilateral TLE-HS or TLE-NL as defined by hippocampal volumetry and signal quantification (122 TLE-HS and 50 TLE-NL) plus a group of 82 healthy individuals. Voxel-based morphometry was performed with VBM8/SPM8 in 3T MRIs. Patients with up to three complex partial seizures and no generalized tonic-clonic seizures in the previous year were considered to have infrequent seizures. Those who did not fulfill these criteria were considered to have frequent seizures.ResultsPatients with TLE-HS had more pronounced GM atrophy, including the ipsilateral mesial temporal structures, temporal lobe, bilateral thalami and pre/post-central gyri. Patients with TLE-NL had more subtle GM atrophy, including the ipsilateral orbitofrontal cortex, bilateral thalami and pre/post-central gyri. Both TLE-HS and TLE-NL showed increased GM volume in the contralateral pons. TLE-HS patients with frequent seizures had more pronounced GM atrophy in extra-temporal regions than TLE-HS with infrequent seizures. Patients with TLE-NL and infrequent seizures had no detectable GM atrophy. In both TLE-HS and TLE-NL, the duration of epilepsy correlated with GM atrophy in extra-hippocampal regions.ConclusionAlthough a diffuse network GM atrophy occurs in both TLE-HS and TLE-NL, this is strikingly more evident in TLE-HS and in patients with frequent seizures. These findings suggest that neocortical atrophy in TLE is related to the ongoing seizures and epilepsy duration, while thalamic atrophy is more probably related to the original epileptogenic process.

WCN 2013 No: 2441 Topic: 7 Neuromuscular disorders The follow-up of the patients with GBS treated with plasmapheresis A. Kuqo, H.V. Doci, L. Buda, M.H. Papajani, S. Grabova, F. Myslimi, A.A. Quka, J. Kruja. Neurology, QSUT, Tirana, Albania Background: GBS is an acute polyneuropathy, a disorder affecting the peripheral nervous system. It can cause life-threatening complications, in particular if the respiratory muscles are affected or if there is autonomic nervous system involvement. The disease is usually triggered by an infection. Treatment consists of attempting to reduce the body's attack on the nervous system by plasmapheresis. Objective: To evaluate the efficacy of PEX in GBS patients. Methods: In our prospective study a group of 17 patients with GBS was evaluated before, immediately after PEX and 1 year later. The evaluation was made using the Hughes functional grading scale for GBS (from Hughes et al., Lancet 1978). Results: We have evaluated the 17 patients. We have found an improvement in 14/17(82.35%) patients immediately after and 1 year after the PEX treatment. We haven't found an improvement in 3/17 patients. In 4 patients the progression of the neurological signs was stopped immediately after the first PEX procedure and in these patients we have found better results. We have found good results even in patients who require assisted ventilation (score 5 of Hughes functional grading scale for GBS). 3/17(17.64%) patients had an improvement even they haven't made all the PEX procedure because of complications. Conclusions: The PEX treatment in GBS patients is efficient. The improvement consisted of good clinical outcome. In some cases the progression of clinical signs was stopped even after only one procedure. doi:10.1016/j.jns.2013.07.1663 Abstract WCN 2013 No: 1004 Topic: 7 Neuromuscular disorders Temporal cortical damage as a prognostic marker in ALS (amyotrophic lateral sclerosis) WCN 2013 No: 1004 Topic: 7 Neuromuscular disorders Temporal cortical damage as a prognostic marker in ALS (amyotrophic lateral sclerosis) M. Albuquerque, H.M.T. Andrade, F.P.G. Bergo, M.C. FrancaJunior, A. Nucci. Neurology, Universidade Estadual de Campinas, Campinas, Brazil; Neurology, Universidade Estadual de Campinas, Campinas, Brazil; Computer Engineering, Universidade Estadual de Campinas