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Identification and characterization of etiology, mechanisms of damage, neuronal dysfunction, and molecular defects in mesial temporal lobe epilepsy and its relationship with response to treatment


Epilepsy affects approximately 1-2% of the population and partial epilepsies with complex partial seizures account for approximately 40% of all epilepsies in adults. The most frequent form of partial epilepsy in adults is temporal lobe epilepsy (TLE). Classical histopathological studies and, more recently, different high-resolution neuroimaging modalities identify hippocampal atrophy and other signs of hippocampal sclerosis (HS) as the most prominent pathological substrate in patients with intractable mesial temporal lobe epilepsy (MTLE). Our aim is to perform a longitudinal study in a series of patients with MTLE and other forms of partial epilepsies. We will evaluate and quantify structural and functional brain abnormalities, using different modalities of magnetic resonance (MR) imaging, and investigate the relationship between these abnormalities and the genetic substrate using molecular genetic techniques. Specifically, we propose (a) to continue the development of MR techniques for evaluating TLE, including the use of functional MRI with simultaneous EEG recording (EEG-fMRI), (b) to study the relationship between the degree of hippocampal damage determined by MR techniques and anti-epileptic drug (AED) resistance in patients with MTLE, (c) to investigate factors related to prognosis for seizure control in patients submitted to surgical treatment for AED resistant MTLE; (d) to identify and characterize molecular genetic defects in patients with MTLE. We believe that this study will help in better understanding the underlying pathogenic mechanisms in MTLE and other forms of partial epilepsies, and consequently, this may allow a better diagnosis and treatment for these patients. (AU)

Scientific publications (6)
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
MIRANDA, PAULO A. V.; FALCAO, ALEXANDRE X.; ROCHA, ANDERSON; BERGO, FELIPE P. G. Object delineation by kappa-connected components. EURASIP JOURNAL ON ADVANCES IN SIGNAL PROCESSING, 2008. Web of Science Citations: 7.
BONILHA, LEONARDO; ALESSIO, ANDRÉA; RORDEN, CHRIS; BAYLIS, GORDON; DAMASCENO, BENITO P.; MIN, LI LI; CENDES, FERNANDO. Extrahippocampal gray matter atrophy and memory impairment in patients with medial temporal lobe epilepsy. Human Brain Mapping, v. 28, n. 12, p. 1376-1390, Dec. 2007.
CLÁUDIA VIANNA MAURER-MORELLI; RAFAEL BREGLIO MARCHESINI; RODRIGO SECOLIN; NEIDE FERREIRA SANTOS; ELIANE KOBAYASHI; FERNANDO CENDES; ISCIA LOPES-CENDES. Linkage study of voltage-gated potassium channels in familial mesial temporal lobe epilepsy. Arquivos de Neuro-Psiquiatria, v. 65, n. 1, p. -, Mar. 2007.
MAURER-MORELLI‚ C. V.; SECOLIN‚ R.; MARCHESINI‚ R. B.; SANTOS‚ N. F.; KOBAYASHI‚ E.; CENDES‚ F.; LOPES-CENDES‚ I. THE SCN2A gene is not a likely candidate for familial mesial temporal lobe epilepsy. Epilepsy Research, v. 71, n. 2/3, p. 233-236, Oct. 2006.
AUDIGIER, ROMARIC; LOTUFO, ROBERTO; FALCÃO, ALEXANDRE. 3D visualization to assist iterative object definition from medical images. Computerized Medical Imaging and Graphics, v. 30, n. 4, p. 217-230, June 2006.
ALESSIO‚ A.; BONILHA‚ L.; RORDEN‚ C.; KOBAYASHI‚ E.; MIN‚ L.L.; DAMASCENO‚ B.P.; CENDES‚ F. Memory and language impairments and their relationships to hippocampal and perirhinal cortex damage in patients with medial temporal lobe epilepsy. Epilepsy & Behavior, v. 8, n. 3, p. 593-600, 2006.

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