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Moreover, the AR and PR peaks are not distinguishable in time, since the maximum signal change in each ROI is not significantly different from its value at the position of the other ROI's peak (p?>?0.3). The effect of ROI size was investigated by reducing the size of the ROIs through the intersection of the thresholded SPMs (p?[http://www.selleckchem.com/products/Romidepsin-FK228.html find more] that the lagged GLM results are also inconclusive using the smaller ROIs (results not shown). Our work represents the first application of DCM to investigate seizure propagation pathways based on EEG-correlated fMRI recorded in humans. Two competing hypotheses for the causal chain leading to epileptic activity propagation in a patient with a giant HH were tested, based on clinically plausible scenarios previously described in the literature. The DCM results yielded propagation from the HH to a temporal�Coccipital, posterior region followed by a frontal, anterior region as the most likely model explaining the data. Although the seizure focus may be the question of interest in most EEG-correlated fMRI studies of epileptic patients, this is not the case in HHs. In fact, the association between gelastic seizures and HHs is one of the strongest anatomical�Cclinical correlations in the field of human epilepsy. This focus location in the HH was also in agreement with the clinical history of our patient, as well as with the seizure reduction observed [http://en.wikipedia.org/wiki/LMTK2 LMTK2] one year after the surgical two-stage hamartoma disconnection. The question of interest in the case [http://www.selleckchem.com/products/U0126.html U0126 in vivo] of HHs is concerned with the pathway of seizure propagation from the HH to an extended brain network. Two alternative pathways have been shown in different patients, probably as a function of the exact location of the hamartoma within the hypothalamus (Kahane et al., 2003?and?Leal et al., 2003). The identification of the specific propagation model in individual patients would open surgical alternatives targeting the underlying propagation pathways, instead of the removal of the hamartoma in high-risk patients. The dynamics of the epileptic activity propagation experienced by our patient was previously investigated through an ERS/ERD analysis of the EEG signal recorded during seizures outside the fMRI scanner (Leal et al., 2009). The involvement of the frontal lobe was always limited to the late phases of the EEG seizure event and was always preceded by left side occipital�Ctemporal spike activity. It was then proposed that antidromic conduction in the fornix formation projecting to the posterior hippocampus could explain the focal slowing and abundant interictal spike activity over the left occipital and posterior temporal lobes. The left cingulate fasciculus would then conduct activity from posterior temporal to frontal lobe, overlapping the Papez circuit.