Epilepsy is rarely a major problem in young cryptogenic ischemic stroke survivors. Early seizures are associated with stroke disability and cortical involvement. Early seizures, cortical signs, and large infarct are independent risk factors for late seizures.

¹⁸FDG-PET coregistered with MRI is highly sensitive to detect TTFCD and greatly improves diagnosis and surgical prognosis of patients with negative MRI.

Purpose This joint practice guideline or procedure standard was developed collaboratively by the European Association of Nuclear Medicine (EANM) and the Society of Nuclear Medicine and Molecular Imaging (SNMMI). The goal of this guideline is to assist nuclear medicine practitioners in recommending, performing, interpreting, and reporting the results of dopaminergic imaging in parkinsonian syndromes. Methods Currently nuclear medicine investigations can assess both presynaptic and postsynaptic function of dopaminergic synapses. To date both EANM and SNMMI have published procedural guidelines for dopamine transporter imaging with single photon emission computed tomography (SPECT) (in 2009 and 2011, respectively). An EANM guideline for D2 SPECT imaging is also available (2009). Since the publication of these previous guidelines, new lines of evidence have been made available on semiquantification, harmonization, comparison with normal datasets, and longitudinal analyses of dopamine transporter imaging with SPECT. Similarly, details on acquisition protocols and simplified quantification methods are now available for dopamine transporter imaging with PET, including recently developed fluorinated tracers. Finally, [ 18 F]fluorodopa PET is now used in some centers for the differential diagnosis of parkinsonism, although procedural guidelines aiming to define standard procedures for [ 18 F]fluorodopa imaging in this setting are still lacking. Conclusion All these emerging issues are addressed in the present procedural guidelines for dopaminergic imaging in parkinsonian syndromes.

Interictal hypometabolism is commonly found in mesio-temporal lobe epilepsy (MTLE), but its pathophysiology remains incompletely understood. We hypothesized that metabolic changes reflect the preferential networks involved by ictal discharges. We analysed the topography of interictal hypometabolism according to electro-clinical patterns in 50 patients with unilateral hippocampal sclerosis (HS) and consistent features of MTLE. Based on electro-clinical correlations, we identified four groups: (i) mesial group (13 cases) characterized by mesial seizure onset without evidence of early spread beyond the temporal lobe; (ii) anterior mesio-lateral group (AML; 18 cases) with early anterior spread involving the anterior lateral temporal cortex and insulo-fronto-opercular areas; (iii) widespread mesio-lateral group (WML; 15 cases) with wide spread (involving both anterior and posterior lateral temporal and perisylvian areas); and (iv) bitemporal (BT) group (four cases) with early contralateral temporal spread. Results of [18F]fluorodeoxyglucose-PET imaging in each group were compared with those of 10 control subjects using statistical parametric mapping software (SPM99). MRI data and surgical outcome in each group were compared with metabolic findings. Hypometabolism was limited to hippocampal gyrus, temporal pole and insula in the mesial group. Gradual involvement of lateral temporal cortex, insula and perisylvian areas was observed in the AML and WML groups. The BT group differed from the others with mild bitemporal involvement, bilateral insular hypometabolism and longer epilepsy duration. MRI structural abnormalities outside of the mesial formations were detected in 65% of the cases. Neither the severity of HS nor temporal atrophy appeared related to the topography of hypometabolism. However, temporal hypometabolism was more extended when temporo-polar signal changes were detected. Among operated patients (n = 43), seizure-free outcome was obtained in 82%. Surgical outcome appeared more favourable in the mesial group. However, the difference between the four groups was not significant. Our results suggest that hypometabolism in MTLE may be related to ictal discharge generation and spread pathways, even if structural changes and epilepsy duration may also play a role.