Simultaneous assay by PET of pre- and postsynaptic markers of dopamine neurotransmission indicated that a striatal dopamine deficit correlated with alcohol craving, which was associated with a high relapse risk.
The hypofrontality theory ofthe pathogenesof schizophrenia predicts that cortical lesions caupsychosis. To test the hypothesis that the state of psychosis in temporal lobe epilepsy is associated with the same striatal supersensitivity that may cause psychosis in schizophrenia, we measured the rate of metabolism of an exogenous analog of dopa in both disorders, using positron emission tomography (PET) ofthe tracer 6-18Flfluoro-L-dopa (18F-dopa) (5,6).We have previously shown that the rate of metabolism of externally administered 18F-dopa is an index ofthe activity of the enzyme responsible for the decarboxylation of dopa to dopamine (EC 4.1.1.28) (7,8). We determined the brain metabolism of 18F-dopa in 31 subjects, including 10 patients with psychotic disorders, of whom 5 had schizophrenia and 5 had a history of complex partial seizures (CPS) with schizophreniform psychosis, and 21 control subjects, of whom 8 had CPS without psychosis and 13 were healthy volunteers.
Among the MRI-suspected LGG, kinetic but not conventional analysis of FET uptake enabled remarkably high sensitivity for detection of HGG. This held true even for lesions with low or diffuse tracer uptake. Lesions with reduced tracer uptake must be interpreted with caution, as they can also harbour HGG tissue.
We aimed to evaluate 68 Ga-DOTATATE PET/CT for the early prediction of time to progression and clinical outcome after a first cycle of peptide receptor radionuclide treatment (PRRT) in a cohort of patients with well-differentiated neuroendocrine tumors. Methods: Thirty-three consecutive patients (22 men and 11 women; mean age 6 SD, 57.8 6 12.1 y) were investigated at baseline and again 3 mo after initiation of the first cycle of PRRT. 68 Ga-DOTATATE receptor expression was assessed using 2 measures of standardized uptake value (SUV): maximum SUV (SUV max ) and tumor-to-spleen SUV ratio (SUV T/S ). Percentage change in SUV scores after PRRT relative to baseline (DSUV) was calculated. After completing 1-3 cycles of PRRT, patients entered the follow-up study, for estimation of time to progression. According to the Response Evaluation Criteria in Solid Tumors, progression was defined on the basis of contrast-enhanced CT. Clinical symptoms, as well as the tumor markers chromogranin A and neuron-specific enolase, were also recorded during regular follow-up visits. Results: The 23 of 31 patients with decreased SUV T/S after the first PRRT cycle had longer progression-free survival than did the 8 of 31 patients with stable or increased scores (median survival not reached vs. 6 mo, P 5 0.002). For the 18 of 33 patients showing a reduction in SUV max , there was no significant difference in progression-free survival (median survival not reached vs. 14 mo, P 5 0.22). Multivariate regression analysis identified SUV T/S as the only independent predictor for tumor progression during follow-up. In the 17 of 33 patients with clinical symptoms before PRRT, DSUV T/S correlated with clinical improvement (r 5 0.52, P , 0.05), whereas DSUV max did not (r 5 0.42, P 5 0.10). Changes in the tumor markers (chromogranin A and neuronspecific enolase) did not predict DSUV scores, clinical improvement, or time to progression. Conclusion: Decreased 68 Ga-DOTATATE uptake in tumors after the first cycle of PRRT predicted time to progression and correlated with an improvement in clinical symptoms among patients with welldifferentiated neuroendocrine tumors; DSUV T/S was superior to DSUV max for prediction of outcome.
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