Enhancing Cerebral Amyloid Angiopathy-Related Inflammation Diagnosis With PET Using Pittsburgh Compound B.

ABSTRACT: Cerebral amyloid angiopathy-related inflammation is a rare encephalopathy characterized by inflammation against amyloid protein accumulated in cerebral small vessels. A 50-year-old man was presented with a subacute consciousness disorder. Brain MRI revealed high intensity lesions in the white matter of the right parietal and occipital lobes on fluid-attenuated inversion recovery sequences and cerebral microbleeds in the right parietal and occipital lobes on T2*-weighted images. Pittsburgh compound B-PET demonstrated accumulation in the right temporoparietal lobe, confirming a potential diagnosis of probable cerebral amyloid angiopathy-related inflammation without brain biopsy. Steroid pulse therapy was initiated, with good results.

Influence of antidepressant use on 123I-MIBG heart and lung uptakes in the diagnosis of Lewy body disease.

OBJECTIVE: The clinical significance of decreased physiological lung uptake of 123I-metaiodobenzylguanidine (MIBG) has not been well investigated. This study aimed to elucidate the association between a decrease in lung MIBG uptake with antidepressant intake and the myocardial MIBG uptake in patients who were clinically diagnosed with Lewy body disease (LBD) and patients who were diagnosed as not having LBD. METHODS: We retrospectively reviewed the heart and lung uptakes on 167 consecutive MIBG scans, antidepressant status, and clinical diagnosis of LBD. The images were visually classified into two groups: decreased lung uptake and preserved lung uptake. A semi-quantitative analysis was performed using the heart-to-mediastinum ratio (H/M), lung-to-mediastinum ratio (L/M), and myocardial washout rate (WR). RESULTS: All 17 patients with decreased lung uptake were on treated with antidepressants, while none of the 150 patients with preserved lung uptake were treated with any antidepressants. Of the 17 patients with decreased lung uptake, 6 patients were clinically diagnosed as LBD and other 11 were clinically diagnosed as non-LBD. There was not significant difference in early H/M, delayed H/M, and myocardial WR between the 11 non-LBD patients with decreased lung uptake and 83 non-LBD patients with preserved lung uptake (2.87 ± 0.69 vs. 2.89 ± 0.44, 3.09 ± 0.48 vs. 2.98 ± 0.59, and 21.8 ± 11.3% vs. 21.1 ± 12.5%, respectively). Moreover, in LBD patients, there were no significant differences in those values between six patients with decreased lung uptake and 67 patients with preserved lung uptake (1.68 ± 0.32 vs. 1.73 ± 0.42, 1.34 ± 0.21 vs. 1.54 ± 0.57, 46.2 ± 22.8% vs. 42.8 ± 21.3%, respectively). CONCLUSIONS: Antidepressants probably blocked MIBG uptake in the lungs, and a decreased lung uptake was not significantly associated with heart uptake. A remarkable decrease in lung uptake can be a signal to check a patient's medication status.

Two Cases of Decreased 123I-Metaiodobenzylguanidine Lung Uptake in Metaiodobenzylguanidine Scintigraphy While Taking Selective Serotonin Reuptake Inhibitor/Serotonin Noradrenaline Reuptake Inhibitor.

ABSTRACT: 123I-metaiodobenzylguanidine scintigraphy is used to differentiate Lewy body disease from other neurodegenerative disorders. We identified 2 cases with remarkably changed pulmonary uptake between 2 metaiodobenzylguanidine scintigraphies; pulmonary uptake was reduced when patients were taking selective serotonin reuptake inhibitor/serotonin noradrenaline reuptake inhibitor and preserved during the medication-naive or withdrawal state, suggesting that pulmonary uptake involves not only the noradrenaline transporter, but also the serotonin transporter. Pulmonary accumulation may affect the heart-to-mediastinum ratio as the region of interest on the planner image is usually placed on the heart and includes part of the lung. Therefore, we should pay attention to the medication state of patients with decreased pulmonary uptake.