Value of MIBG in the differential diagnosis of neurodegenerative disorders

Abstract

I- meta iodobenzylguanidine (MIBG) has a history of over 20 years as a markerof myocardial sympathetic activity and has been used for assessment of various cardiac diseases. Reduced cardiac MIBG uptake in myocardial scintigraphy has been reported in patients with Parkinson’s disease (PD), dementia with Lewy bodies (DLB), pure autonomic failure (PAF), rapid eye movement sleep behavior disorder (RBD), and familial PD linked to SNCA duplication. In 2005, the Dementia with Lewy Bodies Consortium considered 123 I-MIBG myocardial scintigraphy a “supportive” diagnostic tool. Recently, reliable and clear evidence for the usefulness of 123 I-MIBG scintigraphy in the diagnosis of Lewy body disorders has been accumulated, and it has become increasingly popular, whereasreduction of cardiac MIBG accumulation was reported in some cases of atypical parkinsonian syndromes such as progressive supranuclear palsy and multiple system atrophy. In 123 I-N-ù-fl uoropropyl-2â-carbomethoxy-3â-(4-iodophenyl) nortropan (FP-CIT) SPECT-supplemented MIBG scintigraphy of PD and DLB, FP-CIT binding in basal ganglia is closely related to cardiac MIBG uptake. Reduced 123 I-MIBG cardiac uptake might be a “suggestive” feature for Lewy body diseases.