Differential clinical diagnosis of Parkinsonism: precepts and pitfalls of MIBG scintigraphy

Abstract

Lewy-prone neurons are characterized by hyperbranching axons, which innervate to wide areas of brain and body, leading to generalized, poorly somatotopic clinical manifestations such αS mood, motivation, sleep, cognition and autonomic functions. Because αS is enriched in axon terminals, hyperbranching axons provide a heavy αS load to these neurons. Because MIBG is accumulated at axon terminals of cardiac sympathetic nerves, decreased myocardial uptake of MIBG is correlated with degeneration of cardiac sympathetic nerve, induced by αS deposition. Although lower brainstem is rich in αS deposits, upward spread of αS is not consistent. Rather, haphazard development of αS deposits, as multifocal Lewy-body disease may be more plausible. Moreover, decreased myocardial uptake of MIBG may happen even in the absence of Lewy pathology. Although decreased myocardial uptake of MIBG may suggest Lewy pathology, it is time to reconsider this convenient but oversimplified paradigm so that diagnostic accuracy is maximized by referencing to pathology obtained at autopsy.