Normal ‘heart’ in Parkinson's disease: is this a distinct clinical phenotype?

• DOI: 10.1111/ene.13206
• Publication Date: 2016-11-26T05:54:05Z
• Authors: J.‐S. Kim; H.‐E. Park; I.‐S. Park; Y.‐S. Oh; D.‐W. Ryu; I.‐U. Song; Y.‐A. Jung; I. R. Yoo; H.‐S. Choi; P. H. Lee; K.‐S. Lee
• Keywords: Male; Parkinson's disease; 610; REM Sleep Behavior Disorder; normal cardiac sympathetic innervation; Hypotension, Orthostatic; Olfaction Disorders; 03 medical and health sciences; 0302 clinical medicine; Cost of Illness; Humans; Aged; Heart; Parkinson Disease; Middle Aged; 3. Good health; 3-Iodobenzylguanidine; Positron-Emission Tomography; metaiodobenzylguanidine scintigraphy; non-motor features; Female; Radiopharmaceuticals; Cognition Disorders; Constipation

Background and purposeReduction of metaiodobenzylguanidine (MIBG) uptake has been observed in almost all patients with Parkinson's disease (PD), associated with hyposmia, orthostatic hypotension and rapid eye movement sleep behavioral disorder (RBD). In contrast, a subgroup of patients with PD with normal MIBG uptake have been reported to have milder disease and preserved cognition compared with those with lower MIBG. The aim of this study was to investigate whether non‐motor manifestations of PD differ between patients with normal and abnormal myocardial MIBG uptake.MethodsAmong 160 de‐novo cases of PD, 44 had normal MIBG uptake. Twelve candidate non‐motor features were evaluated using questionnaires and laboratory tests.ResultsPatients with decreased MIBG uptake had more constipation, RBD, cognitive impairment, hyposmia and orthostatic hypotension than did those with normal MIBG uptake. On linear regression analysis, orthostatic hypotension, olfactory function and probable RBD were significantly associated with MIBG uptake in PD. The principal component analysis showed that the group with normal MIBG was not associated with non‐motor impairments.ConclusionsThese results suggest that patients with PD with normal MIBG scans have a relatively low disease burden compared with those with abnormal MIBG. Fewer synuclein pathologies in the myocardia and sympathetic ganglia in PD with preserved MIBG uptake might be associated with lower threshold patterns of Braak synuclein pathology for non‐motor manifestations compared with PD with decreased MIBG.