## Abstract Myocardial ^123^Metaiodobenzylguanidine (MIBG) enables the assessment of postganglionic sympathetic cardiac innervation. MIBG uptake is decreased in nearly all patients with Parkinson's disease (PD). Our objective was to evaluate MIBG uptake in patients with genetic PD. We investigated
123I-metaiodobenzylguanidine scintigraphy in Parkinson's disease and related disorders
✍ Scribed by Olivier Rascol; Ludwig Schelosky
- Publisher
- John Wiley and Sons
- Year
- 2009
- Tongue
- English
- Weight
- 672 KB
- Volume
- 24
- Category
- Article
- ISSN
- 0885-3185
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Autonomic dysfunction is common in Lewy body disorders (Parkinson's disease, Dementia with Lewy Bodies, Pure Autonomic Failure, and REM sleep disorder). The loss of post‐ganglionic myocardial sympathetic nerve fibers is a prominent feature of autonomic dysfunction in such disorders. ^123^I‐metaiodobenzylguanidine (MIBG) scintigraphy that visualizes catecholaminergic terminals in vivo is a biomarker used to detect cardiac sympathetic degeneration. Abnormal MIBG uptake has been consistently reported in Lewy body disorders. Some studies agree in the notion that increasing bradykinesia is related with an incremental cardiac sympathetic denervation, whereas tremor is not closely linked to cardiac denervation. “Atypical” parkinsonian syndromes, including Multiple System Atrophy, Progressive Supranuclear Palsy, and others, show modest reductions of cardial MIBG uptake. MIBG scintigraphy is moderately sensitive and specific in differentiating Parkinson's disease from such syndromes. Conversely, its sensitivity and specificity might be better in cognitively impaired patients, helping differential diagnosis between Dementia with Lewy Bodies, and Alzheimer disease. Confounding factors (comorbidities, comedications) should be carefully controlled before analyzing MIBG scintigraphy. © 2009 Movement Disorder Society
📜 SIMILAR VOLUMES
Although we are sympathetic to Reynolds and Slocum's concerns, 1 their editorial errs on several points. The authors cite deference to regulatory (presumably Food and Drug Administration) approval as a constraint. The FDA has long recognized broad physician discretion in using FDAapproved drugs or d
## Abstract The purpose of our study was to prospectively evaluate cardiac [^123^I]metaiodobenzylguanidine (MIBG) uptake in patients with cerebrovascular disease (CVD) who develop clinical symptoms of vascular Parkinsonism (VP). A total of 19 consecutive patients who developed Parkinsonism during t
## Abstract There is substantial evidence to support a role for small vessel disease (SVD) as a cause for vascular parkinsonism (VP). Using [^123^I] FP‐CIT SPECT (single photon emission computed tomography), we have tried to determine whether VP patients have pre‐synaptic dopaminergic function simi
## Abstract To analyze the correlation between muscle sympathetic nerve activity (MSNA) and cardiac ^123^I‐metaiodobenzylguanidine (MIBG) uptake in patients with Parkinson's disease (PD), we measured both parameters in 14 PD patients who were 51 to 82 years of age (mean, 63.1 ± 8.7 years). The dura
## Abstract In the majority of cases, mitochondrial disorders are multisystem conditions that most frequently affect the skeletal muscle, followed by the central nervous system. One of the clinical manifestations of central nervous system involvement is Parkinson's syndrome (PS). Evidence for an as