title: Degeneration of cardiac sympathetic nerve can occur in multiple system atrophy.
abstract: Decreased cardiac uptake of meta-iodobenzylguanidine (MIBG) on [(123)I] MIBG myocardial scintigraphy, a sensitive biological marker for Parkinson's disease (PD), is related to cardiac sympathetic denervation in patients with PD. A slight decrease in cardiac uptake of MIBG has also been reported in some patients with multiple system atrophy (MSA). However, the pathophysiological mechanism accounting for the slight decrease in MIBG uptake in MSA remains to be elucidated. For confirmation, we examined cardiac tissue and sympathetic ganglia from patients with MSA. We immunohistochemically examined each specimen of 15 patients with MSA together with 10 control subjects using antibodies against tyrosine hydroxylase (TH) and neurofilament (NF). The number of TH-immunoreactive nerve fibers in the epicardium was preserved in 8 of 15 patients with MSA as well as in 10 control subjects. The number of TH-immunoreactive, but not of NF-immunoreactive nerve fibers in the epicardium was mildly or moderately decreased in six patients with MSA, of whom four showed a decrease of TH immunoreactivity in the neuronal somata in the sympathetic ganglia. Moreover, TH- and NF-immunoreactive nerve fibers almost entirely disappeared in the heart of one patient with MSA, in whom Lewy body pathology was present in the sympathetic ganglia. These findings suggest that mild degeneration of the cardiac sympathetic nerve can occur in MSA which is closely related to the pathological change of neurons in the sympathetic ganglia, accounting for the slight decrease in cardiac uptake of MIBG. Moreover, concurrent Lewy body pathology in the sympathetic ganglia might accelerate cardiac sympathetic denervation even in MSA.
authors.affiliation: Department of Neurology, Kanto Central Hospital, 6-25-1 Kami-Yoga, Setagaya-ku, Tokyo, 158-8531, Japan. orimo@kanto-ctr-hsp.com
authors.forename: Satoshi
authors.initials: S
authors.lastname: Orimo
authors.forename: Toshiro
authors.initials: T
authors.lastname: Kanazawa
authors.forename: Ayako
authors.initials: A
authors.lastname: Nakamura
authors.forename: Toshiki
authors.initials: T
authors.lastname: Uchihara
authors.forename: Fumiaki
authors.initials: F
authors.lastname: Mori
authors.forename: Akiyoshi
authors.initials: A
authors.lastname: Kakita
authors.forename: Koichi
authors.initials: K
authors.lastname: Wakabayashi
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Takahashi
mesh_terms: D000320:Adrenergic Fibers / Q000378:metabolism / Q000473:pathology*; D000368:Aged; D000369:Aged, 80 and over; D005260:Female; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D002479:Inclusion Bodies / Q000473:pathology; D008297:Male; D008875:Middle Aged; D019578:Multiple System Atrophy / Q000150:complications* / Q000473:pathology; D009206:Myocardium / Q000473:pathology*; D019636:Neurodegenerative Diseases / Q000209:etiology* / Q000378:metabolism; D016900:Neurofilament Proteins / Q000378:metabolism; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
chemical_list: D016900:Neurofilament Proteins; D014446:Tyrosine 3-Monooxygenase