Cerebral glucose metabolism and striatal 18F-Dopa uptake by PET in cases of chorea with or without dementia

Makoto Otsuka, Yuichi Ichiya, Yasuo Kuwabara, Shinichi Hosokawa, Masayuki Sasaki, Toshimitsu Fukumura, Kouji Masuda, Ikuo Goto, Motohiro Kato

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

Cerebral glucose metabolism was studied by positron emission tomography with [18F]fluorodeoxyglucose in 12 patients with chorea due to different underlying diseases. The striatal 18F-Dopa uptake was also studied with 6-l-[18F]fluorodopa in 6 of them. Five of them were diagnosed as Huntington's disease two were as 'sporadic progressive chorea and dementia' with characteristic symptoms and signs of Huntington's disease but no family histories, two were as choreoacanthocytosis, and two had hemichorea caused by suspected vascular lesions in the contralateral striatum revealed by MRI. Caudate and putaminal glucose metabolism decreased in chorea compared to the controls. Hemichorea showed decreased glucose metabolism only in the contralateral striatum. Moreover the glucose metabolism decreased in demented each 7 patients in the frontal, temporal and parietal cortices as well as in the striatum. The caudate and putaminal 18F-Dopa uptake in patients with chorea showed no difference with that in the controls. The pathogenetic mechanism of chorea may involve decreased glucose metabolism and normal presynaptic dopaminergic activity in the striatum, and that of the demented state in chorea may also involve an additional decrease of the glucose metabolism in the frontal, temporal and parietal cortices.

Original languageEnglish
Pages (from-to)153-157
Number of pages5
JournalJournal of the Neurological Sciences
Volume115
Issue number2
DOIs
Publication statusPublished - Jan 1 1993

Fingerprint

Corpus Striatum
Chorea
Dihydroxyphenylalanine
Dementia
Glucose
Parietal Lobe
Huntington Disease
Frontal Lobe
Temporal Lobe
Neuroacanthocytosis
Fluorodeoxyglucose F18
Positron-Emission Tomography
Signs and Symptoms
Blood Vessels

All Science Journal Classification (ASJC) codes

  • Neurology
  • Clinical Neurology

Cite this

Cerebral glucose metabolism and striatal 18F-Dopa uptake by PET in cases of chorea with or without dementia. / Otsuka, Makoto; Ichiya, Yuichi; Kuwabara, Yasuo; Hosokawa, Shinichi; Sasaki, Masayuki; Fukumura, Toshimitsu; Masuda, Kouji; Goto, Ikuo; Kato, Motohiro.

In: Journal of the Neurological Sciences, Vol. 115, No. 2, 01.01.1993, p. 153-157.

Research output: Contribution to journalArticle

Otsuka, M, Ichiya, Y, Kuwabara, Y, Hosokawa, S, Sasaki, M, Fukumura, T, Masuda, K, Goto, I & Kato, M 1993, 'Cerebral glucose metabolism and striatal 18F-Dopa uptake by PET in cases of chorea with or without dementia', Journal of the Neurological Sciences, vol. 115, no. 2, pp. 153-157. https://doi.org/10.1016/0022-510X(93)90218-N
Otsuka, Makoto ; Ichiya, Yuichi ; Kuwabara, Yasuo ; Hosokawa, Shinichi ; Sasaki, Masayuki ; Fukumura, Toshimitsu ; Masuda, Kouji ; Goto, Ikuo ; Kato, Motohiro. / Cerebral glucose metabolism and striatal 18F-Dopa uptake by PET in cases of chorea with or without dementia. In: Journal of the Neurological Sciences. 1993 ; Vol. 115, No. 2. pp. 153-157.
@article{12b1c17c666f42e6adb515a2e7d37512,
title = "Cerebral glucose metabolism and striatal 18F-Dopa uptake by PET in cases of chorea with or without dementia",
abstract = "Cerebral glucose metabolism was studied by positron emission tomography with [18F]fluorodeoxyglucose in 12 patients with chorea due to different underlying diseases. The striatal 18F-Dopa uptake was also studied with 6-l-[18F]fluorodopa in 6 of them. Five of them were diagnosed as Huntington's disease two were as 'sporadic progressive chorea and dementia' with characteristic symptoms and signs of Huntington's disease but no family histories, two were as choreoacanthocytosis, and two had hemichorea caused by suspected vascular lesions in the contralateral striatum revealed by MRI. Caudate and putaminal glucose metabolism decreased in chorea compared to the controls. Hemichorea showed decreased glucose metabolism only in the contralateral striatum. Moreover the glucose metabolism decreased in demented each 7 patients in the frontal, temporal and parietal cortices as well as in the striatum. The caudate and putaminal 18F-Dopa uptake in patients with chorea showed no difference with that in the controls. The pathogenetic mechanism of chorea may involve decreased glucose metabolism and normal presynaptic dopaminergic activity in the striatum, and that of the demented state in chorea may also involve an additional decrease of the glucose metabolism in the frontal, temporal and parietal cortices.",
author = "Makoto Otsuka and Yuichi Ichiya and Yasuo Kuwabara and Shinichi Hosokawa and Masayuki Sasaki and Toshimitsu Fukumura and Kouji Masuda and Ikuo Goto and Motohiro Kato",
year = "1993",
month = "1",
day = "1",
doi = "10.1016/0022-510X(93)90218-N",
language = "English",
volume = "115",
pages = "153--157",
journal = "Journal of the Neurological Sciences",
issn = "0022-510X",
publisher = "Elsevier",
number = "2",

}

TY - JOUR

T1 - Cerebral glucose metabolism and striatal 18F-Dopa uptake by PET in cases of chorea with or without dementia

AU - Otsuka, Makoto

AU - Ichiya, Yuichi

AU - Kuwabara, Yasuo

AU - Hosokawa, Shinichi

AU - Sasaki, Masayuki

AU - Fukumura, Toshimitsu

AU - Masuda, Kouji

AU - Goto, Ikuo

AU - Kato, Motohiro

PY - 1993/1/1

Y1 - 1993/1/1

N2 - Cerebral glucose metabolism was studied by positron emission tomography with [18F]fluorodeoxyglucose in 12 patients with chorea due to different underlying diseases. The striatal 18F-Dopa uptake was also studied with 6-l-[18F]fluorodopa in 6 of them. Five of them were diagnosed as Huntington's disease two were as 'sporadic progressive chorea and dementia' with characteristic symptoms and signs of Huntington's disease but no family histories, two were as choreoacanthocytosis, and two had hemichorea caused by suspected vascular lesions in the contralateral striatum revealed by MRI. Caudate and putaminal glucose metabolism decreased in chorea compared to the controls. Hemichorea showed decreased glucose metabolism only in the contralateral striatum. Moreover the glucose metabolism decreased in demented each 7 patients in the frontal, temporal and parietal cortices as well as in the striatum. The caudate and putaminal 18F-Dopa uptake in patients with chorea showed no difference with that in the controls. The pathogenetic mechanism of chorea may involve decreased glucose metabolism and normal presynaptic dopaminergic activity in the striatum, and that of the demented state in chorea may also involve an additional decrease of the glucose metabolism in the frontal, temporal and parietal cortices.

AB - Cerebral glucose metabolism was studied by positron emission tomography with [18F]fluorodeoxyglucose in 12 patients with chorea due to different underlying diseases. The striatal 18F-Dopa uptake was also studied with 6-l-[18F]fluorodopa in 6 of them. Five of them were diagnosed as Huntington's disease two were as 'sporadic progressive chorea and dementia' with characteristic symptoms and signs of Huntington's disease but no family histories, two were as choreoacanthocytosis, and two had hemichorea caused by suspected vascular lesions in the contralateral striatum revealed by MRI. Caudate and putaminal glucose metabolism decreased in chorea compared to the controls. Hemichorea showed decreased glucose metabolism only in the contralateral striatum. Moreover the glucose metabolism decreased in demented each 7 patients in the frontal, temporal and parietal cortices as well as in the striatum. The caudate and putaminal 18F-Dopa uptake in patients with chorea showed no difference with that in the controls. The pathogenetic mechanism of chorea may involve decreased glucose metabolism and normal presynaptic dopaminergic activity in the striatum, and that of the demented state in chorea may also involve an additional decrease of the glucose metabolism in the frontal, temporal and parietal cortices.

UR - http://www.scopus.com/inward/record.url?scp=0027481846&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027481846&partnerID=8YFLogxK

U2 - 10.1016/0022-510X(93)90218-N

DO - 10.1016/0022-510X(93)90218-N

M3 - Article

C2 - 8482976

AN - SCOPUS:0027481846

VL - 115

SP - 153

EP - 157

JO - Journal of the Neurological Sciences

JF - Journal of the Neurological Sciences

SN - 0022-510X

IS - 2

ER -