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Diminution of basal ganglia dopaminergic function may play an important role in the generation of akinetic mutism in a patient with anterior cerebral arterial infarct.

Authors
  • Yang, Chun-Pai
  • Huang, Wei-Shih
  • Shih, Hsu-Tzu
  • Lin, Chun-Yi
  • Lu, Ming-Kuei
  • Kao, Chia-Hung
  • Hsieh, Te-Chun
  • Huang, Kai-Ju
  • Lee, Ying-Hsuan
  • Tsai, Chon-Haw
Type
Published Article
Journal
Clinical Neurology and Neurosurgery
Publisher
Elsevier
Publication Date
Sep 01, 2007
Volume
109
Issue
7
Pages
602–606
Identifiers
PMID: 17543443
Source
Medline
License
Unknown

Abstract

We report the clinical features and dopamine transporter [2-[[2-[[[3-(4-chlorophenyl)-8-methyl-8-azabicyclo[3.2.1]oct-2-yl]methyl](2-mercaptoethyl)amino]ethyl]amino]ethanethiolato(3-)-N2,N20,S2,S20]oxo-[1R-(exo-exo)]-[99mTc] technetium([99mTc]TRODAT-1) image finding in an 86-year-old woman with akinetic mutism due to infarction of bilateral anterior cerebral arterial territories. TRODAT-1 is a cocaine analogue that can be labeled with technetium-99m and bound to the dopamine transporter (DAT) site. It reflects primarily the integrity of presynaptic dopamine neuron terminals. With the evolution of the clinical features, the TRODAT SPECT images change from bilateral diminution of radioactivity uptake at the 81st-day check point to normal pattern at the 6-month one when the akinetic mute manifestations were nearly gone. This novel illustration suggests that the akinetic mutism caused by anterior cerebral arterial infarct is closely linked to the perturbation of the subcortical dopaminergic system. And the amelioration of the clinical features concordantly evolved with the restoration of the dopaminergic function.

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