我们报告了一例86岁女性患者的临床特征和多巴胺转运体情况，患者由于双侧性大脑前动脉梗塞导致运动不能性缄默。采用了[２-[[２-[[[３-(4-chlorophenyl）-８-甲基methyl-８-azabicyclo[3.2.1]辛oct-２-yl]甲基]（２-mercaptoethyl）氨基]乙基]氨基]ethanethiolato（３-）N2,N20,S2,S20]氧oxo-[1R-(exo-exo-exo)]-[99mTc]锝([99mTc]TRODAT-1)影像学技术。TRODAT-1是一种可卡因同型物，能用锝-99m标记，并与多巴胺转运体（DAT）位点结合。它主要反映多巴胺神经元终末突触前的完整性。
这种新的实例说明运动不能性缄默由大脑前动脉梗塞所引起，与皮质下多巴胺能系统的波动密切相关。

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.