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[高血糖所致继发性阵发性运动诱发性运动障碍患者99mTc ECD SPECT成像的发作期改变]

[Ictal alteration of 99mTc ECD SPECT imaging in a patient with secondary paroxysmal kinesigenic dyskinesia caused by hyperglycemia].

作者信息

Saiki Misuzu, Saiki Shinji, Gondo Yuichiro, Murata Ken-ya, Sakai Koichiro, Hirose Genjiro

机构信息

Department of Neurology, Kanazawa Medical University, 1-1 Daigaku, Uchinada, Kahoku, Ishikawa 920-0293, Japan.

出版信息

Rinsho Shinkeigaku. 2005 Apr;45(4):312-6.

PMID:15912801
Abstract

We described a 61-year-old man with diabetes mellitus who presented with hyperglycemia related paroxysmal kinesigenic dyskinesia (PKD) with sudden development of paroxysmal unilateral involuntary movements (IMs) of his neck and the left extremities. Ictal 99mTc-ethylcysteinate dimer SPECT (ECD-SPECT) revealed a hyperperfusion over the contralateral frontal cortex and a hypoperfusion over the contralateral basal ganglia. Immediate correction of hyperglycemia after admission resulted in a marked improvement of IMs and a return to normal cerebral blood flow on interictal ECD-SPECT imaging. These findings suggest that dysfunction of the indirect pathway through the basal ganglia lead to an imbalance of the cortico-striato-thalamo-cortical circuit and may have contributed to the cause of PKD in this case.

摘要

我们描述了一名61岁的糖尿病男性患者,他出现了与高血糖相关的阵发性运动诱发性运动障碍(PKD),突然出现颈部和左上肢阵发性单侧不自主运动(IMs)。发作期99mTc-乙基半胱氨酸二聚体单光子发射计算机断层扫描(ECD-SPECT)显示对侧额叶皮质血流灌注增加,对侧基底节血流灌注减少。入院后立即纠正高血糖导致IMs明显改善,发作间期ECD-SPECT成像显示脑血流恢复正常。这些发现表明,通过基底节的间接通路功能障碍导致皮质-纹状体-丘脑-皮质回路失衡,可能是该病例中PKD的病因。

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