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安非他酮在帕金森病脑多巴胺转运体成像中导致误诊。

Bupropion Causes Misdiagnosis in Brain Dopamine Transporter Imaging for Parkinsonism.

作者信息

Honkanen Emma A, Kemppainen Nina, Noponen Tommi, Seppänen Marko, Joutsa Juho, Kaasinen Valtteri

机构信息

Department of Neurology, University of Turku.

Division of Clinical Neurosciences, Turku University Hospital.

出版信息

Clin Neuropharmacol. 2019 Sep/Oct;42(5):181-183. doi: 10.1097/WNF.0000000000000359.

Abstract

OBJECTIVE

The objective of this study was to report long-lasting effects of bupropion on brain dopamine transporter (DAT) in a patient with depression and parkinsonism.

METHODS

The patient was a 52-year old man who had been treated with 150 mg/d of bupropion for depression. The patient developed cognitive problems, bradykinesia, and reduced stride length for which he was scanned with [I]FP-CIT single photon emission computed tomography after the recommended 1-week discontinuation of bupropion. Levodopa treatment trial was initiated without a response. Eleven months later, the patient was scanned for a second time after a 1-month stoppage of bupropion.

RESULTS

The first scan was abnormal with left putamen specific binding ratio of 1.99 (SDs from the reference value mean, -2.40), right putamen of 2.27 (SD, -1.84), left caudate of 2.33 (SD, -2.26), and right caudate of 2.29 (SD, -2.18). The second scan (after 1-month discontinuation) was normal, and specific binding ratios had increased from 5.2% to 31.7% in all striatal regions as compared with the first scan. Brain magnetic resonance imaging and [F]fluorodeoxyglucose positron emission tomography imaging were normal, and there was no levodopa response or other features supporting neurodegenerative parkinsonism.

CONCLUSIONS

Bupropion has previously generally been discontinued 1 week prior DAT imaging, which meets the recommended, albeit arbitrary, time interval of 5 plasma clearance half-lives before the scan. One-week discontinuation of bupropion before DAT imaging may be insufficiently short. Our case shows that longer medication washout and rescan may be needed when there is contradiction between the imaging result and clinical outcome in patients with medications affecting DAT binding.

摘要

目的

本研究的目的是报告安非他酮对一名患有抑郁症和帕金森症患者脑多巴胺转运体(DAT)的长期影响。

方法

该患者为一名52岁男性,曾接受每日150毫克安非他酮治疗抑郁症。患者出现认知问题、运动迟缓以及步幅减小,在按推荐停用安非他酮1周后,接受了[I]FP-CIT单光子发射计算机断层扫描。启动左旋多巴治疗试验但无反应。11个月后,在停用安非他酮1个月后对患者进行了第二次扫描。

结果

第一次扫描异常,左侧壳核特异性结合率为1.99(相对于参考值均值的标准差,-2.40),右侧壳核为2.27(标准差,-1.84),左侧尾状核为2.33(标准差,-2.26),右侧尾状核为2.29(标准差,-2.18)。第二次扫描(在停药1个月后)正常,与第一次扫描相比,所有纹状体区域的特异性结合率从5.2%增加到了31.7%。脑磁共振成像和[F]氟脱氧葡萄糖正电子发射断层扫描成像均正常,且无左旋多巴反应或其他支持神经退行性帕金森症的特征。

结论

以前在DAT成像前1周通常会停用安非他酮,这符合扫描前5个血浆清除半衰期这一推荐的、尽管是任意的时间间隔。在DAT成像前停用安非他酮1周可能不够短。我们的病例表明,当影响DAT结合的药物在患者中成像结果与临床结果存在矛盾时,可能需要更长时间的药物洗脱和重新扫描。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4643/6791561/89a150dba481/wnf-42-181-g001.jpg

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