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甲基苯丙胺和可卡因加速HIV痴呆症进程。

Acceleration of HIV dementia with methamphetamine and cocaine.

作者信息

Nath A, Maragos W F, Avison M J, Schmitt F A, Berger J R

机构信息

Department of Neurology, University of Kentucky, Lexington 40526-0284, USA.

出版信息

J Neurovirol. 2001 Feb;7(1):66-71. doi: 10.1080/135502801300069737.

DOI:10.1080/135502801300069737
PMID:11519485
Abstract

We report a patient with rapidly accelerating HIV dementia accompanied by seizures and an unusual movement disorder despite highly potent antiretroviral therapy. This clinical constellation was associated with the non-parenteral use of methamphetamine and cocaine. Fractional enhancement time on post contrast magnetic resonance imaging studies revealed a progressive breakdown of the blood brain barrier particularly in the basal ganglia. The movement disorder but not the dementia responded to a combination of dopamine replacement and anticholinergic therapy. While the movement disorder may have been unmasked by concomitant anticonvulsant therapy, we suggest in this instance, that prior drug abuse synergized with HIV to cause a domino effect on cerebral function. Careful attention and analysis to histories of remote non-injecting drug abuse may help substantiate our hypothesis.

摘要

我们报告了一名患者,尽管接受了高效抗逆转录病毒治疗,但仍出现快速进展的HIV痴呆,并伴有癫痫发作和一种不寻常的运动障碍。这一临床症状群与非肠道外使用甲基苯丙胺和可卡因有关。对比增强磁共振成像研究中的分数增强时间显示血脑屏障逐渐破坏,尤其是在基底神经节。多巴胺替代疗法和抗胆碱能疗法联合使用对运动障碍有效,但对痴呆无效。虽然运动障碍可能是由同时进行的抗惊厥治疗所引发,但在这种情况下,我们认为既往药物滥用与HIV协同作用,对脑功能产生了多米诺效应。对既往非注射吸毒史进行仔细关注和分析可能有助于证实我们的假设。

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Evidence for long-term neurotoxicity associated with methamphetamine abuse: A 1H MRS study.与甲基苯丙胺滥用相关的长期神经毒性证据:一项氢质子磁共振波谱研究。
Neurology. 2000 Mar 28;54(6):1344-9. doi: 10.1212/wnl.54.6.1344.
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Cerebrovascular changes in the basal ganglia with HIV dementia.伴有HIV痴呆的基底节区脑血管变化。
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Impact of HIV-1 tat protein on methamphetamine-induced inhibition of vesicular monoamine transporter2-mediated dopamine transport and methamphetamine conditioned place preference in HIV-1 tat transgenic mice.
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