Gonzalez Raul, Rippeth Julie D, Carey Catherine L, Heaton Robert K, Moore David J, Schweinsburg Brian C, Cherner Mariana, Grant Igor
HIV Neurobehavioral Research Center, University of California, San Diego, 150 W. Washington Street, 2nd Floor, San Diego, CA 92103, USA.
Drug Alcohol Depend. 2004 Nov 11;76(2):181-90. doi: 10.1016/j.drugalcdep.2004.04.014.
Abuse of the stimulant drug methamphetamine is associated with neural injury and neuropsychological (NP) deficits, while the residual effects of marijuana use remain uncertain. We sought to determine if methamphetamine dependent persons who also met criteria for marijuana abuse or dependence evidenced different NP performance than those with dependence for methamphetamine alone. We examined three groups that did not differ significantly on important demographic factors: (1) subjects with a history of methamphetamine dependence and history of marijuana abuse/dependence (METH+/MJ+, n=27); (2) methamphetamine dependent subjects without history of marijuana abuse/dependence (METH+/MJ-, n=26); (3) a control group with minimal or no drug use (n=41). A comprehensive NP battery was administered and performance was quantified for five cognitive ability areas. The METH+/MJ- group generally demonstrated the greatest NP impairment, with statistically significant differences observed between the METH+/MJ- and control group in learning, retention/retrieval, and a summary score of global NP performance. The METH+/MJ+ group did not differ significantly from the control or METH+/MJ- group on any NP ability. However, there was a significant linear trend in the global NP score suggesting that the METH+/MJ+ performed intermediate to the control and METH+/MJ- groups. Based on these findings, we cannot conclude that there is a protective effect of marijuana use in methamphetamine users; however, marijuana use clearly did not appear to exacerbate methamphetamine neurotoxicity. Further investigations are needed to determine if the emerging literature, suggesting that certain cannabinoids might have neuroprotective actions, is generalizable to community-dwelling substance abusers.
兴奋剂甲基苯丙胺的滥用与神经损伤和神经心理学(NP)缺陷有关,而使用大麻的残留影响尚不确定。我们试图确定,同时符合大麻滥用或依赖标准的甲基苯丙胺依赖者,与仅对甲基苯丙胺有依赖的人相比,是否表现出不同的NP表现。我们研究了三组在重要人口统计学因素上无显著差异的人群:(1)有甲基苯丙胺依赖史和大麻滥用/依赖史的受试者(甲基苯丙胺+/大麻+,n = 27);(2)无大麻滥用/依赖史的甲基苯丙胺依赖受试者(甲基苯丙胺+/大麻-,n = 26);(3)药物使用极少或无药物使用的对照组(n = 41)。实施了一套全面的NP测试,并对五个认知能力领域的表现进行了量化。甲基苯丙胺+/大麻-组总体表现出最大的NP损伤,甲基苯丙胺+/大麻-组与对照组在学习、记忆保持/提取以及全球NP表现的综合评分方面存在统计学上的显著差异。甲基苯丙胺+/大麻+组在任何NP能力上与对照组或甲基苯丙胺+/大麻-组均无显著差异。然而,全球NP评分存在显著的线性趋势,表明甲基苯丙胺+/大麻+组的表现介于对照组和甲基苯丙胺+/大麻-组之间。基于这些发现,我们不能得出大麻使用对甲基苯丙胺使用者有保护作用的结论;然而,大麻使用显然似乎并未加剧甲基苯丙胺的神经毒性。需要进一步研究,以确定新兴文献中表明某些大麻素可能具有神经保护作用的观点,是否适用于社区居住的药物滥用者。