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Psychopharmacol Bull. 2021 Jan 12;51(1):94-109.
This comprehensive review discusses the adverse effects known today about marijuana, for either medical or recreational use. It reviews the role of cannabis in the treatment of chronic pain, cognitive and neurological adverse effects, special cases and addiction.
Cannabinoids work through the endocannabinoids system and inhibit the release of GABA and glutamate in the brain, impact neuromodulation, as well as dopamine, acetylcholine and norepinephrine release. They affect reward, learning and pain. The use of cannabis is increasing nationally and world-wide for both recreational and medicinal purposes, however, there is relatively only low quality evidence to the efficacy and adverse effects of this. Cannabis and its derivatives may be used for treatment of chronic pain. They are via CB1 receptors that are thought to modulate nociceptive signals in the brain. CB2 receptors in the DRG likely affect pain integration in the afferent pathways, and peripherally CB2 also affects noradrenergic pathways influencing pain. A large proportion of users may see more than 50% of chronic pain alleviation compared with placebo. Cannabis affects cognition, most notably executive function, memory and attention, and may deteriorate the boundary between emotional and executive processing. Cannabis impairs memory in the short run, which become more significant with chronic use, and may also be accompanied by poorer effort, slower processing and impacted attention. It is generally believed that long-term use and earlier age are risk factor for neurocognitive deficits; neuroimaging studies have shown reduced hippocampal volume and density. Executive functions and memory are worse in adolescent users versus adults. Cannabis addiction is different and likely less common than other addictive substances, but up to 10% of users meet criteria for lifetime cannabis dependence. Addiction patterns may be linked to genetic and epigenetic differences. It is still unclear whether abstinence reverses patterns of addiction, and more research is required into this topic.
Cannabis use has become more abundant for both medical and recreational use. It carries likely benefits in the form of analgesia, anti-emesis and improved appetite in chronic patients. The evidence reviewing adverse effects of this use are still limited, however, exiting data points to a clear link with neurocognitive deterioration, backed by loss of brain volume and density. Addiction is likely complex and variable, and no good data exists to support treatment at this point. It is becoming clear that use in earlier ages carries a higher risk for long-term deficits. As with any other drug, these risks should be considered alongside benefits prior to a decision on cannabis use.
本文全面讨论了当前已知的大麻的不良反应,包括医用和娱乐用。本文综述了大麻在治疗慢性疼痛、认知和神经不良反应、特殊病例和成瘾方面的作用。
大麻通过内源性大麻素系统发挥作用,抑制大脑中 GABA 和谷氨酸的释放,影响神经调节以及多巴胺、乙酰胆碱和去甲肾上腺素的释放。它们影响奖赏、学习和疼痛。大麻的使用在全国乃至全球范围内都在增加,无论是出于娱乐还是医疗目的,但对于其疗效和不良反应,只有相对较低质量的证据。大麻及其衍生物可用于治疗慢性疼痛。通过 CB1 受体,大麻被认为可以调节大脑中的伤害性信号。DRG 中的 CB2 受体可能影响传入通路中的疼痛整合,而外周 CB2 也影响影响疼痛的去甲肾上腺素途径。与安慰剂相比,很大一部分使用者的慢性疼痛缓解率可能超过 50%。大麻影响认知,最明显的是执行功能、记忆和注意力,可能会损害情绪和执行处理之间的边界。大麻在短期内会损害记忆,而随着慢性使用,记忆损害会更加明显,并且可能还伴有较差的努力、较慢的处理和注意力受损。一般认为,长期使用和较早年龄是神经认知缺陷的危险因素;神经影像学研究显示海马体积和密度减少。青少年使用者的执行功能和记忆力比成年人差。与其他成瘾物质相比,大麻成瘾不同,可能不太常见,但多达 10%的使用者符合终生大麻依赖的标准。成瘾模式可能与遗传和表观遗传差异有关。目前还不清楚戒断是否能逆转成瘾模式,需要对此进行更多研究。
大麻的使用无论是医用还是娱乐用都变得更加普遍。它在慢性患者中可能具有镇痛、止吐和改善食欲的作用。然而,关于这种使用的不良反应的现有数据仍然有限,但现有的数据表明,与大脑体积和密度的丧失相吻合,它与神经认知恶化有明显的联系。成瘾可能是复杂的,而且因人而异,目前还没有很好的数据支持这一点。很明显,早期使用大麻会增加长期缺陷的风险。与任何其他药物一样,在决定使用大麻之前,应该权衡利弊,考虑这些风险。