Obsessive-Compulsive Disorder, Impulse Control Disorders and Drug Addiction Common Features and Potential Treatments

Obsessive-Compulsive Disorder, Impulse Control Disorders and Drug Addiction Common Features and Potential Treatments
复制标题

DOI:
10.2165/11591790-000000000-00000
复制
发表时间:
2011-01-01
期刊:
影响因子:
11.5
通讯作者:
Yuecel, Murat
Yuecel, Murat
中科院分区:
医学1区
文献类型:
--
作者:
Fontenelle, Leonardo F.;Oostermeijer, Sanne;Yuecel, Murat

文献摘要

被引文献

相似文献

强迫性、冲动性和成瘾行为的基本概念是重叠的,这可能有助于解释为什么外行人会互换使用这些表达方式。尽管已经进行了大量的研究工作来更好地描述和理清这些行为,但临床医生和科学家仍然无法清楚地区分它们。因此,强迫症(OCD)、冲动控制障碍(ICD)和物质相关障碍(SUD)在不同层面上有重叠,包括现象学、共病、神经回路、神经认知、神经化学和家族史。在这篇综述中,我们总结了这些问题,特别强调阿片类药物系统在 OCD、ICD 和 SUD 的病理生理学和治疗中的作用。我们假设,随着强迫症的进展和慢性化,由冲动“皮疹”过程驱动的强迫症相关行为(例如检查、清洗、排序和囤积等)的比例随着更多腹侧纹状体回路的参与变得突出而增加。相反,随着 SUD 和 ICD 的进展,由强迫性“习惯”过程驱动的 SUD 和 ICD 相关行为的比例随着更多背侧纹状体回路的参与变得突出而增加。我们并不是说,随着时间的推移,ICD 会变成 OCD,反之亦然。相反,我们提出,随着时间的推移,这些疾病可能会获得另一种疾病的特质。换句话说,ICD/SUD 患者可能会出现“强迫性冲动”,而 OCD 患者可能会表现出“冲动性冲动”。我们的模型有许多潜在的影响。从理论上讲,表现出冲动或成瘾特征的强迫症患者可以通过药物来治疗,以解决潜在驱动力的质量和神经系统的参与问题。例如,用于减少或预防成瘾(例如酗酒)复发的药物,其通过阿片样物质(例如丁丙诺啡和纳曲酮)、谷氨酸(例如托吡酯)、血清素(例如昂丹司琼)或γ-氨基丁酸(例如巴氯芬和托吡酯)系统调节皮质-中脑边缘多巴胺系统,可能被证明对某些形式的强迫症有一定的好处。根据现有证据,我们建议对这些疾病患者的治疗必须考虑到疾病的潜在动机和神经生物学的改变。我们为未来临床试验可能考虑对强迫症患者进行的具体治疗提供初步指南。例如,明智的做法可能是在患有 SUD 和 ICD 共病的患者中测试纳曲酮,在患有 ICD 和饮食失调的患者中测试托吡酯,在患有抽动秽语综合征的患者中测试巴氯芬。这些试验还可以包括旨在评估潜在冲动性的量表(例如巴拉特冲动量表),以检查该结构是否可以预测对作用于奖励系统的药物的反应。
The basic concepts underlying compulsive, impulsive and addictive behaviours overlap, which may help explain why laymen use these expressions interchangeably. Although there has been a large research effort to better characterize and disentangle these behaviours, clinicians and scientists are still unable to clearly differentiate them. Accordingly, obsessive-compulsive disorder (OCD), impulse control disorders (ICD) and substance-related disorders (SUD) overlap on different levels, including phenomenology, comorbidity, neurocircuitry, neurocognition, neurochemistry and family history. In this review we summarize these issues with particular emphasis on the role of the opioid system in the pathophysiology and treatment of OCD, ICD and SUD. We postulate that with progression and chronicity of OCD, the proportion of the OCD-related behaviours (e.g. checking, washing, ordering and hoarding, among others) that are driven by impulsive 'rash' processes increase as involvement of more ventral striatal circuits becomes prominent. In contrast, as SUD and ICD progress, the proportion of the SUD- and ICD-related behaviours that are driven by compulsive 'habitual' processes increase as involvement of more dorsal striatal circuits become prominent. We are not arguing that, with time, ICD becomes OCD or vice versa. Instead, we are proposing that these disorders may acquire qualities of the other with time. In other words, while patients with ICD/SUD may develop 'compulsive impulsions', patients with OCD may exhibit 'impulsive compulsions'. There are many potential implications of our model. Theoretically, OCD patients exhibiting impulsive or addictive features could be managed with drugs that address the quality of the underlying drives and the involvement of neural systems. For example, agents for the reduction or prevention of relapse of addiction (e.g. heavy drinking), which modulate the cortico-mesolimbic dopamine system through the opioid (e.g. buprenorphine and naltrexone), glutamate (e.g. topiramate), serotonin (e.g. ondansetron) or y-aminobutyric acid (e.g. baclofen and topiramate) systems, may prove to show some benefit in certain forms of OCD. Based on the available evidence, we suggest that the treatment of patients with these disorders must account for alterations in the underlying motivations and neurobiology of the condition. We provide an initial guide to the specific treatments that future clinical trials might consider in patients with OCD. For example, it might be wise to test naltrexone in patients with co-morbid SUD and ICD, topiramate in patients with comorbid ICD and eating disorders, and baclofen in patients with co-morbid Tourette's syndrome. These trials could also include scales aimed at assessing underlying impulsivity (e.g. Barratt Impulsiveness Scale) to check whether this construct might predict response to drugs acting on the reward system.