Kellner Michael
University Hospital Hamburg-Eppendorf, Dept of Psychiatry and Psychotherapy, Anxiety Spectrum Disorders Unit, Hamburg, Germany.
Dialogues Clin Neurosci. 2011;13(4):485-93. doi: 10.31887/DCNS.2011.13.4/mkellner.
Experimental neurochemical provocation of panic attacks in susceptible human subjects has considerably expanded our knowledge of the pathophysiology and psychopharmacology of panic disorder. Some panicogens also elicit short-lived panic-like states in healthy man. This offers the opportunity to assess the anti-panic action of drugs in proof-of-concept studies. However, from current data it is still unclear whether experimental panic in healthy man is a valid translational model. Most such studies in healthy volunteers have been performed using a cholecystokinin tetrapeptide (CCK-4) challenge. While CCK-4 panic was blocked by alprazolam pretreatment, escitalopram showed negative results in healthy man. Preliminary findings on novel investigational drugs and a few problematic results will be reviewed. Small sample sizes in many panic provocation studies, lack of dose-response aspects, and still-insufficient knowledge about the biological underpinning of experimental and spontaneous panic limit the interpretation of existing findings and should inspire further research.
在易感人群中通过实验性神经化学方法诱发惊恐发作,极大地拓展了我们对惊恐障碍病理生理学和精神药理学的认识。一些致惊恐物质也会在健康人身上引发短暂的惊恐样状态。这为在概念验证研究中评估药物的抗惊恐作用提供了机会。然而,从目前的数据来看,尚不清楚健康人身上的实验性惊恐是否是一个有效的转化模型。大多数针对健康志愿者的此类研究是使用胆囊收缩素四肽(CCK-4)激发试验进行的。虽然阿普唑仑预处理可阻断CCK-4诱发的惊恐,但艾司西酞普兰在健康人身上却得出了阴性结果。本文将对新型研究药物的初步研究结果以及一些有问题的结果进行综述。许多惊恐激发研究样本量小、缺乏剂量反应方面的研究,且对实验性惊恐和自发性惊恐的生物学基础了解仍不足,这些都限制了对现有研究结果的解读,也应促使进一步开展研究。