Panic disorder: Neurobiology and mechanisms of cardiac risks

有些人会反复发作，往往是莫名其妙的焦虑，这是非常不愉快的，并伴有身体症状，如出汗，心悸，震颤和窒息的感觉。在几个月或几年的时间内反复发作，形成了恐慌症诊断的基础。直到最近，人们才意识到，尽管恐慌症令人痛苦和致残，但它并不构成生命危险。患者往往担心他们有心脏病，因为他们的症状的性质，但已经放心，这不是事实。然而，最近的流行病学研究表明，恐慌症患者的心脏风险增加。本研究的假设如下：这种恐慌症的特征是大脑化学信使血清素的释放增加，这是通过药物治疗逆转的最广泛使用的一类药物对这种疾病，选择性血清素再摄取阻滞剂，在神经系统的自动刺激部分的变化，具有首要的重要性，在遗传易感性恐慌症，和调节心脏病风险。在治疗过程中体重增加是一个很常见的问题，这是由于抑制大脑5-羟色胺的释放。我们将使用最先进的临床科学方法测试所有这些主张。惊恐障碍有一个重要的心脏方面，需要更好地了解心脏保护惊恐障碍患者实现。我们对心脏风险机制的研究应该提供这一点。我们还将提供非常直接，有效的测量恐慌症患者大脑中化学信使的释放，使用我们独特的方法。这将为惊恐障碍的脑化学异常和选择性5-羟色胺再摄取抑制剂的作用机制提供新的认识。

Some people are subject to episodes of recurring, often inexplicable anxiety which are very unpleasant and accompanied by physical symptoms such as sweating, palpitations, tremor and a sensation of suffocation. Recurring attacks over a period of months, or years, forms the basis for the diagnosis of panic disorder. It has until recently been felt that although panic disorder was distressing and disabling, it did not constitute a risk to life. Sufferers often fear that they have heart disease, because of the nature of their symptoms, but have been reassured that this is not the case. Recent epidemiological studies, however, indicate that there is an increased risk of heart risk in patients with panic disorder. Our hypotheses in this research are as follows: That panic disorder is characterised by increased release of the brain chemical messenger, serotonin, which is reversed by drug treatment with the most widely used class of drugs for this disorder, selective serotonin reuptake blockers That changes in an automatic stimulatory part of the nervous system, has primary importance in the disorder, in both genetically predisposing to panic disorder, and in mediating heart risk. That weight gain during therapy, a very common problem, is due to inhibition of brain serotonin release. We will test all these propositions using state of the art clinical scientific methods. Panic disorder has an important cardiological dimension which needs to be better understood for cardiac protection to be achieved in panic disorder patients. Our study of the mechanisms of cardiac risk should provide this. We will also provide very direct, valid measurements of chemical messenger release in the brain of panic disorder sufferers, using our unique methods. These should give a new understanding of the brain chemistry abnormalities of panic disorder, and the mechanism of action of the selective serotonin reuptake inhibitors.