San Diego State University, San Diego, CA, USA.
J Sex Med. 2009 Oct;6(10):2901-9. doi: 10.1111/j.1743-6109.2009.01421.x. Epub 2009 Aug 11.
This is the second case report of a woman with bipolar disorder type I who noted the onset of persistent genital arousal disorder (PGAD) symptoms after abrupt cessation of paroxetine. With the worsening of PGAD symptoms, she developed severe depression and suicidal thoughts, resulting in her undergoing electroconvulsive therapy (ECT) as management.
To describe a case of PGAD and develop hypotheses to explain the beneficial actions of ECT on PGAD based on 4 years of ECT administration.
Patient self-report after obtaining consent, as well as literature review.
After the fourth ECT, the patient's PGAD symptoms abated serendipitously. She was placed on ECT on demand for the treatment of her PGAD. With each ECT treatment, PGAD symptoms immediately disappeared, relapsing slowly over time until the next ECT was administered. The patient has, thus far, received a total of 30 treatments of ECT. Side effects continue to be minimal and include brief short-term memory loss, headache, and muscle aches.
ECT is known to induce cerebral excitatory and inhibitory neurotransmitter changes after acute and chronic administration. Sexual arousal is stimulated by the action of hypothalamic and limbic dopamine, noradrenaline, melanocortin, and oxytocin, and inhibited by serotonin, cerebral opioids, and endocannabinoids. Based on the patient's bipolar disorder, the mechanism of action of ECT and the observation of ECT effectiveness on her PGAD, we hypothesize the following: (i) bipolar disorder led to central hyperactive dopamine release, an important component in the pathophysiology of her PGAD; (ii) central serotonin deficiency after selective serotonin-reuptake inhibitor (SSRI) withdrawal resulted in a lack of inhibition of sexual excitement; (iii) ECT resulted in lowering of the hyperstimulated central dopamine release; and (iv) ECT led to an increase in sexual inhibition by stimulating serotonin activity. Further research in the central control of sexual arousal is needed.
这是第二位报告的女性患者，她患有 I 型双相情感障碍，在突然停止服用帕罗西汀后出现持续性生殖器唤醒障碍（PGAD）症状。随着 PGAD 症状的恶化，她出现严重的抑郁和自杀念头，最终接受了电休克治疗（ECT）。
描述一例 PGAD 病例，并根据 4 年的 ECT 管理经验，提出解释 ECT 对 PGAD 有益作用的假说。
患者在获得同意后进行自我报告，以及文献回顾。
第四次 ECT 后，患者的 PGAD 症状意外地减轻了。她因 PGAD 接受按需 ECT 治疗。每次 ECT 治疗后，PGAD 症状立即消失，但随着时间的推移会逐渐复发，直到下一次 ECT 治疗。迄今为止，该患者共接受了 30 次 ECT 治疗。副作用持续轻微，包括短暂的短期记忆丧失、头痛和肌肉疼痛。
ECT 在急性和慢性给药后已知会引起大脑兴奋性和抑制性神经递质的变化。性唤起受下丘脑和边缘多巴胺、去甲肾上腺素、黑色素皮质素和催产素的作用刺激，受 5-羟色胺、脑内阿片类物质和内源性大麻素的抑制。基于患者的双相情感障碍、ECT 的作用机制以及 ECT 对其 PGAD 的有效性观察，我们提出以下假说：（i）双相情感障碍导致中枢多巴胺释放过度活跃，这是她 PGAD 病理生理学的重要组成部分；（ii）选择性 5-羟色胺再摄取抑制剂（SSRI）停药后导致中枢 5-羟色胺缺乏，从而缺乏对性兴奋的抑制；（iii）ECT 导致过度刺激的中枢多巴胺释放降低；（iv）ECT 通过刺激 5-羟色胺活性增加性抑制。需要进一步研究中枢性性唤起的控制。
