Milnacipran for the treatment of chronic pain
Milnacipran for the treatment of chronic pain
复制标题
米那普仑用于治疗慢性疼痛
DOI：
10.1002/hup.521
复制
发表时间：
2003
期刊：
影响因子：
--
通讯作者：
H. Higuchi
中科院分区：
文献类型：
--
作者：
M. Kamata;Shingo Naito;Hitoshi Takahashi;H. Higuchi
三环类抗抑郁药(TCAs)是治疗慢性疼痛最常用的抗抑郁药。TCA对去甲肾上腺素和5-羟色胺的影响，这两种单胺被认为是抑郁症病因学的关键，对于它们对慢性疼痛的影响也很重要(Barkin和Fawcett，2001)。TCA阻断了其他与慢性疼痛治疗无关的神经受体。正是这些不相关的神经受体的拮抗作用产生了众所周知的TCA的不良反应，这些不良反应损害了患者的依从性(Barkin和Fawcett，2001)。米那普兰是一种选择性的5-羟色胺和去甲肾上腺素再摄取抑制剂(SNRI)，已在大鼠下丘脑中被证明可以抑制去甲肾上腺素和5-羟色胺的再摄取，其效力相似(Moret等人，1985)。在选择性和绝对亲和力方面，米那西普兰与丙咪嗪相似(Moret等人，1985年)。此外，米那西普兰不与突触后受体相互作用，这被认为是其良好耐受性的原因(Kasper等人，1996)。我们假设米那普兰在治疗慢性疼痛方面将被证明特别有效。有一些关于使用米兰西普兰治疗慢性疼痛的报告(Shimamoto等人，2002年；丰福县，2003年；宇都宫等人，2002年)。我们增加了一例慢性疼痛通过米那普兰治疗缓解的病例报告。一位72岁的家庭主妇患舌痛2个月。尽管她的胃口很好，但疼痛还是导致了她进食困难。她咨询了耳鼻喉科医生，但没有发现舌头、鼻子和喉咙异常。用维生素制剂和非类固醇抗炎药治疗疼痛的努力收效甚微。她被转介到我们精神病科。舌痛现在已经持续了3个多月，她被诊断为慢性舌痛。没有观察到抑郁症状，但她确实遭受了轻微的失眠。使用三唑仑0.25 mg/d治疗失眠，获得了良好的睡眠。安定4 mg/d治疗3周并未改善舌痛。安定停用，患者开始服用米那西普兰50 mg/d。疼痛在2周内明显消退。自从米那西普兰开始使用后的一个月里，她几乎没有感觉到疼痛。自米那西普兰开始以来，医疗方案没有任何变化。米那西普兰似乎缓解了这名患者的慢性疼痛，尽管她年龄较大，但对药物的耐受性很好。有研究表明，治疗慢性疼痛的理想抗抑郁剂是同时调节去甲肾上腺素和5-羟色胺，但缺乏与TCA相关的非治疗性突触效应(Barkin和Fawcett，2001)。因此，在慢性疼痛的药物治疗中，SNRIs可能是TCAs的有效替代品。文拉法辛，另一种SNRI，已经被报道在治疗慢性疼痛方面有帮助(Songer和Schulte，1996)。米那西普兰是日本唯一可用的SNRI。由于米那普兰不是通过肝脏中的细胞色素P-450系统代谢的(Puozzo和Leonard，1996)，它还有一个额外的优势，即不良药物相互作用的风险很低。虽然这位患者的慢性疼痛通过米那普兰的治疗得到了改善，但这位患者没有进行任何形式的疼痛量化。在进一步的研究中，使用某种形式的疼痛量化可能会有所帮助，例如视觉模拟标尺，以了解疼痛程度。我们建议进一步研究米那普兰对慢性疼痛的疗效。
Tricyclic antidepressants (TCAs) are the most commonly studied antidepressants in the treatment of chronic pain. The effect of the TCAs on both norepinephrine and serotonin, the two monoamines believed to be key in the aetiology of depression, is also important for their effect on chronic pain (Barkin and Fawcett, 2001). The TCAs block other neuroreceptors unrelated to the treatment of chronic pain. It is the antagonism of these unrelated neuroreceptors that produces the well-known adverse effects of the TCAs, and these adverse effects compromise patient compliance (Barkin and Fawcett, 2001). Milnacipran is a selective serotonin and norepinephrine reuptake inhibitor (SNRI) that has been shown in the rat hypothalamus to inhibit the reuptake of both norepinephrine and serotonin with similar potency (Moret et al., 1985). With respect both to selectivity and absolute affinity, milnacipran is similar to imipramine (Moret et al., 1985). Furthermore, milnacipran does not interact with post-synaptic receptors and this is thought to be responsible for its favourable tolerance profile (Kasper et al., 1996). We hypothesized that milnacipran would prove particularly effective in the treatment of chronic pain. There have been a few reports on the use of milancipran for chronic pain (Shimamoto et al., 2002; Toyofuku, 2003; Utsunomiya et al., 2002). We add a case report of chronic pain ameliorated by treatment with milnacipran. A 72-year-old housewife suffered from glossal pain for 2 months. The pain caused difficulty in eating, even though she had a good appetite. She consulted an otolaryngologist, but no tongue, nose or throat abnormality was found. Efforts to treat the pain with a vitamin preparation and nonsteroidal antiinflammatory drugs were of little effect. She was referred to our Department of Psychiatry. The tongue pain had now persisted for over 3 months, and she was diagnosed with chronic glossal pain. Depressive symptoms were not observed, but she did suffer slight insomnia. Triazolam 0.25 mg/day was used to treat the insomnia, and she achieved sound sleep. Treatment with diazepam 4 mg/day for 3 weeks did not improve the tongue pain. The diazepam was stopped and the patient was started on milnacipran 50 mg/day. The pain subsided markedly within 2 weeks. She has felt little pain in the month since milnacipran was started. No changes in the medical regimen have been introduced since the start of the milnacipran. Milnacipran appears to have alleviated this patient’s chronic pain, and the drug was well tolerated despite her age. It has been suggested that the ideal antidepressant agent for the management of chronic pain would modulate both norepinephrine and serotonin but lack the nontherapeutic synaptic effect associated with the TCAs (Barkin and Fawcett, 2001). Accordingly, the SNRIs may be useful alternatives to the TCAs in the pharmacological treatment of chronic pain. Venlafaxine, another SNRI, has already been reported to be helpful in the treatment of chronic pain (Songer and Schulte, 1996). Milnacipran is the sole SNRI which available in Japan. Because milnacipran is not metabolized via the cytochrome P-450 system in the liver (Puozzo and Leonard, 1996), it has the additional advantage of a low risk for adverse drug interactions. Although this patient’s chronic pain was ameliorated by the treatment with milnacipran, no form of quantification of pain was performed in this patient. In a further study, it may be helpful to use some form of quantification of pain, such as a visual analogue scale, to understand the pain level. We suggest that milnacipran should be studied further for its effectiveness in the treatment of chronic pain.