Henderson Theodore A
Neuro-Luminance, The Synaptic Space, Neuro-Laser Foundation, Centennial, CO, USA.
Neural Regen Res. 2016 Feb;11(2):195-200. doi: 10.4103/1673-5374.177708.
While controversial, ketamine has emerged as an effective treatment for refractory depression. Serial infusions have been performed 3 times per week, but our practical experience has challenged this precept concerning infusion frequency. Depression is associated with neuron loss, reduced synapse numbers, and dearborization of dendrites. Ketamine appears to potently induce mechanisms which reverse these neurodegenerative processes. Ketamine not only blocks the glutamate receptor, it activates eukaroyotic elongation factor 2 (eEF2). This, in turn, activates brain-derived neurotrophic factor (BDNF) protein synthesis. This is thought to underlie ketamine's enduring benefits. In addition, ketamine alters glycogen synthase kinase-3 (GSK-3) phosphorylation, probably responsible for its rapid antidepressant effect. Notably, inhibition of the BDNF receptor does not block the immediate benefits of ketamine, but does prevent the enduring effects. Neuro-Luminance Ketamine Infusion Centers have been treating patients with serial ketamine infusions for over three years. Our methods differ from what is often reported, as we perform infusions only once per week and generally do not perform more than five infusions. Data from 100 patients showed that 80% of the patients responded. The baseline Quick Inventory of Depressive Symptomatology-Self Report (QIDS-SR) score was 17.8 ± 2.8. Responders to ketamine showed a drop in QIDS-SR score of 10.8 ± 3.5, while non-responders showed a 0.8 ± 1.8 change. Moreover, they often had persistent benefits over several months. Recently, it was proposed that psychotomimetic effects are necessary during a ketamine infusion to yield effective antidepressant benefits. Yet, only one patient in our clinic has experienced hallucinations in three years. Nevertheless, 80% of our patients show clinical improvement. Further studies of clinical methods for ketamine infusion therapy are encouraged.
尽管存在争议,但氯胺酮已成为治疗难治性抑郁症的有效方法。以往每周进行3次连续输注,但我们的实际经验对这种关于输注频率的观念提出了挑战。抑郁症与神经元丧失、突触数量减少以及树突脱失有关。氯胺酮似乎能有效诱导逆转这些神经退行性过程的机制。氯胺酮不仅能阻断谷氨酸受体,还能激活真核生物延伸因子2(eEF2)。这进而激活脑源性神经营养因子(BDNF)的蛋白质合成。这被认为是氯胺酮持久疗效的基础。此外,氯胺酮会改变糖原合酶激酶-3(GSK-3)的磷酸化,这可能是其快速抗抑郁作用的原因。值得注意的是,抑制BDNF受体会阻断氯胺酮的即时疗效,但不会阻止其持久疗效。神经发光氯胺酮输注中心用连续氯胺酮输注治疗患者已超过三年。我们的方法与通常报道的不同,因为我们每周仅进行一次输注,且一般不超过5次输注。来自100名患者的数据显示,80%的患者有反应。抑郁症状快速自评量表(QIDS-SR)的基线评分为17.8±2.8。氯胺酮治疗有反应者的QIDS-SR评分下降了10.8±3.5,而无反应者的评分变化为0.8±1.8。此外,他们在数月内往往有持续的疗效。最近有人提出,氯胺酮输注期间产生有效的抗抑郁疗效需要有拟精神病效应。然而,在我们诊所三年来只有一名患者出现幻觉。尽管如此,我们80%的患者有临床改善。鼓励对氯胺酮输注治疗的临床方法进行进一步研究。