In a recent review, Xin-Ke Li
[1] expounded the neuroimaging research progress of electroconvulsive therapy (ECT) for major depressive disorder. The authors concluded that the neurobiological mechanism of ECT may be to modulate the functional activity and connectivity or neural structural plasticity of specific brain regions to normal levels for therapeutic effect. We fully agree with the authors and hereby elaborate on the importance and potential of ECT for major depressive disorder.
It was in the course of the Prince s wanderings, in search of experience of men and things, that he came to the court of Queen Frivola, where he was extremely well received
We had met in the second grade. She was missing a tooth, I was missing my friends. I had just moved across the continent to find cold metal swings and cold smirking4 faces outside the foreboding doors of P.S. 174, my new school. I asked her if I could see her Archie comic book, even though I didn’t really like comics; she said yes, even though she didn’t really like to share. Maybe we were both looking for a smile. And we found it. We found someone to giggle5 with late at night, someone to slurp6 hot chocolate with on the cold winter days when school was canceled and we would sit together by the bay window, watching the snow endlessly falling.
ECT mainly achieves therapeutic effects by increasing the synthesis and uptake of norepinephrine in the body and improving the sensitivity of serotonergic neurons. The prevailing view on the mechanism of ECT is that a cascade of reactions is triggered by electrical stimulation of specific areas of the brain. Consequently, neuronal synaptic plasticity and the levels of various neurotrophic factors and synaptic cleft transmitters are altered. Therefore, ECT has a significant therapeutic effect on a variety of mental disorders[2]. A series of studies have proved that ECT is especially suitable for major depressive disorder[3], manic acute episodes, and schizophrenia, especially some acute patients, those with acute affective symptoms, and catatonic patients[3,4].
But the little love lump refused. My kingdom is not of this world, he said. And within he felt all love, all joy, all peace... the gentle touch of the Wumpalump.
In general, ECT has played a very important role in the treatment of some depressive disorders, especially major depressive disorders. In the past decade, however, the role of physical therapy in some neuropsychiatric disorders has been underestimated or partially ignored. Most practitioners only consider ECT when a patient has failed to respond to many medication therapies. Such attempts can last months or years, delaying treatment while also increasing the patient's mental instability and prolonging their suffering. And due to a series of reasons such as ideology[9] and social environment, the role of ECT has not been fully exerted. ECT should not be seen as a last resort for psychiatric treatment.
The authors declare no potential conflicts of interest with respect to the research, authorship, or publication of this article.
ECT has the function of regulating the neuroinflammatory response. When subjected to external stress, there is an inflammatory response that activates indole-amine 2,3-dioxygenase and degrades TRP to kynurenine (KYN), which is metabolized to kynurenic acid (KYNA) and 3-hydroxykynurenine (3-HK). Then, KYNA and 3-HK are converted to quinolinic acid[5]. 3-HK and quinolinic acid have neurotoxic effects on the central nervous system, while KYNA is neuroprotective. Major depressive disorder exacerbates the immune inflammatory response, leading to an increase in BDNF. Several studies have shown that ECT increases KYNA levels[6]. This suggests that ECT may have neuroprotective effects.
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In addition, accumulating neuroimaging evidence suggests that ECT modulates medial temporal and prefrontal cortical regions in major depressive disorder. Source-based morphometry (a multivariate statistical approach for structural data analysis) revealed that the medial temporal lobe network (including the hippocampus and parahippocampal cortex) was significantly increased after ECT[7]. What’s more, a study shows that brain plasticity is induced by changes in gray matter volume (GMV) during treatment for schizophrenia[8]. GMV was determined using voxel-based morphometry wholebrain analysis. These studies provide a broader perspective on the mechanism of action of ECT in the treatment of depression.
the Curriculum Reform Project of Taizhou University in 2021, No. xkg2021087.
Ma ML contributed to the conception of the research and wrote the letter; He LP contributed to the revision of the letter; all authors approved the final manuscript for submission.
But she felt sure that her father was leaving her for ever, so she was very sad when the bell rang sharply for the second time, and warned them that the time had come for them to part
Mei-Lin Ma 0000-0002-5689-7756; Lian-Ping He 0000-0002-9627-5599.
Wang LL
Wang TQ
Wang LL
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World Journal of Clinical Cases2022年16期