I am not a Psych. student or someone who has extensive knowledge on this subject, but from searching this forum, I gathered that our problem has something to do with our desensitized 5-HT1A receptors. And so, searching the web about the effects of psychotherapy on the brain, I was intrigued by what I found:
What do you guys think?Molecular psychodynamics
All these studies, however, have investigated the brain changes on the whole brain systems level. To understand the more basic mechanisms related to psychotherapy, possible molecular and cellular changes should also be studied. So far, only 2 Finnish studies have measured molecular level changes after psychotherapy, and in this way directly tested the hypothesis put forth by Kandel2 that psychotherapy could lead to changes in gene expression through learning, by altering the strength of synaptic connections between nerve cells and inducing morphological changes in neurons. Interestingly, in both studies, the psychotherapy that was used was psychodynamic.
In the study by Lehto and colleagues,20 19 depressive outpatients received psychodynamic psychotherapy for 12 months. Of the patients, 8 were classified as having atypical depression. Midbrain serotonin transporter and striatum dopamine transporter densities were recorded using SPECT brain imaging with the [123I]nor-β-CIT radioligand before and after psychotherapy. The researchers showed that midbrain serotonin transporter density significantly increased during psychotherapy in patients with atypical depression, but not among patients with standard depression. There were no changes in the levels of striatum dopamine transporter. Because of the subgroup finding, these results are difficult to interpret, and one of the shortcomings of this study is the lack of a control group.
In the other Finnish study, patients with MDD were randomized to receive either short-term psychodynamic psychotherapy or fluoxetine. Before being treated and after 4 months of treatment, they underwent a brain scan with PET using [carbonyl-11C]WAY-100635 (measures the density of serotonin type 1A [5-HT1A] receptors) and [11C]raclopride (measures density of dopamine type 2/3 receptors). In the 2 published papers, the researchers reported that the clinical outcome in both treatment groups was similar in terms of standard symptom ratings (symptom remission was achieved in 59% of the patients and 77% of the patients met criteria for response).17,21 However, an analysis of the change in the 5-HT1A receptor density in the treatment groups revealed a significant increase in the psychotherapy group compared with the medication group, for which no change was detected (Figure). Fluoxetine increased [11C]raclopride binding in the lateral thalamus; no change was seen in the group that received psychotherapy.
Several previous studies have found changes in 5-HT1A receptor binding in MDD that is not reversed by SSRI treatment.22-27 This could mean that the recovery process in MDD after psychotherapy is different from recovery after medication. Currently, the clinical implications of these findings are unknown, but they may be related to the finding that suggests that the relapse rate for MDD is lower in patients treated with psychotherapy than in those treated with antidepressants.28
Conclusion
Although still preliminary, the studies using neuroimaging for measuring change caused by psychotherapy will in the long run lead to a more refined understanding of how different psychotherapies work. This may lead to a development in which specific modes of psychotherapy can be designed to target specific brain circuits.1 In addition, neurobiological research may help refine psychological theories about the change processes.
- See more at: http://www.psychiatrictimes.com/psychot ... yQjTr.dpuf
