scholarly journals The Hypothesis on the Prediction of Treatment Response with Buspirone Augmentation along with Serotonergic Antidepressant in Patients with Major Depressive Disorder Using Loudness Dependence of Auditory Evoked Potentials: Two Cases and Review of the Literature for Evidence

2020 ◽  
Vol 17 (3) ◽  
pp. 222-224
Author(s):  
Young-Min Park

Some studies have shown that augmenting buspirone with antidepressant has similar efficacy as the combination with two antidepressants in patients with major depressive disorder (MDD). Some researchers assume that the antidepressant boosting effect of buspirone is revealed under a poop-out state, which means a phenomenon where some patients having an initial response to an antidepressant may worsen or not improve any more even though they continue treatment because of serotonin depletion. Loudness dependence of auditory evoked potential (LDAEP) is a reliable marker of central serotonergic activity, and is inversely correlated with central serotonergic activity. Thus LDAEP will be a biological marker for prediction of treatment response with buspirone augmentation with SSRI because it can measure central serotonergic activity such as serotonin depletion. Two cases will be introduced and the literature evidence about whether LDAEP can predict the treatment response of buspirone augmentation in patients with MDD will be reviewed.

2020 ◽  
Vol 10 (11) ◽  
pp. 789
Author(s):  
Yang Rae Kim ◽  
Young-Min Park

Mismatch negativity (MMN) and loudness dependence of auditory evoked potentials (LDAEP), which are event-related potentials, have been investigated as biomarkers. MMN indicates the pre-attentive function, while LDAEP may be an index of central serotonergic activity. This study aimed to test whether MMN and LDAEP are useful biological markers for distinguishing patients with bipolar disorder (BD) and major depressive disorder (MDD), as well as the relationship between MMN and LDAEP. Fifty-five patients with major depressive episodes, aged 20 to 65 years, who had MDD (n = 17), BD type II (BIID) (n = 27), and BD type I (BID) (n = 11), were included based on medical records. Patients with MDD had a higher MMN amplitude than those with BID. In addition, the MMN amplitude in F4 positively correlated with the Korean version of mood disorder questionnaire scores (r = 0.37, p = 0.014), while the MMN amplitude in F3 correlated negatively with LDAEP (r = −0.30, p = 0.024). The odds ratios for the BID group and some variables were compared with those for the MDD group using multinomial logistic regression analysis. As a result, a significant reduction of MMN amplitude was found under BID diagnosis compared to MDD diagnosis (p = 0.015). This study supported the hypothesis that MMN amplitude differed according to MDD, BIID, and BID, and there was a relationship between MMN amplitude and LDAEP. These findings also suggested that BID patients had a reduced automatic and pre-attentive processing associated with serotonergic activity or N-methyl-D-aspartate receptor.


2019 ◽  
Vol 9 (10) ◽  
pp. 253
Author(s):  
Bun-Hee Lee ◽  
Young-Min Park ◽  
Seung-Hwan Lee ◽  
Miseon Shim

Background: Proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α), are associated with the pathophysiology of major depressive disorder (MDD). Several studies have reported that increased TNF-α might be associated with tryptophan depletion, which eventually could result in MDD. However, other studies revealed that TNF-α increased serotonin firing in raphe. Therefore, whether TNF-α increases or decreases serotonin activity remains unclear. Here, we aimed to determine the relationship between serum TNF-α level and central serotonergic activity using the loudness dependence of auditory evoked potentials (LDAEP) and standardized low-resolution brain electromagnetic tomography (sLORETA), as well as to evaluate the effects of antidepressants on TNF-α levels. Methods: LDAEP, serum TNF-α level, and depression severity were measured in 64 MDD outpatients pre and post 3 months of treatment. Results: Pretreatment TNF-α levels were negatively correlated with the pretreatment N1 sLORETA-LDAEP, P2 sLORETA-LDAEP, and N1/P2 sLORETA-LDAEP (p < 0.05). In multiple regression analysis for N1/P2 sLORETA-LDAEP, lower N1/P2 sLORETA-LDAEP was significantly related to higher TNF-α (CE = −0.047, p = 0.017) when all subjects were dichotomized based on the median TNF-α level (7.16 pg/mL) into pretreatment low- and high-TNF-α groups. In addition, the pretreatment Beck Depression Inventory, P2 LDAEP, and N1/P2 sLORETA-LDAEP were greater in the high-TNF-α groups than in the low-TNF-α groups (p < 0.05). Moreover, the posttreatment TNF-α level was significantly decreased compared to the pretreatment TNF-α level (z = −2.581, p = 0.01). However, the posttreatment TNF-α levels were not associated with posttreatment LDAEP. Conclusions: Higher TNF-α level is associated with decreased LDAEP, which could indicate compensatory elevation of central serotonin activity in outpatients with MDD, although this effect disappeared and TNF-α level was reduced after three months of antidepressant treatment.


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