High efficiency of left superior frontal gyrus and the symptom features of major depressive disorder.

Objectives: Major depressive disorder (MDD) patients with anhedonia tend to have a poor prognosis. The underlying imaging basis for anhedonia in MDD remains largely unknown. The relationship between nodal properties and anhedonia in MDD patients need to be further investigated. Herein, this study aims to explore differences of cerebral functional node characteristics in MDD patients with severe anhedonia (MDD-SA) and MDD patients with mild anhedonia (MDD-MA) before and after the antidepressant treatment.

Methods: Ninety participants with current MDD were recruited in this study. 24-Item Hamilton Depression Scale (HAMD-24) and Snaith-Hamilton Pleasure Scale (SHAPS) were used to assess the severity of depression and anhedonia at baseline and the end of 6-months treatment. The MDD patients who scored above the 25th percentile on the SHAPS were assigned to an MDD-SA group (19), while those who scored below the 25th percentile were assigned to an MDD-MA group (18). All patients in the 2 groups received antidepressant treatment. Functional magnetic resonance imaging (fMRI) images of all the patients were collected at baseline and the end of 6-months treatment. Graph theory was applied to analyze the patients' cerebral functional nodal characteristics, which were measured by efficiency (e) and degree (k).

Results: Repeated measures 2-factor ANCOVA showed significant main effects on group on the e and k values of left superior frontal gyrus (LSFG) (0.003 and 0.008, respectively), and on the e and k values of left medial orbital-frontal gyrus (LMOFG) (=0.004 and 0.008, respectively). Compared with the MDD-MA group, the significantly higher e and k values of the LSFG (0.015 and 0.021, respectively), and the significantly higher e and k values of the LMOFG (=0.015 and 0.037, respectively) were observed in the MDD-SA group at baseline. Meanwhile, higher SHAPS scores could result in higher e and k values of LSFG (=0.019 and 0.026, respectively), and higher e value of LMOFG (0.040) at baseline; higher SHAPS scores could result in higher e values of LSFG (0.049) at the end of 6-months treatment. The multiple linear regression analysis revealed that sex were negatively correlated with the e and k values of LSFG (= -0.014, =0.004; =-1.153, =0.001, respectively). The onset age of MDD was negatively correlated with the k value of LSFG (=-0.420, =0.034) at the end of 6-months treatment. We also found that SHAPS scores at baseline were positively correlated with the HAMD-24 scores (=0.387, =0.022) at the end of 6-months treatment.

Conclusions: There are obvious differences in nodal properties between the MDD-SA and the MDD-MA patients, such as the high e of LSFG in the MDD-SA patients, which may be associated with the severity of anhedonia. These nodal properties could be potential biomarkers for the prognosis of MDD. The increased e and k values in the LSFG of MDD-SA patients may underlie a compensatory mechanism or protective mechanism. The mechanism may be an important component of the pathological mechanism of MDD-SA. The poor prognosis in the MDD-SA patients suggests that anhedonia may predict a worse prognosis in MDD patients. Sex and onset age of MDD may affect the nodal properties of LSFG at baseline and the end of 6-months treatment.