Abstract
The present study aimed to examine the neural mechanisms underlying the ability to process the mental rotation with mirrored stimuli for different depressive tendencies with psychomotor retardation. Using functional near-infrared spectroscopy (fNIRS), we measured brain cortex activation of participants with higher and lower depressive tendencies while performing a left-right paradigm of object mental rotation or a same-different paradigm of subject mental rotation. Behavioral data revealed no differences in reaction time and rotation speed. The fNIRS data revealed a higher deactivation of oxyhemoglobin (HbO) change for the higher depression group in the perceptual stage of object mental rotation with mirrored stimuli in the superior external frontal cortex (BA46), inferior frontal gyrus (BA45), premotor cortex (BA6), and primary motor cortex (BA4) (study 1). In addition, there existed a significant difference between the two groups in premotor cortex (BA6) in subject mental rotation with mirrored stimuli (study 2). These results suggest that the neural mechanism of higher depression individuals connected with psychomotor retardation exists in the frontal and motor areas when processing object mental rotation with mirrored stimuli, and the motor cortex when processing subject mental rotation.
Highlights
Individuals with depression have difficulties in emotion and cognition, presenting depressive mood for more than 2 weeks, being anhedonia, being bias toward negative information, an inhibition disorder to information, and being psychomotor retardation
Twenty-seven participants were assigned to the lower depression tendencies group whose Z score was less than 0, while 13 participants were in the higher group whose Z score was greater than 0
The independent samples t-test showed no significant difference in the reaction time of the perceptual stage and rotation speed of the rotation stage, ts < 1
Summary
Individuals with depression have difficulties in emotion and cognition, presenting depressive mood for more than 2 weeks, being anhedonia, being bias toward negative information, an inhibition disorder to information, and being psychomotor retardation. Individuals with depression disorder have some specific brain cortex. Brain structures altered in depression are part of several connectivity networks, such as in the Default Mode Network (DMN) and the Cognitive Control Network (CCN) (Gudayol-Ferré et al, 2015). Yan et al (2019) found reduced rather than increased functional connectivity within the default mode network for major depressive disorder. Region-specific fNIR leads show patients with unipolar depression had lower hemodynamic activation in the left dorsolateral prefrontal cortex (DLPFC), orbitofrontal cortex (OFC), bilateral ventrolateral prefrontal cortex (VLPFC), and left inferior frontal gyrus (IFG) relative to healthy population (Feng et al, 2021). Patients with bipolar disorder showed more deactivation in the medial prefrontal cortex than those with unipolar depression (Rodríguez-Cano et al, 2017). The information processing of depressive person involves the frontal cortex, and the deactivation might be presented
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