Abstract
Background
Psychomotor retardation (PMR) is a clinically significant but under-investigated neuropsychiatric manifestation of major depressive disorder (MDD). Its neuroanatomical features remain poorly understood. This study aims to examine differences in gray matter volume (GMV) alterations between MDD patients with and without PMR.
Methods
The study enrolled 107 first-episode, treatment-naïve MDD patients (diagnosed per DSM-IV criteria) and 112 age- and sex-matched healthy controls. Participants were divided into two clinical subgroups based on the retardation factor score of the 17-item Hamilton Depression Rating Scale: an MDD with retardation (MDD-WR) group (score ≥ 8, n = 51) and an MDD without retardation (MDD-WoR) group (score < 8, n = 56). Structural MRI scans were obtained for all participants.
Results
Compared with healthy controls, the MDD-WR group showed significantly smaller GMV in the bilateral posterior cerebellum and left calcarine gyrus. In contrast, the MDD-WoR group demonstrated larger GMV in the left postcentral gyrus (PoCG) and right angular gyrus. Among all of the MDD patients, patients of the MDD-WR group had smaller GMV in the right PoCG, right superior frontal gyrus, and left olfactory bulb compared with the MDD-WoR group.
Conclusion
Our findings identify distinct neuroanatomical patterns of GMV changes in MDD patients with PMR compared with those without PMR. This provides novel insights into the neural basis of PMR in MDD.
Keywords: gray matter volume, major depressive disorder, psychomotor retardation, structural MRI
Introduction
Major depressive disorder (MDD) is a clinically heterogeneous psychiatric condition characterized by persistent and profound low mood, and it frequently results in significant impairment in social functioning [1]. Empirical evidence indicates that psychomotor retardation (PMR) is most common among patients with current depressive episodes [2]. Clinically, PMR appears as generalized psychomotor slowing, including delayed speech and movement, along with cognitive impairment [3,4]. Patients with PMR exhibit more severe clinical characteristics than those without PMR, including longer illness duration, increased suicide risk, and more frequent episodes [3]. However, the neural mechanisms behind PMR in MDD remain poorly understood. Emerging evidence suggests that fronto-striatal networks may contribute to reduced spontaneous movement in MDD patients with psychomotor dysfunction [4]. Neuroimaging studies have found reduced gray matter volume (GMV) in the bilateral caudate nuclei as a potential link to psychomotor dysfunction in depression. However, treatment-associated increases in striatal volume did not predict improvements in psychomotor symptoms [5]. A recent large-scale cohort study further demonstrated that MDD patients with PMR have poor compensatory cortico-caudate and cortico-cortical connectivity in motor networks. This may lead to psychomotor disturbances when patients are depressed [2]. Altogether, these findings suggest that the striatum could be a potential vulnerability factor in PMR pathogenesis. They also point to the involvement of higher cortical regions associated with voluntary motor control. Nevertheless, there is a clear lack of direct structural comparisons between MDD patients with and without PMR. This critical gap in past research precludes clear conclusions about potential gray matter morphological differences between these subgroups. It also limits our understanding of the regional neuroanatomical features that may underlie their clinical heterogeneity.
In neuroimaging research, voxel-based morphometry (VBM) is a reliable method for assessing between-group variations in regional GMV and how these variations relate to phenotypic characteristics [6]. The present study utilized VBM to examine GMV abnormalities in patients with MDD, with a specific focus on comparing those with and without PMR. We hypothesized that GMV differences in different brain regions would be observed in PMR and non-PMR patients, and that these structural abnormalities may represent the neuropathological substrate underlying depression with PMR.
Methods
Participants
This study recruited 219 participants aged 18–60 years, including 112 healthy controls and 107 patients with MDD. Baseline demographic and clinical data, including age, gender, years of education, and illness duration, were systematically collected for all participants. MDD diagnoses were independently confirmed by two senior psychiatrists using structured clinical interviews following DSM-IV criteria.
Patients were recruited at the Department of Psychiatry, First Affiliated Hospital of Kunming Medical University, between February 2012 and July 2015. Inclusion criteria for the patient group included: (a) meeting DSM-IV diagnostic criteria for MDD, with a 17-item Hamilton Depression Rating Scale (HDRS-17) score greater than or equal to 18; (b) age 18–60 years; (c) right-handed; (d) first depressive episode; and (e) medication-naïve. Exclusion criteria were: (a) comorbid psychiatric disorders; (b) history of organic brain disease or severe systemic illness; (c) pregnancy or perinatal status; (d) prior systematic psychotherapy or brain stimulation therapy; and (e) contraindications for MRI.
Healthy controls were recruited through community and institutional advertisements, and matched to patients by age and gender. Inclusion criteria for healthy controls were: (a) no organic brain disease or severe systemic illness; (b) no DSM-IV Axis I or Axis II psychiatric diagnoses; and (c) no family history of mental illness. Exclusion criteria for health controls were the same as those for patients.
The study protocol was approved by the Institutional Review Board of the First Affiliated Hospital of Kunming Medical University [Ethics Review L No. 50 (2016)]. Written informed consent was obtained from all participants before enrollment.
Clinical assessment of patients
To stratify the patient cohort, we used the cumulative scores from items 1, 7, 8, and 14 of the HDRS-17. The patient cohort was divided into two subgroups: 56 participants with scores ranging from 0 to 8 were categorized as ‘Major Depressive Disorder without Retardation’ (MDD-WoR). The remaining 51 patients with scores greater than or equal to 8 were classified as ‘Major Depressive Disorder with Retardation’ (MDD-WR).
MRI data acquisition
All participants had MRI scans at the Department of Medical Imaging, First Affiliated Hospital of Kunming Medical University. Scans were done utilizing a 3.0 Tesla Philips Achieva MRI system with an eight-channel head coil. First, conventional scans were conducted to exclude participants with significant organic brain abnormalities. Next, high-resolution three-dimensional T1-weighted structural images were acquired using a fast spoiled gradient recalled echo sequence with the following imaging parameters: repetition time = 7.38 ms; echo time = 3.40 ms; flip angle = 8°; slice thickness = 1.2 mm (no inter-slice gap); number of slices = 230; field of view = 250 × 250 mm; and matrix size = 256 × 256. The total acquisition time for each scan was 6 min and 53 s. All imaging data were collected under standardized conditions to ensure consistency across participants.
Voxel-based morphometry
Image preprocessing was done on a Matlab 2016a platform (MathWorks, Natick, Massachusetts, USA) using the SPM12 and CAT12 toolboxes after converting the original DICOM images to NIfTI format [7]. T1-weighted images were spatially normalized using the DARTEL algorithm. The data were then automatically segmented into gray matter, white matter, and cerebrospinal fluid. After Jacobian modulation, all gray matter images were smoothed with a full width at half maximum of 8-mm Gaussian kernel. Manual quality control was strictly implemented at each stage of the preprocessing to ensure data integrity.
Statistical analysis
Statistical analyses were conducted using SPSS (version 26.0 for Windows, IBM Corp., Armonk, New York, USA). Normality of data distribution was tested for illness duration in the two patient subgroups, as well as for age, years of education, and HDRS-17 scores across all groups. These variables were then compared using two-sample t-tests or one-way analysis of variance, with results presented as mean ± SD (x̄±s). Categorical variables, including gender, were analyzed using the chi-squared test. A two-tailed P value less than 0.05 was set as the threshold for statistical significance.
Analysis of covariance (ANCOVA) was performed to compare the whole-brain GMV differences across the three groups, with total intracranial volume, years of education, age, and gender included as covariates. Post-hoc pairwise comparisons were then conducted to examine GMV differences between each group. GMV abnormalities were reported using Gaussian random field correction, with significance thresholds set at Pvoxel level < 0.001 and Pcluster level < 0.05.
Regions of interest (ROIs) were identified based on GMV differences between the MDD-WR and MDD-WoR groups. Maximum voxel values from these ROIs were extracted and adjusted, followed by bivariate correlation analysis to examine the relationship between GMV values and HDRS-17 scores.
Results
Demographic and clinical characteristics
The demographic and clinical characteristics of all participants are presented in Table 1. No statistically significant differences were observed in age or gender across the three groups (P > 0.05). Similarly, the duration of illness did not differ significantly between the two MDD subgroups. However, the HDRS-17 scores were significantly lower in the MDD-WoR group than in the MDD-WR group (P < 0.05). Additionally, years of education were significantly lower in both MDD subgroups compared with healthy controls (P < 0.05).
Table 1.
Demographic and clinical characteristics of participants
| MDD-WR (n = 51) |
MDD-WoR (n = 56) |
HC (n = 112) |
F、χ2 or t | P value | |
|---|---|---|---|---|---|
| Age (years) | 30.5 ± 7.7 | 31.3 ± 7.4 | 30.6 ± 7.2 | 0.189 | 0.828a |
| Sex (man/female) | 10/41 | 20/36 | 33/79 | 2.788 | 0.248b |
| Years of education (years) | 11.7 ± 3.7 | 12.3 ± 4.4 | 14.9 ± 4.0 | 13.777 | <0.001a |
| Duration of illness (month) | 9.7 ± 16.1 | 8.8 ± 10.8 | – | 0.337 | 0.737c |
| HDRS-17 | 25.3 ± 4.6 | 21.3 ± 3.1 | – | – | – |
| Total internal volume (mm3) | 1270.4 ± 120.8 | 1332.2 ± 133.3 | 1331.4 ± 111.8 | 5.136 | 0.007a |
ANCOVA, analysis of covariance; HC, healthy controls; .HDRS-17, 17-item Hamilton Depression Rating Scale; MDD, major depressive disorder; MDD-WoR, MDD without retardation; MDD-WR, MDD with retardation.
The P value was obtained by analyses of variance.
The P value was obtained by a chi-square test. P = 0.136 (MDD-WR vs. MDD-WoR).
The P value was obtained by a two-tailed, two-sample t-test.
Gray matter volume abnormalities across groups
Results of the GMV analysis across the three groups are presented in Table 2 and Fig. 1. ANCOVA identified significant intergroup differences in the right postcentral gyrus (PoCG). Specifically, the MDD-WR group showed significantly smaller GMV in the left olfactory bulb, right superior frontal gyrus (SFG), and right PoCG compared with the MDD-WoR group. Furthermore, relative to healthy controls, the MDD-WR group demonstrated lower GMV in the bilateral posterior lobe of the cerebellum and left calcarine sulcus. In contrast, the MDD-WoR group had larger GMV in the left PoCG and right angular gyrus compared with healthy controls.
Table 2.
Significant group differences in gray matter volume
| Cluster location | Hemisphere | MNI (X, Y, Z) | Number of voxels | F or T value | ||
|---|---|---|---|---|---|---|
| ANCOVA | ||||||
| Postcentral gyrus | R | 48 | –23 | 60 | 51 | 13.1599 |
| MDD-WR vs. MDD-WoR | ||||||
| Olfactory bulbs | L | –6 | 25 | –11 | 71 | –4.2113 |
| Superior frontal gyrus | R | 13 | 37 | 55 | 166 | –4.1199 |
| Postcentral gyrus | R | 48 | –22 | 60 | 260 | –5.1269 |
| MDD-WR vs. HC | ||||||
| Cerebellum posterior lobe | L | –37 | –55 | –40 | 85 | –3.806 |
| Calcarine | L | –1 | –84 | –9 | 46 | –3.8267 |
| Cerebellum posterior lobe | R | 37 | –58 | 40 | 72 | –3.9931 |
| MDD-WoR vs. HC | ||||||
| Postcentral gyrus | L | –36 | –36 | 60 | 62 | 3.9141 |
| Angular gyrus | R | 54 | -48 | 30 | 42 | 3.8508 |
X, Y, Z, coordinates of peak locations in the MNI space. T value represents the statistic value of two-sample t-tests at Gaussian random field corrected P < 0.001 (voxel level) and P < 0.05 (cluster level). F value represents the statistic value of one-way analysis of variance.
ANCOVA, one-way analysis of variance; HC, healthy controls; MDD, major depressive disorder; MDD-WoR, MDD without retardation; MDD-WR, MDD with retardation.
Fig. 1.
Statistical maps illustrating group differences in GMV. Statistical maps show GMV differences in patients with MDD-WR or MDD-WoR compared with HCs. (a) Group differences in GMV within the right postcentral gyrus across all three groups. (b–d) Regions where MDD-WR patients show smaller GMV compared with MDD-WoR patients. (e–j) Regions where MDD-WR patients show smaller GMV compared with HCs. (h and i) Regions where MDD-WR patients show larger GMV compared with HCs. Red and blue indicate regions with significantly larger and smaller GMV, respectively (P < 0.05, GRF corrected). GMV, gray matter volume; HCs, healthy controls; MDD, major depressive disorder; MDD-WoR, MDD without retardation; MDD-WR, MDD with retardation.
Correlation between gray matter volume values and clinical characteristics
GMV values of ROIs and HDRS-17 scores were normally distributed with homogenous variance. Thus, Pearson correlation analyses are presented in Fig. 2. Statistically significant negative linear correlations between total HDRS-17 scores and GMV values in the right SFG (r = −0.237, P = 0.014) and right PoCG (r = −0.238, P = 0.014) were observed in patients with MDD (see Fig. 2). However, subgroup analysis of MDD patients did not show significant associations. No statistically significant correlations were found between HDRS-17 scores and GMV values in other cerebral regions.
Fig. 2.
Correlation between HDRS-17 scores and GMV values. (a) Negative linear correlations between total HDRS-17 scores and GMV values in the right SFG. (b) Negative linear correlations between total HDRS-17 scores and GMV values in the right PoCG. GMV, gray matter volume; HDRS-17, 17-item Hamilton Depression Rating Scale; PoCG, postcentral gyrus; SFG, superior frontal gyrus.
Discussion
The current study found a significant smaller GMV in the right SFG in the MDD-WR group compared with the MDD-WoR group. The SFG is a critical component of the dorsolateral prefrontal cortex and is crutial for cognitive control and emotional regulation processes [8,9]. Furthermore, empirical evidence has found a significant association between SFG dysfunction and anhedonia [10], a core symptom of MD. The smaller GMV observed in the SFG may therefore represent a neuropathological mechanism underlying MD. Since PMR may be a more distinctive feature of MD than anhedonia [11], combining these findings with our results suggests that smaller SFG GMV may also be a specific pathological mechanism of the MDD-WR subgroup.
Subgroup comparisons showed a significantly smaller GMV in the left olfactory bulb of the MDD-WR group compared with the MDD-WoR group. This observation is consistent with clinical evidence of smaller olfactory bulb GMV in MDD patients [12]. Neuroanatomical studies have identified the olfactory bulb projections to emotion-related brain regions, including the piriform cortex (PirC) and amygdala (Amg). Experimental evidence from rodent models demonstrates that olfactory bulbectomy induces anhedonia – this effect may be mediated by indirect olfactory bulb projections to the nucleus accumbens (NAc) via the PirC. Given the NAc’s central role in the reward pathway, olfactory bulb inhibition may lead to NAc hypofunction and subsequent anhedonia [13]. Our previous studies found significant functional differences in the NAc between the MD and NMD groups [14]. Since PMR is a hallmark feature of MD, the observed smaller in left olfactory bulb GMV in the MDD-WR group compared with the MDD-WoR group may indicate more severe anhedonia in the MDD-WR group.
The present study also observed significantly smaller GMV in the right PoCG in the MDD-WR group compared with the MDD-WoR group. Previous research has linked PoCG abnormalities to MDD severity [15]. Additionally, sleep efficiency in MDD patients has shown a positive association with regional activity in the PoCG [16]. Notably, the PoCG has also been involved in suicide risk assessment in mood disorders [17]. Since MD is characterized by greater disease severity, more severe sleep disturbances, and elevated suicide risk compared with NMD [18], these findings suggest that the PoCG may represent a neural substrate associated with these clinical features of MD. Considering PMR is a core feature of MD [11] and the observed negative correlation between this brain region and HDRS-17 total scores, the current findings, together with previous evidence, suggest that the clinical characteristics of the MDD-WR group, particularly disease severity, might be linked to the observed smaller GMV in the PoCG.
The present study further observed a significantly smaller GMV within the bilateral cerebellum of the MDD-WR group compared with healthy controls. Our findings align with previous studies demonstrating reduced cerebellar GMV in MDD patients, suggesting that cerebellar structural changes may contribute to the pathophysiology of depression [19]. Supporting this, recent perfusion SPECT imaging studies have found hypoperfusion in the cerebellum and other brain regions in MDD-WR patients, further linking cerebellar dysfunction to PMR pathogenesis [20]. Given the phenotypic similarities between MDD-WR and MD [11], these findings suggest that cerebellar structural abnormalities may be a neurobiological substrate for PMR in MDD-WR.
Moreover, the current study revealed significantly smaller GMV in the calcarine gyrus in MDD-WR patients and healthy controls. The calcarine gyrus is located in the primary visual cortex and plays a pivotal role in initial visual information processing [21]. Empirical evidence has documented impaired neural responses to visual emotional stimuli and reduced emotional expressivity in MD patients [22]. Since PMR is a core diagnostic feature of MD, the identified structural abnormalities in the calcarine gyrus may reflect disruptions in visual feedback-mediated motor regulation processes [23], potentially contributing to the neuropathological mechanisms underlying PMR.
The present study also found a significantly larger GMV in the right angular gyrus in the MDD-WoR group compared with healthy controls. A previous study found that the angular gyrus is associated with the pathogenesis of depression [19]. The angular gyrus is a key component of the posterior DMN [24]. Clinical studies have found a positive correlation between improved PMR and enhanced connectivity within the posterior DMN [25], suggesting that targeted modulation of posterior DMN regions may represent a potential therapeutic strategy for PMR. However, the mechanisms through which angular gyrus modulation improves PMR remain unclear and require further study.
This study has several limitations to consider. First, its cross-sectional design prevents establishing causal relationships. Second, the assessment of PMR was limited to a single scale-based measure. The current study employed the PMR subscale of the HDRS-17 for patient classification. Future studies should integrate quantitative assessment tools to enhance the robustness of these findings. Third, the years of education were lower in the MDD patients group than that in the healthy controls, and years of education are known to correlate with cognitive performance. The absence of cognitive function assessments in this study limits our ability to fully explore the relationship between PMR and cognitive impairment in depressed patients. Subsequent studies should aim to provide additional evidence to better delineate the relationship between the observed brain region alterations and PMR.
In summary, this study found that depressed patients with PMR have smaller GMV in multiple brain regions compared with both healthy controls and depressed patients without PMR. These brain regions are associated with key clinical features of depression, suggesting that these structural abnormalities may serve as the neuropathological substrate underlying depression with PMR.
Acknowledgements
We thank our participants and their families for their cooperation. We would also like to thank all the staff involved in the study. We thank Jingting Yan for providing language help and writing assistance.
This work was supported by the National Natural Science Foundation of China (Grant No. 82260277), the Yunnan fundamental research projects (Grant No. 202301AT070126), the Yunnan Revitalization Talent Support Program and Yunnan Clinical Medical Center for Mental Disorders (2024YNLCYXZX0006), and Academician Song Weihong Workstation in Yunnan Province (202305AF150180).
All authors contributed to and approved the final manuscript. Y.W. and L.Y. analyzed the data and drafted the manuscript. X.L. and J.L. conducted the study. Y.Z. contributed to data management. Z.S. organized the study and finalized the manuscript.
Conflicts of interest
The authors declare no conflicts of interest.
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