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ABSTRACT Neuroeconomic findings show that interoceptive sensitivity contributes to the typical overweighting of prospective losses over gains known as “loss aversion.” Whether the latter is related to the morphometric properties of the insula—a key node for interoception—remains, however, debated, due to previous conflicting evidence of both positive and negative correlations between their respective metrics. We combined a well‐established behavioral modeling approach with a comprehensive morphometric protocol to explore both a linear and quadratic relationship between loss aversion and distinct voxel‐based and surface‐based cortical features in a sample of 208 healthy young individuals. Both univariate and multivariate analyses highlighted a positive quadratic (i.e., U‐shaped) relationship between loss aversion and distinct morphometric features of the posterior insula and somatosensory‐parietal cortex. These results first suggest that previous inconsistent findings might reflect methodological differences across studies, facilitating the detection of either the descending or ascending sectors of a U‐shaped relationship between loss aversion and structural features. Moreover, they provide novel insights into the interoceptive modulation of choice‐related evaluations guiding decision‐making towards or away from loss avoidance, thus paving the way to studies investigating alterations of this mechanism in neuro‐psychiatric conditions and its susceptibility to different types of intervention including neuromodulation. Univariate and multivariate analyses highlighted a positive, “U‐shaped”, quadratic relationship between loss aversion and posterior insular/somatosensory morphometric features. These results provide novel insights into the interoceptive modulation of choice‐related evaluations guiding decision‐making towards or away from loss avoidance, paving the way to studies investigating alterations of this mechanism in neuro‐psychiatric conditions.

Aims The aim of this study is to investigate differences in gray matter volume and cortical complexity between Parkinson's disease with depression (PDD) patients and Parkinson's disease without depression (PDND) patients. Methods A total of 41 PDND patients, 36 PDD patients, and 38 healthy controls (HC) were recruited and analyzed by Voxel‐based morphometry (VBM) and surface‐based morphometry (SBM). Differences in gray matter volume and cortical complexity were compared using the one‐way analysis of variance (ANOVA) and correlated with the Hamilton Depression Scale‐17 (HAMD‐17) scores. Results PDD patients exhibited significant cortical atrophy in various regions, including bilateral medial parietal–occipital–temporal lobes, right dorsolateral temporal lobes, bilateral parahippocampal gyrus, and bilateral hippocampus, compared to HC and PDND groups. A negative correlation between the GMV of left precuneus and HAMD‐17 scores in the PDD group tended to be significant (r = −0.318, p = 0.059). Decreased gyrification index was observed in the bilateral insular and dorsolateral temporal cortex. However, there were no significant differences found in fractal dimension and sulcal depth. Conclusion Our research shows extensive cortical structural changes in the insular cortex, parietal–occipital–temporal lobes, and hippocampal regions in PDD. This provides a morphological perspective for understanding the pathophysiological mechanism underlying depression in Parkinson's disease. The first row of pictures shows extensive cortical volume loss in Parkinson's disease with depression patients, primarily concentrated in the parietal–occipital–temporal lobes, parahippocampal gyrus, and hippocampus. The second row of pictures shows decreased gyrification index in the insula.

Background A dual‐syndrome hypothesis, which states the cognitive impairments in Parkinson's disease (PD) are attributable to frontostriatal dopaminergic dysregulation and cortical disturbance—each associated with attention/executive and memory/visuospatial dysfunction, respectively—has been widely accepted. This multisystem contribution also underlies highly heterogeneous progression rate to dementia. Methods Nondemented PD patients who underwent [123I]N‐ω‐fluoropropyl‐2β‐carbomethoxy‐3β‐(4‐iodophenyl) nortropane ([123I]FP‐CIT) SPECT and neuropsychological examinations were enrolled. Patients who agreed to participate and age‐ and sex‐matched healthy controls (HCs) also underwent 7‐T MRI. Patients were classified as cognitively normal (PD‐CN) or mild cognitive impairment (PD‐MCI) following the level II criteria of Movement Disorder Society Guideline. Results A total of 155 patients (PD‐CN/PD‐MCI 74/81) were enrolled, whereas 76 patients (PD‐CN/PD‐MCI 35/41) and 56 HCs underwent 7 T‐MRI. The caudate [123I]FP‐CIT uptake in PD was correlated with the performance of attention/working memory (trail‐making test [TMT]‐A and symbol digit modality test) and executive (TMT‐B) domains. In contrast, the regional cortical thickness in the left frontotemporal and right frontal lobes in PD was correlated with performance of memory (Hopkins verbal learning test‐revised delayed recall) and visuospatial (judgment of line orientation) domains. Moreover, compared to 37 HCs with a Montreal Cognitive Assessment score of >25, PD‐CN patients showed broad occipitoparietal cortical thinning. Conclusions We demonstrated distinctive impairments of dopaminergic frontostriatal deficits and cortical degeneration as neural bases for the dual‐syndrome hypothesis. Our findings suggest that occipitoparietal lobe thinning occurs at a cognitively normal stage, and additional frontotemporal lobe thinning underlies impairments in the memory and visuospatial domains at the PD‐MCI stage.

Aims To extract vertex‐wise features of the hippocampus and amygdala in Parkinson's disease (PD) with mild cognitive impairment (MCI) and normal cognition (NC) and further evaluate their discriminatory efficacy. Methods High‐resolution 3D‐T1 data were collected from 68 PD‐MCI, 211 PD‐NC, and 100 matched healthy controls (HC). Surface geometric features were captured using surface conformal representation, and surfaces were registered to a common template using fluid registration. The statistical tests were performed to detect differences between groups. The disease‐discriminatory ability of features was also tested in the ensemble classifiers. Results The amygdala, not the hippocampus, showed significant overall differences among the groups. Compared with PD‐NC, the right amygdala in MCI patients showed expansion (anterior cortical, anterior amygdaloid, and accessory basal areas) and atrophy (basolateral ventromedial area) subregions. There was notable atrophy in the right CA1 and hippocampal subiculum of PD‐MCI. The accuracy of classifiers with multivariate morphometry statistics as features exceeded 85%. Conclusion PD‐MCI is associated with multiscale morphological changes in the amygdala, as well as subtle atrophy in the hippocampus. These novel metrics demonstrated the potential to serve as biomarkers for PD‐MCI diagnosis. Overall, these findings from this study help understand the role of subcortical structures in the neuropathological mechanisms of PD cognitive impairment. We introduced a conformal representation method to calculate vertex‐wise features in the hippocampus and amygdala in PD‐MCI and PD‐NC. Compared with PD‐NC, the amygdala of PD‐MCI showed both global and subfields' alterations (expanded anterior cortical, anterior amygdaloid, and accessory basal areas and atrophied basolateral ventromedial area), with only atrophy found in the right hippocampal subiculum. The novel features from the above regions achieved accuracy exceeding 85% in classification tasks.

Background Bulimia nervosa is a recurrent eating disorder with uncertain pathogenesis. Recently, there has been growing interest in using neuroimaging techniques to explore brain structural and functional alterations in bulimia nervosa, but the findings of previous studies have a great number of inconsistencies. Methods Here, we collected anatomical and resting‐state functional magnetic resonance imaging data from 43 bulimia nervosa patients and 34 matched healthy controls (HCs). We applied a surface‐based morphology analysis to explore brain cortical morphology differences and a novel surface‐based functional connectivity (FC) analysis to investigate functional abnormalities. Principal component analysis was performed to analyze the behavioral data of the participants. We further analyzed the relationships between abnormalities in cortical characteristics or FC and clinical features. Results We observed increased greater sulcal depth in the right superior temporal gyrus (STG) and the right medial orbitofrontal cortex (mOFC) in bulimia nervosa patients than in the HCs. Additionally, the patients exhibited increased FC between the right STG and right ventral tegmental area but decreased function between the right mOFC and right putamen, which was significantly negatively correlated with the first principal component reflecting the severity of bulimia nervosa symptom. Conclusions Our findings provide evidence of neuroanatomical and functional abnormalities in bulimia nervosa patients. Moreover, the FC between the right mOFC and right putamen was associated with symptom severity of bulimia nervosa, which may be a neural marker and involved in the neuropathological mechanism of bulimia nervosa. We conducted a novel surface‐based FC analysis based on surface morphology alterations in BN, PCA to analyze the behavioral data of the participants and further explored the relationships between neuroimaging findings and principal component. Altered FC based on surface morphology alterations was related with related to the severity of BN symptom. Our findings provided further evidence that reward processing and body image processing may be involved in BN.

To measure the changes in cerebral cortical thickness in patients with herpes zoster (HZ) and postherpetic neuralgia (PHN) by surface-based morphometry (SBM) and further estimate its correlation with clinical scores. Twenty-nine HZ patients, 30 PHN patients and 30 well-matched healthy controls (HCs) were included. Magnetic resonance imaging (MRI) data from all subjects were collected and then analyzed by SBM. The changes in cortical thickness among the HZ, PHN and HC groups were analyzed by ANOVA and correlated with clinical scores. The thickness of the bilateral primary visual cortex (V1, V2) and right primary visual cortex (V3), left somatosensory cortex (L3A), right anterior cingulate gyrus and medial prefrontal cortex (RS32) increased in PHN group, and the thickness the left insular and frontal opercular cortex (LFOP4), left motor cortex (L3B), and right superior temporal visual cortex (RSTV) were decreased in the HZ and PHN groups compared to the HC group. The thickness measurements of RS32, LFOP4, and (L3B) in HZ and PHN patients were correlated with the duration of disease. In HZ and PHN patients, the Hamilton Anxiety Scale (HAMA) and Hamilton Depression Scale (HAMD) scores were significantly positively correlated. Changes in cortical thickness in the areas related to sensory, motor, and cognitive/emotional changes in patients with PHN affect the neuroplasticity process of the brain, which may be the reason for the transformation of HZ into PHN and provide a possible explanation for the neuropathological mechanism of pain persistence in PHN patients.

ABSTRACT Background Heroin and methamphetamine are two widely abused drugs that have profound effects on brain morphology and functioning. This study aims to (1) identify brain structural differences between heroin and methamphetamine users; (2) examine how these drugs differentially affect the topology and functional connectivity of key brain networks; and (3) characterize associations between morphological alterations and clinical symptoms, including anxiety and depression. Methods In this study, we collected T1‐weighted magnetic resonance imaging data from 26 heroin‐abstinent (HA) patients, 24 methamphetamine‐abstinent (MA) patients, and 32 healthy controls (HC). All participants were in early abstinence (< 6 months) to minimize acute intoxication and withdrawal confounds while capturing residual brain alterations. Four surface‐based morphological features, including cortical thickness (CT), fractal dimension (FD), gyrification index (GI), and sulcal depth (SD), were analyzed, and morphological brain networks were constructed using Jensen‐Shannon divergence with 210 cortical regions from the Brainnetome Atlas. Results Both patient groups showed brain tissue thinning in hearing‐related areas (temporal cortex) and reduced depth in visual processing regions. Heroin users specifically exhibited atrophy in somatosensory cortex regions associated with touch sensation whereas methamphetamine users demonstrated distinctive cortical folding alterations in motor cortex areas related to movement control. Network analysis revealed that heroin users had widespread connection problems affecting brain communication efficiency, while methamphetamine users showed localized damage in specific brain hubs important for memory, attention, and visual processing. Clinical correlations revealed that morphological changes were significantly associated with drug use patterns (frequency and dosage) and psychological symptoms, with anxiety scores negatively correlating with SD in heroin users and depression scores positively correlating with morphological measures in methamphetamine users. Conclusions Our findings demonstrate distinct neurobiological signatures of heroin and methamphetamine addiction that persist during early abstinence. Heroin primarily causes widespread network disruption, while methamphetamine leads to focal hub damage. The observed associations between brain morphology and clinical symptoms indicate the practical importance of these structural alterations. These distinct patterns may inform the development of substance‐specific treatment approaches. Our morphological brain network analysis of 82 participants reveals that these substances leave dramatically different fingerprints that persist even in recovery, with heroin causing global network collapse through increased path lengths across the entire cortex, while methamphetamine selectively damages temporal parietal, and visual processing centers.

Mentalising ability, indexed as the ability to understand others' beliefs, feelings, intentions, thoughts and traits, is a pivotal and fundamental component of human social cognition. However, considering the multifaceted nature of mentalising ability, little research has focused on characterising individual differences in different mentalising components. And even less research has been devoted to investigating how the variance in the structural and functional patterns of the amygdala and hippocampus, two vital subcortical regions of the “social brain”, are related to inter‐individual variability in mentalising ability. Here, as a first step toward filling these gaps, we exploited inter‐subject representational similarity analysis (IS‐RSA) to assess relationships between amygdala and hippocampal morphometry (surface‐based multivariate morphometry statistics, MMS), connectivity (resting‐state functional connectivity, rs‐FC) and mentalising ability (interactive mentalisation questionnaire [IMQ] scores) across the participants (N=24). In IS‐RSA, we proposed a novel pipeline, that is, computing patching and pooling operations‐based surface distance (CPP‐SD), to obtain a decent representation for high‐dimensional MMS data. On this basis, we found significant correlations (i.e., second‐order isomorphisms) between these three distinct modalities, indicating that a trinity existed in idiosyncratic patterns of brain morphometry, connectivity and mentalising ability. Notably, a region‐related mentalising specificity emerged from these associations: self‐self and self‐other mentalisation are more related to the hippocampus, while other‐self mentalisation shows a closer link with the amygdala. Furthermore, by utilising the dyadic regression analysis, we observed significant interactions such that subject pairs with similar morphometry had even greater mentalising similarity if they were also similar in rs‐FC. Altogether, we demonstrated the feasibility and illustrated the promise of using IS‐RSA to study individual differences, deepening our understanding of how individual brains give rise to their mentalising abilities. A trinity existed in idiosyncratic patterns of brain morphometry, connectivity and mentalising ability, that is, three distinct modalities shared one essence.

Major depressive disorder (MDD) tends to emerge during adolescence; however, neurobiological research in adolescents has lagged behind that in adults. This study aimed to characterize gray matter (GM) structural alterations in adolescents with MDD using comprehensive morphological analyses. This study included 93 adolescent MDD patients and 77 healthy controls. Voxel-based morphometry (VBM), deformation-based morphometry (DBM), and surface-based morphometry (SBM) methods were used to analyze GM morphological alterations in adolescent MDD patients. Sex-by-group and age-by-group interactions, as well as the relationships between altered GM structure and clinical characteristics were also analyzed. Whole-brain VBM and DBM analyses revealed GM atrophy in the left thalamus and bilateral midbrain in adolescent MDD patients. Whole-brain SBM analysis revealed that adolescent MDD patients, relative to controls, showed decreased thickness in the left postcentral gyrus and left precentral gyrus; increased thickness in the bilateral superior temporal gyrus, left parahippocampal gyrus and right lateral orbitofrontal gyrus; and decreased fractal dimension in the right lateral occipital gyrus. A significant sex-by-group interaction effect was found in the fractal dimension of the left lateral occipital gyrus. The volume of the left thalamus and the thickness of the left superior temporal gyrus were correlated with the duration of disease in adolescent MDD patients. This study suggested that adolescent MDD had GM morphological abnormalities in the frontal-limbic, subcortical, perceptual network and midbrain regions, with some morphological abnormalities associated with disease duration and sex differences. These findings provide new insight into the neuroanatomical substrates underlying adolescent MDD.

•This study offers the first evidence of compensatory neuroplastic remodeling in the contralateral prefrontal cortex of children with drug-resistant epilepsy before hemispherotomy.•Cortical thickness of the anterior cingulate gyrus emerges as the strongest predictor of motor recovery after surgery.•An abnormal increase in gray-matter volume within the temporal pole and adjacent temporal regions forecasts poorer functional outcomes.•Integrating VBM and SBM provides a comprehensive map of gray-matter alterations across the pre- and postoperative phases. Hemispherotomy (HS) is an effective treatment option to control seizures for children with pharmacoresistant epilepsy. We aimed to explore the alteration of the gray matter structure before and after surgery and identify the specific brain regions associated with preoperative neuropsychological development and postoperative motor development. We conducted a retrospective study of magnetic resonance imaging (MRI) results, clinical parameters and follow-up data in 46 children who underwent hemispherotomy (HS) at our hospital between 2018 and 2022, and 32 controls were included. Voxel-based morphometry (VBM) and surface-based morphometry (SBM) techniques were employed to quantify the alteration of the gray matter structure. We used Spearman rank correlation and logistic regression models to analyze the influence of different factors on neuropsychological development and motor outcome. 46 children with pharmacoresistant epilepsy undergoing hemispherotomy and 32 control subjects were recruited for this study. The patients were divided into two groups according to their surgical side: 29 patients with the left hemispherotomy (13 females, 17 months [IQR, 26 months]) and 17 patients with the right hemispherotomy (11 females, 19 months [IQR, 27.5 months]). Finally, 36 patients completed 13.80±1.54 months (LHS)/ 11.53±1.73 months (RHS) of follow-up, and 89.0 % remained completely seizure-free (outcome scale class IA). The prefrontal cortex showed a positive correlation with neuropsychological development before surgery. Cortical thickness (CT) of the anterior cingulate gyrus was an independent protective factor [OR=18.19, 95 % CI (1.56–212.43), P = 0.021] for motor function prognosis after surgery, while gray matter volume (GMV) of the temporal pole of the middle temporal gyrus was an independent risk factor [OR=0.07, 95 % CI (0.01–0.85), P = 0.037] after surgery. Preoperative remodeling of prefrontal cortical gray matter structures in the contralateral hemisphere was performed for functional compensation. After surgery, the prefrontal and cingulate cortices resumed the normal developmental trajectories, with the cingulate cortex determining postoperative motor outcome. However, there is irreversible gray matter damage to the temporal lobe, leading to corresponding functional developmental deficits.