Perigenual Anterior Cingulate Cortex Research Articles

Atlas-based structural analysis of prefrontal cortex atrophy in major depressive disorder: Correlations with severity and episode frequency

BackgroundCurrent models of major depressive disorder (MDD) primarily focus on the structural and functional changes in key prefrontal areas responsible for emotional regulation. Among these regions some sections such as the dorsal prefrontal area, has received limited attention regarding its structural abnormalities in MDD. This study aims to evaluate volumetric abnormalities in brain regions associated with markers of depression severity and episode frequency. MethodsThe study included 33 MDD patients and 33 healthy subjects. Using an atlas-based method, we measured the volumes of several key brain regions based on MRI data. The regions of interest included prefrontal and posterior sections of the middle frontal gyrus (MFG) and superior frontal gyrus (SFG). Additionally, we evaluated the volumes of the dorsal anterior cingulate cortex (dACC), perigenual (rostral) anterior cingulate cortex (pgACC), subgenual cingulate cortex (sgACC), posterior cingulate cortex (PCC), hippocampus (HPC), and parahippocampus (paraHPC). Hamilton Depression Scale (HAM-D) scores and count of the depressive episodes of patients were also obtained. A regression analysis with sex as the confounding factor has been made. ResultsAnalysis of covariances, controlling for sex, showed significant atrophy in the sgACC in the depression group: F(1, 63) = 4.013, p = 0.049 (left) and F(1, 63) = 8.786, p < 0.004 (right). Poisson regression, also controlling for sex, found that each additional depressive episode was associated with a significant reduction in left posterior MFG volume (0.952 times, 95 % CI, 0.906 to 1.000; p = 0.049). ConclusionsFindings in this study highlight the structural abnormalities in MDD patients in correlation to either current depression severity or chronicity of the disease.

General mechanisms of task engagement in the primate frontal cortex

Staying engaged is necessary to maintain goal-directed behaviors. Despite this, engagement exhibits continuous, intrinsic fluctuations. Even in experimental settings, animals, unlike most humans, repeatedly and spontaneously move between periods of complete task engagement and disengagement. We, therefore, looked at behavior in male macaques (macaca mulatta) in four tasks while recording fMRI signals. We identified consistent autocorrelation in task disengagement. This made it possible to build models capturing task-independent engagement. We identified task general patterns of neural activity linked to impending sudden task disengagement in mid-cingulate gyrus. By contrast, activity centered in perigenual anterior cingulate cortex (pgACC) was associated with maintenance of performance across tasks. Importantly, we carefully controlled for task-specific factors such as the reward history and other motivational effects, such as response vigor, in our analyses. Moreover, we showed pgACC activity had a causal link to task engagement: transcranial ultrasound stimulation of pgACC changed task engagement patterns.

Dynamical and individualised approach of transcranial ultrasound neuromodulation effects in non-human primates

Low-frequency transcranial ultrasound stimulation (TUS) allows to alter brain functioning with a high spatial resolution and to reach deep targets. However, the time-course of TUS effects remains largely unknown. We applied TUS on three brain targets for three different monkeys: the anterior medial prefrontal cortex, the supplementary motor area and the perigenual anterior cingulate cortex. For each, one resting-state fMRI was acquired between 30 and 150 min after TUS as well as one without stimulation (control). We captured seed-based brain connectivity changes dynamically and on an individual basis. We also assessed between individuals and between targets homogeneity and brain features that predicted TUS changes. We found that TUS prompts heterogenous functional connectivity alterations yet retain certain consistent changes; we identified 6 time-courses of changes including transient and long duration alterations; with a notable degree of accuracy we found that brain alterations could partially be predicted. Altogether, our results highlight that TUS induces heterogeneous functional connectivity alterations. On a more technical point, we also emphasize the need to consider brain changes over-time rather than just observed during a snapshot; to consider inter-individual variability since changes could be highly different from one individual to another.

Resting-state amygdala subregion and precuneus connectivity provide evidence for a dimensional approach to studying social anxiety disorder

Social anxiety disorder (SAD) is a prevalent and disabling mental health condition, characterized by excessive fear and anxiety in social situations. Resting-state functional magnetic resonance imaging (fMRI) paradigms have been increasingly used to understand the neurobiological underpinnings of SAD in the absence of threat-related stimuli. Previous studies have primarily focused on the role of the amygdala in SAD. However, the amygdala consists of functionally and structurally distinct subregions, and recent studies have highlighted the importance of investigating the role of these subregions independently. Using multiband fMRI, we analyzed resting-state data from 135 participants (42 SAD, 93 healthy controls). By employing voxel-wise permutation testing, we examined group differences of fMRI connectivity and associations between fMRI connectivity and social anxiety symptoms to further investigate the classification of SAD as a categorical or dimensional construct. Seed-to-whole brain functional connectivity analysis using multiple ‘seeds’ including the amygdala and its subregions and the precuneus, revealed no statistically significant group differences. However, social anxiety severity was significantly negatively correlated with functional connectivity of the precuneus - perigenual anterior cingulate cortex and positively correlated with functional connectivity of the amygdala (specifically the superficial subregion) - parietal/cerebellar areas. Our findings demonstrate clear links between symptomatology and brain connectivity in the absence of diagnostic differences, with evidence of amygdala subregion-specific alterations. The observed brain-symptom associations did not include disturbances in the brain’s fear circuitry (i.e., disturbances in connectivity between amygdala - prefrontal regions) likely due to the absence of threat-related stimuli.

Preliminary evidence that ketamine alters anterior cingulate resting-state functional connectivity in depressed individuals

Activity changes within the anterior cingulate cortex (ACC) are implicated in the antidepressant effects of ketamine, but the ACC is cytoarchitectonically and functionally heterogeneous and ketamine’s effects may be subregion specific. In the context of a double-blind randomized placebo-controlled crossover trial investigating the clinical and resting-state fMRI effects of intravenous ketamine vs. placebo in patients with treatment resistant depression (TRD) vs. healthy volunteers (HV), we used seed-based resting-state functional connectivity (rsFC) analyses to determine differential changes in subgenual ACC (sgACC), perigenual ACC (pgACC) and dorsal ACC (dACC) rsFC two days post-infusion. Across cingulate subregions, ketamine differentially modulated rsFC to the right insula and anterior ventromedial prefrontal cortex, compared to placebo, in TRD vs. HV; changes to pgACC-insula connectivity correlated with improvements in depression scores. Post-hoc analysis of each cingulate subregion separately revealed differential modulation of sgACC-hippocampal, sgACC-vmPFC, pgACC-posterior cingulate, and dACC-supramarginal gyrus connectivity. By comparing rsFC changes following ketamine vs. placebo in the TRD group alone, we found that sgACC rsFC was most substantially modulated by ketamine vs. placebo. Changes to sgACC-pgACC, sgACC-ventral striatal, and sgACC-dACC connectivity correlated with improvements in anhedonia symptoms. This preliminary evidence suggests that accurate segmentation of the ACC is needed to understand the precise effects of ketamine’s antidepressant and anti-anhedonic action.

The incidence of schizophrenia in the context of growing up in urbanised vs. green areas – a narrative review

The neurodevelopmental theory of schizophrenia describes multiple risk factors of this serious mental disorder. These include genetic factors that generally have biological roots, as well as factors related to the upbringing in a specific environment during childhood and adolescence of a person who will develop schizophrenia in adulthood. The neurodevelopmental hypothesis also implies the existence of protective factors. The paper discusses selected environmental risk factors and protective factors of schizophrenia in the context of ecopsychiatry. Urbanicity has for decades been a factor indicated as one that increases the risk of schizophrenia. Contemporary research helps understand how growing up in an urban environment affects brain development, with a particular focus on grey matter volume changes in the dorsolateral prefrontal cortex and the perigenual anterior cingulate cortex. The impact of air pollution as a risk factor for schizophrenia is also the subject of discussions. Exposure to outdoor air pollutants containing particulate matter and ultrafine particulate matter, gases, organic compounds, and metals can lead to neurotoxicity and neuropathology. Air pollution can affect the brain through such mechanisms as inflammation and oxidative stress. On contrary, higher exposure to green spaces has been suggested to reduce the incidence of schizophrenia. Some research indicates a dose-response association between the level of exposure to green space in childhood and a lower risk of developing schizophrenia in the future. The presented review of selected publications indicates that exposure to a certain environment in childhood and adolescence modulates the risk of schizophrenia. Environments heavily transformed by human activity (urbanisation) and characterised by a high level of chemical contamination (toxins, air pollution, smog) are a risk factor for schizophrenia. Protective factors, on the other hand, include direct contact with the natural environment from childhood through adolescence to adulthood.

Functional dysconnectivity of anterior cingulate subregions in schizophrenia and psychotic and nonpsychotic bipolar disorder.

Aberrant resting-state functional connectivity (FC) of anterior cingulate cortex (ACC) has been implicated in the pathophysiology of schizophrenia and bipolar disorder (BP). This study investigated the subregional FC of ACC across schizophrenia and psychotic (PBP) and nonpsychotic BP (NPBP) and the relationship between brain functional alterations and clinical manifestations. A total of 174 first-episode medication-naive patients with schizophrenia (FES), 80 patients with PBP, 77 patients with NPBP and 173 demographically matched healthy controls (HCs) underwent resting-state functional magnetic resonance imaging. Brain-wide FC of ACC subregions was computed for each individual, and compared between the groups. General intelligence was evaluated using the short version of the Wechsler Adult Intelligence Scale. Relationships between FC and various clinical and cognitive variables were estimated using the skipped correlation. The FES, PBP and NPBP groups showed differing connectivity patterns in the left caudal, dorsal and perigenual ACC. Transdiagnostic dysconnectivity was found in the subregional ACC associated with cortical, limbic, striatal and cerebellar regions. Disorder-specific dysconnectivity in FES was identified between the left perigenual ACC and bilateral orbitofrontal cortex, and the left caudal ACC coupling with the default mode network (DMN) and visual processing region was correlated with psychotic symptoms. In the PBP group, FC between the left dorsal ACC and the right caudate was correlated with psychotic symptoms, and FC connected with the DMN was associated with affective symptoms. The current findings confirmed that subregional ACC dysconnectivity could be a key transdiagnostic feature and associated with differing clinical symptomology across schizophrenia and PBP.

Regional superficial amygdala resting-state functional connectivity in adults infers childhood maltreatment severity.

Childhood maltreatment (CM) is a potential risk factor for some neuropsychiatric disorders in adulthood (e.g. depression and anxiety) and alters trajectories of brain development. Accumulating evidence suggests that functional connectivity of the limbic system, especially the amygdala, is highly associated with childhood maltreatment, although not all studies have found this. These inconsistent results may be due to differential alterations of amygdala resting-state functional connectivity (rsFC) following childhood maltreatment. Our aim was to investigate the relationship between the rsFC of amygdala subregions and CM severity, as well as to develop a stable rsFC-based model for inferring the severity of CM. In this study, we employed the Childhood Trauma Questionnaire (CTQ) to assess CM severity in each individual. We explored the relationship between the rsFC of amygdala subregions (i.e. centromedial -CMA, basolateral -BLA, superficial-SFA amygdala) and CM experience in a discovery dataset of n=110 healthy Chinese participants by linear multiple regression analysis. Subsequent dimensional and categorical approach were performed to elucidate the relationship between rsFCs and CM severity and CM subtypes, respectively. A support vector regression model was then conducted to validate the associations between rsFCs and total CTQ scores. Moreover, we also verified the model into another independent replication dataset (n=38). Our findings suggested that childhood maltreatment was negatively associated with rsFC between the right superficial amygdala and perigenual anterior cingulate cortex (pgACC)/postcentral gyrus (PCG) but not the other two amygdala subregions. Moreover, SFA-pgACC coupling was more associated with physical neglect whereas the SFA-PCG was more related to emotional neglect. In addition, supervised machine learning confirmed that using these two rsFCs as predictors could stably estimate continuous maltreatment severity in both discovery and replication datasets. The current study supports that the rsFCs of superficial amygdala are related to childhood maltreatment and which may be a potential biomarker for the effects of childhood maltreatment-related psychiatric disorders (i.e. depression and anxiety).

A Brain Mechanism for Hate.

A Brain Mechanism for Hate.

Perigenual anterior cingulate cortex and its structural covariance as predictors for future body fat gain in young adults

This study aimed to examine whether baseline gray matter (GM) volume and structural covariance patterns could predict body fat gain over 1 to 2 years in a relatively large sample. Voxel-based morphometry (VBM) analysis was applied to examine the association between baseline GM volume and body fat gain in 502 participants over 1 to 2 years. Furthermore, this study tested whether the structural covariances between the regions identified as seeds from VBM analysis and the rest of the brain were associated with future body fat gain. A significant positive association was observed between baseline GM volume in the perigenual anterior cingulate cortex (pgACC) and body fat gain over 1 to 2 years. Furthermore, relative to those with lower future body fat gain, pgACC covaried more extensively with the middle frontal gyrus, middle temporal gyrus, inferior temporal gyrus, and cerebellum in participants with higher future body fat gain. Using VBM and structural covariance network analysis, the current study revealed that higher GM volume of pgACC and its increased structural covariances with specific brain regions were associated with future weight gain, which may guide the development of more effective prevention and treatment interventions for obesity.

Learning whom to cooperate with: neurocomputational mechanisms for choosing cooperative partners.

Cooperation is fundamental for survival and a functioning society. With substantial individual variability in cooperativeness, we must learn whom to cooperate with, and often make these decisions on behalf of others. Understanding how people learn about the cooperativeness of others, and the neurocomputational mechanisms supporting this learning, is therefore essential. During functional magnetic resonance imaging scanning, participants completed a novel cooperation-partner-choice task where they learned to choose between cooperative and uncooperative partners through trial-and-error both for themselves and vicariously for another person. Interestingly, when choosing for themselves, participants made faster and more exploitative choices than when choosing for another person. Activity in the ventral striatum preferentially responded to prediction errors (PEs) during self-learning, whereas activity in the perigenual anterior cingulate cortex (ACC) signaled both personal and vicarious PEs. Multivariate pattern analyses showed distinct coding of personal and vicarious choice-making and outcome processing in the temporoparietal junction (TPJ), dorsal ACC, and striatum. Moreover, in right TPJ the activity pattern that differentiated self and other outcomes was associated with individual differences in exploitation tendency. We reveal neurocomputational mechanisms supporting cooperative learning and show that this learning is reflected in trial-by-trial univariate signals and multivariate patterns that can distinguish personal and vicarious choices.

Cortical thickness in default mode network hubs correlates with clinical features of dissociative seizures

BackgroundDissociative seizures (DS) are a common subtype of functional neurological disorder (FND) with an incompletely understood pathophysiology. Here, gray matter variations and their relationship to clinical features were investigated. MethodsForty-eight patients with DS without neurological comorbidities and 43 matched clinical control patients with syncope with structural brain MRIs were identified retrospectively. FreeSurfer-based cortical thickness and FSL FIRST-based subcortical volumes were used for quantitative analyses, and all findings were age and sex adjusted, and corrected for multiple comparisons. ResultsGroups were not statistically different in cortical thickness or subcortical volumes. For patients with DS, illness duration was inversely correlated with cortical thickness of left-sided anterior and posterior cortical midline structures (perigenual/dorsal anterior cingulate cortex, superior parietal cortex, precuneus), and clusters at the left temporoparietal junction (supramarginal gyrus, postcentral gyrus, superior temporal gyrus), left postcentral gyrus, and right pericalcarine cortex. Dissociative seizure duration was inversely correlated with cortical thickness in the left perigenual anterior cingulate cortex, superior/middle frontal gyri, precentral gyrus and lateral occipital cortex, along with the right isthmus-cingulate and posterior-cingulate, middle temporal gyrus, and precuneus. Seizure frequency did not show any significant correlations. ConclusionsIn patients with DS, illness duration inversely correlated with cortical thickness of left-sided default mode network cortical hubs, while seizure duration correlated with left frontopolar and right posteromedial areas, among others. Etiological factors contributing to neuroanatomical variations in areas related to self-referential processing in patients with DS require more research inquiry.

Cross-lagged Relationships Between Depressive Symptoms and Altered Default Mode Network Connectivity Over the Course of Adolescence

BackgroundAlthough the peak onset of depressive symptoms occurs during adolescence, very few studies have directly examined depression-related changes in resting-state (RS) default mode network activity during adolescence, controlling for potential neural markers of risk. MethodsThis study used data from a longitudinal adolescent cohort to investigate age-specific, persistent (i.e., lagged), and dynamic associations between RS functional connectivity within the default mode network and depressive symptoms during adolescence using a random intercept cross-lagged panel framework. The Neuroventure sample consisted of 151 adolescents ages 12–14 at study entry without any neurological illness who were assessed three times during a 5-year follow-up with 97% follow-up across the three assessments. Depressive symptoms were measured using the depression subscale of the Brief Symptoms Inventory. RS functional magnetic resonance imaging data were collected using a 3T Siemens Magnetom Trio scanner in a single 6-minute sequence. ResultsAfter controlling for relationships between random intercepts, future depression risk was predicted by RS couplings in the perigenual anterior cingulate cortex and anterior dorsomedial prefrontal cortex (β = −0.69, p = .014) and in the left inferior parietal lobule and anterior superior frontal gyrus (β = −0.43, p = .035). Increases in depressive symptoms at previous time points significantly predicted changes in functional connectivity between the posterior cingulate cortex and the precuneus and posterior middle temporal gyrus (β = 0.37, p = .039) and between the dorsal precuneus and posterior middle temporal gyrus (β = 0.47, p = .036). ConclusionsThis study was able to disassociate the RS brain markers of depression from those that appear to follow early-onset depression.

Abnormal functional connectivity of the anterior cingulate cortex subregions mediates the association between anhedonia and sleep quality in major depressive disorder

BackgroundThe anterior cingulate cortex (ACC) is a crucial region in the pathophysiology of major depressive disorder (MDD). However, the relationship between functional alterations of the ACC subregions, anhedonia and sleep quality remains unclear in MDD patients. MethodsThe resting-state functional connectivity (rsFC) of ACC subregions was measured in 41 first-episode medication-naïve MDD patients and 63 healthy controls who underwent functional magnetic resonance imaging. Between-group differences were examined using two-sample t-test. Furthermore, correlation and mediation analyses were carried out to investigate the relationships between the aberrant rsFC of ACC subregions, anhedonia and sleep quality in the patients and controls. ResultsCompared to healthy controls, the MDD patients exhibited increased rsFC of ACC subregions to areas of the anterior default mode network (DMN) and showed decreased rsFC of the right subgenual ACC to left precuneus (PCUN), which belongs to the posterior DMN. In MDD group, the sleep quality and consummatory anhedonia are correlated with some rsFC, which involves the angular gyrus (ANG) and superior frontal gyrus (SFG). More importantly, the rsFC between the right perigenual ACC and left SPG mediates the association between anhedonia and sleep quality in MDD. LimitationsThe cross-sectional design and the subjective questionaries for assessment. ConclusionThese findings confirm the functional alterations of the ACC subregions and reveal the mediating role of ACC subregions in sleep and reward dysfunction in MDD.

The mutuality of social emotions: How the victim's reactive attitude influences the transgressor's emotional responses

Would a transgressor be guiltier or less after receiving the victim's forgiving or blaming attitude? Everyday intuitions and empirical evidence are mixed in this regard, leaving how interpersonal attitudes shape the transgressor's reactive social emotions an open question. We combined a social interactive game with multivariate pattern analysis of fMRI data to address this question. Participants played an interactive game in an fMRI scanner where their incorrect responses could cause either high or low pain stimulation to an anonymous co-player. Following incorrect responses, participants were presented with the co-player's (i.e., the victim's) attitude towards the harm (Blame, Forgive, or Neutral). Behaviorally, the victim's attitude and the severity of harm interactively modulated the transgressor's social emotions, with expectation violation serving as a mediator. While unexpected forgiveness following severe harm amplified the participants’ guilt, unexpected blame following minor harm reduced the participants’ guilt and increased their anger. This role of expectation violation was supported by multivariate pattern analysis of fMRI, revealing a shared neural representation in ventral striatum in the processing of victim's attitude-induced guilt and anger. Moreover, we identified a neural re-appraisal process of guilt in the transgressor, with the involvement of area related to self-conscious processing (i.e., perigenual anterior cingulate cortex) before knowing the victim's attitude transiting to the involvement of other-regarding related area (i.e., temporoparietal junction) after knowing the victim's attitude. These findings uncover the neurocognitive bases underlying the transgressor's social emotional responses, and highlight the importance of the mutuality of social emotions.

Alteration of grey matter volume is associated with pain and quality of life in children with sickle cell disease

Pain is the most common symptom experienced by patients with sickle cell disease (SCD) and is associated with poor quality of life. We investigated the association between grey matter volume (GMV) and the frequency of pain crises in the preceding 12 months and SCD-specific quality of life (QOL) assessed by the PedsQLTM SCD module in 38 pediatric patients with SCD. Using voxel-based morphometry methodology, high-resolution T1 structural scans were preprocessed using SPM and further analyzed in SPSS. The whole brain multiple regression analysis identified that perigenual anterior cingulate cortex (ACC) GMV was negatively associated with the frequency of pain crises (r=-0.656, P=0.003). A two-group t-test analysis showed that the subgroup having pain crisis/crises in the past year also showed significantly lower GMV at left supratemporal gyrus than the group without any pain crisis (p=0.024). The further 21 pain-related regions of interest (ROI) analyses identified a negative correlation between pregenual ACC (r=-0.551, P=0.001), subgenual ACC (r=-0.540, P=0.001) and the frequency of pain crises. Additionally, the subgroup with poorer QOL displayed significantly reduced GMV in the parahippocampus (left: P=0.047; right: P=0.024). The correlations between the cerebral structural alterations and the accentuated pain experience and QOL suggests a possible role of central mechanisms in SCD pain.

Neural signatures of bullying experience and social rejection in teenagers.

Relational bullying in schools is one of the most frequent forms of violence and can have severe negative health impact, e.g. depression. Social exclusion is the most prominent form of relational bullying that can be operationalized experimentally. The present study used MR-based perfusion imaging (pCASL) to investigate the neural signatures of social exclusion and its relationship with individually different extent of previous bullying experience. Twenty-four teenagers reporting bullying experience at different extent were scanned during a virtual ball-tossing (Cyberball game). Our findings showed that social exclusion (relative to social inclusion) activated frontal brain areas: sub- and perigenual anterior cingulate cortex (sg/pgACC), left inferior frontal cortex (IFG), and dorsolateral prefrontal cortex. Positive relationship between exclusion-specific signal increase and individually different extents of prior bullying experience was for the first time observed in left IFG and sgACC. This suggests that more frequent prior experience has conditioned greater mentalizing and/or rumination, in order to cope with the situation. While this interpretation remains speculative, the present data show that the experience of being bullied partly sensitizes the neural substrate relevant for the processing of social exclusion.

Controlling one’s world: Identification of sub-regions of primate PFC underlying goal-directed behavior

SummaryImpaired detection of causal relationships between actions and their outcomes can lead to maladaptive behavior. However, causal roles of specific prefrontal cortex (PFC) sub-regions and the caudate nucleus in mediating such relationships in primates are unclear. We inactivated and overactivated five PFC sub-regions, reversibly and pharmacologically: areas 24 (perigenual anterior cingulate cortex), 32 (medial PFC), 11 (anterior orbitofrontal cortex, OFC), 14 (rostral ventromedial PFC/medial OFC), and 14-25 (caudal ventromedial PFC) and the anteromedial caudate to examine their role in expressing learned action-outcome contingencies using a contingency degradation paradigm in marmoset monkeys. Area 24 or caudate inactivation impaired the response to contingency change, while area 11 inactivation enhanced it, and inactivation of areas 14, 32, or 14-25 had no effect. Overactivation of areas 11 and 24 impaired this response. These findings demonstrate the distinct roles of PFC sub-regions in goal-directed behavior and illuminate the candidate neurobehavioral substrates of psychiatric disorders, including obsessive-compulsive disorder.

Altered Posterior Cerebellar Lobule Connectivity With Perigenual Anterior Cingulate Cortex in Women With Primary Dysmenorrhea.

Objectives: This study aimed to investigate the potential connectivity mechanism between the cerebellum and anterior cingulate cortex (ACC) and the cerebellar structure in primary dysmenorrhea (PDM).Methods: We applied the spatially unbiased infratentorial template (SUIT) of the cerebellum to obtain anatomical details of cerebellar lobules, upon which the functional connectivity (FC) between the cerebellar lobules and ACC subregions was analyzed and the gray matter (GM) volume of cerebellar lobules was measured by using voxel-based morphometry (VBM) in 35 PDM females and 38 age-matched healthy females. The potential relationship between the altered FC or GM volume and clinical information was also evaluated in PDM females.Results: PDM females showed higher connectivity between the left perigenual ACC (pACC) and lobule vermis_VI, between the left pACC and left lobule IX, and between right pACC and right cerebellar lobule VIIb than did the healthy controls. Compared with healthy controls, no altered GM volume was found in PDM females. No significant correlation was found between altered cerebellum–ACC FC and the clinical variables in the PDM females.Conclusion: PDM females have abnormal posterior cerebellar connectivity with pACC but no abnormal structural changes. ACC–cerebellar circuit disturbances might be involved in the PDM females.

Distinct Basal Brain Functional Activity and Connectivity in the Emotional-Arousal Network and Thalamus in Patients With Functional Constipation Associated With Anxiety and/or Depressive Disorders.

Functional constipation (FC) is a common gastrointestinal disorder. Anxiety and/or depressive disorders are common in patients with FC (FCAD). Brain dysfunction may play a role in FC, but the contribution of comorbid anxiety and/or depression in patients with FC is poorly understood. Sixty-five FC patients and 42 healthy controls (HCs) were recruited, and a hierarchical clustering algorithm was used to classify FC patients into FCAD and patients without anxiety/depressive status (FCNAD) based on neuropsychological assessment. Resting-state functional magnetic resonance imaging measures including fractional amplitude of low-frequency fluctuation (fALFF) and functional connectivity were used to investigate brain functional differences. Thirty-seven patients were classified as FCAD, and 28 patients were classified as FCNAD; as compared with HC, both groups showed decreased activity (fALFF) in the perigenual anterior cingulate cortex (pACC), dorsomedial prefrontal cortex (DMPFC), and precuneus; enhanced precentral gyrus-thalamus connectivity and attenuated precuneus-thalamus connectivity in FCAD/FCNAD highlighted the thalamus as a critical connectivity node in the brain network (pFWE < .05). In comparison with FCNAD/HC, the FCAD group also had decreased fALFF in the orbitofrontal cortex (OFC) and thalamus, and increased OFC-hippocampus connectivity. In the FCNAD group, brain activities (pACC/DMPFC) and connection (precuneus-thalamus) had correlations only with symptoms; in the FCAD group, brain activities (OFC, pACC/DMPFC) and connectivities (OFC-hippocampus/precentral gyrus-thalamus) showed correlations with both constipation symptoms and anxiety/depressive status ratings. Mediation analysis indicated that the relationship between abdominal distension and OFC activity was completely mediated by anxiety in FCAD. These findings provide evidence of differences in brain activity and functional connectivity between FCAD and FCNAD, potentially providing important clues for improving treatment strategies.