Cingulate Research Articles

18 kDa Translocator protein (TSPO) is upregulated in rat brain after peripheral nerve injury and downregulated by diroximel fumarate

Neuroimmune signaling is a key process underlying neuropathic pain. Clinical studies have demonstrated that 18 kDa translocator protein (TSPO), a putative marker of neuroinflammation, is upregulated in discrete brain regions of patients with chronic pain. However, no preclinical studies have investigated TSPO dynamics in the brain in the context of neuropathic pain and in response to analgesic treatments. We used positron emission tomography-computed tomography (PET-CT) and [18F]-PBR06 radioligand to measure TSPO levels in the brain across time after chronic constriction injury (CCI) of the sciatic nerve in both male and female rats. Up to 10 weeks post-CCI, TSPO expression was increased in discrete brain regions, including medial prefrontal cortex, somatosensory cortex, insular cortex, anterior cingulate cortex, motor cortex, ventral tegmental area, amygdala, midbrain, pons, medulla, and nucleus accumbens. TSPO was broadly upregulated across these regions at 4 weeks post CCI in males, and 10 weeks in females, though there were regional differences between the sexes. Using immunohistochemistry, we confirmed TSPO expression in these regions. We further demonstrated that TSPO was upregulated principally in microglia in the nucleus accumbens core, and astrocytes and endothelial cells in the nucleus accumbens shell. Finally, we tested whether TSPO upregulation was sensitive to diroximel fumarate, a drug that induces endogenous antioxidants via nuclear factor E2-related factor 2 (Nrf2). Diroximel fumarate alleviated neuropathic pain and reduced TSPO upregulation. Our findings indicate that TSPO is upregulated over the course of neuropathic pain development and is resolved by an antinociceptive intervention in animals with peripheral nerve injury.

Distinct 5-HT receptor subtypes regulate claustrum excitability by serotonin and the psychedelic, DOI

Recent evidence indicates that neuronal activity within the claustrum (CLA) may be central to cellular and behavioral responses to psychedelic hallucinogens. The CLA prominently innervates many cortical targets and displays exceptionally high levels of serotonin (5-HT) binding. However, the influence of serotonin receptors, prime targets of psychedelic drug action, on CLA activity remains unexplored. We characterize the CLA expression of all known 5-HT subtypes and contrast the effects of 5-HT and the psychedelic hallucinogen, 2,5-dimethoxy-4-iodoamphetamine (DOI), on excitability of cortical-projecting CLA neurons. We find that the CLA is particularly enriched with 5-HT2C receptors, expressed predominantly on glutamatergic neurons. Electrophysiological recordings from CLA neurons that project to the anterior cingulate cortex (ACC) indicate that application of 5-HT inhibits glutamate receptor-mediated excitatory postsynaptic currents (EPSCs). In contrast, application of DOI stimulates EPSCs. We find that the opposite effects of 5-HT and DOI on synaptic signaling can both be reversed by inhibition of the 5-HT2C, but not 5-HT2A, receptors. We identify specific 5-HT receptor subtypes as serotonergic regulators of the CLA excitability and argue against the canonical role of 5-HT2A in glutamatergic synapse response to psychedelics within the CLA-ACC circuit.

The links among age, sex, and glutathione: A cross-sectional magnetic resonance spectroscopy study

Glutathione (GSH) is a brain marker for oxidative stress and has previously been associated with cerebral amyloid deposition and memory decline. However, to date, no study has examined the links among GSH, sex, age, amyloid, and Apolipoprotein E (APOE) genotype in a large non-clinical cohort of older adults. We performed APOE genotyping, magnetic resonance spectroscopy (MRS) as well as simultaneous positron emission tomography with the radiotracer Flutemetamol (Amyloid-PET), in a group of older adults. The final analysis set comprised 140 healthy older adults (mean age: 64.7 years) and 49 participants with mild cognitive impairment (mean age: 71.4 years). We recorded metabolites in the posterior cingulate cortex (PCC) by a GSH-edited MEGAPRESS sequence. Structural equation modeling revealed that higher GSH levels were associated with female sex, but neither APOE- epsilon 4 carrier status nor age showed significant associations with GSH. Conversely, older age and the presence of an APOE4 allele, but not sex, are linked to higher global amyloid load. Our results suggest that the PCC shows sex-specific GSH alterations in older adults.

Altered cingulate gyrus subregions functional connectivity in chronic insomnia disorder with anxiety

BackgroundChronic insomnia disorder (CID) is commonly associated with mood disorders. The cingulate gyrus (CG) plays a critical role in the pathophysiology of CID and anxiety. However, the specific characteristics of altered brain networks in the CG in CID with anxiety remain unclear. This study aimed to investigate the characteristics of CG functional connectivity (FC) in CID with and without anxiety. Methods: Resting-state functional magnetic resonance imaging was conducted on 92 CID and 36 healthy controls (HC). CID was divided into CID with anxiety (CID-A, N = 37) and CID without anxiety (CID-NA, N = 55) groups based on anxiety scores. Using the Human Brainnetome Atlas, the subregion CG FC network was constructed. ResultsCompared with HC, CID showed significantly decreased CG FC with the precuneus, middle frontal gyrus (MFG), and hippocampus, while showing significantly increased CG FC with the middle temporal gyrus (MTG)/superior temporal gyrus (STG). In contrast, CID-A showed significantly decreased CG FC with the salience network (insular, putamen) and default mode network (MTG/STG and inferior parietal lobule), while showing significantly increased CG FC with the thalamus and MFG compared to CID-NA. Further, CID-A and CID-NA could be classified with 84.21 % accuracy by using the CG FCs as features. Among these features, the CG FC with MFG, thalamus, and putamen had the highest contribution weights. ConclusionThis study revealed specific changes in the brain network of the CG subregion in CID-A. Understanding these CG FC alterations can help identify potential biomarkers specific to CID-A, which may be valuable for early detection and differentiation from other CID subtypes.

Hyperactivity and altered functional connectivity of the ventral striatum in schizophrenia compared with bipolar disorder: A resting state fMRI study

BackgroundSchizophrenia patients frequently present with structural and functional abnormalities of the ventral striatum (VS). Methodswe examined basal activation state and functional connectivity (FC) in four subregions of the bilateral ventral striatum: left inferior ventral striatum (VSi_L), left superior ventral striatum(VSs_L), right inferior ventral striatum(VSi_R), and right superior ventral striatum(VSs_R). Resting-state functional magnetic resonance images were obtained from 62 schizophrenia patients (SCH), 57 bipolar disorder (BD) patients, and 26 healthy controls (HCs). ResultsThe schizophrenia group exhibited greater fALFF in bilateral VS subregions compared to BD and HC groups as well as greater FC between the bilateral VSi and multiple brain regions, including the thalamus, putamen, posterior cingulate gyrus (PCC), frontal cortex and caudate. Moreover, the fALFF values of the bilateral ventral striatum were positively correlated with the severity of positive symptoms. We also found the functional connectivity between the bilateral inferior ventral striatum and some brain regions aforementioned were positively correlated with the severity of negative symptoms. ConclusionThese findings confirm a crucial contribution of ventral striatum dysfunction, especially of the bilateral VSi in schizophrenia. Functionally dissociated regions of the ventral striatum are differentially disturbed in schizophrenia.

Symptom Persistence Relates to Volume and Asymmetry of the Limbic System after Mild Traumatic Brain Injury.

Background: Persistent symptoms have been reported in up to 50% of the 27 million people with mild traumatic brain injuries (mTBI) every year. MRI findings are currently limited by low diagnostic and prognostic sensitivities, constraining the value of imaging in the stratification of patients following mTBI. Limbic system structures are promising brain regions in offering prognostic factors for symptom persistence following mTBI. The objective of this study was to associate volume and symmetry of limbic system structures with the presence and persistence of common symptoms in patients with mTBI. Methods: This study focused on 524 adults (aged 18-82), 58% female, with 82% injured in motor vehicle accidents and 28% reporting loss of consciousness (LOC). Magnetic resonance imaging (MRI) data included a sagittal 3D T1-weighted sequence with 1.2 mm slice thickness, with voxel sizes of 0.93 mm × 0.93 mm × 1.2 mm, obtained a median of 156 days after injury. Symptom diagnosis and persistence were collected retrospectively from patient medical records. Intracranial volume-adjusted regional volumes per side utilizing automated volumetric analysis (NeuroQuant®) were used to calculate total volume, laterality index, and side-independent asymmetry. Covariates included age, sex, LOC, and days from injury. Limbic volumetrics did not relate to symptom presentation, except the (-) association between headache presence and thalamus volume (adjusted odds ratio = 0.51, 95% confidence interval = 0.32, 0.85). Headache, balance problems, anxiety, and depression persistence was (-) associated with thalamus volume (hazard ratio (HR) 1.25 to 1.94). Longer persistence of balance problems was associated with (-) lateral orbitofrontal cortex volume (HR = 1.33) and (+) asymmetry of the hippocampus (HR = 0.27). Persistence of cognitive deficits was associated with (+) asymmetry in the caudal anterior cingulate (HR = 0.67). Depression persistence was associated with (+) asymmetry in the isthmus of the cingulate gyrus (HR = 5.39). Persistence of anxiety was associated with (-) volume of the parahippocampal gyrus (HR = 1.67), orbitofrontal cortex (HR > 1.97), and right-biased laterality of the entorhinal cortex (HR = 0.52). Conclusions: Relative volume and asymmetry of the limbic system structures in patients with mTBI are associated with the persistence of symptoms, particularly anxiety. The conclusions of this study are limited by the absence of a reference group with no mTBI.

The interplay of ADHD, social media usage, and dopamine receptors in adolescents: A literature review

ADHD is a neurodevelopmental disorder marked by symptoms such as inattentiveness, hyperactivity, and impulsivity, with a prevalence rate exceeding 5%. The pathophysiology of ADHD includes cognitive and functional brain abnormalities, particularly in the anterior cingulate gyrus and dorsolateral prefrontal cortex, as well as decreased activity in the frontostriatal region. Diagnosis involves comprehensive assessments based on behavioral criteria outlined in the DSM-5. Treatment primarily includes stimulant medications, which are effective in about 70% of patients, and non-stimulant options such as atomoxetine and antidepressants. The review explores the effects of social media on adolescents, highlighting both negative impacts, such as social isolation, depression, and cyberbullying, and positive aspects, such as enhanced communication and knowledge sharing. Adolescents with ADHD are particularly vulnerable to behavioral addictions due to their poor impulse control, making them susceptible to excessive social media use. Additionally, the role of D2-dopamine receptors in ADHD is discussed, noting that genetic components like the DRD2 gene can affect dopamine neurotransmission, impacting attention and pleasure experiences. The pleasure principle, as proposed by Freud, is also analyzed in the context of ADHD, suggesting that individuals with ADHD may engage in behaviors that provide immediate gratification to avoid discomfort. Therefore, this review underscores the correlation between ADHD symptoms, social media usage, dopamine receptor function, and the underlying psychological drives in adolescents, providing a comprehensive understanding of these interrelated factors.

Neural correlates of anhedonia in young adults with subthreshold depression: A graph theory approach for cortical-subcortical structural covariance

BackgroundAnhedonia is an enduring symptom of subthreshold depression (StD) and predict later onset of major depressive disorder (MDD). Brain structural covariance describes the inter-regional distribution of morphological changes compared to healthy controls (HC) and reflects brain maturation and disease progression. We investigated neural correlates of anhedonia from the structural covariance. MethodsT1-weighted brain magnetic resonance images were acquired from 79 young adults (26 StD, 30 MDD, and 23 HC). Intra-individual structural covariance networks of 68 cortical surface area (CSAs), 68 cortical thicknesses (CTs), and 14 subcortical volumes were constructed. Group-level hubs and principal edges were defined using the global and regional graph metrics, compared between groups, and examined for the association with anhedonia severity. ResultsGlobal network metrics were comparable among the StD, MDD, and HC. StD exhibited lower centralities of left pallidal volume than HC. StD showed higher centralities than HC in the CSAs of right rostral anterior cingulate cortex (ACC) and pars triangularis, and in the CT of left pars orbitalis. Less anhedonia was associated with higher centralities of left pallidum and right amygdala, higher edge betweenness centralities in the structural covariance (EBSC) of left postcentral gyrus-parahippocampal gyrus and LIPL-right amygdala. More anhedonia was associated with higher centralities of left inferior parietal lobule (LIPL), left postcentral gyrus, left caudal ACC, and higher EBSC of LIPL-left postcentral gyrus, LIPL-right lateral occipital gyrus, and left caudal ACC-parahippocampal gyrus. LimitationsThis study has a cross-sectional design. ConclusionsStructural covariance of brain morphologies within the salience and limbic networks, and among the salience-limbic-default mode-somatomotor-visual networks, are possible neural correlates of anhedonia in depression.

A neurometabolic mechanism involving dmPFC/dACC lactate in physical effort-based decision-making.

Motivation levels vary across individuals, yet the underlying mechanisms driving these differences remain elusive. The dorsomedial prefrontal cortex/dorsal anterior cingulate cortex (dmPFC/dACC) and the anterior insula (aIns) play crucial roles in effort-based decision-making. Here, we investigate the influence of lactate, a key metabolite involved in energy metabolism and signaling, on decisions involving both physical and mental effort, as well as its effects on neural activation. Using proton magnetic resonance spectroscopy and functional MRI in 63 participants, we find that higher lactate levels in the dmPFC/dACC are associated with reduced motivation for physical effort, a relationship mediated by neural activity within this region. Additionally, plasma and dmPFC/dACC lactate levels correlate, suggesting a systemic influence on brain metabolism. Supported by path analysis, our results highlight lactate's role as a modulator of dmPFC/dACC activity, hinting at a neurometabolic mechanism that integrates both peripheral and central metabolic states with brain function in effort-based decision-making.

Neural populations in macaque anterior cingulate cortex encode social image identities

The anterior cingulate cortex gyrus (ACCg) has been implicated in prosocial behaviors and reasoning about social cues. While this indicates that ACCg is involved in social behavior, it remains unclear whether ACCg neurons also encode social information during goal-directed actions without social consequences. To address this, we assessed how social information is processed by ACCg neurons in a reward localization task. Here we show that neurons in the ACCg of female rhesus monkeys differentiate the identities of conspecifics in task images, even when identity was task-irrelevant. This was in contrast to the prearcuate cortex (PAC), which has not been strongly linked to social behavior, where neurons differentiated identities in both social and nonsocial images. Many neurons in the ACCg also categorically distinguished social from nonsocial trials, but this encoding was only slightly more common in ACCg compared to the PAC. Together, our results suggest that ACCg neurons are uniquely sensitive to social information that differentiates individuals, which may underlie its role in complex social reasoning.

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.

Understanding the Changes in Brain Activation When Viewing Products with Differences in Attractiveness.

Product design and attractiveness are pivotal factors that determine people's positive reactions when viewing a product and may eventually affect their purchasing choices. Comprehending how people assess product design is crucial. Various studies have explored the link between product attractiveness and consumer behavior, but these were predominantly behavioral studies that offered limited insight into the neural processes underlying perceptions of product attractiveness. Gaining a deeper understanding of these neural mechanisms is valuable, as it enables the formulation of more objective design guidelines based on brain activity, enhancing product appeal and, ultimately, spurring consumer purchases. In our study, we sought to (1) elucidate the neural network engaged when individuals evaluate highly attractive product images, (2) delineate the neural network activated during the evaluation of less attractive product images, and (3) contrast the differences in neural networks between evaluations of highly and less attractive images. We utilized fMRI to investigate the neural activation patterns elicited by viewing product images of varying attractiveness levels. The results indicated distinct neural activations in response to the two types of attractive images. Highly attractive product images elicited activity in the anterior cingulate cortex (ACC) and the occipital pole, whereas less attractive product images stimulated the insula and the inferior frontal gyrus (IFG). The findings of this project provide some of the first insights of its kind and valuable insights for future product design, suggesting that incorporating more positive and rewarding elements could enhance product appeal. This research elucidates the neural correlates of people's responses to product attractiveness, revealing that highly attractive designs activate reward-related brain regions, while less attractive designs engage areas associated with emotional processing. These findings offer a neuroscientific basis for further studies on developing design strategies that align with consumers' innate preferences, potentially transforming product design and marketing practices. By leveraging this knowledge, designers can craft products that not only meet functional needs but also resonate more deeply on an esthetic level, thereby enhancing consumer engagement and purchase likelihood.

Large-scale meta-analyses and network analyses of neural substrates underlying human escalated aggression

Escalated aggression represents a frequent and severe form of violence, sometimes manifesting as antisocial behavior. Driven by the pressures of modern life, escalated aggression is of particular concern due to its rising prevalence and its destructive impact on both individual well-being and socioeconomic stability. However, a consistent neural circuitry underpinning it remains to be definitively identified. Here, we addressed this issue by comparing brain alterations between individuals with escalated aggression and those without such behavioral manifestations. We first conducted a meta-analysis to synthesize previous neuroimaging studies on functional and structural alterations of escalated aggression (325 experiments, 2997 foci, 16,529 subjects). Following-up network and functional decoding analyses were conducted to provide quantitative characterizations of the identified brain regions. Our results revealed that brain regions constantly involved in escalated aggression were localized in the subcortical network (amygdala and lateral orbitofrontal cortex) associated with emotion processing, the default mode network (dorsal medial prefrontal cortex and middle temporal gyrus) associated with mentalizing, and the salience network (anterior cingulate cortex and anterior insula) associated with cognitive control. These findings were further supported by additional meta-analyses on emotion processing, mentalizing, and cognitive control, all of which showed conjunction with the brain regions identified in the escalated aggression. Together, these findings advance the understanding of the risk biomarkers of escalated aggressive populations and refine theoretical models of human aggression.

Biomarkers of Internet Gaming Disorder-A Narrative Review.

Since game mechanics and their visual aspects have become more and more addictive, there is concern about the growing prevalence of Internet gaming disorder (IGD). In the current narrative review, we searched PubMed and Google Scholar databases for the keywords "igd biomarker gaming" and terms related to biomarker modalities. The biomarkers we found are grouped into several categories based on a measurement method and are discussed in the light of theoretical addiction models (tripartite neurocognitive model, I-PACE). Both theories point to gaming-related problems with salience and inhibition. The first dysfunction makes an individual more susceptible to game stimuli (raised reward seeking), and the second negatively impacts resistance to these stimuli (decreased cognitive control). The IGD patients' hypersensitivity to reward manifests mostly in ventral striatum (VS) measurements. However, there is also empirical support for a ventral-to-dorsal striatal shift and transition from goal-directed to habitual behaviors. The deficits in executive control are demonstrated in parameters related to the prefrontal cortex (PFC), especially the dorsolateral prefrontal cortex (DLPFC). In general, the connection of PFC with reward under cortex nuclei seems to be dysregulated. Other biomarkers include reduced P3 amplitudes, high-frequency heart rate variability (HRV), and the number of eye blinks and saccadic eye movements during the non-resting state. A few studies propose a diagnostic (multimodal) model of IGD. The current review also comments on inconsistencies in findings in the nucleus accumbens (NAcc), anterior cingulate cortex (ACC), and precuneus and makes suggestions for future IGD studies.

Functional near-infrared spectroscopy-based neurofeedback training targeting the dorsolateral prefrontal cortex induces changes in cortico-striatal functional connectivity

Due to its central role in cognitive control, the dorso–lateral prefrontal cortex (dlPFC) has been the target of multiple brain modulation studies. In the context of the present pilot study, the dlPFC was the target of eight repeated neurofeedback (NF) sessions with functional near infrared spectroscopy (fNIRS) to assess the brain responses during NF and with functional and resting state magnetic resonance imaging (task-based fMRI and rsMRI) scanning. Fifteen healthy participants were recruited. Cognitive task fMRI and rsMRI were performed during the 1st and the 8th NF sessions. During NF, our data revealed an increased activity in the dlPFC as well as in brain regions involved in cognitive control and self-regulation learning (pFWE < 0.05). Changes in functional connectivity between the 1st and the 8th session revealed increased connectivity between the posterior cingulate cortex and the dlPFC, and between the posterior cingulate cortex and the dorsal striatum (pFWE < 0.05). Decreased left dlPFC-left insula connectivity was also observed. Behavioural results revealed a significant effect of hunger and motivation on the participant control feeling and a lower control feeling when participants did not identify an effective mental strategy, providing new insights on the effects of behavioural factors that may affect the NF learning.

The moderating role of information processing speed in the relationship between brain remodeling and episodic memory in amnestic mild cognitive impairment.

The role of information processing speed (IPS) on relationships between episodic memory (EM) and central remodeling features in amnestic mild cognitive impairment (aMCI) was investigated. Neuropsychological evaluations and multimodal magnetic resonance imaging were performed on 48 patients diagnosed with aMCI and 50 healthy controls (HC). Moderation models explored the moderating effect of IPS on associations between EM and imaging features at single-region, connectivity, and network levels. IPS significantly enhanced the positive correlations between recall and cortical thickness of left inferior temporal gyrus. IPS also notably amplified negative correlations between recognition and functional connectivity (FC) of left inferior parietal lobe and right occipital, as well as between recall/recognition and nodal clustering coefficient of left anterior cingulate cortex. IPS functioned as a moderator of associations between recall and neuroimaging metrics at the "single region-connectivity-network" level, providing new insights for cognitive rehabilitation in aMCI patients. aMCI patients exhibited brain functional and structural remodeling alterations. IPS moderated relations between episodic memory and brain remodeling metrics. Therapy targeted at IPS can be considered for improving episodic memory in aMCI.

Effects of Head-Only Exposure to 900 MHz GSM Electromagnetic Fields in Rats: Changes in Neuronal Activity as Revealed by c-Fos Imaging without Concomitant Cognitive Impairments.

Over the last two decades, animal models have been used to evaluate the physiological and cognitive effects of mobile phone exposure. Here, we used a head-only exposure system in rats to determine whether exposure to 900 MHz GSM electromagnetic fields (EMFs) induces regional changes in neuronal activation as revealed by c-Fos imaging. In a first study, rats were exposed for 2 h to brain average specific absorption rates (BASARs) ranging from 0.5 to 6 W/kg. Changes in neuronal activation were found to be dose-dependent, with significant increases in c-Fos expression occurring at BASAR of 1 W/kg in prelimbic, infralimbic, frontal, and cingulate cortices. In a second study, rats were submitted to either a spatial working memory (WM) task in a radial maze or a spatial reference memory (RM) task in an open field arena. Exposures (45 min) were conducted before each daily training session (BASARs of 1 and 3.5 W/kg). Control groups included sham-exposed and control cage animals. In both tasks, behavioral performance evolved similarly in the four groups over testing days. However, c-Fos staining was significantly reduced in cortical areas (prelimbic, infralimbic, frontal, cingulate, and visual cortices) and in the hippocampus of animals engaged in the WM task (BASARs of 1 and 3.5 W/kg). In the RM task, EMF exposure-induced decreases were limited to temporal and visual cortices (BASAR of 1 W/kg). These results demonstrate that both acute and subchronic exposures to 900 MHz EMFs can produce region-specific changes in brain activity patterns, which are, however, insufficient to induce detectable cognitive deficits in the behavioral paradigms used here.

Correlation between semiautomated magnetic resonance imaging volumetry of the cingulate gyrus and interictal epileptiform discharge lateralization in dogs with idiopathic epilepsy.

Brain imaging suggests the involvement of the limbic system, particularly the cingulate gyrus (GC), in dogs with idiopathic epilepsy (IE). A correlation exists between the side of interictal epileptiform discharges (IEDs) and the volume of the ipsilateral GC (GCe) in dogs with IE. Dogs admitted to the neurological consultation (32 with epileptic seizures and 13 control) were included. This retrospective, blinded study followed the International Veterinary Epilepsy Task Force recommendations for diagnosing IE at the Tier III confidence level. The IE group included 18 and 14 dogs with IEDs in the left and right hemispheres, respectively (median age: 36 months, median weight: 19.5 kg), whereas the control group included 13 dogs (median age: 32 months, median weight: 20 kg). Whole-brain and GC-volumetric assessments were performed by a semiautomated method. In the control group, the volume of the GC was: left, from 743.63 to 1001.61 mm3, right, from 789.35 to 1015.86 mm3. In the study group, the volume of the GC was: left, from 720.88 to 1054.9 mm3 and right, from 566.29 to 987.77 mm3. In dogs with IE, GCe volume was significantly lower than the mean volume of the GC in the control group relative to total intracranial volume (TIV; P = .00044). Alterations in the volume of the GC provide insights into structural changes during IE. The use of semiautomatic volumetry provides an advantage by reducing the potential for human error.

Altered individual-level morphological similarity network in children with growth hormone deficiency

BackgroundAccumulating evidences indicate regional grey matter (GM) morphology alterations in pediatric growth hormone deficiency (GHD); however, large-scale morphological brain networks (MBNs) undergo these patients remains unclear.ObjectiveTo investigate the topological organization of individual-level MBNs in pediatric GHD.MethodsSixty-one GHD and 42 typically developing controls (TDs) were enrolled. Inter-regional morphological similarity of GM was taken to construct individual-level MBNs. Between-group differences of topological parameters and network-based statistics analysis were compared. Finally, association relationship between network properties and clinical variables was analyzed.ResultsCompared to TDs, GHD indicated a disturbance in the normal small-world organization, reflected by increased Lp, γ, λ, σ and decreased Cp, Eglob (all PFDR < 0.017). Regarding nodal properties, GHD exhibited increased nodal profiles at cerebellum 4-5, central executive network-related left inferior frontal gyrus, limbic regions-related right posterior cingulate gyrus, left hippocampus, and bilateral pallidum, thalamus (all PFDR < 0.05). Meanwhile, GHD exhibited decreased nodal profiles at sensorimotor network -related bilateral paracentral lobule, default-mode network-related left superior frontal gyrus, visual network -related right lingual gyrus, auditory network-related right superior temporal gyrus and bilateral amygdala, right cerebellum 3, bilateral cerebellum 10, vermis 1-2, 3, 4-5, 6 (all PFDR < 0.05). Furthermore, serum markers and behavior scores in GHD group were correlated with altered nodal profiles (P ≤ 0.046, uncorrected).ConclusionGHD undergo an extensive reorganization in large-scale individual-level MBNs, probably due to abnormal cortico-striatal-thalamo-cerebellum loops, cortico-limbic-cerebellum, dorsal visual-sensorimotor-striatal, and auditory-cerebellum circuitry. This study highlights the crucial role of abnormal morphological connectivity underlying GHD, which might result in their relatively slower development in motor, cognitive, and linguistic functional within behavior problem performance.

The virtual disengagement hypothesis: A neurophysiological framework for reduced empathy on social media.

Social media is a hotbed of interpersonal conflict and aggression. Platforms such as Twitter and Instagram are used by more than 62% of the global population, facilitating billions of user interactions every day. However, many of these exchanges involve hostile, insensitive, and antisocial behaviors. This raises the question: is empathy blunted on social media? Substantial evidence demonstrates that humans tend to behave more rudely in virtual settings, but considering the scarcity of physiological data collected under these circumstances, it remains unclear how the neural systems guiding social cognition and empathy may function differently in online interactions. We propose the "Virtual Disengagement Hypothesis," a conceptual framework to explain the prevalence of hostility online. It posits that interactions occurring on social media omit social cues that facilitate the assessment of a social partner's affective state, such as facial expressions and vocal tone, and thus fail to sufficiently recruit brain circuitry involved in empathy, such as the anterior cingulate cortex, insula, and prefrontal cortex. Additionally, interactions on social media occur asynchronously and in a "replayed" context, which may further limit recruitment of empathy systems. As a result of this diminished sensitivity to others' states, users may be predisposed to inconsiderate or outright antisocial behaviors. Given the massive and growing base of users on these platforms, we urge researchers to expand efforts that focus on neuroimaging in virtual settings with a particular emphasis on developing social media-relevant behavioral designs.