Brain Sciences最新文献

Objective: Genetic and environmental factors influence the expression of personality pathology and subsequent treatment efforts. This study associates genetics with a contemporary nosology of personality pathology represented in the Alternative Model for Personality Disorders (AMPD). We hypothesized traits from Criterion B of the AMPD would differ between genotypes of the catechol-O-methyltransferase (COMT) polymorphism (rs4680/Val158Met variation), given this genetic marker's role in the metabolism of dopamine and norepinephrine, especially in the prefrontal cortex. Methods: The Personality Inventory for DSM-V (PID-5) was used to quantify personality traits, and the Genomind platform was used to identify the genotypes of the Val158Met COMT polymorphism in 84 psychiatric outpatients. Results: One of the five Criterion B personality domains and three of the twenty-five traits were significantly different among genotypes. Met/Met carriers had significantly higher pathological scores on the broad domain of negative affect and specific traits of perceptual dysregulation and separation insecurity, while the Val/Val carriers had significantly higher scores on the restricted affectivity trait. The COMT Val158Met polymorphism's association with personality pathology was sexually dimorphic, with the two domains and nine traits significantly different across genotypes in males, but no differences were found in females. A substantial improvement in the regression of domains/traits score when gene-sex interactions were included further confirmed the dimorphism, e.g., the R-squared (adjusted) for the psychoticism improved from 0.03 (p = 0.15) to 0.19 (p < 0.001). Conclusions: Findings offer preliminary support for a link, potentially dimorphic across sexes, between the COMT Val158Met polymorphism and personality pathology as represented by the AMPD.

Background/Objectives: This study aimed to examine the effect of different forgetting strategies on intentional forgetting, specifically comparing the passive decay strategy ('forgetting by keeping the mind blank') and the active rehearsal strategy ('forgetting by rehearsing other words'). Methods: An item-method directed forgetting paradigm was used in a between-subjects design while the electroencephalogram (EEG) was recorded. Results: Behavioral results showed that both strategies produced a robust directed forgetting (DF) effect, but participants in the active rehearsal group recognized more to-be-remembered (TBR) words. Event-related potential (ERP) results indicated that both groups exhibited a DF effect in the cue-induced P2-P3 complex. Compared to the passive decay group, the active rehearsal group did not show a DF effect in the cue-induced later positive component (LPC); instead, a significant DF effect appeared in the P600 during the test phase. Time-frequency results showed that the passive decay group exhibited a significant DF effect in the 9-25 Hz frequency band during the late stage of cue processing, while the active rehearsal group showed a reversed DF effect in the 8-16 Hz frequency band during the mid-stage of cue processing. Conclusions: These findings indicate that forgetting strategies do not affect the recognition performance of to-be-forgotten (TBF) words. The active rehearsal strategy led participants to shift attention from TBF to TBR words, resulting in better TBR recognition performance in this group.

Background/Objectives: Precise identification of seizure onset zones (SOZs) and their propagation pathways is essential for effective epilepsy surgery and other interventional therapies and is typically achieved through invasive electrophysiological recordings such as intracranial electroencephalography (EEG). Previous research has demonstrated that analyzing information flow patterns, particularly in high-frequency oscillations (>80 Hz) using parametric and Wilson algorithm (WL)-based nonparametric Granger causality (GC), is valuable for SOZ identification. In this study, we analyzed scalp EEG recordings from epilepsy patients using an alternative nonparametric GC approach based on spectral density matrix factorization via the Janashia-Lagvilava algorithm (JLA). The aim of this study is to evaluate the effectiveness of JLA-based matrix factorization in nonparametric GC for noninvasively identifying seizure onset zones from ictal EEG recordings in patients with drug-resistant epilepsy. Methods: Two regions of interest (ROIs) in pairs were isolated across different time epochs in six patients referred for presurgical evaluation. To apply the nonparametric Granger causality (GC) estimation approach to the EEG recordings from these regions, the cross-power spectral density matrix was first computed using the multitaper method and subsequently factorized using the JLA. This factorization yielded the transfer function and noise covariance matrix required for GC estimation. GC values were then obtained at different prediction time steps (measured in milliseconds). These estimates were used to confirm the visually suspected seizure onset regions and their propagation pathways. Results: JLA-based spectral factorization applied within the Granger causality framework successfully identified SOZs and their propagation patterns from scalp EEG recordings, demonstrating alignment with positive surgical outcomes (Engel Class I) in all six cases. Conclusions: JLA-based spectral factorization in nonparametric Granger causality shows strong potential not only for accurate SOZ localization to support diagnosis and treatment, but also for broader applications in uncovering information flow patterns in neuroimaging and computational neuroscience.

Background/objectives: Post-varicella arteriopathy (PVA) is a significant cause of pediatric arterial ischemic stroke (AIS) that typically involves previously healthy children within 12 months of primary varicella infection, mostly with a monophasic course. Diagnosis is based on clinical and imaging findings, and cerebrospinal fluid analysis may confirm it; treatment is empirical and heterogeneous. We describe a typical case of PVA and present a systematic review of its clinical, radiological, therapeutic, and outcome features.

Methods: Following PRISMA 2020 and AMSTAR-2 guidelines, data on demographics, clinical presentation, imaging, laboratory confirmation, treatment, and outcomes were extracted across databases (PubMed, Embase, Scopus).

Results: Forty-seven studies, encompassing 312 pediatric patients, were included. Mean age was 4 years with a median latency of 3.82 months from varicella to neurologic symptoms. Common presentation included hemiparesis, language impairment, and seizures. Imaging findings showed unilateral focal involvement of anterior circulation arteries, basal ganglia infarctions, and, rarely, bilateral or posterior circulation involvement. CSF VZV-DNA PCR and anti-VZV IgG were positive in 39% and 48% of tested patients. Treatment included intravenous acyclovir (34%), corticosteroids (20%), and low-dose aspirin (77%); two patients underwent acute reperfusion therapy (rt-PA or thrombectomy). Outcomes tended to be moderately favorable: 43% achieved full recovery, 45% had residual deficit, and 11% experienced recurrence. Prothrombotic state was reported, and it may influence disease severity.

Conclusions: PVA is a rare distinct cause of pediatric stroke, with a generally favorable prognosis quoad vitam. Standardized guidelines and prospective studies are needed to establish evidence-based management. Clinicians should maintain a high suspicion for its diagnosis.

Background: Numerical cognition and motor performance rely on overlapping brain systems, yet the extent of their reciprocal interaction remains unclear. This systematic review explores how number processing influences motor execution and how motor activity shapes numerical cognition, emphasizing the neural mechanisms underlying these associations.

Methods: A comprehensive search of Scopus, PubMed, MEDLINE, SPORTDiscus, PsycINFO, and SpringerLink, as well as journal citations and conference proceedings (up to August 2025), identified experimental studies examining the interplay between numerical cognition and motor performance in healthy adults. Both randomized and non-randomized designs were included. Two reviewers independently screened, extracted data, and assessed study quality following PRISMA and Cochrane Risk of Bias guidelines.

Results: Twelve studies met the inclusion criteria. Most showed that numerical stimuli facilitated motor responses, with congruent number-movement pairings yielding faster reactions and more efficient kinematics. Mental calculation often enhanced motor output (e.g., force, jump height), though interferences emerged under high cognitive load. Conversely, motor actions consistently biased numerical judgments, aligning with spatial-numerical associations.

Conclusions: Evidence suggests a predominant pattern of facilitation, likely reflecting shared networks between cognitive and motor resources. These findings advance theoretical understanding and highlight promising translational applications in education, sport, and neurorehabilitation.

Background/Objectives: Tinnitus causes significant cognitive and emotional distress; however, its clinical assessment mostly relies on subjective measures without evaluation of objective indices. In this narrative review, we examined the potential of electroencephalography (EEG)-based neurophysiological markers as objective biomarkers in tinnitus assessment. Methods: The Web of Science, PubMed, EMBASE, and MEDLINE databases were searched to identify research articles on EEG-based analysis of individuals with tinnitus. Studies in which treatment and control groups were compared across four analytical domains (spectral power analysis, functional connectivity, microstate analysis, and entropy measures) were included. Qualitative synthesis was conducted to elucidate neurophysiological mechanisms, methodological characteristics, and clinical implications. Results: Analysis of 18 studies (n = 1188 participants) revealed that tinnitus is characterized by distributed neural dysfunction that extends beyond the auditory system. Spectral power analyses revealed sex-dependent, frequency-specific abnormalities across distributed brain regions. Connectivity analyses demonstrated elevated long-range coupling in high-frequency bands concurrent with diminished low-frequency synchronization. Microstate analyses revealed alterations in spatial configuration and transition probabilities. Entropy quantification indicated elevated complexity, particularly in the frontal and auditory cortices. Conclusions: EEG-derived neurophysiological markers demonstrate associations with tinnitus in group analyses and show potential for elucidating pathophysiological mechanisms. However, significant limitations, including low spatial resolution, small sample sizes, methodological heterogeneity, and lack of validation for individual-level diagnosis or treatment prediction, highlight the need for cautious interpretation. Standardized analytical protocols, larger validation studies, multimodal neuroimaging integration, and demonstration of clinical utility in prospective trials are required before EEG markers can be established as biomarkers for tinnitus diagnosis and management.

Background/Objectives: The use of theta-burst stimulation (TBS) over the dorsolateral prefrontal cortex (DLPFC) to modulate cognitive function is gaining increasing interest, since it is more time-efficient than standard repetitive transcranial magnetic stimulation. However, the impact of TBS protocols on specific cognitive processes, such as emotional attention, remains understudied. This study aimed to examine the differential effect of continuous TBS (cTBS) over the left and right DLPFC on the facilitation of attention towards emotional (i.e., pleasant and distressing) versus neutral stimuli. Methods: In this randomized controlled trial, ninety-one healthy young adults were randomly allocated to receive either real or sham stimulation over the right or left DLPFC (i.e., left/right real cTBS and left/right sham cTBS), and then completed a computerized dot-probe task that included distressing, pleasant, and neutral images. Results: Participants who received real cTBS showed slower response times to probes replacing neutral images compared to emotional images, whereas no differences were found between stimuli in the sham conditions. No hemisphere-dependent effects were observed for distressing or pleasant images, suggesting that cTBS modulated attentional performance in a comparable manner when administered over the left or right DLPFC. Conclusions: These findings contribute to the literature on emotional attention, underscoring the role of DLPFC in attentional control, which is a valuable cognitive target for advancing the design and implementation of cTBS protocols.

Background/Objectives: Rapid postural reactions are critical for preventing falls, yet the neural systems supporting these responses are not fully understood, particularly with respect to aging and neurological disorders. Understanding how the brain detects, interprets, and responds to balance disturbances is essential for developing new interventions. This scoping review aimed to synthesize evidence from neuroimaging studies to identify the cortical and subcortical mechanisms underlying reactive balance and to characterize how these mechanisms are altered by aging and pathology. Methods: A structured search of EMBASE, PubMed, and CINAHL (7 November 2024) identified studies examining neural activity during experimentally induced balance perturbations. Sixty-one studies met inclusion criteria (EEG n = 45; MRI n = 9; fNIRS n = 8; PET n = 1) and were analyzed for patterns of regional activation and age- or disease-related differences. Results: Evidence converges on a distributed network supporting reactive balance. Sensorimotor, premotor, supplementary motor, and prefrontal cortices show consistent involvement, while cerebellar, brainstem, and basal ganglia structures contribute to rapid, automatic responses. Aging and neurological conditions commonly heighten cortical activation, suggesting reduced automaticity and increased reliance on compensatory control. Conclusions: Reactive balance emerges from coordinated activity across cortico-subcortical systems that are altered by aging and pathology. Further research incorporating multimodal imaging approaches and more ecologically realistic perturbation paradigms is needed to clarify mechanistic pathways and inform precision-based fall-prevention strategies.

Background: Recent research suggests that damage to right hemisphere regions homotopic to the left hemisphere language network affects language abilities to a greater extent than previously thought. However, few studies have investigated acute disruption of language after lesion to the right hemisphere. Here, we examined lesion correlates of acute speech deficits following left and right hemisphere ischemic stroke to clarify the neural architecture underlying early language dysfunction. Methods: We retrospectively analyzed 410 patients (225 left, 185 right hemisphere lesions) from the Stroke Outcome Optimization Project dataset. Presence and severity of speech deficits was measured using the National Institute of Health Stroke Scale Best Language subscore within 48 h of onset. Manual lesion masks were derived from clinical MRI scans and normalized to MNI space. Lesion-symptom mapping was conducted using voxelwise and region-of-interest analyses with permutation correction (5000 iterations; p < 0.05), controlling for total lesion volume. Results: Speech deficits were observed in 53.7% of the cohort (58.2% left, 48.1% right hemisphere lesions). In the full sample, the presence of speech deficits was associated with bilateral subcortical and perisylvian damage, including the external and internal capsules, insula, putamen, and superior fronto-occipital fasciculus. Severity of speech deficits localized predominantly to left hemisphere structures, with peak associations in the external capsule (Z = 6.39), posterior insula (Z = 5.64), and inferior fronto-occipital fasciculus (Z = 5.43). In the right hemisphere cohort, the presence and severity of speech deficits were linked to homologous regions, including the posterior insula (Z = 3.70) and external capsule (Z = 3.63), although with smaller effect sizes relative to the left hemisphere cohort. Right hemisphere lesions resulted in milder deficits despite larger lesion volumes compared with left hemisphere lesions. Conclusions: Acute speech impairment following right hemisphere stroke is associated with damage to a homotopic network encompassing perisylvian cortical and subcortical regions analogous to the dominant left hemisphere language network. These findings demonstrate that damage to the right hemisphere consistently results in acute speech deficits, challenging the traditional left-centric view of post-stroke speech impairment. These results have important implications for models of bilateral language representation and the neuroplastic mechanisms supporting language recovery.

Background: Emotional prosody refers to the variations in pitch, pause, melody, rhythm, and stress of pronunciation conveying emotional meaning during speech. Although several studies demonstrated that the cerebellum is involved in the network subserving recognition of emotional facial expressions, there is only preliminary evidence suggesting its possible contribution to recognising emotional prosody by modulating the activity of cerebello-prefrontal circuits. The present study aims to further explore the role of the left and right cerebellum in the recognition of emotional prosody in a sample of healthy individuals who were required to identify emotions (happiness, anger, sadness, surprise, disgust, and neutral) from vocal stimuli selected from a validated database (EMOVO corpus). Methods: Anodal transcranial Direct Current Stimulation (tDCS) was used in offline mode to modulate cerebellar activity before the emotional prosody recognition task, and functional near-infrared spectroscopy (fNIRS) was used to monitor stimulation-related changes in oxy- and deoxy- haemoglobin (O2HB and HHB) in prefrontal areas (PFC). Results: Right cerebellar stimulation reduced reaction times in the recognition of all emotions (except neutral and disgust) as compared to both the sham and left cerebellar stimulation, while accuracy was not affected by the stimulation. Haemodynamic data revealed that right cerebellar stimulation reduced O2HB and increased HHB in the PFC bilaterally relative to the other stimulation conditions. Conclusions: These findings are consistent with the involvement of the right cerebellum in modulating emotional processing and in regulating cerebello-prefrontal circuits.