Frontiers in Neuroscience最新文献

[This corrects the article DOI: 10.3389/fnins.2024.1237245.].

Introduction: Sleep-related hypermotor epilepsy (SHE) is a rare epileptic syndrome characterized by nocturnal seizures that predominantly arise during sleep, featuring complex motor behaviors. Pathogenic variants in the nitrogen permease regulator-like 3 (NPRL3) gene and other regulators of the mTOR pathway have been linked to diverse epilepsy phenotypes, including SHE. SHE is challenging to diagnose due to its diverse presentations, overlap with non-epileptic sleep disorders, and semiological similarities to functional/dissociative seizures (FDS).

Case report: We present the case of a 61-year-old woman with a lifelong history of nocturnal paroxysmal events and focal epilepsy. She experienced stereotyped nocturnal episodes of focal motor seizures with retained consciousness, characterized by hyperkinetic activity and asymmetric posturing. Despite multiple antiseizure medications (ASMs), only carbamazepine (CBZ) provided long-term seizure freedom. Genetic testing revealed a novel heterozygous mutation in the NPRL3 gene.

Discussion: This case highlights the diagnostic challenges of SHE and the importance of genetic testing in drug-resistant epilepsy. The identified NPRL3 mutation shows the genetic complexity of SHE and its implications for treatment.

Introduction: The rapid spread of misinformation during the COVID-19 pandemic has raised important questions about how individuals evaluate false information, particularly when it conflicts with strongly held prior attitudes. Understanding the neural mechanisms underlying the processing of vaccine-related misinformation may clarify why such beliefs persist despite corrective information.

Methods: Using functional magnetic resonance imaging (fMRI), we examined neural responses to COVID-19 vaccine misinformation and factual information in vaccine-receptive participants (N = 29). During scanning, participants were presented with a series of vaccine-related statements-both accurate and false-and indicated their level of agreement. Analyses focused on the influence of prior beliefs and attitude congruence on neural activation.

Results: Contrary to our hypotheses, exposure to attitude-incongruent misinformation did not elicit significant activation in emotional processing regions such as the amygdala or precuneus. However, when participants made attitude-incongruent responses-endorsing misinformation or rejecting accurate information-we observed increased activation in the left dorsolateral prefrontal cortex (DLPFC), dorsomedial prefrontal cortex (DMPFC), intraparietal sulcus (IPS), and middle frontal gyrus (MFG), regions associated with decision-making, moral reasoning, memory integration, and cognitive control.

Discussion: These findings suggest that conflicts between incoming information and prior attitudes engage effortful, higher-order cognitive systems rather than affective processing. Resolving such conflicts appears to rely on decision-making and control mechanisms that manage uncertainty and cognitive dissonance. Due to recruitment limitations, the present study focused exclusively on vaccine-receptive individuals. Future research should investigate whether vaccine-resistant individuals exhibit similar or distinct neural patterns, which may provide further insight into the persistence of misinformation in the context of negative prior attitudes.

Objective: To explore the clinical features and treatment approaches for leukoencephalopathy with calcifications and cysts (LCC).

Methods: We retrospectively analyzed a 22-year-old male patient with genetically confirmed LCC admitted to Qingdao University Affiliated Hospital in April 2019. The patient's clinical presentation, imaging characteristics, treatment course, and outcomes were summarized alongside a comprehensive literature review.

Results: The patient underwent resection of bilateral frontal lobe cysts followed later by resection of a parietal lobe cyst. Postoperative pathology confirmed LCC with calcification and cystic changes. No severe postoperative complications occurred. Follow-up imaging demonstrated gradual cyst regression and symptom resolution. Genetic testing identified heterozygous SNORD118 variants (n.3C>T and n.74G>A).

Conclusion: Surgical resection is an effective treatment for LCC cysts causing significant mass effect or neurological deficits, requiring regular follow-up. For smaller, asymptomatic cysts without mass effect, treatment with VEGF inhibitors (e.g., bevacizumab) may be beneficial. Management should be individualized.

Objective: To examine prefrontal hemodynamic changes in patients with post-stroke anxiety (PSA), both at rest and during cognitive task engagement, with the aim of elucidating the underlying neural mechanisms of PSA and identifying potential neural correlates for clinical application.

Methods: Fifty patients with PSA and 45 post-stroke patients without anxiety symptoms were recruited. PSA was diagnosed using the Hamilton Anxiety Rating Scale (HAMA ≥ 7), and comorbid depression was screened using the 17-item Hamilton Depression Rating Scale (HAMD-17 ≥ 8). Patients with significant cognitive impairment were excluded. Functional near-infrared spectroscopy (fNIRS) was used to measure resting-state functional connectivity in the frontopolar cortex (FPC) and dorsolateral prefrontal cortex (DLPFC), as well as task-evoked activation during the verbal fluency task (VFT). Demographic and clinical characteristics showed no significant differences between groups except for stroke type. Between-group comparisons were conducted to identify PSA-related differences in prefrontal network characteristics. Subgroup analyses were performed to explore the influence of comorbid depression on neural alterations.

Results: There were no significant differences between the PSA and non-PSA groups in demographic or clinical characteristics, including age, sex, and disease duration (P > 0.05). Compared to the non-PSA group, patients with PSA exhibited significantly reduced activation in the bilateral FPC during the VFT (P < 0.05). Within the PSA group, those with comorbid depression showed further reductions in activation in the bilateral FPC and the left DLPFC (P < 0.05). No significant differences in resting-state functional connectivity were observed between groups (P > 0.05).

Conclusion: Reduced activation in the bilateral FPC may represent a key neural substrate associated with post-stroke anxiety. In addition, altered activation patterns in the bilateral FPC and left DLPFC may reflect neural correlates related to depressive symptoms in patients with PSA, providing candidate targets for future mechanistic and clinical studies.

Each year, approximately 2.9 million people in the United States sustain a traumatic brain injury (TBI), many of whom go on to experience chronic secondary complications such as post-traumatic epilepsy (PTE) and sleep-wake disturbances. These outcomes arise from complex secondary injury processes, including neuroinflammation, oxidative stress, and disruptions in neuroendocrine signaling. While inflammatory and excitotoxic mechanisms have been extensively studied, growing evidence highlights sex hormone dysregulation-particularly involving estrogen, progesterone, and testosterone-as an important yet underrecognized contributor to post-TBI physiology. Clinical and preclinical studies indicate that TBI can alter systemic and brain-derived hormone levels, influencing neuroinflammation, glial activation, neuronal survival, and synaptic plasticity. These hormone-related changes have been associated with altered seizure susceptibility and disrupted sleep architecture, suggesting that sex hormone dysregulation may represent one interacting pathway influencing both outcomes. Additionally, the bidirectional relationship between epilepsy and sleep-where seizures disrupt sleep architecture and sleep loss increases cortical excitability-may further compound vulnerability after TBI. Given the heterogeneity of injury mechanisms and hormonal responses across individuals, these relationships remain incompletely understood but biologically plausible. This narrative review examines how TBI-related alterations in estrogen, progesterone, and testosterone may intersect with sleep regulation and seizure susceptibility. We summarize their physiological roles in the brain, evaluate how post-injury disruptions may shape chronic outcomes, and highlight how early identification of hormonal abnormalities could inform future research on therapeutic strategies. By addressing this understudied interface between endocrine, neural, and behavioral dysfunction, we aim to advance understanding of modifiable pathways that may contribute to long-term morbidity after TBI.

Background: Impaired attention is a key feature of HIV-associated brain damage, and people living with HIV (PLWH) often have potential visual-auditory perceptual deficits. This study aimed to explore functional alterations in divided attention in PLWH using a parallel audio-visual spatiotemporal task with multimodal functional magnetic resonance imaging (fMRI) and to explore candidate neuroimaging markers of HIV-related attention impairment.

Methods: Thirty-one cognitively unimpaired PLWH and 34 healthy controls (HC) completed a divided attention task during fMRI via a modified Posner paradigm. Behavioral performance and task-related brain activation were compared between the two groups. Seed-based whole-brain functional connectivity (FC) maps were computed in resting-state fMRI (rs-fMRI) using a priori anatomical regions of interest (ROIs) from the audiovisual attention network, defined based on previous independent fMRI studies employing similar spatial-temporal attention paradigms.

Results: The PLWH showed lower accuracy than HC. Task-related brain activation was more extensive in PLWH, including increased activation in occipital/temporal lobes, plus frontal/parietal lobes, insula, and limbic system. Using a priori anatomical regions of interest from the audiovisual attention network as seeds, PLWH exhibited increased resting-state FC between these frontal-parietal-temporal-insular regions and bilateral posterior cerebellar lobules VIII-IX, as well as with multimodal associative cortices. Within the PLWH group, percent BOLD signal change showed significant positive correlations with HIV infection duration in a subset of task-difference ROIs-7 regions identified under spatial cueing and 13 regions identified under temporal cueing.

Conclusion: The HIV impairs audio-visual divided attention, with fMRI revealing neural alterations in cognitively unimpaired PLWH. These findings suggest that task-related activation patterns and resting-state connectivity measures may serve as sensitive candidate markers of HIV-related brain involvement and help identify individuals at increased risk of cognitive decline, although longitudinal studies are needed to establish their prognostic value.

The global rise in non-communicable diseases, alongside an aging population, is expected to increase the prevalence of motor impairments and, therefore, the need for assistive care. Upper limb impairments can significantly affect independent living and increase long-term care costs. Wearable assistive devices incorporating electrical stimulation (ES) offer a promising solution to support independence and help alleviate pressures on both formal and informal care provision. The development of hybrid systems, which integrate aspects of robotics and electrical stimulation, aim to overcome the limitations associated with single-modality devices. However, there is limited information on the most appropriate electrical stimulation protocols to use, or on what challenges may be faced in doing so. Correspondingly, this narrative review addresses this gap through assessing the role of electrical stimulation in upper limb assistive technology. By evaluating user requirements and identifying challenges with current stimulation strategies, this review highlights the potential benefits of exploring alternative protocols, beyond conventional functional electrical stimulation (FES) techniques, for upper limb assistance. In particular, addressing practical difficulties of stimulation is likely to be critical for successful user uptake and minimizing device abandonment. The paper subsequently reviews several stimulation strategies which may offer novel research directions and opportunities in the development of upper limb assistive technologies.

Background: Social cognition impairments-including difficulties in recognizing personally familiar faces-occur early in mild cognitive impairment (MCI) and can lead to social withdrawal, reduced motivation, and secondary depression. Face recognition is central to social cognition, yet its neural basis in MCI remains insufficiently understood. This study examined whether task-based fMRI during famous face recognition could capture early alterations in the parahippocampal gyrus (PHG) and posterior cingulate cortex (PCC), key nodes supporting semantic access and internally directed cognition within the default mode network (DMN).

Methods: Thirty-two participants (20 healthy controls, 12 MCI) completed two fMRI tasks: famous vs. non-famous face judgment and face vs. object categorization. A 2 × 2 factorial analysis assessed Group and Task effects, and small-volume correction was applied to PHG and PCC.

Results: Behavioral accuracy was comparable between groups; however, whole-brain analyses revealed markedly reduced activation in the left PHG and PCC in the MCI group during socially meaningful face processing. ROI analyses further demonstrated that the left PHG reduction remained significant after FWE correction, whereas PCC showed a weaker reduction that did not survive correction for multiple comparisons.

Conclusion: These findings suggest early alterations in PHG-PCC networks that precede observable behavioral decline in MCI. In particular, reduced activation in the left PHG may reflect early disruptions in semantic access and internally directed processing. Assessing these socially relevant neural circuits alongside established amyloid and tau biomarkers may provide complementary functional insight into early cognitive vulnerability in individuals at risk for dementia.