Frontiers in Neurology最新文献

Introduction: Spinocerebellar ataxias (SCA) form a group of dominantly inherited neurodegenerative diseases represented by progressive cerebellar ataxia and various other neurological deficits. SCA3 is the most prevalent type globally and represents 28% of the autosomal dominant cerebellar ataxias in The Netherlands. The associated oculomotor disorders, with distance esotropia as its hallmark, cause diplopia and often present early. To gain further insight into this, we examined eye movements made during a continuous visual stimulus tracking task (SONDA; Standardized Oculomotor and Neuro-Ophthalmic Disorder Assessment).

Methods: Thirteen genetically confirmed SCA3 cases underwent SONDA, both monocularly and binocularly. As a reference, we used previously collected data from 36 monocularly and 13 binocularly measured healthy subjects.

Results: SCA3 cases were well capable of tracking the moving stimulus, but they performed the task differently. More specifically, their eyes were not synchronized in their movements, and they made multiple small saccades in response to a large stimulus jump instead of a larger saccade followed by a small corrective saccade. The saccadic amplitude distribution shape was related to the severity of the oculomotor disorder, suggesting that the saccadic amplitude distribution could be used as a biomarker of disease severity.

Conclusion: Overall, this study highlights that eye-tracking during a standardized task can give valuable insights into how eye movements are affected in SCA3 and provides suggestions for potential biomarkers for severity and the associated treatment options. Longitudinal research is needed to elaborate on these findings and validate the proposed biomarkers.

Background: Fabry disease (FD) is a lysosomal storage disorder that causes glycosphingolipid deposition in the vascular endothelium. Early neurovascular involvement is difficult to detect because conventional magnetic resonance imaging (MRI) findings overlap with age-related small- and large-vessel changes. We hypothesized that integrating microvascular and macrovascular MRI markers could improve the detection of FD-related vasculopathy.

Methods: In a prospective case-control study, 26 genetically confirmed FD patients and 26 age- and sex-matched healthy controls underwent three-Tesla MRI (3 T MRI), including high-resolution vessel wall imaging. The macrovascular metrics included the basilar artery (BA) diameter, BA tortuosity index (BATI), and a composite BA degeneration index (BADI). The microvascular markers included the perivascular space (PVS) burden (Potter scale), white matter lesion severity (modified Fazekas scale), and global cerebral atrophy. Associations with FD were assessed using multivariable logistic regression, adjusting for age, sex, and vascular risk factors. Correlations between microvascular and macrovascular markers and age-stratified analyses were also performed.

Results: Patients with FD exhibited a larger BA diameter, higher PVS burden in the basal ganglia and centrum semiovale, and greater cerebral atrophy than controls, while Fazekas scores were similar. Both PVS burden and BA diameter were independently associated with FD after adjustment, and the PVS burden remained significant after controlling for vascular risk factors. In patients with FD, but not in controls, the PVS burden correlated positively with the BADI, indicating coupled microvascular and macrovascular remodeling. Age-stratified analyses revealed steeper increases in BA metrics and PVS burden with advancing age in patients with FD, suggesting accelerated vascular degeneration.

Conclusion: Combining the PVS burden with posterior circulation remodeling indices (BA diameter/BADI) reveals the disease-specific coupling of microvascular and macrovascular degeneration in FD. This quantitative MRI approach may enable earlier diagnosis, more precise risk stratification, and monitoring of therapeutic responses in clinical practice.

Objective: To assess the synergistic effect of acupuncture combined with antidepressants in the treatment of mild-to-moderate depressive disorders.

Methods: Our systematic search identified randomized controlled trials evaluating acupuncture combined with antidepressants for mild-to-moderate depression across eight databases, with records retrieved from each database's establishment until October 29, 2025. Independent researchers critically reviewed the literature, recorded relevant data, and assessed the quality of research. Data were analyzed using RevMan 5.4, Stata 17.0, and TSA 0.9.5.10.

Results: The study included a total of 975 patients across 15 trials. Meta-analysis revealed that compared with antidepressants alone, acupuncture combined with antidepressants could significantly improve patients' HAMD-24 scores (MD = -1.43, 95% CI [-1.88, -0.98], p < 0.00001), HAMD-17 scores (MD = -2.80, 95% CI [-3.97, -1.62], p < 0.00001), early efficacy (MD = -2.00, 95% CI [-2.62, -1.38], p < 0.00001), total effective rate (MD = 2.44, 95% CI [1.65, 3.63], p < 0.00001), SDS scores (MD = -4.16, 95% CI [-5.70, -2.62], p < 0.00001), TESS scores (MD = -3.63, 95% CI [-5.50, -1.76], p = 0.0001) as well as the SERS scores (MD = -3.01, 95% CI [-3.79, -2.23], P<0.00001). Although there is publication bias in HAMD-24 and total effective rate, the trim-and-fill test has confirmed the robustness of the results. Trial sequential analysis (TSA) results demonstrated that acupuncture combined with antidepressants was significantly superior to antidepressants alone in improving HAMD-24 scores, HAMD-17 scores, early efficacy, total effective rate, SDS scores, TESS scores as well as the SERS scores. Moreover, TSA confirmed that the sample sizes for all outcomes were sufficient to support the robustness of these conclusions.

Conclusion: Acupuncture combined with antidepressants demonstrates a clear synergistic effect in treating mild to moderate depression. The combined therapy not only significantly outperformed antidepressants alone on primary efficacy endpoints but also demonstrated early therapeutic advantages as early as one week post-treatment, while markedly reducing medication-related side effects.

Systematic review registration: https://www.crd.york.ac.uk/PROSPERO/view/CRD42025641858, Identifier CRD42025641858.

Introduction: Vestibular migraine (VM) remains an under-recognized condition despite its relative high prevalence and substantial impact on the interictal burden of migraine. We quantified vestibular dysfunctions and interictal migraine burden and evaluated whether dizziness contributes to the migraine interictal burden of VM.

Methods: We conducted a retrospective observational study of consecutive patients fulfilling the Bárány Society and the International Classification of Headache Disorders, 3rd edition, criteria for VM who attended our outpatient clinic between December 2024 and April 2025. Multidimensional assessments included the Headache Impact Test-6 (HIT-6), Migraine Interictal Burden Scale-4 (MIBS-4), Dizziness Handicap Inventory (DHI), Self-Rating Depression Scale (SDS), Video Head Impulse Test (v-HIT), and posturography (Romberg ratio). Association between MIBS-4 and the other assessments were analyzed using Spearman's correlation and stepwise multiple linear regression.

Results: Seventy-five patients were included {median age 37 years [interquartile range (IQR): 27-47]; 74.3% female; 26.7% with aura}. The median HIT-6 score was 62 (IQR: 58-65) and the median MIBS-4 was 4.0 (IQR: 1.0-7.0), with 41.3% of patients exhibiting severe interictal burden (MIBS-4 ≥5). The median DHI score was 20 (IQR: 12-36), and the Romberg ratio was 1.45 (IQR: 1.03-1.97). Vestibular-ocular reflex gains were largely normal, whereas 73.3% of patients exhibited catch-up saccade (CUS) abnormalities. In univariable analyses, MIBS-4 correlated positively with HIT-6 (ρ = 0.414, p < 0.001), DHI (ρ = 0.419, p < 0.001), and SDS (ρ = 0.433, p < 0.001). In multivariable analysis, high HIT-6 scores (β = 0.265, p = 0.016) and high DHI total scores (β = 0.250, p = 0.019) independently predicted high MIBS-4.

Conclusion: In patients with VM during the interictal period, vestibular functions were largely normal except for abnormalities in the v-HIT CUS, whereas subjective dizziness assessed by DHI significantly contributed to the high degree of migraine interictal burden. The dizziness experienced in VM resembled that of persistent postural-perceptual dizziness. These results indicate that vestibular rehabilitation might be effective in alleviating migraine interictal burden in patients with VM.

Background: Migraine is a common comorbidity in patients with epilepsy, with a comorbidity rate ranging from 9.3 to 34.7%. Transcutaneous auricular vagus nerve stimulation (taVNS) is an emerging therapy used in both epilepsy and migraine treatment. However, there are currently no randomized controlled studies (RCTs) using taVNS for epilepsy complicated with migraine.

Objective: In this study, we evaluated the effect of taVNS as an adjuvant therapy on patients with comorbid epilepsy and migraine.

Methods: Forty comorbid patients (taVNS n = 20, tanVNS n = 20) were recruited and randomly grouped. The taVNS group received the true stimulus, whereas the tanVNS group received a pseudostimulus. Outcome assessment was performed at baseline and 24 weeks after initiation. We used t-test and non-parametric tests to analyse the data.

Results: The frequencies of migraine attacks and seizures significantly decreased in the taVNS group from baseline to 24 weeks (migraine attack frequency, p = 0.002; seizure frequency, p = 0.004), and so did in Self-Rating Anxiety Scale (SAS) score (p < 0.001) and Self-Rating Depression Scale (SDS) score (p < 0.001). The QOLIE-31 scores increased after 24 weeks of taVNS treatment (p = 0.028). Moreover, taVNS reduced the EEG power spectrum in four frequency bands at 16 electrode locations in comparison between groups (p < 0.05).

Conclusion: In comorbid patients in our groups, taVNS can decrease the frequency of seizures, improve mood and quality of life, and reduce the EEG power spectrum.

Speech production and comprehension are coordinated by a large-scale language network. The dynamic balance of intrahemispheric and interhemispheric connectivity within this network is essential for normal language processing. Stroke often significantly disrupts both the functional integrity and dynamic balance of the language network, leading to language deficits (aphasia). However, the brain's adaptive potential to compensate for lesions in post-stroke aphasia (PSA) remains incompletely understood. A key unresolved question is whether recovery of language function in PSA is primarily facilitated by compensatory mechanisms within the left hemisphere, increased recruitment ("upregulation") in the right hemisphere, or both. Building on prior research, we defined a language network encompassing canonical language areas. We employed resting-state functional magnetic resonance imaging (rs-fMRI) to quantify functional connectivity (FC) and investigated differences in intrahemispheric and interhemispheric connectivity within this network between 32 patients with PSA and 70 healthy controls (HCs). Furthermore, we examined the association between altered connectivity patterns at baseline and subsequent improvement in language function in the PSA group. Compared to the HCs, the patients with PSA exhibited increased intrahemispheric FC at baseline. Crucially, this increased intrahemispheric FC was positively correlated with the magnitude of language function improvement from baseline to follow-up. In addition, intrahemispheric FC was significantly higher than interhemispheric FC in the PSA group at baseline. These findings suggest that aberrant connectivity within the language network represents a neural substrate of language impairment in PSA and that heightened intrahemispheric connectivity within the residual left hemisphere language network may predict better recovery of language function in patients with subacute PSA. Collectively, network-based pathology analysis enhances our understanding of the neural mechanisms underlying both lesion effects and functional recovery in PSA.

Sleep constitutes an essential physiological process that is vital for maintaining physical and mental wellbeing. However, the science of sleep focusing on basic questions such as "how" we sleep and "why" we sleep is still not clear. Over the past decade, substantial progress has also been made in elucidating the interactions between sleep and other biological processes, providing insights into the basic questions of sleep. Among these, emerging evidence highlights the microbiota-gut-brain axis (MGBA) as a pivotal bidirectional network that connects gut microorganisms with the central nervous system to regulate sleep architecture and homeostasis. This interaction is inherently bidirectional: sleep deprivation alters gut motility, mucosal integrity, and microbial composition, while microbial metabolites in turn influence neurotransmission (γ-aminobutyric acid, serotonin), immune-endocrine balance, and inflammatory signaling. In this article, we will review recent studies about MGBA-targeted therapeutic strategies for sleep disorders, such as probiotics, prebiotics, and fecal microbiota transplantation, which aim to restore microbial homeostasis and improve sleep quality. Furthermore, we discuss emerging interventions that modulate microbial metabolites and neuroimmune-endocrine signaling, as well as innovative pharmacological approaches targeting MGBA dysfunction. Collectively, we hope this review will contribute to a deeper understanding of MGBA-mediated mechanisms in sleep disorders promises to inform novel preventive and therapeutic strategies, ultimately improving clinical outcomes and quality of life for affected individuals.

Background: Post-stroke depression (PSD) is one of the most common neuropsychiatric complications among stroke survivors, with a substantial impact on functional recovery and quality of life. This study aimed to investigate the association between the systemic immune-inflammation index (SII) at admission and the occurrence of PSD in patients with acute ischemic stroke (AIS).

Methods: We prospectively enrolled 318 consecutive patients with first-ever AIS admitted to our hospital between August 2024 and March 2025. Venous blood samples were collected at admission, and SII was calculated as neutrophil count × platelet count/lymphocyte count. At 3 months post-stroke, depressive symptoms were assessed using the 17-item Hamilton Depression Rating Scale (HAMD-17). Patients with a HAMD-17 score >7 were diagnosed with PSD and categorized accordingly into PSD and non-PSD groups.

Results: At the 3-month follow-up, 98 patients (30.82%) were diagnosed with PSD. Compared with the non-PSD group, patients in the PSD group had significantly higher SII values [658.66 (468.73-958.90) vs. 476.71 (362.73-646.83), p < 0.001]. In multivariate logistic regression analysis, after adjusting for potential confounders, patients in the highest SII tertile had a significantly increased risk of developing PSD compared with those in the lowest tertile (OR = 3.502, 95% CI: 1.582-7.752, p = 0.002). Receiver operating characteristic (ROC) curve analysis identified an optimal SII cut-off value of 602.503 for predicting PSD, with a sensitivity of 0.582, a specificity of 0.700, and an area under the curve (AUC) of 0.659 (95% CI: 0.592-0.726, p < 0.001).

Conclusion: Elevated SII levels at admission are positively associated with the development of PSD in AIS patients, suggesting that SII may serve as a valuable inflammatory biomarker for early identification of patients at high risk for PSD.