New neurological symptoms in neuro-oncology patients are usually attributed to the tumor or its treatment. A diagnosis of functional neurological disorder (FND) is often only considered when investigations do not reveal a cause and medical management fails. The consequences to neuro-oncology patients of comorbid FND have not been elaborated.
We performed a single-center retrospective case study of adult neuro-oncology patients with an intracranial tumor who presented acutely with FND and required expedited investigations. Data recorded were tumor type, investigations, adverse life events, medical interventions, and outcomes. This was combined with a systematic literature review.
Ten patients met our study criteria. Six had functional seizures, two had functional hemiparesis, and two had functional speech disorders. FND symptoms started prior to tumor diagnosis in three patients; between diagnosis and tumor treatment in three patients; and after treatment commenced in four patients. Two patients were thrombolyzed for a presumed stroke. Three patients had either their tumor surgery or chemoradiotherapy delayed. Diagnosis and management of FND enabled tumor treatment to restart. The systematic review identified 43 patients. Thirty-nine had functional seizures, and four had motor FND. All FNDs except one started after tumor treatment commenced.
Acute FND can occur at any stage of a brain tumor illness. The FND may lead to unnecessary medical interventions and can disrupt tumor treatment. Although acute FND improved with diagnosis and explanation, many neuro-oncology patients require a multidisciplinary tumor–FND pathway to manage acute FND and avoid delays to tumor treatment.
This study was conducted to investigate the effects of positive psychotherapy-based education on pain, psychological resilience, and mental well-being after lumbar canal stenosis surgery.
A randomized controlled experimental study was conducted with 66 participants (33 control, 33 experimental) at the Brain and Neurosurgery Department of Medical Center X between March 2025 and July 2025. The control group received no intervention, while the experimental group received 8 weeks of psychoeducation based on positive psychotherapy. Pretests were administered to the control and experimental groups in March 2025. The training of the experimental group was administered between April 2025 and May 2025. Data collection tools included the Descriptive Characteristics Form, Pain Scale, Brief Resilience Scale, and Mental Well-Being Scale. It was determined that the data showed normal distribution, and parametric tests were used in the analyses. Chi-square and Fisher's exact tests were used to compare the descriptive characteristics of the patients in the experimental and control groups. A t-test was applied to the dependent and independent groups to determine the effect of the training.
In the study, no statistically significant difference was found in the comparison of the pretest pain, psychological resilience, and mental well-being scales of the control and experimental groups (p = 0.259, p = 0.177, p = 0.428). In the study, a statistically significant difference was found in the comparison of the posttest pain, psychological resilience, and mental well-being scales of the control and experimental groups (p = 0.001). In the study, a statistically significant difference was found in the pretest–posttest pain, psychological resilience and mental well-being scale total score averages of the experimental group (p = 0.001).
Positive psychotherapy-based education was effective in reducing pain and increasing psychological resilience, and mental well-being in patients after lumbar spinal stenosis surgery. Based on these findings, positive psychotherapy-based education can be recommended as an adjunct to pharmacological treatment for not only physical but also psychological recovery.
The pathogenesis of Parkinson's disease (PD) is closely linked to ferroptosis, yet the mechanism by which ferroptosis-related proteins modulate PD risk through genetic variations remains unclear.
We performed two-sample Mendelian randomization (MR) analyses using protein quantitative trait loci (pQTLs) from the UKB-PPP and deCODE studies as instrumental variables, combined with PD genome-wide association study (GWAS) data. The inverse variance weighting (IVW) method served as the primary analytical approach to identify PD-associated proteins. To assess the role of ferroptosis-related proteins in PD, a two-step MR mediation analysis was conducted, followed by multiple sensitivity analyses. Transcriptomic datasets were analyzed to confirm the differential expression of genes encoding prioritized proteins. Publicly available single-cell RNA sequencing data were utilized to investigate cell-type-specific expression patterns and functional pathways of key proteins.
A total of 210 proteins significantly associated with PD were identified (p<0.05). Mediation analysis demonstrated that CCNE1 mediated 44.17% of the neuroprotective effect (β = −0.503, p = 5.8 × 10−4) through upregulating PARP16 expression (β = 0.318, p = 2.36 × 10−18), with CCNE1's differential expression further validated in transcriptomic datasets. Single-cell analysis demonstrated that CCNE1 and PARP16 are specifically highly expressed in neurons (p < 0.05), with neurons being significantly enriched in neural survival and synaptic plasticity pathways. The cell interaction network revealed that neurons specifically communicate with astrocytes via the NRG3-ERBB4 pathway.
This study provides the first molecular insight into how CCNE1 exerts neuroprotective effects through the regulation of the ferroptosis key protein PARP16, offering a novel perspective for PD mechanism research.
To investigate the correlation between serum 25-hydroxyvitamin D3 (25-(OH)D3) levels and anxiety disorders in adolescents, and to assess the potential impact of vitamin D status on pediatric anxiety disorders, thereby providing clinical evidence for diagnosis and treatment.
This study included 124 adolescents with anxiety disorders who visited the pediatric outpatient department of Jingzhou First People's Hospital from January 2020 to December 2022 as the experimental group and 131 healthy adolescents who underwent physical examinations during the same period as the control group. Serum 25-(OH)D3 levels were compared between the two groups. Simple linear regression analysis was conducted to evaluate the predictive capacity of 25-(OH)D3 levels on anxiety scores in the experimental group. Additionally, 86 adolescents with anxiety disorders and 25-(OH)D deficiency or insufficiency in the experimental group received vitamin D supplementation for 12 weeks, and changes in anxiety scores before and after supplementation were analyzed to assess the effect of 25-(OH)D3 levels on anxiety disorders.
The mean serum 25-(OH)D3 level in the experimental group [(16.48 ± 6.53) ng/ml] was significantly lower than that in the control group [(22.95 ± 7.25) ng/ml], with a statistically significant difference (p < 0.05). The prevalence of vitamin D deficiency and insufficiency was higher in the experimental group (69.35%) than in the control group (36.64%), with a statistically significant difference (p < 0.05). Furthermore, in the experimental group, anxiety scores were negatively correlated with serum 25-(OH)D3 levels, indicating that lower 25-(OH)D3 levels were associated with higher anxiety scores. After vitamin D supplementation, adolescents with anxiety disorders and 25-(OH)D deficiency or insufficiency exhibited reduced anxiety scores.
Vitamin D deficiency may represent a potential risk factor for anxiety disorders in adolescents and demonstrate some predictive value for these conditions. Vitamin D supplementation could potentially alleviate anxiety symptoms in adolescents.
Depression is a global burden that causes mortality and morbidity in patients and affects millions of people worldwide. Conventional treatment of depression has limited efficacy in addressing cognitive symptoms. Probiotics, particularly psychobiotics, offer promise by modulating the gut–brain axis and improving both depressive symptoms and cognitive function. This meta-analysis provides insights into the potential of probiotics in alleviating depression-related symptoms and cognitive deficits in comparison with placebo.
A thorough literature search was performed using online resources such as PubMed, Embase, Cochrane, and Google Scholar. The seven randomized control trials (RCTs) met the inclusion criteria. The study was conducted in compliance with the PRISMA guidelines.
Patients receiving probiotics had significant alleviation of cognitive symptoms (p = 0.01; SMD, −0.90; 95% confidence interval [CI], −1.59 to −0.21; I2 = 82%) in comparison to placebo. Likewise, the probiotic group had a significant reduction in depressive symptoms compared to the placebo group (p = 0.03; SMD, −0.55; 95% CI, −1.04 to −0.06; I2 = 79%). Both results favored the probiotic group over the placebo group.
In conclusion, research has demonstrated that probiotic supplementation can be a highly effective supplementary treatment for depression by effectively addressing psychological symptoms and cognitive problems. Its therapeutic potential in clinical settings should be explored by additional research to better understand its mechanisms.
Chronic stress can have significant impacts on both physical and mental health, including affecting learning and memory processes. Research has shown that exposure to stress during prenatal and neonatal stages can have long-lasting effects on individuals. The objective of this study is to investigate how prenatal stress influences an organism's response to adult stress in terms of memory and learning processes. This comprehensive approach aims to examine the impact of prenatal and adult stress on cognitive functions and gene expression in specific brain regions.
The study involved subjecting pregnant female rats to restraint stress, followed by exposing male offspring to chronic unpredictable stress (CUS) and social instability stress in adulthood for 3 weeks. The researchers then assessed passive avoidance, active avoidance, and spatial learning and memory using the shuttle box and Morris Water Maze tasks, respectively. Additionally, the expression levels of glutamate receptors, brain-derived neurotrophic factor (BDNF), tropomyosin receptor kinase B (TrkB), and Toll-like receptors (TLR2/4) genes in the rats' hippocampus and prefrontal cortex were analyzed.
According to our data, exposure to prenatal maternal stress led to impairments in learning and memory. These disorders are exacerbated in prenatally stressed rats exposed to adulthood stress. TLR2 and TLR4 mRNA levels were significantly elevated. In contrast, the expression of BDNF and TrkB and NMDA and AMPA receptor genes decreased compared to the control.
Collectively, these results indicate that exposure to stressors during the prenatal period is associated with potential long-term impairments in memory formation and/or retrieval, which may persist into adulthood and be exacerbated by chronic stress experienced later in life.
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