Acta neurologica Belgica最新文献

Background and objectives: Acute traumatic subdural hematomas (aTSDH) represent a frequent and critical neurosurgical emergency, associated with a significant risk of mortality. Elderly patients with symptomatic aTSDH may benefit from early antifibrinolytic therapy (EAFT). We aim to investigate whether EAFT can improve clinical outcomes in aTSDH patients and to explore the factors influencing mortality, using data from a nationwide, multicenter, prospective cohort study.

Methods: Multicenter, prospective cohort study at 30 trauma centers from 2023 to 2024 enrolled 963 patients diagnosed aTSDH. After screening, 297 patients aged 60 years or older met inclusion criteria. The primary outcome was 90-day mortality. Secondary outcomes included vascular occlusion, brain rebleeding, sepsis, gastrointestinal bleeding, and renal failure.

Results: A total of 297 aTSDH patients were identified, of whom 195 received EAFT, and 102 were in the control group. After propensity score matching (PSM), 80 patients in each group were compared. There were no significant differences in 90-day mortality (before PSM, P = 0.439; after PSM, P = 0.828). The difference between the two group in the incidence of brain rebleeding, sepsis, gastrointestinal bleeding, and renal failure were similar before and after PSM. The EAFT group had a significantly higher incidence of vascular occlusion compared to the control group (before PSM, P = 0.014; after PSM, P = 0.027). In multivariate logistic regression (odds ratio [95% confidence interval]), increased 90-day mortality was predicted by larger hematoma volume (2.329 [1.123-4.830], P = 0.023) and greater midline shift (2.251 [1.065-4.755], P = 0.034). Sensitivity analysis indicated that there was heterogeneity in the treatment effects between the two groups across different midline shift categories (before PSM, P = 0.012; after PSM, P = 0.043).

Conclusion: EAFT may not significantly reduce mortality in elderly aTSDH patients and could potentially increase the risk of vascular occlusion. Therefore, its use in this population should be approached with caution, carefully assessing the potential risks.

Background: Parkinson's disease (PD) is one of the most common progressive neurological disorders characterized by the loss of dopaminergic neurons in the substantia nigra of the midbrain. In recent years, PIAS family proteins have been proposed as key factors in the development of neurodegenerative diseases. The aim of this study was to investigate the expression levels of PIAS family genes in patients with PD and compare them with those in the healthy control group.

Methods: The expression of PIAS family genes in the peripheral blood cells was investigated by RT-qPCR technique and the results were statistically analyzed using R software.

Results: PIAS4 gene expression was significantly lower in PD patients compared to the control group (p = 0.016), while we found no significant change in the expression of other PIAS genes between PD patients and healthy control group. Considering gender, the expression of PIAS3 was higher in males than that in females (p = 0.024). Also, significant downregulations in PIAS3 and PIAS4 genes were observed with increasing age, especially in men regardless of being patient or healthy (p = 0.04 and 0.001, respectively). In the correlation analysis, there were significant positive pairwise correlations between PIAS family members. Also, significant negative correlations between the expression of PIAS3 and PIAS4 genes with age were found.

Conclusion: These findings show that part of the disruption of immune system regulation occurring in PD is probably related to the expression of PIAS family genes and that these proteins, especially PIAS4, can play an important role in the inflammatory and pathophysiological mechanisms of PD.

Background: Botulinum toxin is now used to treat a variety of neurological and non-neurological disorders. Despite the fact that injections of botulinum neurotoxin may significantly reduce the involuntary muscular contractions associated with focal dystonia and hemifacial spasm (HFS), it is less certain whether the motor effect would result in an improvement in health-related quality of life (HR-QoL).Our goal was to evaluate how botulinum toxin affected individuals with cervical dystonia and hemifacial spasm in terms of their quality of life, self-esteem, pain, sleep, and depression.

Methods: This is a prospective study that included 40 patients diagnosed with cervical dystonia or hemifacial spasm treated with Botulinum toxin. Quality of life, self-esteem, pain, sleep and depression were all assessed in the studied patients by self-reporting questionnaires to assess the impact of botulinum toxin on them.

Results: The quality of life with its components (physical, physical role, emotional role, vitality, mental health, social functioning and pain) showed significant improvement at the end of follow up compared to baseline with p values ≤ 0.001. Also, there was a significant improvement of self-esteem score, depression score, at the end of follow up period compared to baseline assessment with p value 0.012, < 0.001 respectively. Moreover, there was a significant improvement of all pain scales and sleep quality scores with p values < 0.05 except the habitual sleep efficiency.

Conclusion: botulinum toxin is an effective therapy for motor and non-motor manifestations associated with focal cervical dystonia and hemifacial spasm as well as the quality of life and to conclude that its effectiveness is dependent not only on the elimination of physical symptoms, but also on improving the patients' and their families' emotional and social status to help providing the drug to all eligible patients.

Background: Scales and questionnaires measure various variables, such as health symptoms, functionality, and quality of life. The Headache Needs Assessment (HANA) survey evaluates the chronic impact of migraine on quality of life, focusing on frequency and bothersomeness.

Objective: This study aimed to adapt and validate the Turkish version of the HANA, a concise and practical tool for assessing tension-type headache-related needs.

Methods: A total of 86 individuals with tension-type headaches were included in the test phase, while 79 participants with tension-type headaches were involved in the retest phase. Exploratory and Confirmatory Factor Analyses (EFA and CFA) were used to assess structural validity. Reliability was evaluated using Intraclass Correlation Coefficients (ICC) and Cronbach's α, and convergent validity was tested by correlating HANA scores with the Henry Ford Hospital Headache Disability Inventory (HDI) and Headache Impact Test-6 (HIT-6).

Results: Test-retest reliability was strong (ICC 0.789-0.840), and internal consistency was high (α = 0.882-0.913). Good correlations with HDI (r = 0.545; p = 0.000) and HIT-6 (r = 0.484; p = 0.000) supported convergent validity, while it was observed a low correlation with Visual Analog Scale (r = 0.342; p = 0.001). There were no floor or ceiling effects observed.

Conclusion: The Turkish version of the HANA is a valid and reliable tool in individuals with tension-type headache that is easy to administer in both clinical and research contexts.

Clinicaltrials:

Gov number: NCT06675292.

Human MutT homolog 1 (MTH1) plays a crucial role in sanitizing oxidized DNA precursors by enzymatically hydrolyzing oxidized nucleotides. The absence of MTH1 activity in the cells results in the accumulation of oxidized nucleotides within the nucleus and mitochondria, leading to mutations, abnormal proteins, and neurodegeneration (in the central nervous system). It has garnered interest as a potential target for anticancer treatment through targeted inhibitor molecules but remains largely understudied in other neurological disorders. This review explores the understanding of MTH1 expression in glioma and its potential role in neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and Huntington's disease concerning disease mechanism and prognosis. Neurodegeneration, activation of glial cells, and mitochondrial dysfunction are common mechanisms involved in the progression of these diseases. This review also tries to identify the unexplored associations and research gaps that can reveal novel applications of the enzyme in epilepsy, in which MTH1 is studied less. The influence of the ROS environment and cell type on MTH1 expression and function is crucial to be studied for elucidating its role in a multitude of CNS pathologies. The involvement of microglial cell-mediated inflammatory responses through ROS production in epileptogenesis in mouse models highlights the interplay between oxidative stress and neuroinflammation in epilepsy. The possible existence of a similar association between MTH1 expression and pathogenesis of the discussed neurological disorders in vivo demands further exploration preclinically and in patient samples.