Revue neurologique最新文献

Introduction: Functional neurological disorders (FND) are a frequent reason for consultation in neurology, characterized by symptoms that can impair various functions, without any identifiable lesion. Diagnosis plays a key role in patient adherence to treatment and the improvement of outcomes. However, the diversity of terms used to describe FND and etiological uncertainties reflect a lack of consensus, which may affect communication between healthcare professionals and patients. This raises the question of how healthcare providers explain the diagnosis of FND.

Objective: To explore similarities and differences in the language used by physicians, physiotherapists, and psychologists to explain FND to patients.

Method: An exploratory qualitative study was conducted using individual semi-structured interviews with physicians, physiotherapists, and psychologists who had encountered at least one case of FND in the course of their practice.

Results: FND are associated with heterogeneous conceptualizations among healthcare professionals, ranging from psychological to neurological approaches. Despite this diversity marked by uncertainty, recognizing symptoms while reassuring patients remains essential. Diagnosis disclosure constitutes a complex process for clinicians due to its potential impact on patients, requiring appropriate communication to foster therapeutic alliance. This step requires an interprofessional dynamic, which is sometimes hindered by communication challenges and inconsistent narratives that disrupt care pathways. In this context, developing a common language emerges as a key imperative.

Conclusion: This study highlights the importance of establishing coordinated care pathways for FND patients, which rely on harmonized communication among healthcare practitioners. Although resources exist, their implementation appears to be limited.

Lecanemab, the first anti-amyloid therapy approved by the European Medicines Agency, has demonstrated a statistically and clinically significant but moderate slowing of decline in early Alzheimer's disease (AD). In contrast, its long-term impact on the disease course is not formally established. Any benefit, therefore, needs to be carefully weighed against its adverse effects and practical constraints, which must be discussed with patients and caregivers within a shared decision-making process (SMD). However, applying SDM in this context is challenging due to treatment complexity, cognitive impairment and the involvement of care partners. Supported decision-making, which aims to assist individuals with decisional limitations in participating in important choices, has been promoted as a relevant approach. In this bicentric study conducted in France, we evaluated a simulated supported decision-making process in 25 patients with early AD who were eligible for lecanemab and faced the decision to choose anti-amyloid immunotherapy. We created a written decision aid using a consensus-based method to provide clear, accurate, and scientifically validated information to patients and care partners. After a one-week reflection period, both patients and care partners demonstrated a good overall understanding of the information provided, though care partners showed higher levels of comprehension and retention. The treatment was considered acceptable by most patients and their care partners. While patients ultimately remain the decision-makers, these findings highlight the central role of care partners in strengthening supported decision-making, notably through frameworks such as the French "trusted person" model.

Background: Hardware-related infections may follow primary deep brain stimulation (DBS) implantation or implantable pulse generator (IPG) replacement with challenging management in fluctuating Parkinson's disease (PD) patients.

Objectives: We aimed to investigate the incidence, risk factors, management and outcome of DBS-related infections in PD.

Methods: We performed a ten-year retrospective cohort study including all consecutive PD patients who underwent primary DBS implantation surgery and IPG replacement respectively. Incidence and risk factors of infections were analyzed in both cohorts using survival analysis, and infectious and neurological management was reported.

Results: The incidence of DBS-related infections was 11.3 (95%CI 6.3-18.7) per 1000 person-year following primary DBS implantation (293 patients) and 20.7 (95%CI 10.7-36.2) per 1000 person-year following IPG replacement (217 procedures in 188 patients). Infections were associated with a shorter disease duration before primary DBS implantation, but longer disease, DBS duration and a greater number of procedures for IPG replacement. Following DBS implantation, surgical management consisted in partial (3/15, 20%) or total (8/15, 53%) hardware removal, with good outcome in 12 (80%) patients. Infections resulted in increased short-term neurological worsening and challenging therapeutic management for total hardware removal and advanced PD patients.

Conclusions: We found low incidence of DBS-related infections following primary DBS implantation or IPG replacement in PD patients, depending on PD duration. Our study highlights that patient-specific and multidisciplinary management in expert center resulted in good outcome and high rates of reimplantation following primary implantation-related infection, whereas PD patients with IPG replacement-associated infection had more severe outcome and challenging management.

Stress exposure, whether acute or chronic, is now recognized to be a determinant of epileptogenic vulnerability. Psychological stress or trauma may not only precipitate seizures but also actively contribute to the development of epilepsy, a concept that in the clinical setting could be termed "psychoepileptogenesis". Recent evidence from both animal models and clinical studies supports the role of emotional stress in facilitating epileptogenesis, particularly within limbic structures such as the amygdala and hippocampus. In rodent models, chronic stress has been shown to lower seizure thresholds and promote epileptogenesis through mechanisms involving brain-derived neurotrophic factor (BDNF) and dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis. Human studies reinforce these findings: individuals exposed to trauma or suffering from post-traumatic stress disorder (PTSD) exhibit an elevated risk of developing epilepsy, especially temporal lobe epilepsy (TLE), with structural and functional neuroimaging revealing changes in limbic and paralimbic circuits. These converging lines of evidence suggest that psychoepileptogenesis is a plausible, albeit complex, phenomenon. Further research is needed to identify biomarkers of vulnerability and evaluate whether early interventions targeting stress pathways might alter the course of epileptogenesis.