Revue Neurologique[JOURNAL]
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200 papers
Non-infectious environmental risk factors of multiple sclerosis: Mechanisms and intervention windows for prevention.
Rival M, Thouvenot E
Rev Neurol (Paris) · 2026 May · PMID 41986183 · Publisher ↗
The trajectory of multiple sclerosis (MS) is shaped by complex interactions between genetic susceptibility and environmental factors. This review examines modifiable non-infectious determinants across the life course and...
The trajectory of multiple sclerosis (MS) is shaped by complex interactions between genetic susceptibility and environmental factors. This review examines modifiable non-infectious determinants across the life course and proposes integrated prevention strategies. Key factors include vitamin D deficiency, low UV exposure, smoking, adolescent obesity, air pollution, and chemical environmental exposures. Mendelian randomization studies support the causality of several determinants, particularly low vitamin D and high BMI. Adolescence emerges as a critical susceptibility window where the maturing immune system is uniquely sensitive to metabolic and environmental triggers. Among validated interventions, vitamin D supplementation stands out for its ability to reduce disease activity in early MS. Effective prevention requires both individual actions and structural public health policies, such as air quality regulations and urban "walkability". Future efforts should prioritize multimodal strategies targeting high-risk youths through the educational system (physical activity, weight management, and smoking prevention). These holistic approaches offer broad-spectrum benefits, reducing the burden of MS while preventing comorbidities, including cardiovascular, metabolic but also cancer.
Imaging myelin content changes: A bridge between tissue and clinics.
Galbusera R, Stadelmann C, Granziera C
Rev Neurol (Paris) · 2026 May · PMID 41986182 · Publisher ↗
The development of remyelinating therapies is becoming an increasingly important strategy in the treatment of diseases such as multiple sclerosis. In this context, reliable measurement of myelin content is essential for...
The development of remyelinating therapies is becoming an increasingly important strategy in the treatment of diseases such as multiple sclerosis. In this context, reliable measurement of myelin content is essential for the objective assessment of therapeutic efficacy. Over the past two decades, quantitative MRI has emerged as a method of choice for this purpose, supported by several postmortem validation studies that combine MRI with histology, the latter serving as the reference standard. In this review, we summarize the most relevant quantitative MRI contrasts sensitive to myelin changes and describe the mechanisms by which each contrast provides an estimate of myelin content. In addition, we outline the key steps involved in histological myelin quantification, highlighting the different methodological approaches as well as their limitations and potential pitfalls.
Remyelination and neuroprotection translational trials: Lessons from optic neuritis.
Louapre C, Beigneux Y, Maestri F … +2 more , Meyniel C, Touitou V
Rev Neurol (Paris) · 2026 May · PMID 41966939 · Publisher ↗
Multiple sclerosis disease-modifying treatments have reduced inflammatory activity but have limited impact on progressive neurodegeneration. In this context, remyelination and neuroprotection appear as key therapeutic go...
Multiple sclerosis disease-modifying treatments have reduced inflammatory activity but have limited impact on progressive neurodegeneration. In this context, remyelination and neuroprotection appear as key therapeutic goals. The visual pathway offers an attractive translational model, as optic neuritis recapitulates the demyelinating and neurodegenerative features of multiple sclerosis while providing accessible functional and structural readouts through visual evoked potentials and optical coherence tomography. Over the past two decades, several clinical trials have evaluated remyelinating and neuroprotective agents using optic neuritis as a model. However, so far, no phase 3 trial has met its primary endpoint for either indication. This review synthesises the preclinical rationale, clinical trial evidence, and methodological lessons from these studies. Key challenges include the timing of intervention, heterogeneity in baseline damage, variability of electrophysiological assessments, and uncertain clinical impact of surrogate markers. Addressing these limitations through refined trial design, outcome measure harmonisation, and combined therapeutic strategies will be essential for future translational success.
Contrasting genetic architectures of multiple sclerosis susceptibility and outcome phenotypes.
Sorella MY, Ding Y, Garcia AM … +4 more , Ygonia M, Wang L, Jacobs BM, Harroud A
Rev Neurol (Paris) · 2026 May · PMID 41935914 · Publisher ↗
Multiple sclerosis (MS) is characterized by substantial clinical heterogeneity, yet the factors governing long-term outcomes remain poorly understood. Over the past two decades, genome-wide association studies have ident...
Multiple sclerosis (MS) is characterized by substantial clinical heterogeneity, yet the factors governing long-term outcomes remain poorly understood. Over the past two decades, genome-wide association studies have identified an increasing number of genetic variants influencing MS susceptibility, predominantly implicating immune pathways. Whether these same variants also shape disease course after onset is a question with direct implications for risk prediction, causal inference, and drug development in patients with established disease. This review examines the relationship between MS susceptibility genetics and disease outcomes, synthesizes emerging efforts to identify genetic determinants of severity, neuroimaging phenotypes, and treatment response, and considers how these findings inform our understanding of the mechanisms driving disease heterogeneity.
The evolutionary origins of multiple sclerosis.
Barrie W
Rev Neurol (Paris) · 2026 May · PMID 41935913 · Publisher ↗
There are two main evolutionary theories for why modern humans develop multiple sclerosis (MS). The first, antagonistic pleiotropy, argues that genetic variants that predispose people to MS are protective against infecti...
There are two main evolutionary theories for why modern humans develop multiple sclerosis (MS). The first, antagonistic pleiotropy, argues that genetic variants that predispose people to MS are protective against infections; this explains why these genetic variants persist at high frequency. The second, the Old Friends hypothesis, argues that reduced exposure to ancient, co-evolved micro-organisms like helminths results in immune dysregulation and overreactions to harmless infections and substances; this explains why MS prevalence increases with sanitation. Here, I assess these theories in the light of recent ancient DNA (aDNA) studies. These suggest that populations from the Pontic-Caspian Steppe which migrated across Eurasia in the Bronze Age evolved a strong pro-inflammatory immune response due to increased zoonotic infections resulting from their pastoralist lifestyle. It is possible that this may have occurred in a context of high levels of anti-inflammatory helminth infections, which resulted in a balanced pro- and anti- inflammatory response. In the modern sanitary world, with a lower helminth burden, the immune system 'overshoots' the level of inflammation required. This explains why genetic risk for MS is higher in northern Europe where people have higher genetic ancestry from the ancient Steppe population, and why disease penetrance is increasing.
The genetic architecture of multiple sclerosis in 2026: From susceptibility to disease progression.
Bourguiba-Hachemi S, Paris J, Gourraud PA … +1 more , Vince N
Rev Neurol (Paris) · 2026 May · PMID 41934071 · Publisher ↗
The genetics of multiple sclerosis (MS) has advanced dramatically through the combined impact of high-throughput genotyping, large biobank resources, worldwide collaborations, and powerful computational analyses. Over th...
The genetics of multiple sclerosis (MS) has advanced dramatically through the combined impact of high-throughput genotyping, large biobank resources, worldwide collaborations, and powerful computational analyses. Over the past two decades, genome-wide association studies (GWAS) have significantly reshaped our understanding of the genetic architecture of complex multifactorial diseases such as MS. The number of MS susceptibility-associated genomic regions is now more than 200, underscoring its highly polygenic nature. Within the major histocompatibility complex (MHC), the HLA-DRB1*15:01 allele and its extended haplotypes remain the most robust and reproducible risk factors. This historical association reflects a long-standing link between antigen presentation, immune regulation, and central nervous system autoimmunity. Beyond the MHC, common non-HLA loci implicate a wide network of immune pathways involving T-cell and B-cell activation, cytokine signaling, and antigen presentation. Moreover, rare variant analyses and family-based designs, although limited in power, have uncovered additional susceptibility genes, such as PRF1, CYP27B1, and NLRP1, shedding light on distinct mechanisms of immune modulation and metabolic regulation. The step forward will be now to explore diverse genetic ancestry populations, bearing differences in risk allele frequencies; multi-ethnic and family-based designs are needed to disentangle true genetic effects from environmental confounders. In parallel, progress has been made toward MS progression, as variants potentially influencing disability accumulation and neurodegeneration were identified. These findings have deepened our understanding of MS pathophysiology. They now provide a foundation for future integrative models that combine genetics, environment, and multi-omics data to elucidate disease heterogeneity and guide personalized therapeutic strategies.
Brain atrophy in multiple sclerosis: Mechanisms, measurement, and clinical translation.
Koubiyr I, Schoonheim MM
Rev Neurol (Paris) · 2026 May · PMID 41934070 · Publisher ↗
Multiple sclerosis (MS) features extensive neurodegenerative pathology, in addition to the well-known neuro-inflammatory lesions. Recent breakthroughs highlight the importance of slow physical and cognitive progression i...
Multiple sclerosis (MS) features extensive neurodegenerative pathology, in addition to the well-known neuro-inflammatory lesions. Recent breakthroughs highlight the importance of slow physical and cognitive progression in MS, which can continue despite effective slowing of lesion formation through high efficacy treatment. These types of progression seem driven to a large extent by neurodegenerative changes in MS, highlighting the need for more research to achieve clinical implementation with clear cut-off scores and monitoring strategies. This mini review outlines possible mechanisms underlying neurodegeneration, how to measure these processes on MRI and how we can move towards implementation.
Diagnostic pitfalls and complex cases in MS.
Cobo-Calvo Á, Rovira À, Tintore M
Rev Neurol (Paris) · 2026 May · PMID 41927390 · Publisher ↗
Accurate diagnosis of multiple sclerosis (MS) remains a significant clinical challenge despite major advances in imaging, fluid biomarkers, and diagnostic criteria. Over the past decades, the diagnostic framework has shi...
Accurate diagnosis of multiple sclerosis (MS) remains a significant clinical challenge despite major advances in imaging, fluid biomarkers, and diagnostic criteria. Over the past decades, the diagnostic framework has shifted from a primarily clinical assessment to one increasingly grounded in biological and paraclinical evidence. The introduction of the 2024 McDonald criteria represents a notable evolution, incorporating novel biomarkers such as the central vein sign, paramagnetic rim lesions, and the kappa free light chain index, and expanding anatomical regions for dissemination in space. The new criteria also represent a paradigm shift away from dissemination in time and offer new options to confirm the diagnosis. These innovations aim to enhance diagnostic precision and allow earlier recognition of both relapsing and progressive MS. However, substantial pitfalls persist, especially in patients whose presentations diverge from classical MS patterns. In this review, we discuss a series of complex and illustrative cases that underscore the breadth of diagnostic uncertainty, including hereditary small-vessel disease mimicking demyelination, multifocal white matter lesions later identified as primary central nervous system lymphoma, fulminant demyelinating episodes, solitary progressive lesions consistent with solitary sclerosis, and progressive phenotypes newly classifiable under the 2024 McDonald criteria. Across these scenarios, atypical features (such as strong family history, tumor-like infiltration, or isolated lesions) emphasize the importance of maintaining a broad differential diagnosis and recognizing the many disorders capable of imitating MS on clinical, radiological, or pathological grounds. Collectively, these cases highlight the need for structured, multidisciplinary diagnostic strategy that combines clinical expertise with advanced imaging, cerebrospinal fluid biomarkers, and, when necessary, extended investigations including genetic testing or biopsy. While the 2024 McDonald criteria constitute a major advance, careful interpretation remains essential to avoid misdiagnosis. Understanding these pitfalls is crucial for improving diagnostic accuracy and ensuring timely initiation of appropriate therapy.
Target trial emulation for causal inference using observational data in neurology.
Gavoille A, Nourredine M, Subtil F … +2 more , Kalincik T, Vukusic S
Rev Neurol (Paris) · 2026 May · PMID 41927389 · Publisher ↗
Most clinical questions in neurology are inherently causal, yet observational studies have long been interpreted in terms of associations rather than causal effects of well-defined interventions. This limitation has cont...
Most clinical questions in neurology are inherently causal, yet observational studies have long been interpreted in terms of associations rather than causal effects of well-defined interventions. This limitation has contributed to persistent biases in neurology research, including inappropriate covariate adjustment, temporal misalignment, immortal-time bias, and susceptible depletion. Recent developments in causal inference offer a formal framework to overcome these issues through counterfactual reasoning, causal diagrams, and g-methods. The target trial emulation approach translates these concepts into a practical strategy: investigators first specify the protocol of the randomized trial that would ideally address their question, and then emulate this protocol using observational data. This requires explicit definition of eligibility, treatment strategies, assignment procedures, time zero, follow-up, outcomes, causal contrasts, and handling of intercurrent events, together with prespecified causal assumptions and an appropriate analysis plan. By aligning the design of observational studies with the structure of randomized trials, target trial emulation reduces design-related bias, clarifies the causal question, and provides a transparent foundation for real-world evidence generation. Validation studies, including recent work in multiple sclerosis, have demonstrated good concordance between emulated trials using observational data and randomized controlled trials. Target trial emulation therefore represents an essential complement to randomized evidence, particularly for questions that are difficult or impossible to address through randomization, and has the potential to substantially improve causal inference in neurology.
Adaptive trials and new designs.
Wade C, Apap Mangion S, Chataway J
Rev Neurol (Paris) · 2026 May · PMID 41927388 · Publisher ↗
Neurological therapeutics are advancing rapidly, yet many neurodegenerative diseases still lack effective disease-modifying treatments, in part because traditional trial designs are ill-suited to slowly progressive, hete...
Neurological therapeutics are advancing rapidly, yet many neurodegenerative diseases still lack effective disease-modifying treatments, in part because traditional trial designs are ill-suited to slowly progressive, heterogeneous disorders. Adaptive methods and multi-arm approaches have improved early-phase efficiency but remain limited when used within isolated trials. Multi-arm multi-stage (MAMS) platform designs offer a more powerful solution by evaluating multiple interventions concurrently against a shared control, incorporating interim analyses to stop futile arms early, and enabling addition of new treatments and biomarkers over time within a single, continuous phase-3-capable infrastructure. Experience from oncology and infectious disease demonstrates the feasibility and impact of these platforms. Emerging neurological MAMS trials - such as MND-SMART, ACT-PD, AD-SMART and OCTOPUS in progressive multiple sclerosis - show that these designs can accelerate evaluation, reduce cost and participant burden, and remain responsive to scientific advances.
Therapeutic updates in NMOSD and MOGAD: From present practice to future promise.
Elosua-Bayés I, Cobo-Calvo A
Rev Neurol (Paris) · 2026 May · PMID 41927387 · Publisher ↗
Aquaporin-4-IgG-positive neuromyelitis optica spectrum disorder (AQP4+NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) are rare, antibody-mediated inflammatory disorders of the central n...
Aquaporin-4-IgG-positive neuromyelitis optica spectrum disorder (AQP4+NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) are rare, antibody-mediated inflammatory disorders of the central nervous system (CNS). Although historically grouped under the umbrella of multiple sclerosis, both entities differ markedly in pathophysiology, clinical course, prognosis and therapeutic requirements. The identification of disease-specific autoantibodies has not only refined diagnostic accuracy but has also highlighted fundamental differences in therapeutic strategy, particularly regarding the need for and choice of long-term immunosuppression. While acute management of both conditions relies on similar approaches, the long-term treatment paradigms diverge. Sustained immunosuppression may not be required for all patients with MOGAD, whereas AQP4+NMOSD typically demands continuous therapy, in which agents directed against complement activation, IL-6 signaling, and B-cell-mediated pathways form the cornerstone of relapse prevention. The rarity of these disorders continues to challenge the conduct of large, rigorous therapeutic trials. Nonetheless, innovative targeted therapies have already been developed and transformed the therapeutic landscape in NMOSD while more off-label approaches are being investigating in MOGAD. This review synthesizes current evidence on established and investigational therapies in NMOSD and MOGAD, providing an updated framework to inform clinical practice and guide future research in these complex, antibody-mediated CNS disorders.
NMOSD and MOGAD: Updates on diagnostic criteria.
Marignier R, Leal Rato M
Rev Neurol (Paris) · 2026 May · PMID 41927386 · Publisher ↗
Recently, diagnostic criteria for demyelinating diseases, including multiple sclerosis, have been updated with a focus on imaging and fluid markers. The upcoming criteria for neuromyelitis optica (NMO) introduce several...
Recently, diagnostic criteria for demyelinating diseases, including multiple sclerosis, have been updated with a focus on imaging and fluid markers. The upcoming criteria for neuromyelitis optica (NMO) introduce several clinico-radiological updates, and highlight the need for accurate determination of AQP4-IgG status. Furthermore, seronegative NMO is now considered a syndrome distinct from AQP4-IgG disease. The MOG-antibody associated disease (MOGAD) criteria have been validated in different populations, and a clear role for case-by-case expert review has emerged in light of some limitations to clinical application of the criteria. The impact and the limitations of these criteria will be discussed in this mini-review.
Evolving MS diagnostic criteria: Progress and challenges.
Lebrun-Frenay C
Rev Neurol (Paris) · 2026 May · PMID 41927385 · Publisher ↗
The 2024 update to the McDonald criteria for multiple sclerosis aims to be more inclusive, covering paediatric and elderly patients, as well as those with atypical symptoms or comorbidities. These criteria emphasise obje...
The 2024 update to the McDonald criteria for multiple sclerosis aims to be more inclusive, covering paediatric and elderly patients, as well as those with atypical symptoms or comorbidities. These criteria emphasise objective evidence of central nervous system involvement through clinical signs and biomarkers from fluid analysis or imaging. Several new biomarkers have been added, although some are not yet widely accessible but are expected to be implemented soon: kappa-free light chains in cerebrospinal fluid, which are more reproducible and cost-effective than oligoclonal bands, along with advanced imaging techniques such as the central vein sign and paramagnetic rim lesions on susceptibility-weighted imaging. Cases with incidental magnetic resonance imaging hyperintensities, identified as radiologically isolated syndrome (RIS), may also be classified as preclinical MS if they show T2 lesions in at least two typical locations and meet other specific biomarker criteria. Careful, step-by-step evaluation is essential to prevent misdiagnosis, especially in paediatric and late-onset MS, and in cases with comorbidities. The inclusion of RIS individuals or those with atypical presentations marks a crucial shift in the MS spectrum, requiring expertise and the use of specific biomarkers.
Contribution of new imaging sequences to the diagnosis of multiple sclerosis.
Moccia M, Cocozza S
Rev Neurol (Paris) · 2026 May · PMID 41927384 · Publisher ↗
The 2024 revision of the McDonald criteria reinforces the central role of magnetic resonance imaging (MRI) in diagnosing multiple sclerosis (MS). Key updates include the addition of the optic nerve as a fifth typical reg...
The 2024 revision of the McDonald criteria reinforces the central role of magnetic resonance imaging (MRI) in diagnosing multiple sclerosis (MS). Key updates include the addition of the optic nerve as a fifth typical region for dissemination in space (DIS), requiring dedicated orbital MRI with high-resolution coronal fat-suppressed T2/STIR sequences. The central vein sign (CVS), defined as a vein traversing a T2/FLAIR lesion, offers high diagnostic specificity and can substitute for dissemination in time (DIT) or cerebrospinal fluid analysis. Paramagnetic rim lesions (PRLs), although not necessarily seen in every person with MS, indicate chronic active lesions and carry prognostic significance, correlating with greater disability over time, and supporting the diagnosis of MS in some specific cases. Consensus protocols now advocate baseline whole-brain and whole-spinal cord imaging, optimized 3D T2-FLAIR for lesion detection, and susceptibility-weighted imaging for CVS and PRLs, ideally at 3T but feasible at 1.5T with protocol optimization. These advances align imaging with MS pathobiology, reduce misdiagnosis risk - particularly in older patients or those with vascular comorbidities - and support differential diagnosis from mimics such as MOG-antibody disease and neuromyelitis optica spectrum disorder. While CVS and PRLs remain adjunctive due to limited availability in some settings, their integration into routine practice enhances diagnostic confidence and prognostic stratification. Overall, the 2024 McDonald criteria promote a flexible, yet biology-informed framework, combining clinical aspects with imaging to guide early diagnosis.
Neuroimaging confirms selective cerebral involvement in primary lateral sclerosis and predilection to brain regions with high metabolic activity.
Kleinerova J, Tahedl M, Finegan E … +8 more , Siah WF, Hengeveld JC, Doherty MA, Hardiman O, McLaughlin RL, Hutchinson S, Tan EL, Bede P
Rev Neurol (Paris) · 2026 Jun · PMID 41925483 · Publisher ↗
BACKGROUND: Primary lateral sclerosis (PLS) is a low incidence motor neuron disease manifesting in progressive limb spasticity, gait impairment, bulbar dysfunction and often in pseudobulbar affect. Varying degree of fron...
BACKGROUND: Primary lateral sclerosis (PLS) is a low incidence motor neuron disease manifesting in progressive limb spasticity, gait impairment, bulbar dysfunction and often in pseudobulbar affect. Varying degree of frontotemporal involvement has also been recently confirmed. Postmortem data is scarce in PLS and disease burden patterns are best characterised in vivo by purpose-designed neuroimaging protocols. METHODS: A large prospective neuroimaging study has been undertaken to explore cerebral involvement patterns in PLS using a both structural T1-weighted data and diffusion MRI data. Neuroimaging data were complemented by genetic screening and comprehensive clinical profiling. Brain involvement patterns have been first characterised by standard morphometric and diffusivity analyses. Resulting disease burden maps were then correlated to physiological mitochondrial density (MitoD) maps. In an additional, region-of-interest analysis, brain regions with significant topological associations between neurodegeneration and MitoD were ranked based on their r-values. RESULTS: Grey matter degeneration in PLS is not limited to the motor cortex, but also encompasses frontotemporal, caudate, thalamic, cerebellar and cingulate regions. Voxelwise statistics confirm topological associations between atrophy and physiological mitochondrial density. The most significant associations between neurodegeneration and MitoD were detected in the cerebellum, superior temporal lobe, precentral gyrus, inferior operculum, and orbitofrontal gyrus. Similarly, white matter degeneration is not limited to the corticospinal tracts, but includes the corpus callosum, frontotemporal association fibres, the cingulum, cerebellar peduncles, and the fornix. Anatomical associations were also detected between diffusivity alterations and focal MitoD. DISCUSSION: PLS is associated with a selective disease burden pattern, and our data suggest that brain regions with high baseline metabolic activity are more likely to succumb to neurodegeneration. Cerebral areas showing the most significant anatomical associations between atrophy and mitochondrial density (precentral gyrus, cerebellum, frontotemporal regions) are pathognomonic brain regions of PLS driving its core clinical manifestations.
Prospective comparative study of two educational games used to teach neurological semiology.
Mazoyer J, Madec T, Zeidan S … +4 more , Garcin B, Baltaze S, Josse L, Degos B
Rev Neurol (Paris) · 2026 Jun · PMID 41896099 · Publisher ↗
INTRODUCTION: Neurological semiology is often considered to be difficult to learn. The "Neurological hat game (NHG)" and the "Neurospeed game (NSG)" are two educational games that have both proven their effectiveness as...
INTRODUCTION: Neurological semiology is often considered to be difficult to learn. The "Neurological hat game (NHG)" and the "Neurospeed game (NSG)" are two educational games that have both proven their effectiveness as a teaching method. The aim of this study was to compare the effectiveness of these two games. METHODS: We performed a prospective study, during which we randomly assigned either the NHG or the NSG to third-year medical students at the Sorbonne Paris Nord University in November 2021. In both groups, students answered 20 multiple choice questions (MCQ) before and after the game. We compared the progression of average MCQ scores before and after the games, between the two groups of students. At the end of the games, the students were asked to complete a satisfaction survey. RESULTS: A total of 156 students were included, 76 for the NSG and 80 for the NHG. In both groups, the average MCQ score improved after the game, compared with the average MCQ score before the game. The difference in the progression of MCQ averages between the two games was not statistically significant (P=0.65). Among the 156 students, 140 answered the satisfaction survey (63 NSG and 77 NHG). Responses to the questionnaire were mostly positive, with no difference between the two groups. CONCLUSIONS: This study showed that the NSG and the NHG are two playful tools for teaching neurological semiology. Both are equally effective and popular with students. Further studies are needed to confirm the effectiveness of these teaching methods on long-term learning.
"Time is Brain" also in multiple sclerosis: Fifteen years later, a fully consolidated concept.
Maarouf A, Audoin B, Pelletier J
Rev Neurol (Paris) · 2026 Jun · PMID 41876285 · Publisher ↗
Abstract loading — click title to view on PubMed.
Balint syndrome as the initial presentation of neuromyelitis optica spectrum disorder.
Billet N, Donat S, Grosset-Janin C … +4 more , Androdias G, Pique J, Marignier R, Nicolas P
Rev Neurol (Paris) · 2026 Apr · PMID 41850923 · Publisher ↗
Abstract loading — click title to view on PubMed.
Changing nosology, unknown epidemiology: What do we know about functional neurological disorders in the community?
Mounir Alaoui O, Roze E, Daubigney A … +2 more , Amieva H, Garcin B
Rev Neurol (Paris) · 2026 Apr · PMID 41807222 · Publisher ↗
OBJECTIVE: To estimate the epidemiology of functional neurological disorders (FND) in the general population through a systematic literature review and to assess the quality of the included studies. BACKGROUND: FND are c...
OBJECTIVE: To estimate the epidemiology of functional neurological disorders (FND) in the general population through a systematic literature review and to assess the quality of the included studies. BACKGROUND: FND are characterized by motor and/or sensory symptoms that relate to functional rather than structural abnormalities. Although these disorders are common in neurology, their epidemiology is not well documented. METHODS: Following the Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines, we searched PubMed and Embase for articles reporting on the incidence or prevalence of FND in adults, published in French or English between 1972 and 2022. We used The Joanna Briggs Institute Prevalence Critical Appraisal Tool to assess the quality of the studies. This study was registered under the ID CRD42023434331 in the PROSPERO database. RESULTS: Out of 4260 screened articles, 27 were included, primarily from India, the US, and Europe. The prevalence estimates for hysteria, conversion disorders or FND ranged from 37.2 to 6900 per 100,000, with an incidence ranging from 10.7 to 186. Functional dissociative seizures had a prevalence of 23.8 to 890 and an incidence of 0.91 to 4.9. Functional motor disorders had an incidence of 3.9 to 5.0. Most cases involved young women. Only eight studies were rated as high quality. Overall, the rapidly changing nosology and diagnostic criteria complicate the interpretations of existing data. DISCUSSION: Our findings highlight the urgent need for large-scale, rigorous studies targeting the multiple forms of FND to obtain reliable epidemiological data necessary to develop an adequate health policy for FND.
Calprotectin as an immune-dysregulation biomarker in amyotrophic lateral sclerosis: Insights for diagnosis and therapy.
Mendon A, Jain S, Mishra N … +1 more , Bagwe Parab S
Rev Neurol (Paris) · 2026 Jun · PMID 41791963 · Publisher ↗
Motor neuron degeneration is a defining feature of amyotrophic lateral sclerosis (ALS), a progressive and fatal neurodegenerative disorder. Early diagnosis remains challenging due to the absence of reliable and validated...
Motor neuron degeneration is a defining feature of amyotrophic lateral sclerosis (ALS), a progressive and fatal neurodegenerative disorder. Early diagnosis remains challenging due to the absence of reliable and validated biomarkers. Calprotectin, a well-established inflammatory marker in various neuroinflammatory conditions, has paradoxically been found at reduced levels in the blood of ALS patients in a limited number of studies, raising the hypothesis of immune dysregulation rather than classical neuroinflammation. However, these findings are primarily derived from small patient cohorts and have yet to be independently replicated. This review critically assesses the emerging role of calprotectin in ALS by comparing it with other candidate biomarkers, including vascular endothelial growth factor (VEGF), apolipoprotein A1 (ApoA1), interleukin-8 (IL-8), interleukin-7 (IL-7), and interleukin-10 (IL-10). While calprotectin may reflect a distinct immunological profile, its standalone diagnostic value remains unclear. Nonetheless, its integration into a multi-analyte biomarker panel could enhance diagnostic precision and biological insight. The review also explores underlying immunological mechanisms, including receptor interactions (RAGE, TLR4, CD33), cellular mediators (microglia, lymphocytes, monocytes), and therapeutic implications. Future research should prioritize mechanistic investigation of calprotectin modulation in ALS, longitudinal validation in larger cohorts, and integration within multimodal biomarker frameworks. A better understanding of disease-specific immune alterations may contribute to earlier diagnosis, stratified patient monitoring, and targeted therapeutic development.
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