• 2015-2024close
• Open Access close
• Restricted close
• Open Source close
• CA close
• Frontiers in Neurology close
• Neuroinformatics close

l'étiopathogenèse est encore débattue. Il représente une pathologie stimulante et intrigante pour les cliniciens d'un point de vue diagnostique et thérapeutique, en particulier pour les aspects liés à son évolution et au développement de la compensation vestibulaire (1,2).Comme l'indique le titre, ce thème de recherche intitulé « Vestibulopathie unilatérale aiguë : présentation clinique, schémas instrumentaux, évolution et prise en charge » couvre certains des multiples aspects associés à la perte de la fonction de l'un des deux labyrinthes à la lumière des dernières directives internationales (3,4). etiopatogénesis todavía se debate. Representa una patología desafiante e intrigante para los clínicos desde el punto de vista diagnóstico y terapéutico, particularmente por los aspectos vinculados a su evolución y al desarrollo de la compensación vestibular (1,2).Como indica el título, este Tema de Investigación titulado "Vestibulopatía Unilateral Aguda: Presentación Clínica, Patrones Instrumentales, Evolución y Manejo" abarca algunos de los múltiples aspectos asociados a la pérdida de la función de uno de los dos laberintos a la luz de las últimas directrices internacionales (3,4). etiopathogenesis is still debated. It represents a challenging and intriguing pathology for clinicians from a diagnostic and therapeutic point of view, particularly for the aspects linked to its evolution and the development of vestibular compensation (1,2).As the title indicates, this Research Topic entitled "Acute Unilateral Vestibulopathy: Clinical Presentation, Instrumental Patterns, Evolution, and Management" covers some of the multiple aspects associated with losing the function of one of the two labyrinths in the light of the latest international guidelines (3,4). لا يزال التسبب في المرض موضع نقاش. إنه يمثل مرضًا صعبًا ومثيرًا للاهتمام للأطباء من وجهة نظر تشخيصية وعلاجية، خاصة بالنسبة للجوانب المرتبطة بتطوره وتطوير التعويض الدهليزي (1،2). وكما يشير العنوان، فإن موضوع البحث هذا بعنوان "اعتلال الدهليزي الحاد أحادي الجانب: العرض السريري، والأنماط الآلية، والتطور، والإدارة" يغطي بعض الجوانب المتعددة المرتبطة بفقدان وظيفة أحد المتاهتين في ضوء أحدث الإرشادات الدولية (3،4).

Introduction: Cognitive impairment and orthostatic hypotension (OH) are common, disabling Parkinson disease (PD) symptoms that are strongly correlated. Whether the relationship is causative or associative remains unknown. OH may occur without classic orthostatic symptoms of cerebral hypoperfusion (i.e., lightheadedness or dizziness). Whether longitudinal differences in cognition occur between symptomatic and asymptomatic OH patients has not been explored. Objectives: We characterized the prevalence of OH, orthostatic symptoms, and cognitive impairment among PD patients and compared cognition between patients with and without OH, and between patients with symptomatic and asymptomatic OH. Methods: Our cross-sectional, retrospective, observational study included 226 clinically diagnosed PD patients who underwent repeated standardized evaluations. Among these, 62 had longitudinal follow-up of > 3.5 years. We compared longitudinal Montreal Cognitive Assessment (MoCA) scores between patients remaining OH-free (n = 14) and those without baseline OH that developed OH (n = 28), matched for age, sex, education, and PD duration. We also compared MoCA scores between groups with asymptomatic OH (n = 13) and symptomatic OH (n = 13) matched for the same factors. Results: In the cross-sectional analysis, OH patients had worse cognition. In the longitudinal analysis (mean follow-up = 5.3 years), OH patients had worse cognitive decline (p = 0.027). Cognitive impairment was similar between asymptomatic and symptomatic OH patients in the cross-sectional and longitudinal analyses. Conclusions: OH is associated with cognitive impairment in PD. Further studies are needed in larger cohorts to expand our findings and to determine whether treating OH can prevent or delay cognitive dysfunction.

Pediatric-onset multiple sclerosis (POMS) may represent a model of vulnerability to damage occurring during a period of active maturation of the human brain. Whereas adaptive mechanisms seem to take place in the POMS brain in the short-medium term, natural history studies have shown that these patients reach irreversible disability, despite slower progression, at a significantly younger age than adult-onset MS (AOMS) patients. We tested for the first time whether significant brain alterations already occurred in POMS patients in their early adulthood and with no or minimal disability (n = 15) in comparison with age- and disability-matched AOMS patients (n = 14) and to normal controls (NC, n = 20). We used a multimodal MRI approach by modeling, using FSL, voxelwise measures of microstructural integrity of white matter tracts and gray matter volumes with those of intra- and internetwork functional connectivity (FC) (analysis of variance, p ≤ 0.01, corrected for multiple comparisons across space). POMS patients showed, when compared with both NC and AOMS patients, altered measures of diffusion tensor imaging (reduced fractional anisotropy and/or increased diffusivities) and higher probability of lesion occurrence in a clinically eloquent region for physical disability such as the posterior corona radiata. In addition, POMS patients showed, compared with the other two groups, reduced long-range FC, assessed from resting functional MRI, between default mode network and secondary visual network, whose interaction subserves important cognitive functions such as spatial attention and visual learning. Overall, this pattern of structural damage and brain connectivity disruption in early adult POMS patients with no or minimal clinical disability might explain their unfavorable clinical outcome in the long term.

Progressive supranuclear palsy (PSP) and corticobasal syndrome (CBS; the most common phenotype of corticobasal degeneration) are tauopathies with a relentless course, usually starting in the mid-60s and leading to death after an average of 7 years. There is as yet no specific or disease-modifying treatment. Clinical deficits in PSP are numerous, involve the entire neuraxis, and present as several discrete phenotypes. They center on rigidity, bradykinesia, postural instability, gait freezing, supranuclear ocular motor impairment, dysarthria, dysphagia, incontinence, sleep disorders, frontal cognitive dysfunction, and a variety of behavioral changes. CBS presents with prominent and usually asymmetric dystonia, apraxia, myoclonus, pyramidal signs, and cortical sensory loss. The symptoms and deficits of PSP and CBS are amenable to a variety of treatment strategies but most physicians, including many neurologists, are reluctant to care for patients with these conditions because of unfamiliarity with their multiplicity of interacting symptoms and deficits. CurePSP, the organization devoted to support, research, and education for PSP and CBS, created its CurePSP Centers of Care network in North America in 2017 to improve patient access to clinical expertise and develop collaborations. The directors of the 25 centers have created this consensus document outlining best practices in the management of PSP and CBS. They formed a writing committee for each of 12 sub-topics. A 4-member Steering Committee collated and edited the contributions. The result was returned to the entire cohort of authors for further comments, which were considered for incorporation by the Steering Committee. The authors hope that this publication will serve as a convenient guide for all clinicians caring for patients with PSP and CBS and that it will improve care for patients with these devastating but manageable disorders.

Mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE-HS) may involve extrahippocampal areas of structural damage and dysfunction. The accuracy of medium-term spatial memory can be tested by memory-guided saccades (MGS) to evaluate a functional impairment of the parahippocampal cortex (PHC), while voxel-based morphometry (VBM) analysis can be used to detect a structural damage of the latter region.MGS with 3- and 30-s memorization delays were compared between 7 patients affected by right MTLE-HS (r-MTLE-HS), 6 patients affected by left MTLE-HS, and 13 healthy controls. The same subjects underwent brain MRI for a VBM analysis. Correlation analysis was performed between the results of VBM and MGS and with patients' clinical data.Right MTLE-HS patients showed impaired accuracy of leftward MGS with a 30-s memorization delay; their gray-matter volume was reduced in the right hippocampus and inferior temporal gyrus, and bilaterally in the cerebellum. Left MTLE-HS patients had normal MGS accuracy; their gray-matter volume was reduced in the left hippocampus, in the right-inferior temporal gyrus and corpus callosus, and bilaterally in the insular cortex and in the cerebellum. The difference between right and left parahippocampal volumes correlated with MGS accuracy, while right and left hippocampal volumes did not. Hippocampal and parahippocampal volume did not correlate with clinical variables such as febrile seizures, age at disease onset, disease duration, and seizure frequency.MGS abnormalities suggested the functional involvement of the right PHC in patients with r-MTLE-HS, supporting a right lateralization of spatial memory control and showing a relation between functional impairment and degree of atrophy.

Background: The association between left atrial size and the risk of stroke has not been fully understood. We performed a meta-analysis of prospective cohort studies to determine whether left atrial enlargement (LAE) is associated with an increased risk of stroke. Methods: We searched PubMed, EMBASE, Web of Science, and the Cochrane Library through May 2019. Prospective cohort studies were included if they reported hazard ratios (HRs) and corresponding 95% confidence intervals (CIs) of stroke with respect to LAE. All meta-analyses were performed using a random-effects model. Results: Six studies involving 66,007 participants and 3,549 stroke events were included. Compared with patients without LAE, those with LAE had an increased risk of stroke (adjusted HR 1.68, 95% CI 1.36–2.07). There was also a graded association with stroke relating to LAE (adjusted HR for mild LAE 1.50, 95% CI 0.98–2.28; moderate LAE 1.40, 95% CI 1.12–1.75; and severe LAE 1.59, 95% CI 1.33–1.90). Furthermore, for each increase of 1 cm in left atrial diameter, the odds of stroke were increased by 24% (adjusted HR 1.24, 95% CI 1.03–1.50). Conclusions: Our meta-analysis demonstrated that LAE is associated with an increased and graded risk of stroke.

Embolic stroke of unknown source (ESUS) represents one in five ischemic strokes. Ipsilateral non-stenotic carotid plaques are identified in 40% of all ESUS. In this narrative review, we summarize the evidence supporting the potential causal relationship between ESUS and non-stenotic carotid plaques; discuss the remaining challenges in establishing the causal link between non-stenotic plaques and ESUS and describe biomarkers of potential interest for future research. In support of the causal relationship between ESUS and non-stenotic carotid plaques, studies have shown that plaques with high-risk features are five times more prevalent in the ipsilateral vs. the contralateral carotid and there is a lower incidence of atrial fibrillation during follow-up in patients with ipsilateral non-stenotic carotid plaques. However, non-stenotic carotid plaques with or without high-risk features often coexist with other potential etiologies of stroke, notably atrial fibrillation (8.5%), intracranial atherosclerosis (8.4%), patent foramen ovale (5–9%), and atrial cardiopathy (2.4%). Such puzzling clinical associations make it challenging to confirm the causal link between non-stenotic plaques and ESUS. There are several ongoing studies exploring whether select protein and RNA biomarkers of plaque progression or vulnerability could facilitate the reclassification of some ESUS as large vessel strokes or help to optimize secondary prevention strategies.