6 research outputs found

    Compressive optic neuropathies

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    La pérdida de visión es un síntoma neurológico frecuente referido por los pacientes en la práctica clínica diaria. El diagnóstico de una neuropatía óptica se alcanza a través de la historia clínica, exploración neuroftalmológica y pruebas complementarias. El objetivo de este artículo es revisar las etiologías de las neuropatías ópticas de causa compresiva a través de 2 casos originales. El diagnóstico se apoya fundamentalmente en la RM de cráneo y la intervención precoz mejora el pronóstico de la función visual.Visual loss is a common symptom in clinical neurology. Often the general diagnosis for an optic neuropathy can be established on the basis of clinical history, neurophtalmologic examination and complementary studies. This article presents a review of the etiology of the compressive optic neuropathies through 2 original cases. Diagnosis is based on MRI. An appropriate intervention improves the prognosis of visual function

    Cognitive impairment in multiple sclerosis: diagnosis and monitoring.

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    Cognitive impairment (CI) has a prevalence of 45-70% in people with multiple sclerosis (MS), producing a negative impact on their quality of life, personal life, and work. Early detection of CI has become an important aspect to be considered for an adequate follow-up, to optimize social adaptation and to implement specific cognitive rehabilitation strategies. The aim of this work is to propose a suitable cognitive evaluation of patients with MS based on available and efficient tools for diagnosis and monitoring purposes well supported by literature review and clinical experience. A multidisciplinary panel of professionals from the field of neurology, neuropsychology, and neuroimaging performed a literature review of the topic of cognitive impairment assessment. This was combined and completed with their clinical experience to produce a set of recommendations. Some limitations to cognitive evaluation are described: shortage of time and resources during the neurology consultation, scarceness or absence of specialized professionals' availability, importance of tests adaptation, and doubts about its use to define therapeutic efficiency. We recommend a baseline and annual screening evaluation, and we suggest a baseline and periodic neuropsychological assessment. The latter ought to change to a recommendation with the presence of either positive screening test, or subjective to cognitive complaints, screening-test results and patient or family report mismatch, or in specific social/work situations. Cognitive evaluation should be performed on all patients diagnosed with MS and throughout follow-up. It is necessary to support the creation of multidisciplinary MS teams to optimize the evaluation and follow-up of MS patients

    Activation of Macrophages by Lysophosphatidic Acid through the Lysophosphatidic Acid Receptor 1 as a Novel Mechanism in Multiple Sclerosis Pathogenesis.

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    Multiple sclerosis (MS) is a neuroinflammatory disease whose pathogenesis remains unclear. Lysophosphatidic acid (LPA) is an endogenous phospholipid involved in multiple immune cell functions and dysregulated in MS. Its receptor LPA1 is expressed in macrophages and regulates their activation, which is of interest due to the role of macrophage activation in MS in both destruction and repair. In this study, we studied the genetic deletion and pharmaceutical inhibition of LPA1 in the mouse MS model, experimental autoimmune encephalomyelitis (EAE). LPA1 expression was analyzed in EAE mice and MS patient immune cells. The effect of LPA and LPA1 on macrophage activation was studied in human monocyte-derived macrophages. We show that lack of LPA1 activity induces milder clinical EAE course and that Lpar1 expression in peripheral blood mononuclear cells (PBMC) correlates with onset of relapses and severity in EAE. We see the same over-expression in PBMC from MS patients during relapse compared with progressive forms of the disease and in stimulated monocyte-derived macrophages. LPA induced a proinflammatory-like response in macrophages through LPA1, providing a plausible way in which LPA and LPA1 dysregulation can lead to the inflammation in MS. These data show a new mechanism of LPA signaling in the MS pathogenesis, prompting further research into its use as a therapeutic target biomarker

    Al lado con la persona afectada por Esclerosis Lateral Amiotrófica

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    En port: Un instrumento de cooperación entre servicios y asociaciones para ganar Salud. Trabajar en clave de Recuperación con la persona afectada y sus familias. Y apoyar la labor de la personas cuidadoras. Es una de las estrategias del proyecto "AL LADO" con... Publicado en la página web de la Consejería de Salud y Bienestar Social: Consejería de Salud y Bienestar Social / Ciudadanía / Participar en Salud / 'Al Lado' con... / 'Al Lado' con las personas afectadas por Esclerosis Lateral AmiotróficaYesCuidar y compartir los cuidados son elementos estratégicos para la sostenibilidad y la ganancia en salud. También sabemos que esta forma de gestión de la enfermedad con independencia de su evolución clínica, no puede ser efectiva sin una alianza entre profesionales, personas afectadas empoderadas y familiares, que con su esfuerzo constante constituyen un ejemplo de la colaboración sobre la que pilota el proyecto 'Al Lado ELA'. El interés de la Asociación ELA Andalucía tomando la iniciativa del proyecto, corrobora la importancia de esta alianza. Al Lado ELA, además, pone en valor la ayuda mutua entre iguales y el respeto a los derechos de las personas con enfermedad, incluyendo el derecho a la toma de decisiones en aquellos aspectos que repercuten en su trayectoria de vida. Al mismo tiempo, la receptividad y el alto compromiso de los profesionales implicados en la atención de este proceso, están abriendo cauces para el desarrollo de una mayor sensibilidad para compartir la atención y un aprendizaje para todos. Desde esta convicción, y en el marco del trabajo cooperativo, se ha elaborado un itinerario de atención compartida para ganar en salud y facilitar la labor de las personas cuidadoras. La definición de este itinerario parte de las propias necesidades de las personas afectadas y sus familias, a través de relatos bioráficos que han permitido configurar tanto los hitos clínicos como las vivencias de los distintos síntomas de la enfermedad, a modo de camino que se ha de recorrer de forma genérica y habitual. Junto a ello se describe la red de recursos, con los servicios públicos disponibles, y la red asociativa, además de las experiencias de colaboración existentes en Andalucía

    The cognitive and psychiatric subacute impairment in severe Covid-19.

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    Neurologic impairment persisting months after acute severe SARS-CoV-2 infection has been described because of several pathogenic mechanisms, including persistent systemic inflammation. The objective of this study is to analyze the selective involvement of the different cognitive domains and the existence of related biomarkers. Cross-sectional multicentric study of patients who survived severe infection with SARS-CoV-2 consecutively recruited between 90 and 120 days after hospital discharge. All patients underwent an exhaustive study of cognitive functions as well as plasma determination of pro-inflammatory, neurotrophic factors and light-chain neurofilaments. A principal component analysis extracted the main independent characteristics of the syndrome. 152 patients were recruited. The results of our study preferential involvement of episodic and working memory, executive functions, and attention and relatively less affectation of other cortical functions. In addition, anxiety and depression pictures are constant in our cohort. Several plasma chemokines concentrations were elevated compared with both, a non-SARS-Cov2 infected cohort of neurological outpatients or a control healthy general population. Severe Covid-19 patients can develop an amnesic and dysexecutive syndrome with neuropsychiatric manifestations. We do not know if the deficits detected can persist in the long term and if this can trigger or accelerate the onset of neurodegenerative diseases
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