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1.
Eur J Neurol ; 28(1): 358-360, 2021 01.
Artículo en Inglés | MEDLINE | ID: mdl-32997868

RESUMEN

COVID-19 can occasionally be associated with cranial nerve involvement, but facial palsy, particularly if bilateral, is exceptional. We here report a patient who presented with severe bilateral facial palsy and evidence of SARS-CoV-2 infection preceded by upper respiratory symptoms. He also had serological evidence of coinfection with Epstein-Barr virus, which could have also played a role in his neurological manifestations. PCR in the cerebrospinal fluid was negative for both EBV and SARS-CoV-2, which suggests an indirect, immune-mediated mechanism rather than direct, viral-induced damage. The patient was treated with prednisone 60 mg/24h with a tapering schedule and had a favorable outcome, with an almost complete recovery in 3 weeks. SARS-CoV-2 adds to the list of infectious agents causative of bilateral facial palsy. Coinfection with SARS-CoV-2 is not rare and should be considered in the differential diagnosis.


Asunto(s)
COVID-19/complicaciones , Infecciones por Virus de Epstein-Barr/complicaciones , Parálisis Facial/etiología , Antiinflamatorios/uso terapéutico , Parálisis Facial/diagnóstico por imagen , Humanos , Imagen por Resonancia Magnética , Masculino , Prednisona/uso terapéutico , Recuperación de la Función , Infecciones del Sistema Respiratorio/etiología , Infecciones del Sistema Respiratorio/fisiopatología , Resultado del Tratamiento , Adulto Joven
2.
Maturitas ; 84: 25-31, 2016 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-26653838

RESUMEN

The etiology and pathogenesis of Parkinson's disease (PD) is unknown, aging being the strongest risk factor for brain degeneration. Understanding PD pathogenesis and how aging increases the risk of disease would aid the development of therapies able to slow or prevent the progression of this neurodegenerative disorder. In this review we provide an overview of the most promising therapeutic targets and strategies to delay the loss of dopaminergic neurons observed both in PD and aging. Among them, handling alpha-synuclein toxicity, enhancing proteasome and lysosome clearance, ameliorating mitochondrial disruptions and modifying the glial environment are so far the most promising candidates. These new and conventional drugs may present problems related to their labile nature and to the difficulties in reaching the brain. Thus, we highlight the latest types of drug delivery system (DDS)-based strategies for PD treatment, including DDS for local and systemic drug delivery. Finally, the ongoing challenges for the discovery of new targets and the opportunities for DDS-based therapies to improve and efficacious PD therapy will be discussed.


Asunto(s)
Envejecimiento/fisiología , Encéfalo/fisiopatología , Sistemas de Liberación de Medicamentos , Enfermedad de Parkinson/tratamiento farmacológico , Enfermedad de Parkinson/fisiopatología , alfa-Sinucleína/metabolismo , Antioxidantes/administración & dosificación , Dopamina/administración & dosificación , Agonistas de Dopamina/administración & dosificación , Terapia Genética , Humanos , Cuerpos de Lewy/metabolismo , Lisosomas/metabolismo , Mitocondrias/fisiología , Factores de Crecimiento Nervioso/administración & dosificación , Fármacos Neuroprotectores/administración & dosificación , Estrés Oxidativo , Péptidos/administración & dosificación , Complejo de la Endopetidasa Proteasomal/metabolismo
3.
An Sist Sanit Navar ; 38(1): 79-92, 2015.
Artículo en Español | MEDLINE | ID: mdl-25963461

RESUMEN

Frontotemporal lobar degeneration encompasses three different syndromes, with clinical and pathologic commonalities, making diagnosis difficult in early stages. Three subtypes are recognized: frontotemporal dementia and its three variants, corticobasal syndrome and supranuclear palsy syndrome. The objective of this study is to review the neuropsychological features of each syndrome in order to differentiate amongst subtypes as well as from other forms of dementia. We review multiple studies from the literature, highlighting the main clinical features, neuropathology and changes in brain imaging of each syndrome. Subsequently, we describe the neuropsychological profile compared to other dementias, and how it progresses over time. Although there is an overlap amongst the different subtypes of frontotemporal lobar degeneration, neuropsychological profiles can help identify subtypes and discriminate frontotemporal lobar degeneration from other forms of dementia.


Asunto(s)
Degeneración Lobar Frontotemporal/diagnóstico , Demencia Frontotemporal/diagnóstico , Demencia Frontotemporal/fisiopatología , Degeneración Lobar Frontotemporal/fisiopatología , Humanos , Pruebas Neuropsicológicas , Parálisis Supranuclear Progresiva/diagnóstico , Parálisis Supranuclear Progresiva/fisiopatología
4.
Neurologia ; 28(5): 299-308, 2013 Jun.
Artículo en Inglés, Español | MEDLINE | ID: mdl-21621879

RESUMEN

INTRODUCTION: Prion diseases are neurodegenerative disorders resulting from the accumulation of a misfolded isoform of the cellular prion protein (PrPc). They can occur as acquired, sporadic, or hereditary forms. Although prion diseases show a wide range of phenotypic variations, pathological features and clinical evolution, they are all characterised by a common unfavourable course and a fatal outcome. REVIEW SUMMARY: Some variants, such as kuru, have practically disappeared, while others, for example the variant Creutzfeldt-Jakob (vCJD) or those attributable to iatrogenic causes, are still in force and pose a challenge to current medicine. There are no definitive pre-mortem diagnostic tests, except for vCJD, where a tonsil biopsy detects 100% of the cases. For this reason, diagnostic criteria dependent on statistical probability have had to be created. These require complementary examinations, such as an electroencephalogram (EEG) or the detection of 14-3-3 protein in cerebrospinal fluid (CSF). Only the pulvinar sign in magnetic resonance imaging (MRI) has been included as a vCJD diagnostic criterion. The present review discusses neuroimaging findings for each type of prion disease in patients with a definitive histopathological diagnosis. CONCLUSIONS: The aim is to define the usefulness of these complementary examinations as a tool for the diagnosis of this family of neurodegenerative diseases.


Asunto(s)
Encéfalo/patología , Enfermedades por Prión/patología , Proteínas 14-3-3/líquido cefalorraquídeo , Síndrome de Creutzfeldt-Jakob/diagnóstico , Síndrome de Creutzfeldt-Jakob/patología , Electroencefalografía , Enfermedad de Gerstmann-Straussler-Scheinker/diagnóstico , Enfermedad de Gerstmann-Straussler-Scheinker/patología , Humanos , Insomnio Familiar Fatal/diagnóstico , Insomnio Familiar Fatal/patología , Kuru/diagnóstico , Kuru/patología , Imagen por Resonancia Magnética , Neuroimagen , Proteínas PrPC/líquido cefalorraquídeo , Proteínas PrPC/metabolismo , Enfermedades por Prión/diagnóstico
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