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1.
Eur J Neurol ; 28(1): 358-360, 2021 01.
Article in English | MEDLINE | ID: mdl-32997868

ABSTRACT

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.


Subject(s)
COVID-19/complications , Epstein-Barr Virus Infections/complications , Facial Paralysis/etiology , Anti-Inflammatory Agents/therapeutic use , Facial Paralysis/diagnostic imaging , Humans , Magnetic Resonance Imaging , Male , Prednisone/therapeutic use , Recovery of Function , Respiratory Tract Infections/etiology , Respiratory Tract Infections/physiopathology , Treatment Outcome , Young Adult
2.
Maturitas ; 84: 25-31, 2016 Feb.
Article in English | MEDLINE | ID: mdl-26653838

ABSTRACT

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.


Subject(s)
Aging/physiology , Brain/physiopathology , Drug Delivery Systems , Parkinson Disease/drug therapy , Parkinson Disease/physiopathology , alpha-Synuclein/metabolism , Antioxidants/administration & dosage , Dopamine/administration & dosage , Dopamine Agonists/administration & dosage , Genetic Therapy , Humans , Lewy Bodies/metabolism , Lysosomes/metabolism , Mitochondria/physiology , Nerve Growth Factors/administration & dosage , Neuroprotective Agents/administration & dosage , Oxidative Stress , Peptides/administration & dosage , Proteasome Endopeptidase Complex/metabolism
3.
An Sist Sanit Navar ; 38(1): 79-92, 2015.
Article in Spanish | MEDLINE | ID: mdl-25963461

ABSTRACT

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.


Subject(s)
Frontotemporal Lobar Degeneration/diagnosis , Frontotemporal Dementia/diagnosis , Frontotemporal Dementia/physiopathology , Frontotemporal Lobar Degeneration/physiopathology , Humans , Neuropsychological Tests , Supranuclear Palsy, Progressive/diagnosis , Supranuclear Palsy, Progressive/physiopathology
4.
Neurologia ; 28(5): 299-308, 2013 Jun.
Article in English, Spanish | MEDLINE | ID: mdl-21621879

ABSTRACT

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.


Subject(s)
Brain/pathology , Prion Diseases/pathology , 14-3-3 Proteins/cerebrospinal fluid , Creutzfeldt-Jakob Syndrome/diagnosis , Creutzfeldt-Jakob Syndrome/pathology , Electroencephalography , Gerstmann-Straussler-Scheinker Disease/diagnosis , Gerstmann-Straussler-Scheinker Disease/pathology , Humans , Insomnia, Fatal Familial/diagnosis , Insomnia, Fatal Familial/pathology , Kuru/diagnosis , Kuru/pathology , Magnetic Resonance Imaging , Neuroimaging , PrPC Proteins/cerebrospinal fluid , PrPC Proteins/metabolism , Prion Diseases/diagnosis
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