Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 8.201
Filtrar
1.
Artigo em Inglês | MEDLINE | ID: mdl-34135107

RESUMO

OBJECTIVE: Coronavirus disease (COVID-19) has been associated with a large variety of neurologic disorders. However, the mechanisms underlying these neurologic complications remain elusive. In this study, we aimed at determining whether neurologic symptoms were caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) direct infection or by either systemic or local proinflammatory mediators. METHODS: In this cross-sectional study, we checked for SARS-CoV-2 RNA by quantitative reverse transcription PCR, SARS-CoV-2-specific antibodies, and 49 cytokines/chemokines/growth factors (by Luminex) in the CSF +/- sera of a cohort of 22 COVID-19 patients with neurologic presentation and 55 neurologic control patients (inflammatory neurologic disorder [IND], noninflammatory neurologic disorder, and MS). RESULTS: We detected anti-SARS-CoV-2 immunoglobulin G in patients with severe COVID-19 with signs of intrathecal synthesis for some of them. Of the 4 categories of tested patients, the CSF of IND exhibited the highest level of cytokines, chemokines, and growth factors. By contrast, patients with COVID-19 did not present overall upregulation of inflammatory mediators in the CSF. However, patients with severe COVID-19 (intensive care unit patients) exhibited higher concentrations of CCL2, CXCL8, and vascular endothelium growth factor A (VEGF-A) in the CSF than patients with a milder form of COVID-19. In addition, we could show that intrathecal CXCL8 synthesis was linked to an elevated albumin ratio and correlated with the increase of peripheral inflammation (serum hepatocyte growth factor [HGF] and CXCL10). CONCLUSIONS: Our results do not indicate active replication of SARS-CoV-2 in the CSF or signs of massive inflammation in the CSF compartment but highlight a specific impairment of the neurovascular unit linked to intrathecal production of CXCL8.


Assuntos
Encefalopatias/etiologia , COVID-19/complicações , Citocinas/líquido cefalorraquidiano , Inflamação/etiologia , Acoplamento Neurovascular , SARS-CoV-2/patogenicidade , Adulto , Idoso , Idoso de 80 Anos ou mais , Anticorpos Antivirais/líquido cefalorraquidiano , Encefalopatias/líquido cefalorraquidiano , Encefalopatias/imunologia , Encefalopatias/fisiopatologia , COVID-19/líquido cefalorraquidiano , COVID-19/imunologia , Cuidados Críticos , Estudos Transversais , Citocinas/sangue , Eletroencefalografia , Feminino , Humanos , Imunoglobulina G/líquido cefalorraquidiano , Inflamação/líquido cefalorraquidiano , Inflamação/imunologia , Interleucina-8/líquido cefalorraquidiano , Masculino , Pessoa de Meia-Idade , Acoplamento Neurovascular/imunologia , SARS-CoV-2/imunologia , Índice de Gravidade de Doença , Adulto Jovem
2.
J Cardiothorac Surg ; 16(1): 181, 2021 Jun 23.
Artigo em Inglês | MEDLINE | ID: mdl-34162399

RESUMO

BACKGROUND: During cardiac surgery, micro-air emboli regularly enter the blood stream and can cause cognitive impairment or stroke. It is not clearly understood whether the most threatening air emboli are generated by the heart-lung machine (HLM) or by the blood-air contact when opening the heart. We performed an in vitro study to assess, for the two sources, air emboli distribution in the arterial tree, especially in the brain region, during cardiac surgery with different cannulation sites. METHODS: A model of the arterial tree was 3D printed and included in a hydraulic circuit, divided such that flow going to the brain was separated from the rest of the circuit. Air micro-emboli were injected either in the HLM ("ECC Bubbles") or in the mock left ventricle ("Heart Bubbles") to simulate the two sources. Emboli distribution was measured with an ultrasonic bubble counter. Five repetitions were performed for each combination of injection site and cannulation site, where air bubble counts and volumes were recorded. Air bubbles were separated in three categories based on size. RESULTS: For both injection sites, it was possible to identify statistically significant differences between cannulation sites. For ECC Bubbles, axillary cannulation led to a higher amount of air bubbles in the brain with medium-sized bubbles. For Heart Bubbles, aortic cannulation showed a significantly bigger embolic load in the brain with large bubbles. CONCLUSIONS: These preliminary in vitro findings showed that air embolic load in the brain may be dependent on the cannulation site, which deserves further in vivo exploration.


Assuntos
Aorta , Encefalopatias/etiologia , Procedimentos Cirúrgicos Cardíacos/efeitos adversos , Cateterismo/efeitos adversos , Embolia Aérea/etiologia , Circulação Sanguínea , Pressão Sanguínea , Cateterismo/métodos , Humanos , Técnicas In Vitro , Injeções/métodos
3.
mSphere ; 6(3): e0027021, 2021 06 30.
Artigo em Inglês | MEDLINE | ID: mdl-34160239

RESUMO

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is associated with a wide variety of neurological complications. Even though SARS-CoV-2 is rarely detected in the central nervous system (CNS) or cerebrospinal fluid, evidence is accumulating that SARS-CoV-2 might enter the CNS via the olfactory nerve. However, what happens after SARS-CoV-2 enters the CNS is poorly understood. Therefore, we investigated the replication kinetics, cell tropism, and associated immune responses of SARS-CoV-2 infection in different types of neural cultures derived from human induced pluripotent stem cells (hiPSCs). SARS-CoV-2 was compared to the neurotropic and highly pathogenic H5N1 influenza A virus. SARS-CoV-2 infected a minority of individual mature neurons, without subsequent virus replication and spread, despite angiotensin-converting enzyme 2 (ACE2), transmembrane protease serine 2 (TMPRSS2), and neuropilin-1 (NPR1) expression in all cultures. However, this sparse infection did result in the production of type III interferons and interleukin-8 (IL-8). In contrast, H5N1 virus replicated and spread very efficiently in all cell types in all cultures. Taken together, our findings support the hypothesis that neurological complications might result from local immune responses triggered by virus invasion, rather than abundant SARS-CoV-2 replication in the CNS. IMPORTANCE Infections with the recently emerged severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are often associated with neurological complications. Evidence suggests that SARS-CoV-2 enters the brain via the olfactory nerve; however, SARS-CoV-2 is only rarely detected in the central nervous system of COVID-19 patients. Here, we show that SARS-CoV-2 is able to infect neurons of human iPSC neural cultures but that this infection is abortive and does not result in virus spread to other cells. However, infection of neural cultures did result in the production of type III interferon and IL-8. This study suggests that SARS-CoV-2 might enter the CNS and infect individual neurons, triggering local immune responses that could contribute to the pathogenesis of SARS-CoV-2-associated CNS disease.


Assuntos
Células-Tronco Pluripotentes Induzidas/citologia , Virus da Influenza A Subtipo H5N1/fisiologia , Neurônios/virologia , SARS-CoV-2/fisiologia , Tropismo Viral , Replicação Viral , Animais , Encefalopatias/etiologia , COVID-19/complicações , Chlorocebus aethiops , Cães , Humanos , Virus da Influenza A Subtipo H5N1/imunologia , Cinética , Células Madin Darby de Rim Canino , SARS-CoV-2/imunologia , Células Vero
4.
Rev Paul Pediatr ; 40: e2020415, 2021.
Artigo em Inglês, Português | MEDLINE | ID: mdl-34076204

RESUMO

OBJECTIVE: To perform a systematic literature review to analyze existing data on the neurological effects of coronavirus on newborns. DATA: sources: We followed the guidelines of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) and the Preferred Reporting Items for Systematic Review and Meta-Analysis Protocols (PRISMA-P), and searched the PubMed and Embase platforms for the keywords [brain damage OR pregnancy OR developmental outcomes] and [coronavirus OR SARS-CoV-2 OR SARS-CoV OR MERS-CoV] between January 1, 2000 and June 1, 2020. DATA: synthesis: Twenty-three reports described the course of pregnant women exposed to SARS-CoV-2, SARS-CoV, or MERS-CoV during the gestational period, eight to SARS-CoV-2, eight to SARS-CoV, and seven to MERS-CoV. No data were found on abnormalities in brain development or on a direct link between the virus and neurological abnormalities in the human embryo, fetus, or children. Spontaneous miscarriage, stillbirth, and termination of pregnancy were some complications connected with SARS/MERS-CoV infection. SARS-CoV-2 is not currently associated with complications in the gestational period. CONCLUSIONS: The literature has no data associating exposure to coronavirus during pregnancy with brain malformations and neurodevelopmental disorders. However, despite the lack of reports, monitoring the development of children exposed to SARS-CoV-2 is essential given the risk of complications in pregnant women and the potential neuroinvasive and neurotropic properties found in previous strains.


Assuntos
Encefalopatias/etiologia , Deficiências do Desenvolvimento/etiologia , Efeitos Tardios da Exposição Pré-Natal/virologia , SARS-CoV-2 , Encefalopatias/virologia , Deficiências do Desenvolvimento/virologia , Feminino , Humanos , Transtornos do Neurodesenvolvimento/etiologia , Transtornos do Neurodesenvolvimento/virologia , Gravidez , Efeitos Tardios da Exposição Pré-Natal/etiologia , Fatores de Risco
5.
Int J Mol Sci ; 22(10)2021 May 12.
Artigo em Inglês | MEDLINE | ID: mdl-34066051

RESUMO

Sudden cardiac arrest leads to a significantly increased risk of severe neurological impairment and higher mortality rates in survivors due to global brain tissue injury caused by prolonged whole-body ischemia and reperfusion. The brain undergoes various deleterious cascading events. Among these damaging mechanisms, neuroinflammation plays an especially crucial role in the exacerbation of brain damage. Clinical guidelines indicate that 33 °C and 36 °C are both beneficial for targeted temperature management (TTM) after cardiac arrest. To clarify the mechanistic relationship between TTM and inflammation in transient global ischemia (TGI) and determine whether 36 °C produces a neuroprotective effect comparable to 33 °C, we performed an experiment using a rat model. We found that TTM at 36 °C and at 33 °C attenuated neuronal cell death and apoptosis, with significant improvements in behavioral function that lasted for up to 72 h. TTM at 33 °C and 36 °C suppressed the propagation of inflammation including the release of high mobility group box 1 from damaged cells, the activation and polarization of the microglia, and the excessive release of activated microglia-induced inflammatory cytokines. There were equal neuroprotective effects for TTM at 36 °C and 33 °C. In addition, hypothermic complications and should be considered safe and effective after cardiac arrest.


Assuntos
Temperatura Corporal , Encefalopatias/terapia , Isquemia Encefálica/complicações , Hipotermia Induzida/métodos , Inflamação/terapia , Animais , Encefalopatias/etiologia , Encefalopatias/patologia , Inflamação/etiologia , Inflamação/patologia , Masculino , Ratos , Ratos Sprague-Dawley
7.
Am J Hum Genet ; 108(5): 857-873, 2021 05 06.
Artigo em Inglês | MEDLINE | ID: mdl-33961779

RESUMO

The ALF transcription factor paralogs, AFF1, AFF2, AFF3, and AFF4, are components of the transcriptional super elongation complex that regulates expression of genes involved in neurogenesis and development. We describe an autosomal dominant disorder associated with de novo missense variants in the degron of AFF3, a nine amino acid sequence important for its binding to ubiquitin ligase, or with de novo deletions of this region. The sixteen affected individuals we identified, along with two previously reported individuals, present with a recognizable pattern of anomalies, which we named KINSSHIP syndrome (KI for horseshoe kidney, NS for Nievergelt/Savarirayan type of mesomelic dysplasia, S for seizures, H for hypertrichosis, I for intellectual disability, and P for pulmonary involvement), partially overlapping the AFF4-associated CHOPS syndrome. Whereas homozygous Aff3 knockout mice display skeletal anomalies, kidney defects, brain malformations, and neurological anomalies, knockin animals modeling one of the microdeletions and the most common of the missense variants identified in affected individuals presented with lower mesomelic limb deformities like KINSSHIP-affected individuals and early lethality, respectively. Overexpression of AFF3 in zebrafish resulted in body axis anomalies, providing some support for the pathological effect of increased amount of AFF3. The only partial phenotypic overlap of AFF3- and AFF4-associated syndromes and the previously published transcriptome analyses of ALF transcription factors suggest that these factors are not redundant and each contributes uniquely to proper development.


Assuntos
Encefalopatias/genética , Epilepsia/genética , Rim Fundido/genética , Deficiência Intelectual/genética , Mutação de Sentido Incorreto , Proteínas Nucleares/genética , Osteocondrodisplasias/genética , Adolescente , Sequência de Aminoácidos , Animais , Encefalopatias/etiologia , Criança , Pré-Escolar , Epilepsia/complicações , Evolução Molecular , Feminino , Frequência do Gene , Humanos , Lactente , Masculino , Camundongos , Modelos Moleculares , Proteínas Nucleares/química , Proteínas Nucleares/deficiência , Fenótipo , Estabilidade Proteica , Síndrome , Fatores de Elongação da Transcrição/química , Fatores de Elongação da Transcrição/genética , Adulto Jovem , Peixe-Zebra/genética
8.
Int J Mol Sci ; 22(6)2021 Mar 19.
Artigo em Inglês | MEDLINE | ID: mdl-33808671

RESUMO

Neonatal hypoxic-ischemic encephalopathy (HIE) is an important cause of mortality and morbidity in the perinatal period. This condition results from a period of ischemia and hypoxia to the brain of neonates, leading to several disorders that profoundly affect the daily life of patients and their families. Currently, therapeutic hypothermia (TH) is the standard of care in developing countries; however, TH is not always effective, especially in severe cases of HIE. Addressing this concern, several preclinical studies assessed the potential of stem cell therapy (SCT) for HIE. With this systematic review, we gathered information included in 58 preclinical studies from the last decade, focusing on the ones using stem cells isolated from the umbilical cord blood, umbilical cord tissue, placenta, and bone marrow. Outstandingly, about 80% of these studies reported a significant improvement of cognitive and/or sensorimotor function, as well as decreased brain damage. These results show the potential of SCT for HIE and the possibility of this therapy, in combination with TH, becoming the next therapeutic approach for HIE. Nonetheless, few preclinical studies assessed the combination of TH and SCT for HIE, and the existent studies show some contradictory results, revealing the need to further explore this line of research.


Assuntos
Encefalopatias/etiologia , Encefalopatias/terapia , Terapia Baseada em Transplante de Células e Tecidos , Hipóxia-Isquemia Encefálica/complicações , Transplante de Células-Tronco , Animais , Astrócitos , Encefalopatias/metabolismo , Encefalopatias/patologia , Diferenciação Celular , Transplante de Células-Tronco de Sangue do Cordão Umbilical , Modelos Animais de Doenças , Humanos , Hipotermia Induzida , Recém-Nascido , Transplante de Células-Tronco Mesenquimais , Microglia , Neurogênese , Neurônios , Estresse Oxidativo , Padrão de Cuidado , Transplante de Células-Tronco/métodos
9.
J Stroke Cerebrovasc Dis ; 30(6): 105750, 2021 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-33812174

RESUMO

OBJECTIVE: Vertebral artery compression of the medulla is a rare vascular finding that causes a variety of clinical presentations, from asymptomatic to neurological disability. This article presents the largest literature review to date on medullary compression of the vertebral arteries. METHODS: An English literature search was performed using the PubMed database and the keywords vertebral artery tortuosity, vertebral artery compression, and medullary compression. RESULTS: A comprehensive literature search yielded 68 patients (57% male) with medullary compression by an intracranial vertebral artery (ICVA). The left side of the medulla was compressed in 44, the right side in 19, and bilateral in 7. The most common clinical symptom was weakness - 26 patients (36%) - 6 had quadriparesis and 6 had hemiparesis. 21 patients reported imbalance; 12 various sensory symptoms; 4 patients were asymptomatic. CONCLUSIONS: Understanding the anatomy of the vasculature can help mitigate future debilitating stroke symptoms. Concrete guidelines for revascularization surgery in symptomatic patients may also be effective. Future studies are needed to further clarify the prevalence, natural history, vascular etiology, and treatment of this condition, including asymptomatic patients and the likelihood that they will develop further neurological signs and disability.


Assuntos
Encefalopatias/etiologia , Bulbo/fisiopatologia , Malformações Vasculares/complicações , Artéria Vertebral/anormalidades , Adulto , Idoso , Idoso de 80 Anos ou mais , Encefalopatias/diagnóstico por imagem , Encefalopatias/fisiopatologia , Feminino , Humanos , Masculino , Bulbo/diagnóstico por imagem , Pessoa de Meia-Idade , Paresia/etiologia , Paresia/fisiopatologia , Equilíbrio Postural , Prognóstico , Quadriplegia/etiologia , Quadriplegia/fisiopatologia , Transtornos das Sensações/etiologia , Transtornos das Sensações/fisiopatologia , Malformações Vasculares/diagnóstico por imagem , Malformações Vasculares/fisiopatologia , Artéria Vertebral/diagnóstico por imagem , Artéria Vertebral/fisiopatologia , Adulto Jovem
10.
BMC Neurol ; 21(1): 166, 2021 Apr 20.
Artigo em Inglês | MEDLINE | ID: mdl-33879091

RESUMO

BACKGROUND: We report on a patient with an intracerebral hemorrhage (ICH), who showed delayed development of aphasia, which was demonstrated via follow up diffusion tensor tractography (DTT) to be related to neural degeneration of the arcuate fasciculus (AF). CASE PRESENTATION: A 51-year-old, right-handed male presented with right hemiparesis, which occurred at the onset of a spontaneous ICH in the left corona radiata and basal ganglia. Brain magnetic resonance images showed a hematoma in the left subcortical area at one month after onset and hemosiderin deposits in the left subcortical area at nine years after onset. At four weeks after onset, he exhibited severe aphasia, and Western Aphasia Battery (WAB) testing revealed an aphasia quotient in the 39.6 percentile (%ile). However, his aphasia improved to nearly a normal state, and at three months after onset, his aphasia quotient was in the 90.5 %ile. At approximately eight years after onset, he began to show aphasia, and his aphasia increased slowly with time resulting in a WAB aphasia quotient in the 12.5 %ile at nine years after onset. The integrity of the left AF over the hematoma was preserved on 1-month post-onset DTT. However, the middle portion of the left AF in the middle of the hemosiderin deposits showed discontinuation on 9-year post-onset DTT. The fractional anisotropy value of the left AF was higher on the 9-year post-onset DTT (0.48) than that on the 1-month post-onset DTT (0.35), whereas the mean diffusivity value was lower on the 9-year post-onset DTT (0.10) than that on the 1-month post-onset DTT (0.32). The fiber number of the left AF was decreased to 175 on the 9-year post-onset DTT from 239 on the 1-month post-onset DTT. CONCLUSIONS: We report on a patient with ICH who showed delayed development of aphasia, which appeared to be related to degeneration of the AF in the dominant hemisphere. Our results suggest that DTT would be useful in ruling out neural degeneration of the AF.


Assuntos
Afasia , Encefalopatias , Córtex Cerebral/fisiopatologia , Hemorragia Cerebral/complicações , Vias Neurais/fisiopatologia , Afasia/etiologia , Afasia/fisiopatologia , Encefalopatias/etiologia , Encefalopatias/fisiopatologia , Humanos , Masculino , Pessoa de Meia-Idade
11.
BMJ Case Rep ; 14(3)2021 Mar 24.
Artigo em Inglês | MEDLINE | ID: mdl-33762283

RESUMO

COVID-19 has now emerged from a respiratory illness to a systemic viral illness with multisystem involvement. There is still a lot to learn about this illness as new disease associations with COVID-19 emerge consistently. We present a unique case of a neurological manifestation of a patient with structural brain disease who was COVID-19 positive and developed mental status changes, new-onset seizures and findings suggestive of viral meningitis on lumbar puncture. We also review the literature and discuss our case in the context of the other cases reported. We highlight the value of considering seizures and encephalopathy as one of the presenting features of COVID-19 disease.


Assuntos
Encefalopatias/etiologia , COVID-19/complicações , Convulsões/etiologia , Monofosfato de Adenosina/análogos & derivados , Monofosfato de Adenosina/uso terapêutico , Adulto , Alanina/análogos & derivados , Alanina/uso terapêutico , Anticonvulsivantes/uso terapêutico , Antivirais/uso terapêutico , Encefalopatias/diagnóstico , Encefalopatias/terapia , COVID-19/diagnóstico , COVID-19/terapia , Confusão/complicações , Humanos , Imunização Passiva/métodos , Imageamento por Ressonância Magnética/métodos , Masculino , Reação em Cadeia da Polimerase , Radiografia/métodos , SARS-CoV-2 , Convulsões/terapia , Resultado do Tratamento
12.
Curr Opin Neurol ; 34(3): 423-431, 2021 06 01.
Artigo em Inglês | MEDLINE | ID: mdl-33709973

RESUMO

PURPOSE OF REVIEW: To provide an overview on current knowledge of neurological symptoms and complications of COVID-19, and to suggest management concepts. RECENT FINDINGS: Headache, dizziness, excessive tiredness, myalgia, anosmia/hyposmia, and ageusia/dysgeusia are common nonspecific neurological manifestations during early COVID-19 disease found in the majority of patients. Less frequent but more severe and specific neurological manifestations include Guillain--Barré syndrome, encephalopathy, encephalitis/meningitis, epileptic seizures, and cerebrovascular events. Beyond standard neurological examination, these require a more extensive work-up, including cerebrospinal fluid assessment, neurophysiological evaluation, neuroimaging, and cognitive testing. Symptomatic treatment is advisable unless the neurological complication's immune pathogenesis is proven. SUMMARY: Neurological manifestations of COVID-19 occur during the acute, para-infectious, and 'recovery' phase. Therapeutic management depends on the clinical presentation and neurological work-up.


Assuntos
Anosmia/etiologia , COVID-19/complicações , Doenças do Sistema Nervoso/etiologia , Doenças do Sistema Nervoso/terapia , Encefalopatias/etiologia , Humanos , Doenças do Sistema Nervoso/diagnóstico
15.
Yakugaku Zasshi ; 141(3): 349-357, 2021.
Artigo em Japonês | MEDLINE | ID: mdl-33642503

RESUMO

Folds of the cerebral cortex, which are called gyri and sulci, are one of the most prominent features of the mammalian brain. However, the mechanisms underlying the development and malformation of cortical folds are largely unknown, mainly because they are difficult to investigate in mice, whose brain do not have cortical folds. To investigate the mechanisms underlying the development and malformation of cortical folds, we developed a genetic manipulation technique for the cerebral cortex of gyrencephalic carnivore ferrets. Genes-of-interest can be expressed in the ferret cortex rapidly and efficiently. We also demonstrated that genes-of-interest can be knocked out in the ferret cortex by combining in utero electroporation and the CRISPR/Cas9 system. Using our technique, we found that fibroblast growth factor (FGF) signaling and sonic hedgehog (Shh) signaling are crucial for cortical folding. In addition, we found that FGF signaling and Shh signaling preferentially increased outer radial glial cells and the thickness of upper layers of the cerebral cortex. Furthermore, over-activation of FGF signaling and Shh signaling resulted in polymicrogyria. Our findings provide in vivo data about the mechanisms of cortical folding in gyrencephalic mammals. Our technique for the ferret cerebral cortex should be useful for investigating the mechanisms underlying the development and diseases of the cerebral cortex that cannot be investigated using mice.


Assuntos
Encefalopatias/etiologia , Córtex Cerebral , Animais , Encefalopatias/genética , Encefalopatias/patologia , Sistemas CRISPR-Cas , Córtex Cerebral/citologia , Córtex Cerebral/patologia , Repetições Palindrômicas Curtas Agrupadas e Regularmente Espaçadas , Eletroporação , Furões , Fatores de Crescimento de Fibroblastos/metabolismo , Proteínas Hedgehog/metabolismo , Camundongos , Polimicrogiria/etiologia , Transdução de Sinais
16.
IEEE Pulse ; 12(1): 2-6, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33606616

RESUMO

In March 2020 -still the early days of the U.K.'s COVID-19 crisis-Rhys Thomas, a neurologist at Newcastle University, got a call at home from a concerned colleague. The colleague's cousin was hospitalized, critically ill with COVID-19, and had developed brainstem encephalitis, a severe inflammatory condition of the brain causing a suite of symptoms, from eye problems to balance problems and drowsiness. He wanted to know if Thomas knew anything about these conditions. At the time, the research coming out of Wuhan, China, only suggested a mild whiff of neurological symptoms-headache, dizziness, and the loss of taste and smell. Clearly the virus could affect the brain in some ways, but it wasn't, Thomas thought then, anything serious. But this report sounded much more concerning. Symptoms like this patient's would mean the virus was accessing more of the nervous system than scientists originally thought.


Assuntos
Encefalopatias/etiologia , COVID-19/complicações , Pandemias , SARS-CoV-2 , Encefalopatias/fisiopatologia , Encefalopatias/psicologia , COVID-19/tratamento farmacológico , COVID-19/fisiopatologia , COVID-19/psicologia , Síndrome da Liberação de Citocina/etiologia , Síndrome da Liberação de Citocina/fisiopatologia , Encefalite/etiologia , Encefalite/fisiopatologia , Humanos , Doenças do Sistema Nervoso/etiologia , Doenças do Sistema Nervoso/fisiopatologia , Doenças do Sistema Nervoso/psicologia , SARS-CoV-2/patogenicidade , Acidente Vascular Cerebral/etiologia , Acidente Vascular Cerebral/fisiopatologia
17.
BMC Neurol ; 21(1): 81, 2021 Feb 18.
Artigo em Inglês | MEDLINE | ID: mdl-33602153

RESUMO

BACKGROUND: Erdheim-Chester disease (ECD) is a non-Langerhans histiocytosis that results in multi-organ disease involving the skin, bones, lungs and kidneys. Central nervous system (CNS) involvement occurs in about 50 % of patients, and diabetes insipidus, visual disturbances, and cerebellar ataxia are the most frequent neurological signs. We report a case of Erdheim-Chester disease with central nervous system involvement in the form of enhancing intracranial mass lesions with massive edema. CASE PRESENTATION: The patient presented with vertigo, ataxia, encephalopathy and pyramidal signs. Diagnosis was suggested by xanthomatous skin lesions and a biopsy was compatible with Erdheim-Chester disease demonstrating xanthogranulomas CD68 positive (clone KP1) and CD1a and S100 negative. Testing for BRAF mutation was negative, which precluded treatment with Vemurafenib. Treatment with steroids and interferon resulted in improvement of neurological signs and regression of edema on MRI. CONCLUSIONS: The diagnosis of Erdheim-Chester disease should be considered in intracranial mass lesions. Xanthomatous skin lesions are a clue to the diagnosis.


Assuntos
Encefalopatias/etiologia , Doença de Erdheim-Chester/complicações , Doença de Erdheim-Chester/diagnóstico , Doença de Erdheim-Chester/patologia , Dermatopatias/etiologia , Adulto , Axila/patologia , Biópsia , Encefalopatias/patologia , Feminino , Humanos , Imageamento por Ressonância Magnética , Dermatopatias/patologia
18.
Neurologia (Engl Ed) ; 36(2): 127-134, 2021 Mar.
Artigo em Inglês, Espanhol | MEDLINE | ID: mdl-33549369

RESUMO

OBJECTIVES: Since the beginning of the COVID-19 pandemic, the Spanish Society of Neurology has run a registry of patients with neurological involvement for the purpose of informing clinical neurologists. Encephalopathy and encephalitis were among the most frequently reported complications. In this study, we analyse the characteristics of these complications. PATIENTS AND METHODS: We conducted a retrospective, descriptive, observational, multicentre study of patients with symptoms compatible with encephalitis or encephalopathy, entered in the Spanish Society of Neurology's COVID-19 Registry from 17 March to 6 June 2020. RESULTS: A total of 232 patients with neurological symptoms were registered, including 51 cases of encephalopathy or encephalitis (21.9%). None of these patients were healthcare professionals. The most frequent syndromes were mild or moderate confusion (33%) and severe encephalopathy or coma (9.8%). The mean time between onset of infection and onset of neurological symptoms was 8.02 days. Lumbar puncture was performed in 60.8% of patients, with positive PCR results for SARS-CoV-2 in only one case. Brain MRI studies were performed in 47% of patients, with alterations detected in 7.8% of these. EEG studies were performed in 41.3% of cases, detecting alterations in 61.9%. CONCLUSIONS: Encephalopathy and encephalitis are among the complications most frequently reported in the registry. More than one-third of patients presented mild or moderate confusional syndrome. The mean time from onset of infection to onset of neurological symptoms was 8 days (up to 24hours earlier in women than in men). EEG was the most sensitive test in these patients, with very few cases presenting alterations in neuroimaging studies. All patients treated with boluses of corticosteroids or immunoglobulins progressed favourably.


Assuntos
Encefalopatias/etiologia , COVID-19/complicações , Encefalite Viral/etiologia , Pandemias , SARS-CoV-2/patogenicidade , Corticosteroides/uso terapêutico , Encefalopatias/epidemiologia , Encefalopatias/virologia , COVID-19/epidemiologia , Transtornos Cognitivos/epidemiologia , Coma/epidemiologia , Coma/etiologia , Coma/virologia , Comorbidade , Eletroencefalografia , Encefalite Viral/epidemiologia , Encefalite Viral/virologia , Epilepsia/epidemiologia , Feminino , Humanos , Hipertensão/epidemiologia , Imunoglobulinas Intravenosas/uso terapêutico , Imageamento por Ressonância Magnética , Masculino , Neuroimagem , Sistema de Registros , Síndrome do Desconforto Respiratório/epidemiologia , Síndrome do Desconforto Respiratório/etiologia , Estudos Retrospectivos , SARS-CoV-2/isolamento & purificação , Espanha/epidemiologia , Acidente Vascular Cerebral/epidemiologia
19.
Aging (Albany NY) ; 13(4): 6134-6143, 2021 02 20.
Artigo em Inglês | MEDLINE | ID: mdl-33611310

RESUMO

To investigate the role of P2Y12 receptor-mediated microglia activation in delayed encephalopathy after acute carbon monoxide poisoning (DEACMP), we used static inhalation carbon monoxide to build DEACMP rat model. DEACMP rats were randomly assigned into DEACMP group and intervention group. A control goup was also set. The rats in intervention group received intraperitoneal injection of 100uM suramin (a P2Y12 receptor antagonist). In control group, the escape latency, level of microglia activation and ATP content were similar between different time points. In both DEACMP group and intervention group, the escape latency, level of microglia activation and ATP content were significanlty increased at 21th and 28th day. The hippocampal cells in DEACMP group and intervention group were severely and moderately, respectively, damaged at 21th and 28th day. Meanwhile, compared to control group, both DEACMP group and intervention group had significanlty longer escape latency, higher level of microglia activation and ATP content at 21th and 28th day. Compared to DEACMP group, the intervention group had significantly shorter escape latency and lower level of microglia activation at 21th and 28th day. These results suggested that the microglia activation regulated by ATP through P2Y12 receptor pathway might be closely related to the development of DEACMP.


Assuntos
Encefalopatias/induzido quimicamente , Intoxicação por Monóxido de Carbono/complicações , Microglia/metabolismo , Antagonistas do Receptor Purinérgico P2Y/administração & dosagem , Suramina/administração & dosagem , Animais , Encefalopatias/etiologia , Intoxicação por Monóxido de Carbono/imunologia , Hipocampo/patologia , Masculino , Ratos , Ratos Wistar
20.
Neurol Sci ; 42(2): 479-489, 2021 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-33409828

RESUMO

OBJECTIVE: To describe the clinical, neurological, neuroimaging, and cerebrospinal fluid (CSF) findings associated with encephalopathy in patients admitted to a COVID-19 tertiary reference center. METHODS: We retrospectively reviewed records of consecutive patients with COVID-19 evaluated by a consulting neurology team from March 30, 2020 through May 15, 2020. RESULTS: Fifty-five patients with confirmed SARS-CoV-2 were included, 43 of whom showed encephalopathy, and were further divided into mild, moderate, and severe encephalopathy groups. Nineteen patients (44%) had undergone mechanical ventilation and received intravenous sedatives. Eleven (26%) patients were on dialysis. Laboratory markers of COVID-19 severity were very common in encephalopathy patients, but did not correlate with the severity of encephalopathy. Thirty-nine patients underwent neuroimaging studies, which showed mostly non-specific changes. One patient showed lesions possibly related to CNS demyelination. Four had suffered an acute stroke. SARS-CoV-2 was detected by RT-PCR in only one of 21 CSF samples. Two CSF samples showed elevated white blood cell count and all were negative for oligoclonal bands. In our case series, the severity of encephalopathy correlated with higher probability of death during hospitalization (OR = 5.5 for each increment in the degree of encephalopathy, from absent (0) to mild (1), moderate (2), or severe (3), p < 0.001). CONCLUSION: In our consecutive series with 43 encephalopathy cases, neuroimaging and CSF analysis did not support the role of direct viral CNS invasion or CNS inflammation as the cause of encephalopathy.


Assuntos
Encefalopatias/etiologia , COVID-19/complicações , Adulto , Idoso , Idoso de 80 Anos ou mais , Encefalopatias/líquido cefalorraquidiano , Encefalopatias/diagnóstico por imagem , Encefalopatias/imunologia , COVID-19/mortalidade , COVID-19/terapia , Feminino , Mortalidade Hospitalar , Humanos , Imageamento por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Índice de Gravidade de Doença , Centros de Atenção Terciária
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...