关键词： Posterior reversible encephalopathy syndrome   PRES   Reversible posterior leukoencephalopathy syndrome   Hypertensive encephalopathy   SARS-CoV-2 coronavirus disease 2019  

摘要： • PRES is potentially a complication of severe SARS-CoV-2 infection. • Consider PRES in COVID-19 patients with altered mentation. • Consider tight blood pressure control in ventilated patients with COVID-19. • Hypertensive encephalopathy may prolong ventilator times in COVID-19 patients. [ABSTRACT FROM AUTHOR]

关键词： Traumatic brain injury   TBHQ   Astrocyte   Activation   Nrf-2   Oxidative stress  

摘要： Traumatic brain injury (TBI) is a major leading cause of death and long-term disability. Although astrocytes play a key role in neuroprotection after TBI in the early stage, the overactivation of astrocytes can lead to long-term functional deficits, and the underlying pathophysiological mechanisms remain unclear. In addition, it is unknown whether the nuclear factor erythroid 2-related factor2/haem oxygenase-1 (Nrf-2/HO-1) pathway could elicit a neuroprotective effect by decreasing astrocyte overactivation after TBI. We aimed to study the effects of tert-butylhydroquinone (TBHQ) in reducing astrocyte overactivation after TBI and explored the underlying mechanisms. We first established a controlled cortical impact (CCI) model in rats and performed Haematoxylin and eosin (H&E) staining to observe brain tissue damage. The cognitive function of rats was assessed by modified neurological severity scoring (mNSS) and Morris water maze (MWM) test. Astrocyte and microglia activation was detected by immunofluorescence staining. Oxidative stress conditions were investigated using Western blotting. An enzyme-linked immunosorbent assay (ELISA) was designed to assess the level of the proinflammatory factor tumour necrosis factor-alpha (TNF-alpha). Dihydroethidium (DHE) staining was used to detect reactive oxygen species (ROS). Apoptosis was assessed by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. The results showed that the administration of TBHQ ameliorated motor function and cognitive deficits and decreased the lesion volume. In addition, TBHQ significantly decreased astrocyte overactivation, diminished the pro-inflammatory phenotype M1 and inflammatory cytokines production after TBI, increased Nrf-2 nuclear accumulation, and enhanced the levels of the Nrf-2 downstream antioxidative genes HO-1 and NADPH-quinone oxidoreductase-1 (NQO-1). Furthermore, TBHQ treatment alleviated apoptosis and neuronal death in the cerebral cortex. Overall, our data

关键词： Coronaviruses   Coronavirus disease 2019   COVID-19 neurological complications   Endotheliitis   Environmental neurology   MERS   MERS-CoV   Neuroepidemiology   Neuropathology   Pandemic   SARS   SARS-CoV-1   SARS-CoV-2   Viral neurotropism   Zoonosis  

摘要： A comprehensive review of the neurological disorders reported during the current COVID-19 pandemic demonstrates that infection with SARS-CoV-2 affects the central nervous system (CNS), the peripheral nervous system (PNS) and the muscle. CNS manifestations include: headache and decreased responsiveness considered initial indicators of potential neurological involvement;anosmia, hyposmia, hypogeusia, and dysgeusia are frequent early symptoms of coronavirus infection. Respiratory failure, the lethal manifestation of COVID-19, responsible for 264,679 deaths worldwide, is probably neurogenic in origin and may result from the viral invasion of cranial nerve I, progressing into rhinencephalon and brainstem respiratory centers. Cerebrovascular disease, in particular large-vessel ischemic strokes, and less frequently cerebral venous thrombosis, intracerebral hemorrhage and subarachnoid hemorrhage, usually occur as part of a thrombotic state induced by viral attachment to ACE2 receptors in endothelium causing widespread endotheliitis, coagulopathy, arterial and venous thromboses. Acute hemorrhagic necrotizing encephalopathy is associated to the cytokine storm. A frontal hypoperfusion syndrome has been identified. There are isolated reports of seizures, encephalopathy, meningitis, encephalitis, and myelitis. The neurological diseases affecting the PNS and muscle in COVID-19 are less frequent and include Guillain-Barre syndrome;Miller Fisher syndrome;polyneuritis cranialis;and rare instances of viral myopathy with rhabdomyolysis. The main conclusion of this review is the pressing need to define the neurology of COVID-19, its frequency, manifestations, neuropathology and pathogenesis. On behalf of the World Federation of Neurology we invite national and regional neurological associations to create local databases to report cases with neurological manifestations observed during the on-going pandemic. International neuroepidemiological collaboration may help define the natural his

关键词： MeCP2   Rett syndrome   adenosine deaminase acting on RNA   ADAR   RNA editing  

摘要： Programmable RNA editing is gaining momentum as an approach to repair mutations, but its efficiency in repairing endogenous mutant RNA in complex tissue is unknown. Here we apply this approach to the brain and successfully repair a guanosine-to-adenosine mutation in methyl CpG binding protein 2 RNA that causes the neurodevelopmental disease Rett syndrome. Repair is mediated by hippocampal injections of juvenile Mecp2(317G>A) A mice with an adeno-associated virus expressing the hyperactive catalytic domain of adenosine deaminase acting on RNA 2 and Mecp2 guide. After 1 month, 50% of Mecp2 RNA is recoded in three different hippocampal neuronal populations. MeCP2 protein localization to heterochromatin is restored in neurons to 50% of wild-type levels. Whole-transcriptome RNA analysis of one neuronal population indicates that the majority of off-target editing sites exhibit rates of 30% or less. This study demonstrates that programmable RNA editing can be utilized to repair mutations in mouse models of neurological disease.

关键词： Oxygen   Carbon dioxide   Out-of-hospital cardiac arrest   Brain anoxia-ischemia   Cardio-pulmonary resuscitation   Critical care outcomes  

摘要： Background Exposure to extreme arterial partial pressures of oxygen (PaO2) and carbon dioxide (PaCO2) following the return of spontaneous circulation (ROSC) after out-of-hospital cardiac arrest (OHCA) is common and may affect neurological outcome but results of previous studies are conflicting. Methods Exploratory study of the International Cardiac Arrest Registry (INTCAR) 2.0 database, including 2162 OHCA patients with ROSC in 22 intensive care units in North America and Europe. We tested the hypothesis that exposure to extreme PaO(2)or PaCO(2)values within 24 h after OHCA is associated with poor neurological outcome at discharge. Our primary analyses investigated the association between extreme PaO(2)and PaCO(2)values, defined as hyperoxemia (PaO2 > 40 kPa), hypoxemia (PaO2 < 8.0 kPa), hypercapnemia (PaCO2 > 6.7 kPa) and hypocapnemia (PaCO2 < 4.0 kPa) and neurological outcome. The secondary analyses tested the association between the exposure combinations of PaO2 > 40 kPa with PaCO2 < 4.0 kPa and PaO(2)8.0-40 kPa with PaCO2 > 6.7 kPa and neurological outcome. To define a cut point for the onset of poor neurological outcome, we tested a model with increasing and decreasing PaO(2)levels and decreasing PaCO(2)levels. Cerebral Performance Category (CPC), dichotomized to good (CPC 1-2) and poor (CPC 3-5) was used as outcome measure. Results Of 2135 patients eligible for analysis, 700 were exposed to hyperoxemia or hypoxemia and 1128 to hypercapnemia or hypocapnemia. Our primary analyses did not reveal significant associations between exposure to extreme PaO(2)or PaCO(2)values and neurological outcome (P = 0.13-0.49). Our secondary analyses showed no significant associations between combinations of PaO(2)and PaCO(2)and neurological outcome (P = 0.11-0.86). There was no PaO(2)or PaCO(2)level significantly associated with poor neurological outcome. All analyses were adjusted for relevant co-variates. Conclusions Exposure to extreme PaO(2)or PaCO(2)values in the first 24 h

关键词： Neurological involvement   Kawasaki disease   Intravenous immunoglobulin resistance   Coronary artery lesions   Vasculitis  

摘要： Background Kawasaki disease (KD) is an acute, self-limiting systemic vasculitis that predominately affects children. Neurological involvement is a known complication of KD, however, its association with KD severity remains elusive. We aimed to systematically describe the general manifestations of neurological involvement in KD, determine whether neurological involvement is a marker of disease severity in patients with KD, and assess the relationship of such involvement with intravenous immunoglobulin (IVIG) resistance and coronary artery lesions (CALs). Methods We retrospectively reviewed data from 1582 patients with KD between January 2013 and December 2017. Profiles of patients with neurological symptoms (group A,n = 80) were compared to those of gender- and admission date-matched patients without neurological involvement (group B,n = 512). Multivariate logistic regression analyses were performed to determine whether neurological involvement was significantly associated with IVIG resistance. Results Neurological involvement was observed in 5.1% (80/1582) of patients with KD. The neurological manifestations were diffuse, presenting as headache (13/80, 16.3%), convulsions (14/80, 17.5%), somnolence (40/80, 50.1%), extreme irritability (21/80, 26.3%), signs of meningeal irritation (15/80, 18.8%), bulging fontanelles (7/80, 8.8%), and facial palsy (1/80, 1.3%). Neurological symptoms represented the initial and/or predominant manifestation in 47.5% (38/80) of patients with KD. The incidence of IVIG resistance and levels of inflammatory markers were higher in group A than in group B. However, neurological involvement was not an independent risk factor for IVIG resistance or CALs. Conclusion Rates of neurological involvement were relatively low in patients with KD. Neurological involvement was associated with an increased risk of IVIG resistance and severe inflammatory burden. Our results highlight the need for pediatricians to recognize KD with neurological involvement

关键词： blood brain barrier   cerebrovascular disease   inflammation   interleukins   interleukin-1 alpha   neuroprotective agents   stroke  

摘要： Supplemental Digital Content is available in the text.

摘要： The tendency to engage in addictive behaviors has long been tied to the actions of the dopamine system. Early theories were based on the fact that all addictive drugs and behaviors (such as gambling) increase dopamine levels in the striatum, and the evidence that dopamine signaled reward or reward prediction error. However, with a changing emphasis of addiction away from purely pharmacological models that emphasize tolerance and withdrawal, towards one of behavioral dyscontrol, is there still a place for abnormal dopamine signaling in addiction? Here we recast the dopamine theory of addiction based on the idea that tonic dopamine may index a continuous phenotype that goes from apathy to impulsivity and compulsivity. Higher tonic dopamine signaling would make individuals vulnerable to drug reinforcement and cue-induced craving. We relate this to computational models of dopamine signaling, and review clinical and neuroimaging evidence from Parkinson’s Disease, schizophrenia and bipolar disorder in support of this model.

关键词： Energy expenditure   Neurological diseases   Energy requirement   Alzheimer's disease   Parkinson's disease   Amyotrophic lateral sclerosis   Multiple sclerosis   Cerebral palsy  

摘要： Objectives:It has been reported that in most neurological patients, resting energy expenditure due to hypermetabolism is increased. Physical activity, which is another component of energy expenditure, varies depending on the course of the disease. Different mechanisms are used to explain changes in energy expenditure in this population. Pathological problems of centers that regulate energy balance in the brain, endocrine and metabolic dysfunction, mitochondrial damage, autonomic dysfunction and inflammatory anomalies are thought to be at the root of this situation. In this review study, studies about energy expenditure and energy requirement in neurological diseases have been examined and suggested practices in this field have been presented. Methods:We reviewed articles regarding selected from PubMed, Science Direct, EBSCO, and databases about energy expenditure and neurological diseases. Results:Based on the type of neurological diseases;factors such as stage of the disease, disease complications, metabolic status, mechanical ventilation, body composition, movement restrictions or hyperactivity change energy expenditure and, as a result, nutrition requirement. Determination of the energy requirement is the basic variable for adjusting medical nutrition therapy. Despite an increase in resting energy expenditure as a result of metabolic processes in most neurological disorders, the daily energy expenditure is reported to change based on the restriction of physical activity due to the disorder. Discussion:Determining patient's energy expenditure and energy requirements is regarded as the right approach in terms of improving the patient's quality of life, regulating appropriate medical nutrition treatment and increasing the effectiveness of other treatments.

关键词： 北京大学出版社   文献计量学   《中文核心期刊要目总览》   核心期刊   神经病学   精神病学   专家评审   中华神经医学杂志  

摘要： 《中华神经医学杂志》主编:我们谨此郑重通知:依据文献计量学的原理和方法,经研究人员对相关文献的检索、统计和分析,以及学科专家评审,贵刊《中华神经医学杂志》入编《中文核心期刊要目总览》2017年版(即第8版)之“神经病学与精神病学”类的核心期刊。该书由北京大学出版社出版。