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2.
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue ; 32(4): 483-487, 2020 Apr.
Artigo em Chinês | MEDLINE | ID: mdl-32527358

RESUMO

OBJECTIVE: To investigate the underlying molecular mechanisms of brain injury in rats after cardiac arrest and cardiopulmonary resuscitation (CPR) by observing necroptosis of brain cells and changes of 90 cytokines in brain tissue. METHODS: Sprague-Dawley (SD) rats were divided into Sham group (n = 10) and cardiac arrest group (n = 10) according to random number table method. The model of asphyxia cardiac arrest for 6 minutes followed by CPR model was established. Tracheal intubation in Sham rats were routinely performed without inducing cardiac arrest. Neurological deficit score (NDS) was evaluated, blood samples were collected and rats were sacrificed, then serum S100B level was measured by enzyme linked immunosorbent assay (ELISA) on the third day after CPR. Necroptotic cells in brain were detected by immunofluorescence staining. The levels of 90 cytokines expression in brain were measured by antibody array. The relative ratio of the two groups of protein expression ≥ 1.5 or ≤ 0.5 and P < 0.05 represented the differential expression protein. RESULTS: There were 8 rats successfully resuscitated and 2 died in cardiac arrest group. There were 8 rats selected in Sham group to match the sample size. Compared with Sham group, the NDS score of cardiac arrest group was significantly lower [63.0 (62.5, 64.3) vs. 80.0 (80.0, 80.0), P < 0.01], and the level of serum S100B was significantly higher (ng/L: 47.96±10.16 vs. 16.56±5.60, P < 0.01). More necroptotic cells in cerebral cortex and hippocampus were found in cardiac arrest group [proportion of cells positive for TdT-mediated nick end labeling (TUNEL) and negative for caspase-3: (15.70±0.32)% vs. (8.00±0.28)% in cortex, (20.80±1.35)% vs. (9.00±4.00)% in hippocampus, both P < 0.05]. The levels of inflammatory cytokines [cytokine-induced neutrophil chemoattractant (CINC-2α/ß, CINC-3), interferon-γ (IFN-γ)] and signal protein c-Src kinase (CSK) in brain significantly increased after cardiac arrest as compared to Sham group levels (ratio of cardiac arrest group to Sham group: CINC-2 α/ß was 2.503±0.428, P = 0.024; CINC-3 was 2.369±0.142, P = 0.005; IFN-γ was 3.149±1.362, P = 0.044; CSK was 1.887±0.105, P = 0.001). However, the levels of neuroprotective cytokines ciliary neurotrophic factor (CNTF), glial cell-derived neurotrophic factor receptor (GFR α-1, GFR α-2), growth hormone (GH), growth hormone receptor (GHR), granulocyte-macrophage colony-stimulating factor (GM-CSF) and anti-inflammatory protein interleukin-10 (IL-10) significantly decreased after cardiac arrest (ratio of cardiac arrest group to Sham group: CNTF was 0.341±0.137, P = 0.036; GFRα-1 was 0.461±0.164, P = 0.044; GFRα-2 was 0.447±0.017, P = 0.033; GH was 0.450±0.136, P = 0.024; GHR was 0.508±0.128, P = 0.022; GM-CSF was 0.446±0.130, P = 0.035; IL-10 was 0.502±0.211, P = 0.017). CONCLUSIONS: Necroptosis is involved in brain injury after cardiac arrest. The molecular mechanisms of brain injury may be related to inflammatory response, neurogenesis disorder and impaired survival of nerve cells.


Assuntos
Lesões Encefálicas , Parada Cardíaca , Animais , Encéfalo , Citocinas , Necroptose , Ratos , Ratos Sprague-Dawley
7.
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue ; 32(3): 336-340, 2020 Mar.
Artigo em Chinês | MEDLINE | ID: mdl-32385999

RESUMO

OBJECTIVE: To compare the severity of brain injury between asphyxia and electrical stimulation induced cardiac arrest in rats. METHODS: Forty-two healthy male Sprague-Dawley (SD) rats were randomized into sham group (n = 6), asphyxia group (n = 18) and electrical stimulation group (n = 18). Rats in each group were given invasive mechanical ventilation and femoral blood vessels catheterization for monitoring blood pressure and fluid infusion. In the asphyxia group, the tracheal tube was clamped to induce cardiac arrest, and in the electrical stimulation group, the esophageal electrical stimulation was used to induce cardiac arrest, and cardiopulmonary resuscitation (CPR) was performed 4 minutes after cardiac arrest. In the sham group, only tracheal intubation and femoral artery intubation were performed after anesthesia, but cardiac arrest was not induced. Animals were allowed to survive until 72 hours after resuscitation, and survival analysis was performed using Kaplan-Meier curves. At 24 hours and 72 hours after resuscitation, the neurological deficit score (NDS) was measured. The vena cava blood was collected, and the brain injury associated serum biomarkers, neuron-specific enolase (NSE) and S100B, were detected by enzyme-linked immunosorbent assay (ELISA). The brain tissues were then harvested to perform hematoxylin-eosin (HE) staining for observing pathological changes in the hippocampal CA1 area with light microscopy. RESULTS: Cardiac arrest was successfully induced in both the asphyxia group and the electrical stimulation group, 94.4% (17/18) and 88.9% (16/18) animals were resuscitated successfully in the two groups respectively. Kaplan-Meier curves analysis showed that 72-hour cumulative survival rate was similar in the asphyxia group and the electrical stimulation group (Log-Rank test: χ2 = 0.040, P = 0.841). Both asphyxia group and electrical stimulation group had higher NDS score than sham group at 24 hours after resuscitation (37.50±4.26, 32.17±4.02 vs. 8.33±2.33, both P < 0.01). NDS score showed a downwards trend at 72 hours after resuscitation in both model groups, and the decline was more significant in the electrical stimulation group, which was significantly different as compared with asphyxia group (14.00±2.89 vs. 26.33±4.84, P < 0.05). ELISA results showed that the levels of serum NSE at 24 hours after resuscitation in the asphyxia and electrical stimulation groups were significantly higher than those in the sham group (µg/L: 1.02±0.07, 1.02±0.02 vs. 0.87±0.02, both P < 0.05). NSE kept increasing at 72 hours after resuscitation in the asphyxia group, which showed significant difference as compared with sham group (µg/L: 1.03±0.05 vs. 0.87±0.02, P < 0.01). But it had almost recovered to the normal level in the electrical stimulation group without significant difference as compared with sham group (µg/L: 0.96±0.04 vs. 0.87±0.02, P > 0.05). There was no significant difference in S100B level at different time points after resuscitation among three groups. It was displayed under light microscope that there was no significant neuronal damage in the hippocampal CA1 area in the two model groups at 24 hours after resuscitation as compared with the sham group. At 72 hours, there were certain damages in the hippocampal CA1 area in both model groups, which were more obvious in the asphyxia group. CONCLUSIONS: Both cardiac arrest models induced by asphyxia and electrical stimulation show a certain degree of brain injuries after resuscitation. Brain injuries are more severe in asphyxia-induced cardiac arrest compared with trans-esophageal electrical stimulation method.


Assuntos
Lesões Encefálicas , Reanimação Cardiopulmonar , Parada Cardíaca , Animais , Asfixia , Modelos Animais de Doenças , Estimulação Elétrica , Masculino , Distribuição Aleatória , Ratos , Ratos Sprague-Dawley
8.
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue ; 32(3): 345-349, 2020 Mar.
Artigo em Chinês | MEDLINE | ID: mdl-32386001

RESUMO

OBJECTIVE: To investigate the value and feasibility of early goal directed sedation (EGDS) in patients with acute brain injury. METHODS: A total of 110 patients with acute brain injury who were admitted to intensive care unit (ICU) of the Third Medical Center of the Chinese People's Liberation Army General Hospital from January 2015 to March 2019 were included and randomly divided into EGDS group and standard sedation group (STD) using the random number table. Patients in the EGDS group were sedated by continuous intravenous infusion of dexmedetomidine (initial dose of 0.2 µg×kg-1×min-1) for 72 consecutive hours. Patients in the STD group received intravenous bolus of propofol as appropriate clinically. Richmond agitation-sedation score (RASS) and electroencephalogram bispectral index (BIS) were used to continuously monitor the level of sedation. All patients were given sufentanil for analgesia. Routine treatments such as dehydration and reduction of intracranial pressure with mannitol, hemostasis or antiplatelet therapy were given according to the patients' condition. Vital signs, acute physiology and chronic health evaluation II (APACHE II) score, Glasgow coma scale (GCS) score, BIS value, artery blood gas analysis, duration of mechanical ventilation, analgesic dosage and adverse events were recorded in two groups before and 24, 48, and 72 hours after sedation. RESULTS: (1) Among the 110 patients, patients who received the second surgery due to cerebral hemorrhage, had worsening of cerebral hernia, withdrew during the course of the study, or whose family members abandoned treatment were excluded from the study. Finally, 105 patients were enrolled in the study, including 56 patients in the EGDS group and 49 in the STD group. There was no significant difference in gender, age, types of brain injury, baseline APACHE II or GCS score or rate of mechanical ventilation between the two groups. (2) Compared with before sedation, heart rate (HR) significantly decreased till 72 hours after sedation in both groups, and the decrease in the EGDS groups was more obvious as compared with the STD group (bpm: 70.49±7.53 vs. 79.83±9.48, P < 0.05). Besides HR, significant improvement was found in the APACHE II and GCS scores in the STD group at 72 hours of sedation as compared with before sedation, and no significant difference was found in other indicators. Compared with before sedation, arterial partial pressure of carbon dioxide (PaCO2) was significantly increased from the 24th hour of sedation, mean artery pressure (MAP) was decreased significantly and GCS score, BIS value were increased significantly from the 48th hour of sedation, till 72 hours, which were all improved significantly as compared with the STD group [72-hour PaCO2 (mmHg, 1 mmHg = 0.133 kPa): 40.30±5.98 vs. 31.57±8.20, 72-hour MAP (mmHg): 85.01±8.26 vs. 89.54±9.41, 72-hour GCS score: 8.62±3.34 vs. 7.89±2.74, 72-hour BIS: 60.87±24.79 vs. 56.68±33.43, all P < 0.05]. APACHE II score was significantly lower only at the 72nd hour of sedation as compared with before sedation in the EGDS group, and no significant difference was found as compared with the STD group (17.10±7.05 vs. 18.90±3.32, P > 0.05). Oxygenation index (PaO2/FiO2) was significantly increased only at the 24th hour of sedation in the EGDS group as compared with the STD group (mmHg: 261.05±118.45 vs. 226.45±96.54, P < 0.05). (3) The duration of mechanical ventilation was significantly shorter in the EGDS group than that in the STD group (hours: 20.56±9.03 vs. 27.75±11.23, P < 0.05), and the total administered dose of sufentanil was significantly lower in the EGDS group than that in the STD group (µg: 79.16±26.76 vs. 102.46±35.48, P < 0.05). (4) Compared with the STD group, the incidence of bradycardia in the EGDS group was increased significantly [10.71% (6/56) vs. 6.12% (3/49), P < 0.05], while the incidence of tachycardia was decreased significantly [14.29% (8/56) vs. 38.78% (19/49), P < 0.05], but no significant difference was found in the incidence of hypotension [5.36% (3/56) vs. 4.08% (2/49), P > 0.05]. The incidence of unexpected extubation in the STD group was 4.08% (2/49), which did not occurre in the EGDS group. CONCLUSIONS: EGDS can improve the GCS score and BIS value of patients with acute brain injury, suggesting that the EGDS is safe and feasible, which can help improve neurological function in patients with acute brain injury.


Assuntos
Lesões Encefálicas/tratamento farmacológico , Dexmedetomidina/uso terapêutico , Hipnóticos e Sedativos/uso terapêutico , Objetivos , Humanos , Unidades de Terapia Intensiva , Respiração Artificial
9.
Mol Pharmacol ; 98(1): 13-22, 2020 07.
Artigo em Inglês | MEDLINE | ID: mdl-32350120

RESUMO

Several reports have been published recently demonstrating a beneficial effect of epidermal growth factor receptor (EGFR) inhibitors in improving pathologic and behavioral conditions in neurodegenerative diseases (NDDs) such as Alzheimer's disease and Amyotrophic Lateral Sclerosis (ALS) as well as the brain and spinal cord injuries (SCI). Despite successful therapeutic effects of EGFR inhibition in these pathologic conditions, there is still no report of proof-of-concept studies in well-characterized animal models using recently developed blood-brain barrier (BBB)-penetrating EGFR inhibitors, which is due to previous conflicting reports concerning the level of EGFR or activated EGFR in normal and pathologic conditions that caused target engagement to be a concern in any future EGFR inhibition therapy. In this review, the level of EGFR expression and activation in the developing central nervous system (CNS) compared with the adult CNS will be explained as well as how neuronal injury or pathologic conditions, especially inflammation and amyloid fibrils, induce reactive astrocytes leading to an increase in the expression and activation of EGFR and, finally, neurodegeneration. Furthermore, in this review, we will discuss two main molecular mechanisms that can be proposed as the neuroprotective effects of EGFR inhibition in these pathologic conditions. We will also review the recent advances in the development of BBB-penetrating EGFR inhibitors in cancer therapy, which may eventually be repositioned for NDDs and SCI therapy in the future. SIGNIFICANCE STATEMENT: Based on the lessons from the applications of EGFR inhibitors in oncology, it is concluded that EGFR inhibitors can be beneficial in treatment of neurodegenerative diseases and spinal cord injuries. They carry their therapeutic potentials through induction of autophagy and attenuation of reactive astrocytes.


Assuntos
Lesões Encefálicas/metabolismo , Sistema Nervoso Central/crescimento & desenvolvimento , Doenças Neurodegenerativas/metabolismo , Traumatismos da Medula Espinal/metabolismo , Adulto , Animais , Barreira Hematoencefálica/efeitos dos fármacos , Lesões Encefálicas/tratamento farmacológico , Sistema Nervoso Central/metabolismo , Criança , Reposicionamento de Medicamentos , Receptores ErbB/antagonistas & inibidores , Receptores ErbB/metabolismo , Regulação da Expressão Gênica no Desenvolvimento , Humanos , Terapia de Alvo Molecular , Doenças Neurodegenerativas/tratamento farmacológico , Inibidores de Proteínas Quinases/farmacologia , Inibidores de Proteínas Quinases/uso terapêutico , Traumatismos da Medula Espinal/tratamento farmacológico , Regulação para Cima/efeitos dos fármacos
10.
N Z Med J ; 133(1515): 97-103, 2020 05 22.
Artigo em Inglês | MEDLINE | ID: mdl-32438381

RESUMO

The role of the external clinical advisor is critical to the adjudication of complex claims in the processes of the Accident Compensation Corporation (ACC). This is particularly true of claims for treatment injury that occur during birth, which are often very complicated. In most cases external clinical advisors are non-treating doctors, whose opinion strongly guides the hand of ACC. This viewpoint considers the impact of the role of the external clinical advisor by using extracts from an external clinical advisor's report to show how a power imbalance can be enacted in ACC decision making processes. Also considered are the way that the normal checks and balances in the system, particularly those provided by the Health & Disability Commissioner, are bypassed in most cases. Finally, a recommendation is made to potential external clinical advisors to precisely following the standards set by the Medical Council in all cases when writing reports for ACC.


Assuntos
Traumatismos do Nascimento/etiologia , Compensação e Reparação/legislação & jurisprudência , Prova Pericial/normas , Papel do Médico , Lesões Encefálicas/etiologia , Criança , Tomada de Decisões , Prova Pericial/legislação & jurisprudência , Feminino , Transtornos do Crescimento/complicações , Humanos , Doença Iatrogênica , Recém-Nascido , Consentimento Livre e Esclarecido/legislação & jurisprudência , Masculino , Nova Zelândia , Osteocondrodisplasias/complicações , Gravidez , Complicações na Gravidez/etiologia
11.
Life Sci ; 255: 117815, 2020 Aug 15.
Artigo em Inglês | MEDLINE | ID: mdl-32442450

RESUMO

AIMS: The aim of this study was to investigate the molecular mechanism underlying preterm white matter injury (WMI) via the identification and functional analysis of differentially expressed long non-coding RNAs (lncRNAs) and mRNAs. MAIN METHODS: A neonatal rat model of preterm WMI was established by ligating the common carotid artery and hypoxia induction. RNA sequencing was performed to analyze gene expression profiles of brain samples. Gene Ontology (GO) and Kyoto Encyclopedia of Genes (KEGG) analyses were performed to evaluate functions of target mRNAs. A co-expression network was generated to explore regulatory mechanisms. KEY FINDINGS: In total, 210 lncRNAs and 619 mRNAs were differentially expressed between the preterm WMI group and the sham group. Based on GO and KEGG analyses, enriched pathways included the apoptotic signaling pathway, vascular endothelial growth factor (VEGF) signaling pathway, natural killer cell-mediated cytotoxicity pathway, and the autophagy pathway. SIGNIFICANCE: Differentially expressed lncRNAs and mRNAs in the brain tissues of preterm WMI model were identified, and the biological processes were closely associated with the development of preterm WMI, thus being considered potential targets for future studies.


Assuntos
Lesões Encefálicas/patologia , RNA Longo não Codificante/genética , RNA Mensageiro/genética , Substância Branca/lesões , Animais , Animais Recém-Nascidos , Apoptose/genética , Lesões Encefálicas/genética , Modelos Animais de Doenças , Nascimento Prematuro/patologia , Ratos , Ratos Sprague-Dawley
12.
Eur J Endocrinol ; 183(1): G9-G15, 2020 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-32380474

RESUMO

COVID-19 has changed the nature of medical consultations, emphasizing virtual patient counseling, with relevance for patients with diabetes insipidus (DI) or hyponatraemia. The main complication of desmopressin treatment in DI is dilutional hyponatraemia. Since plasma sodium monitoring is not always possible in times of COVID-19, we recommend to delay the desmopressin dose once a week until aquaresis occurs allowing excess retained water to be excreted. Patients should measure their body weight daily. Patients with DI admitted to the hospital with COVID-19 have a high risk for mortality due to volume depletion. Specialists must supervise fluid replacement and dosing of desmopressin. Patients after pituitary surgery should drink to thirst and measure their body weight daily to early recognize the development of the postoperative syndrome of inappropriate antidiuresis (SIAD). They should know hyponatraemia symptoms. The prevalence of hyponatraemia in patients with pneumonia due to COVID-19 is not yet known, but seems to be low. In contrast, hypernatraemia may develop in COVID-19 patients in ICU, from different multifactorial reasons, for example, due to insensible water losses from pyrexia, increased respiration rate and use of diuretics. Hypernatraemic dehydration may contribute to the high risk of acute kidney injury in COVID-19. IV fluid replacement should be administered with caution in severe cases of COVID-19 because of the risk of pulmonary oedema.


Assuntos
Antidiuréticos/administração & dosagem , Infecções por Coronavirus/terapia , Desamino Arginina Vasopressina/administração & dosagem , Diabetes Insípido Neurogênico/terapia , Hidratação/métodos , Hipernatremia/terapia , Hiponatremia/terapia , Síndrome de Secreção Inadequada de HAD/terapia , Pneumonia Viral/terapia , Lesões Encefálicas/complicações , Infecções por Coronavirus/complicações , Infecções por Coronavirus/prevenção & controle , Infecções por Coronavirus/transmissão , Desidratação/terapia , Diabetes Insípido/complicações , Diabetes Insípido/terapia , Diabetes Insípido Neurogênico/complicações , Gerenciamento Clínico , Humanos , Hiponatremia/etiologia , Hiponatremia/prevenção & controle , Soluções Hipotônicas/uso terapêutico , Procedimentos Neurocirúrgicos , Pandemias/prevenção & controle , Pneumonia Viral/complicações , Pneumonia Viral/prevenção & controle , Pneumonia Viral/transmissão , Complicações Pós-Operatórias/terapia , Guias de Prática Clínica como Assunto , Solução Salina/uso terapêutico , Choque/etiologia , Choque/terapia
13.
Zhen Ci Yan Jiu ; 45(5): 402-6, 2020 May 25.
Artigo em Chinês | MEDLINE | ID: mdl-32447856

RESUMO

OBJECTIVE: To investigate the clinical effect of electroacupuncture at Baihui (GV20) and Shuigou (GV26) points in the treatment of brain injury in patients with sepsis-associated encephalopathy(SAE). METHODS: A total of 70 patients with SAE were randomly divided into control group and treatment group, with 35 patients in each group. The patients in the control group were given routine western medicine treatment, including anti-infective therapy, nerve nutrition, and mechanical ventilation, and those in the treatment group were given electroacupuncture at GV20 and GV26 in addition to the treatment in the control group. The course of treatment was 1 week for both groups. Serum levels of C-reactive protein (CRP), interleukin-6 (IL-6), and neuron-specific enolase (NSE) were measured for both groups, the Montreal Cognitive Assessment (MoCA) scale was used to assess the change in cognitive function, and Glasgow Coma Scale (GCS) score was determined before and after treatment and was used to evaluate treatment outcome after treatment. RESULTS: Both groups had significant reductions in the serum levels of CRP, IL-6, and NSE after 24 h and one week of treatment (P<0.05), and compared with the control group, the treatment group had significant reductions in the levels of CRP, IL-6 and NSE after treatment (P<0.05). The treatment group had significant increases in the total score of MoCA and the scores of all dimensions except attention after one week of treatment (P<0.05), and the treatment group had significantly higher scores than the control group after treatment (P<0.05). Both groups had a significant increase in GCS score after one week of treatment (P<0.05), and the treatment group had a significantly higher GCS score than the control group after treatment (P<0.05). The treatment group had a significantly higher total effective rate than the control group ï¼»88.6% (31/35) vs 57.1% (20/35), P<0.05ï¼½. CONCLUSION: Electroacupuncture at GV20 and GV26 can effectively improve brain injury and effective rate in SAE patients.


Assuntos
Lesões Encefálicas , Eletroacupuntura , Encefalopatia Associada a Sepse , Lesões Encefálicas/terapia , Proteína C-Reativa , Humanos , Fosfopiruvato Hidratase
14.
Rev Med Suisse ; 16(692): 890-893, 2020 May 06.
Artigo em Francês | MEDLINE | ID: mdl-32374531

RESUMO

After a brain lesion, emotional and behavioral disorders affect the quality of life of the patients and their relatives. This article aims to give some cues to manage three problems chosen for their high frequency: apathy, aggression and depression. It will be reviewed how to recognize, to evaluate and to treat them.


Assuntos
Lesões Encefálicas/fisiopatologia , Lesões Encefálicas/psicologia , Encéfalo/fisiopatologia , Emoções , Agressão/psicologia , Apatia , Lesões Encefálicas/terapia , Depressão/complicações , Depressão/terapia , Humanos , Qualidade de Vida
15.
Rev Med Suisse ; 16(692): 894-897, 2020 May 06.
Artigo em Francês | MEDLINE | ID: mdl-32374532

RESUMO

Deficits of episodic memory and subjective memory complaints are common in adults with acquired brain injury. These impairments are likely to have a negative impact on daily activities and vocational integration. Neuropsychological assessments examine their degree of severity, the nature of the impaired processes and the presence of other, associated cognitive or affective symptoms. Cognitive rehabilitation mainly aims at reducing the impact of persisting memory difficulties on everyday life using compensation strategies. Cognitive rehabilitation studies have improved their quality in the last decade, as indicated by the increased number of randomized controlled trials and demonstrated the efficacy of some therapeutic interventions on various variables.


Assuntos
Lesões Encefálicas/diagnóstico , Lesões Encefálicas/reabilitação , Cognição , Transtornos da Memória/diagnóstico , Transtornos da Memória/reabilitação , Memória Episódica , Lesões Encefálicas/psicologia , Humanos , Transtornos da Memória/psicologia , Testes Neuropsicológicos , Ensaios Clínicos Controlados Aleatórios como Assunto
16.
Rev Med Suisse ; 16(692): 901-903, 2020 May 06.
Artigo em Francês | MEDLINE | ID: mdl-32374533

RESUMO

Patients with acquired brain injury often suffer from pathological fatigue that differs from "normal" fatigue in that it appears more quickly and during non-demanding tasks, and recovery is not complete despite rest. It limits physical and cognitive activities, interferes with rehabilitation and return to work. The underlying mechanisms are poorly understood but appear to involve dysfunction of brain interactions. Current management combining physical reconditioning, cognitive compensatory strategies, and treatment of associated factors often leads to significant clinical improvement and promotes socio-professional reintegration. However, the effect remains insufficient in some patients, which underlines the importance of developing new therapeutic approaches based on a better understanding of the underlying neuronal deficits.


Assuntos
Lesões Encefálicas/fisiopatologia , Lesões Encefálicas/reabilitação , Encéfalo/fisiopatologia , Fadiga/complicações , Fadiga/fisiopatologia , Lesões Encefálicas/complicações , Lesões Encefálicas/psicologia , Cognição , Humanos , Descanso
17.
Rev Med Suisse ; 16(692): 907-910, 2020 May 06.
Artigo em Francês | MEDLINE | ID: mdl-32374535

RESUMO

Bladder function is controlled by the autonomic and somatic nervous system in the spinal cord. It is coordinated in the brainstem. Different areas of the brain are involved in the voluntary control of this reflex functioning. Brain lesions often cause an overactive bladder syndrome with increased voiding frequency and urgency. Urinary incontinence, frequently present, may be linked to overactive bladder and associated motor and cognitive disorders. Urinary retention occurs in the acute phase of a hemispherical lesion and following brainstem lesions. The identification, evaluation and treatment of urinary disorders in brain-damaged patients require a global assessment and integrated management taking the other neurological consequences of brain damage into account.


Assuntos
Lesões Encefálicas/complicações , Bexiga Urinária Hiperativa/complicações , Incontinência Urinária/complicações , Lesões Encefálicas/fisiopatologia , Humanos , Reflexo , Bexiga Urinária Hiperativa/fisiopatologia , Incontinência Urinária/fisiopatologia
18.
PLoS Comput Biol ; 16(4): e1007615, 2020 04.
Artigo em Inglês | MEDLINE | ID: mdl-32310962

RESUMO

Sequential sampling models such as the drift diffusion model (DDM) have a long tradition in research on perceptual decision-making, but mounting evidence suggests that these models can account for response time (RT) distributions that arise during reinforcement learning and value-based decision-making. Building on this previous work, we implemented the DDM as the choice rule in inter-temporal choice (temporal discounting) and risky choice (probability discounting) using hierarchical Bayesian parameter estimation. We validated our approach in data from nine patients with focal lesions to the ventromedial prefrontal cortex / medial orbitofrontal cortex (vmPFC/mOFC) and nineteen age- and education-matched controls. Model comparison revealed that, for both tasks, the data were best accounted for by a variant of the drift diffusion model including a non-linear mapping from value-differences to trial-wise drift rates. Posterior predictive checks confirmed that this model provided a superior account of the relationship between value and RT. We then applied this modeling framework and 1) reproduced our previous results regarding temporal discounting in vmPFC/mOFC patients and 2) showed in a previously unpublished data set on risky choice that vmPFC/mOFC patients exhibit increased risk-taking relative to controls. Analyses of DDM parameters revealed that patients showed substantially increased non-decision times and reduced response caution during risky choice. In contrast, vmPFC/mOFC damage abolished neither scaling nor asymptote of the drift rate. Relatively intact value processing was also confirmed using DDM mixture models, which revealed that in both groups >98% of trials were better accounted for by a DDM with value modulation than by a null model without value modulation. Our results highlight that novel insights can be gained from applying sequential sampling models in studies of inter-temporal and risky decision-making in cognitive neuroscience.


Assuntos
Lesões Encefálicas/fisiopatologia , Córtex Pré-Frontal/lesões , Córtex Pré-Frontal/fisiologia , Algoritmos , Teorema de Bayes , Estudos de Casos e Controles , Comportamento de Escolha/fisiologia , Simulação por Computador , Tomada de Decisões/fisiologia , Humanos , Cadeias de Markov , Dinâmica não Linear , Probabilidade , Tempo de Reação , Reforço Psicológico , Recompensa , Fatores de Tempo
19.
Proc Natl Acad Sci U S A ; 117(15): 8616-8623, 2020 04 14.
Artigo em Inglês | MEDLINE | ID: mdl-32229571

RESUMO

In the adult brain, vascular endothelial growth factor D (VEGFD) is required for structural integrity of dendrites and cognitive abilities. Alterations of dendritic architectures are hallmarks of many neurologic disorders, including stroke-induced damage caused by toxic extrasynaptic NMDA receptor (eNMDAR) signaling. Here we show that stimulation of eNMDARs causes a rapid shutoff of VEGFD expression, leading to a dramatic loss of dendritic structures. Using the mouse middle cerebral artery occlusion (MCAO) stroke model, we have established the therapeutic potential of recombinant mouse VEGFD delivered intraventricularly to preserve dendritic architecture, reduce stroke-induced brain damage, and facilitate functional recovery. An easy-to-use therapeutic intervention for stroke was developed that uses a new class of VEGFD-derived peptide mimetics and postinjury nose-to-brain delivery.


Assuntos
Lesões Encefálicas/prevenção & controle , Dendritos/fisiologia , Modelos Animais de Doenças , Mucosa Nasal/metabolismo , Fragmentos de Peptídeos/administração & dosagem , Acidente Vascular Cerebral/complicações , Fator D de Crescimento do Endotélio Vascular/administração & dosagem , Administração Intranasal , Animais , Lesões Encefálicas/etiologia , Lesões Encefálicas/patologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Recuperação de Função Fisiológica
20.
Phys Ther ; 100(5): 747-756, 2020 05 18.
Artigo em Inglês | MEDLINE | ID: mdl-32339243

RESUMO

Beth E. Fisher, PT, PhD, FAPTA, is a physical therapist, educator, and scholar whose clinical career has been shaped by numerous observations and experiences of patients' remarkable potential to recover ideal movement capability. Currently, Dr Fisher is a Professor of Clinical Physical Therapy in the Division of Biokinesiology and Physical Therapy at the University of Southern California. She is Director of the Neuroplasticity and Imaging Laboratory, primarily using transcranial magnetic stimulation to investigate brain-behavior relationships during motor skill learning and motor control in both individuals without disabilities and individuals with neurologic disorders. Dr Fisher previously worked at Rancho Los Amigos Medical Center on the Adult Neurology and Brain Injury Services. During her years as a clinician and rehabilitation specialist, it was her greatest ambition to be a part of developing physical therapist interventions that would maximize neural and behavioral recovery in individuals with pathological conditions affecting the nervous system. Toward this goal, she has continued to consult and teach nationally and internationally on current concepts for the treatment of adults with neurological disorders. It has been her consistent clinical observation not only that patients are limited by impairments that result from their injury, but that movement abnormalities are in part the result of a patient's automatic, implicit tendency to "respond" to those impairments via compensation.


Assuntos
Lesões Encefálicas/reabilitação , Movimento/fisiologia , Doenças do Sistema Nervoso/reabilitação , Plasticidade Neuronal/fisiologia , Fisioterapeutas/tendências , Encéfalo/fisiopatologia , Humanos
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