Base de dados : MEDLINE
Pesquisa : C10.228.140.199.388 [Categoria DeCS]
Referências encontradas : 6 [refinar]
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  1 / 6 MEDLINE  
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[PMID]:28801041
[Au] Autor:Kokkoz Ç; Irik M; Dayangaç HI; Hayran M; Bilge A; Çavus M
[Ad] Endereço:Department of Emergency Medicine, Izmir Cigli State Education Hospital, Turkey. Electronic address: cagrikokkoz@gmail.com.
[Ti] Título:Diagnosis of delayed diffuse axonal Injury.
[So] Source:Am J Emerg Med;35(11):1788.e5-1788.e6, 2017 Nov.
[Is] ISSN:1532-8171
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Diffuse axonal injury is usually caused by head trauma, and patients have significant clinical symptoms during admission to the emergency department. In our case, we present a five-year-old patient who was involved in a car accident. During admission to the emergency department, the patient had no symptoms of trauma. However, 6 h after admission to emergency service, neurological symptoms occurred, and mental status changed. Diffuse axonal injury (DAI) is characterized by diffuse nerve axon injury in the brain and brainstem. This is one of the worst results of a head trauma and occurs in one-third of the patients admitted to the hospital with head trauma. In some studies, it has been reported that diffuse axonal injury is permanent in accelerated and decelerated head traumas without accompanying loss of consciousness. Neurological sequels have occurred in the recovery phase of some patients with diffuse axonal damage. In this study, we present a delayed diffuse axonal injury case accompanying a head trauma.
[Mh] Termos MeSH primário: Acidentes de Trânsito
Lesões Encefálicas Difusas/diagnóstico por imagem
[Mh] Termos MeSH secundário: Lesões Encefálicas Difusas/fisiopatologia
Pré-Escolar
Eletroencefalografia
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Fatores de Tempo
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170813
[St] Status:MEDLINE


  2 / 6 MEDLINE  
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[PMID]:27165893
[Au] Autor:Park S; Czosnyka M; Smielewski P
[Ad] Endereço:Division of Neurosurgery, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK. sp3291@cumc.columbia.edu.
[Ti] Título:Brain Oxygen Relationship to Cerebral Perfusion Pressure Depends on Tip Location and Time Window: Can Brain O2 Be an Adjunctive Modality for Determining Optimal CPP?
[So] Source:Acta Neurochir Suppl;122:133-5, 2016.
[Is] ISSN:0065-1419
[Cp] País de publicação:Austria
[La] Idioma:eng
[Ab] Resumo:Controversy exists regarding the brain tissue oxygen (PbtO2) monitor's optimal tip location and what it actually measures. Recent work [2] identified a "PbtO2 change point" (CPPbt), below which PbtO2 displays pressure-passive behavior, showing significant correlation with optimal cerebral perfusion pressure (CPPopt) as defined by the pressure reactivity index (PRx). This would further support the concept of CPPopt [1] as an individualized target. We endeavored to validate these findings and further explore the relationship between PbtO2 and suboptimal CPP. CPPopt can be determined 55 % of the time [1]. It is undetermined whether PbtO2 can be an adjunctive modality for determining CPPopt.
[Mh] Termos MeSH primário: Contusão Encefálica/metabolismo
Lesões Encefálicas Difusas/metabolismo
Lesões Encefálicas Traumáticas/metabolismo
Encéfalo/metabolismo
Circulação Cerebrovascular/fisiologia
Oxigênio/metabolismo
[Mh] Termos MeSH secundário: Adulto
Pressão Arterial
Encéfalo/irrigação sanguínea
Contusão Encefálica/diagnóstico por imagem
Lesões Encefálicas Difusas/diagnóstico por imagem
Lesões Encefálicas Traumáticas/diagnóstico por imagem
Lesões Encefálicas Traumáticas/fisiopatologia
Seres Humanos
Pressão Intracraniana
Masculino
Meia-Idade
Monitorização Fisiológica
Tomografia Computadorizada por Raios X
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
S88TT14065 (Oxygen)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160512
[St] Status:MEDLINE
[do] DOI:10.1007/978-3-319-22533-3_27


  3 / 6 MEDLINE  
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[PMID]:26926459
[Au] Autor:Esiri M
[Ti] Título:Obituary for Dr Sabina Strich.
[So] Source:Neuropathol Appl Neurobiol;42(2):210-1, 2016 Feb.
[Is] ISSN:1365-2990
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Neurologia/história
Patologia Clínica/história
[Mh] Termos MeSH secundário: Lesões Encefálicas Difusas/patologia
Inglaterra
História do Século XX
História do Século XXI
Seres Humanos
[Pt] Tipo de publicação:BIOGRAPHY; HISTORICAL ARTICLE; JOURNAL ARTICLE; PORTRAITS
[Ps] Nome de pessoa como assunto:Strich S
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160302
[St] Status:MEDLINE
[do] DOI:10.1111/nan.12287


  4 / 6 MEDLINE  
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[PMID]:26774527
[Au] Autor:Muccigrosso MM; Ford J; Benner B; Moussa D; Burnsides C; Fenn AM; Popovich PG; Lifshitz J; Walker FR; Eiferman DS; Godbout JP
[Ad] Endereço:Department of Neuroscience, The Ohio State University, 333 W. 10th Ave, Columbus, OH, United States.
[Ti] Título:Cognitive deficits develop 1month after diffuse brain injury and are exaggerated by microglia-associated reactivity to peripheral immune challenge.
[So] Source:Brain Behav Immun;54:95-109, 2016 May.
[Is] ISSN:1090-2139
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: Traumatic brain injury (TBI) elicits immediate neuroinflammatory events that contribute to acute cognitive, motor, and affective disturbance. Despite resolution of these acute complications, significant neuropsychiatric and cognitive issues can develop and progress after TBI. We and others have provided novel evidence that these complications are potentiated by repeated injuries, immune challenges and stressors. A key component to this may be increased sensitization or priming of glia after TBI. Therefore, our objectives were to determine the degree to which cognitive deterioration occurred after diffuse TBI (moderate midline fluid percussion injury) and ascertain if glial reactivity induced by an acute immune challenge potentiated cognitive decline 30 days post injury (dpi). In post-recovery assessments, hippocampal-dependent learning and memory recall were normal 7 dpi, but anterograde learning was impaired by 30 dpi. Examination of mRNA and morphological profiles of glia 30 dpi indicated a low but persistent level of inflammation with elevated expression of GFAP and IL-1ß in astrocytes and MHCII and IL-1ß in microglia. Moreover, an acute immune challenge 30 dpi robustly interrupted memory consolidation specifically in TBI mice. These deficits were associated with exaggerated microglia-mediated inflammation with amplified (IL-1ß, CCL2, TNFα) and prolonged (TNFα) cytokine/chemokine expression, and a marked reactive morphological profile of microglia in the CA3 of the hippocampus. Collectively, these data indicate that microglia remain sensitized 30 dpi after moderate TBI and a secondary inflammatory challenge elicits robust microglial reactivity that augments cognitive decline. STATEMENT OF SIGNIFICANCE: Traumatic brain injury (TBI) is a major risk factor in development of neuropsychiatric problems long after injury, negatively affecting quality of life. Mounting evidence indicates that inflammatory processes worsen with time after a brain injury and are likely mediated by glia. Here, we show that primed microglia and astrocytes developed in mice 1 month following moderate diffuse TBI, coinciding with cognitive deficits that were not initially evident after injury. Additionally, TBI-induced glial priming may adversely affect the ability of glia to appropriately respond to immune challenges, which occur regularly across the lifespan. Indeed, we show that an acute immune challenge augmented microglial reactivity and cognitive deficits. This idea may provide new avenues of clinical assessments and treatments following TBI.
[Mh] Termos MeSH primário: Lesões Encefálicas Traumáticas/patologia
Lesões Encefálicas Traumáticas/psicologia
Mediadores da Inflamação/metabolismo
Microglia/patologia
[Mh] Termos MeSH secundário: Animais
Astrócitos/metabolismo
Astrócitos/patologia
Lesões Encefálicas Difusas/imunologia
Lesões Encefálicas Difusas/metabolismo
Lesões Encefálicas Difusas/patologia
Lesões Encefálicas Traumáticas/imunologia
Lesões Encefálicas Traumáticas/metabolismo
Quimiocinas/metabolismo
Cognição/fisiologia
Transtornos Cognitivos/metabolismo
Transtornos Cognitivos/patologia
Citocinas/metabolismo
Modelos Animais de Doenças
Inflamação/metabolismo
Masculino
Memória/fisiologia
Camundongos
Camundongos Endogâmicos BALB C
Microglia/metabolismo
Qualidade de Vida
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chemokines); 0 (Cytokines); 0 (Inflammation Mediators)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170802
[Lr] Data última revisão:
170802
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160118
[St] Status:MEDLINE


  5 / 6 MEDLINE  
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[PMID]:26646974
[Au] Autor:Ziebell JM; Rowe RK; Harrison JL; Eakin KC; Colburn T; Willyerd FA; Lifshitz J
[Ad] Endereço:a BARROW Neurological Institute at Phoenix Children's Hospital , Phoenix , AZ , USA.
[Ti] Título:Experimental diffuse brain injury results in regional alteration of gross vascular morphology independent of neuropathology.
[So] Source:Brain Inj;30(2):217-24, 2016.
[Is] ISSN:1362-301X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:PRIMARY OBJECTIVE: A dynamic relationship exists between diffuse traumatic brain injury and changes to the neurovascular unit. The purpose of this study was to evaluate vascular changes during the first week following diffuse TBI. It was hypothesized that pathology is associated with modification of the vasculature. METHODS: Male Sprague-Dawley rats underwent either midline fluid percussion injury or sham-injury. Brain tissue was collected 1, 2 or 7 days post-injury or sham-injury (n = 3/time point). Tissue was collected and stained by de Olmos amino-cupric silver technique to visualize neuropathology or animals were perfused with AltaBlue casting resin before high-resolution vascular imaging. The average volume, surface area, radius, branching and tortuosity of the vessels were evaluated across three regions of interest. RESULTS: In M2, average vessel volume (p < 0.01) and surface area (p < 0.05) were significantly larger at 1 day relative to 2 days, 7 days and sham. In S1BF and VPM, no significant differences in the average vessel volume or surface area at any of the post-injury time points were observed. No significant changes in average radius, branching or tortuosity were observed. CONCLUSIONS: Preliminary findings suggest gross morphological changes within the vascular network likely represent an acute response to mechanical forces of injury, rather than delayed or chronic pathological processes.
[Mh] Termos MeSH primário: Lesões Encefálicas Difusas/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Encéfalo/patologia
Lesões Encefálicas Difusas/anatomia & histologia
Lesões Encefálicas Difusas/lesões
Modelos Animais de Doenças
Masculino
Neuropatologia
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151210
[St] Status:MEDLINE
[do] DOI:10.3109/02699052.2015.1090012


  6 / 6 MEDLINE  
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[PMID]:26414329
[Au] Autor:Olson E; Badder C; Sullivan S; Smith C; Propert K; Margulies SS
[Ad] Endereço:1 Department of Bioengineering, University of Pennsylvania , Philadelphia, Pennsylvania.
[Ti] Título:Alterations in Daytime and Nighttime Activity in Piglets after Focal and Diffuse Brain Injury.
[So] Source:J Neurotrauma;33(8):734-40, 2016 Apr 15.
[Is] ISSN:1557-9042
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We have developed and implemented a noninvasive, objective neurofunctional assessment for evaluating the sustained effects of traumatic brain injury (TBI) in piglets with both diffuse and focal injury types. Derived from commercial actigraphy methods in humans, this assessment continuously monitors the day/night activity of piglets using close-fitting jackets equipped with tri-axial accelerometers to monitor movements of the thorax. Acceleration metrics were correlated (N = 7 naïve piglets) with video images to define values associated with a range of activities, from recumbancy (rest) to running. Both focal (N = 8) and diffuse brain injury (N = 9) produced alterations in activity that were significant 4 days post-TBI. Compared to shams (N = 6) who acclimated to the animal facility 4 days after an anesthesia experience by blurring the distinction between day and night activity, post-TBI time-matched animals had larger fractions of inactive periods during the daytime than nighttime, and larger fractions of active time in the night were spent in high activity (e.g., constant walking, intermittent running) than during the day. These persistent disturbances in rest and activity are similar to those observed in human adults and children post-TBI, establishing actigraphy as a translational metric, used in both humans and large animals, for assessment of injury severity, progressions, and intervention.
[Mh] Termos MeSH primário: Actigrafia/métodos
Lesões Encefálicas Difusas/fisiopatologia
Ritmo Circadiano/fisiologia
Atividade Motora/fisiologia
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Lesões Encefálicas/fisiopatologia
Feminino
Seres Humanos
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170415
[Lr] Data última revisão:
170415
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150929
[St] Status:MEDLINE
[do] DOI:10.1089/neu.2015.4085



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