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[PMID]:28641105
[Au] Autor:Giza CC; Prins ML; Hovda DA
[Ad] Endereço:UCLA Brain Injury Research Center, UCLA Steve Tisch BrainSPORT Program, Department of Neurosurgery, David Geffen School of Medicine, Los Angeles, CA 90095, USA; Division of Pediatric Neurology, Department of Pediatrics, UCLA Mattel Children's Hospital, Los Angeles, CA 90095, USA; Interdepartmental Program for Neuroscience, UCLA, Los Angeles, CA 90095, USA; Interdepartmental Program for Biomedical Engineering, UCLA, Los Angeles, CA 90095, USA. Electronic address: cgiza@mednet.ucla.edu.
[Ti] Título:It's Not All Fun and Games: Sports, Concussions, and Neuroscience.
[So] Source:Neuron;94(6):1051-1055, 2017 Jun 21.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Few items grab the public's attention like sports, from extremes of great victory to injury and defeat. No injury currently arouses stronger interest than concussion. Giza et al., discuss how neuroscience can provide balance between physical activity and TBI, and guide thoughtful discourse and policy.
[Mh] Termos MeSH primário: Traumatismos em Atletas/fisiopatologia
Concussão Encefálica/fisiopatologia
Lesões Encefálicas/fisiopatologia
Lesão Encefálica Crônica/fisiopatologia
[Mh] Termos MeSH secundário: Traumatismos em Atletas/metabolismo
Concussão Encefálica/metabolismo
Lesões Encefálicas/metabolismo
Lesões Encefálicas Traumáticas/metabolismo
Lesões Encefálicas Traumáticas/fisiopatologia
Lesão Encefálica Crônica/metabolismo
Encefalopatia Traumática Crônica/metabolismo
Encefalopatia Traumática Crônica/fisiopatologia
Seres Humanos
Neurociências
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE


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[PMID]:28121021
[Au] Autor:Mitchell C; Bowen A; Tyson S; Butterfint Z; Conroy P
[Ad] Endereço:Division of Neuroscience and Experimental Psychology, University of Manchester MAHSC, Ellen Wilkinson Building, Manchester, UK.
[Ti] Título:Interventions for dysarthria due to stroke and other adult-acquired, non-progressive brain injury.
[So] Source:Cochrane Database Syst Rev;1:CD002088, 2017 01 25.
[Is] ISSN:1469-493X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Dysarthria is an acquired speech disorder following neurological injury that reduces intelligibility of speech due to weak, imprecise, slow and/or unco-ordinated muscle control. The impact of dysarthria goes beyond communication and affects psychosocial functioning. This is an update of a review previously published in 2005. The scope has been broadened to include additional interventions, and the title amended accordingly. OBJECTIVES: To assess the effects of interventions to improve dysarthric speech following stroke and other non-progressive adult-acquired brain injury such as trauma, infection, tumour and surgery. SEARCH METHODS: We searched the Cochrane Stroke Group Trials Register (May 2016), CENTRAL (Cochrane Library 2016, Issue 4), MEDLINE, Embase, and CINAHL on 6 May 2016. We also searched Linguistics and Language Behavioral Abstracts (LLBA) (1976 to November 2016) and PsycINFO (1800 to September 2016). To identify further published, unpublished and ongoing trials, we searched major trials registers: WHO ICTRP, the ISRCTN registry, and ClinicalTrials.gov. We also handsearched the reference lists of relevant articles and contacted academic institutions and other researchers regarding other published, unpublished or ongoing trials. We did not impose any language restrictions. SELECTION CRITERIA: We selected randomised controlled trials (RCTs) comparing dysarthria interventions with 1) no intervention, 2) another intervention for dysarthria (this intervention may differ in methodology, timing of delivery, duration, frequency or theory), or 3) an attention control. DATA COLLECTION AND ANALYSIS: Three review authors selected trials for inclusion, extracted data, and assessed risk of bias. We attempted to contact study authors for clarification and missing data as required. We calculated standardised mean difference (SMD) and 95% confidence interval (CI), using a random-effects model, and performed sensitivity analyses to assess the influence of methodological quality. We planned to conduct subgroup analyses for underlying clinical conditions. MAIN RESULTS: We included five small trials that randomised a total of 234 participants. Two studies were assessed as low risk of bias; none of the included studies were adequately powered. Two studies used an attention control and three studies compared to an alternative intervention, which in all cases was one intervention versus usual care intervention. The searches we carried out did not find any trials comparing an intervention with no intervention. The searches did not find any trials of an intervention that compared variations in timing, dose, or intensity of treatment using the same intervention. Four studies included only people with stroke; one included mostly people with stroke, but also those with brain injury. Three studies delivered interventions in the first few months after stroke; two recruited people with chronic dysarthria. Three studies evaluated behavioural interventions, one investigated acupuncture and another transcranial magnetic stimulation. One study included people with dysarthria within a broader trial of people with impaired communication.Our primary analysis of a persisting (three to nine months post-intervention) effect at the activity level of measurement found no evidence in favour of dysarthria intervention compared with any control (SMD 0.18, 95% CI -0.18 to 0.55; 3 trials, 116 participants, GRADE: low quality, I² = 0%). Findings from sensitivity analysis of studies at low risk of bias were similar, with a slightly wider confidence interval and low heterogeneity (SMD 0.21, 95% CI -0.30 to 0.73, I² = 32%; 2 trials, 92 participants, GRADE: low quality). Subgroup analysis results for stroke were similar to the primary analysis because few non-stroke participants had been recruited to trials (SMD 0.16, 95% CI -0.23 to 0.54, I² = 0%; 3 trials, 106 participants, GRADE: low quality).Similar results emerged from most of the secondary analyses. There was no evidence of a persisting effect at the impairment (SMD 0.07, 95% CI -0.91 to 1.06, I² = 70%; 2 trials, 56 participants, GRADE: very low quality) or participation level (SMD -0.11, 95% CI -0.56 to 0.33, I² = 0%; 2 trials, 79 participants, GRADE: low quality) but substantial heterogeneity on the former. Analyses of immediate post-intervention outcomes provided no evidence of any short-term benefit on activity (SMD 0.29, 95% CI -0.07 to 0.66, I² = 0%; 3 trials, 117 participants, GRADE: very low quality); or participation (SMD -0.24, 95% CI -0.94 to 0.45; 1 study, 32 participants) levels of measurement.There was a statistically significant effect favouring intervention at the immediate, impairment level of measurement (SMD 0.47, 95% CI 0.02 to 0.92, P = 0.04, I² = 0%; 4 trials, 99 participants, GRADE: very low quality) but only one of these four trials had a low risk of bias. AUTHORS' CONCLUSIONS: We found no definitive, adequately powered RCTs of interventions for people with dysarthria. We found limited evidence to suggest there may be an immediate beneficial effect on impairment level measures; more, higher quality research is needed to confirm this finding.Although we evaluated five studies, the benefits and risks of interventions remain unknown and the emerging evidence justifies the need for adequately powered clinical trials into this condition.People with dysarthria after stroke or brain injury should continue to receive rehabilitation according to clinical guidelines.
[Mh] Termos MeSH primário: Lesão Encefálica Crônica/complicações
Disartria/terapia
Terapia da Linguagem
Fonoterapia
Acidente Vascular Cerebral/complicações
[Mh] Termos MeSH secundário: Adulto
Idoso
Disartria/etiologia
Seres Humanos
Meia-Idade
Ensaios Clínicos Controlados Aleatórios como Assunto
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170126
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD002088.pub3


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[PMID]:28001756
[Au] Autor:Naeser MA; Martin PI; Ho MD; Krengel MH; Bogdanova Y; Knight JA; Yee MK; Zafonte R; Frazier J; Hamblin MR; Koo BB
[Ad] Endereço:1 VA Boston Healthcare System (12-A) , Boston, Massachusetts.
[Ti] Título:Transcranial, Red/Near-Infrared Light-Emitting Diode Therapy to Improve Cognition in Chronic Traumatic Brain Injury.
[So] Source:Photomed Laser Surg;34(12):610-626, 2016 Dec.
[Is] ISSN:1557-8550
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: We review the general topic of traumatic brain injury (TBI) and our research utilizing transcranial photobiomodulation (tPBM) to improve cognition in chronic TBI using red/near-infrared (NIR) light-emitting diodes (LEDs) to deliver light to the head. tPBM improves mitochondrial function increasing oxygen consumption, production of adenosine triphosphate (ATP), and improving cellular energy stores. Nitric oxide is released from the cells increasing regional blood flow in the brain. Review of published studies: In our previously published study, 11 chronic TBI patients with closed-head TBI caused by different accidents (motor vehicle accident, sports-related, improvised explosive device blast injury) and exhibiting long-lasting cognitive dysfunction received 18 outpatient treatments (Monday, Wednesday, Friday for 6 weeks) starting at 10 months to 8 years post-TBI. LED therapy is nonthermal, painless, and noninvasive. An LED-based device classified as nonsignificant risk (FDA cleared) was used. Each LED cluster head (5.35 cm diameter, 500 mW, 22.2 mW/cm ) was applied for 9 min 45 sec (13 J/cm ) using 11 locations on the scalp: midline from front-to-back hairline and bilaterally on frontal, parietal, and temporal areas. Testing was performed before and after transcranial LED (tLED; at 1 week, 1 month, and at 2 months after the 18th treatment) and showed significant improvements in executive function and verbal memory. There were also fewer post-traumatic stress disorder (PTSD) symptoms reported. Ongoing studies: Ongoing, current studies involve TBI patients who have been treated with tLED using either 26 J/cm per LED location on the head or treated with intranasal only (iLED) using red (633 nm) and NIR (810 nm) diodes placed into the nostrils. The NIR iLED is hypothesized to deliver photons to the hippocampus, and the red 633 nm iLED is believed to increase melatonin. Results have been similar to the previously published tLED study. Actigraphy sleep data showed increased time asleep (on average one additional hour per night) after the 18th tLED or iLED treatment. LED treatments may be performed in the home. Sham-controlled studies with veterans who have cognitive dysfunction from Gulf War Illness, blast TBI, and TBI/PTSD are currently ongoing.
[Mh] Termos MeSH primário: Lesões Encefálicas Traumáticas/terapia
Lesão Encefálica Crônica/radioterapia
Transtornos Cognitivos/terapia
Terapia com Luz de Baixa Intensidade
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161222
[St] Status:MEDLINE
[do] DOI:10.1089/pho.2015.4037


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[PMID]:27951605
[Au] Autor:Müller T
[Ti] Título:[The Brain-Injured Relationship: Neuropsychological Rehabilitation Counselling and Therapy of Couples and Families].
[Ti] Título:Die hirnverletzte Beziehung ­ Neurorehabilitationspsychologische Beratung und Therapie von Paaren und Familien..
[So] Source:Fortschr Neurol Psychiatr;84(12):739-747, 2016 Dec.
[Is] ISSN:1439-3522
[Cp] País de publicação:Germany
[La] Idioma:ger
[Ab] Resumo:A brain-injured patient's system of relationships is severely disbalanced, and seeks a new equilibrium very much like a kinetic mobile sculpture responding to an impulse. Thus, it is not only the deficits in the patients and their environment and resources that define the success of participation in the process of rehabilitation. Fundamentally, it relies on stable and adjustable relationships as well as trustful communication in the patients' social systems. Negotiating participation is a concerted, interactive adjustment process for everyone involved in dealing with a disruptive life event. Dysfunction in relationships and communication, which frequently is a direct or indirect consequence of brain injuries, puts at risk the sustainability of progress reached during rehabilitation. In this system of relationships often heavily burdened, neuropsychological rehabilitation counseling is needed to secure the long-term success of rehabilitation.
[Mh] Termos MeSH primário: Lesões Encefálicas/psicologia
Lesões Encefálicas/reabilitação
Lesão Encefálica Crônica/psicologia
Lesão Encefálica Crônica/reabilitação
Aconselhamento
Terapia de Casal
Relações Familiares
Terapia Familiar
Casamento
[Mh] Termos MeSH secundário: Adaptação Psicológica
Comunicação
Mecanismos de Defesa
Avaliação da Deficiência
Pesar
Seres Humanos
Qualidade de Vida/psicologia
Apoio Social
Teoria de Sistemas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161213
[St] Status:MEDLINE


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[PMID]:27725141
[Au] Autor:Riley ET
[Ad] Endereço:Department of Anesthesiology, Preoperative, and Pain Medicine, Stanford University School of Medicine, Stanford, California, USA. Electronic address: edriley@stanford.edu.
[Ti] Título:Chronic Traumatic Encephalopathy and Professional Athletes: Suicides are Contagious.
[So] Source:World Neurosurg;94:576-577, 2016 10.
[Is] ISSN:1878-8769
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Atletas
Encefalopatia Traumática Crônica
[Mh] Termos MeSH secundário: Lesão Encefálica Crônica
Seres Humanos
Suicídio
[Pt] Tipo de publicação:LETTER; COMMENT
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161012
[St] Status:MEDLINE


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[PMID]:27395469
[Au] Autor:Takahata K; Tabuchi H; Mimura M
[Ad] Endereço:Department of Functional Brain Imaging Research, Clinical Research Cluster, National Institute of Radiological Sciences.
[Ti] Título:[Late-onset Neurodegenerative Diseases Following Traumatic Brain Injury: Chronic Traumatic Encephalopathy (CTE) and Alzheimer's Disease Secondary to TBI (AD-TBI)].
[So] Source:Brain Nerve;68(7):849-57, 2016 Jul.
[Is] ISSN:1881-6096
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease, which is associated with mild repetitive traumatic brain injury (TBI). This long-term and progressive symptom due to TBI was initially called punch-drunk syndrome or dementia pugilistica, since it was believed to be associated with boxing. However, serial neuropathological studies of mild repetitive TBI in the last decade have revealed that CTE occurs not only in boxers but also in a wider population including American football players, wrestlers, and military personnel. CTE has gained large public interest owing to dramatic cases involving retired professional athletes wherein serious behavioral problems and tragic incidents were reported. Unlike mild repetitive TBI, a single episode of severe TBI can cause another type of late-onset neuropsychiatric disease including Alzheimer's disease (AD). Several epidemiological studies have shown that a single episode of severe TBI is one of the major risk factors of AD. Pathologically, both AD and CTE are characterized by abnormal accumulations of hyperphosphorylated tau proteins. However, recent neuropathological studies revealed that CTE demonstrates a unique pattern of tau pathology in neurons and astrocytes, and accumulation of other misfolded proteins such as TDP-43. Currently, no reliable biomarkers of late-onset neurodegenerative diseases following TBI are available, and a definitive diagnosis can be made only via postmortem neuropathological examination. Development in neuroimaging techniques such as tau and amyloid positron emission tomography imaging might not only enable early diagnosis of CTE, but also contribute to the interventions for prevention of late-onset neurodegenerative diseases following TBI. Further studies are necessary to elucidate the mechanisms of neurodegeneration in the living brain of patients with TBI.
[Mh] Termos MeSH primário: Doença de Alzheimer/etiologia
Lesões Encefálicas Traumáticas/etiologia
Lesão Encefálica Crônica/complicações
[Mh] Termos MeSH secundário: Idade de Início
Boxe
Intervenção Médica Precoce
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[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:160711
[St] Status:MEDLINE
[do] DOI:10.11477/mf.1416200517


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[PMID]:27333673
[Au] Autor:Gregory S
[Ti] Título:ADMITTED. The NFL A link between football and brain trauma.
[So] Source:Time;187(11):18, 2016 Mar 28.
[Is] ISSN:0040-781X
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Concussão Encefálica/complicações
Lesão Encefálica Crônica/etiologia
Futebol Americano/lesões
Revelação da Verdade
[Mh] Termos MeSH secundário: Seres Humanos
Sociedades
Estados Unidos
[Pt] Tipo de publicação:NEWS
[Em] Mês de entrada:1609
[Cu] Atualização por classe:160623
[Lr] Data última revisão:
160623
[Sb] Subgrupo de revista:K
[Da] Data de entrada para processamento:160624
[St] Status:MEDLINE


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[PMID]:27245243
[Au] Autor:Doherty CP; O'Keefe E; Wallace E; Loftus T; Keaney J; Kealy J; Humphries MM; Molloy MG; Meaney JF; Farrell M; Campbell M
[Ad] Endereço:From the Department of Neurology, Health Care Centre, Hospital 5, St James's Hospital, Dublin, Ireland (CPD, EW); Smurfit Institute of Genetics, Trinity College Dublin, University of Dublin, Dublin, Ireland (EO, JK, JoK, MMH, MC); Department of Neuropathology, Beaumont Hospital, Dublin, Ireland (TL,
[Ti] Título:Blood-Brain Barrier Dysfunction as a Hallmark Pathology in Chronic Traumatic Encephalopathy.
[So] Source:J Neuropathol Exp Neurol;75(7):656-62, 2016 Jul.
[Is] ISSN:1554-6578
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Chronic traumatic encephalopathy (CTE) is a neurodegenerative condition associated with repetitive mild traumatic brain injury. In recent years, attention has focused on emerging evidence linking the development of CTE to concussive injuries in athletes and military personnel; however, the underlying molecular pathobiology of CTE remains unclear. Here, we provide evidence that the blood-brain barrier (BBB) is disrupted in regions of dense perivascular p-Tau accumulation in a case of CTE. Immunoreactivity patterns of the BBB-associated tight junction components claudin-5 and zonula occludens-1 were markedly discontinuous or absent in regions of perivascular p-Tau deposition; there was also immunohistochemical evidence of a BBB in these foci. Because the patient was diagnosed premortem clinically as having progressive supranuclear palsy (PSP), we also compromised that the CTE alterations appear to be distinct from those in the brain of a patient with PSP. This report represents the first description of BBB dysfunction in a pathologically proven CTE case and suggests a vascular component in the postconcussion cascade of events that may ultimately lead to development of a progressive degenerative disorder. BBB dysfunction may represent a correlate of neural dysfunction in live subjects suspected of being at risk for development of CTE.
[Mh] Termos MeSH primário: Barreira Hematoencefálica/diagnóstico por imagem
Lesão Encefálica Crônica/diagnóstico por imagem
Encefalopatia Traumática Crônica/diagnóstico por imagem
[Mh] Termos MeSH secundário: Barreira Hematoencefálica/metabolismo
Lesão Encefálica Crônica/complicações
Lesão Encefálica Crônica/metabolismo
Encefalopatia Traumática Crônica/etiologia
Encefalopatia Traumática Crônica/metabolismo
Evolução Fatal
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160602
[St] Status:MEDLINE
[do] DOI:10.1093/jnen/nlw036


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[PMID]:27209674
[Au] Autor:Kerins C
[Ti] Título:CTE - Learning what we don't know.
[So] Source:J Med Assoc Ga;105(1):16-7, 2016.
[Is] ISSN:0025-7028
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Lesão Encefálica Crônica
Medicina Esportiva/tendências
[Mh] Termos MeSH secundário: Boxe/lesões
Futebol Americano/lesões
Seres Humanos
[Pt] Tipo de publicação:EDITORIAL
[Em] Mês de entrada:1606
[Cu] Atualização por classe:160523
[Lr] Data última revisão:
160523
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160524
[St] Status:MEDLINE


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[PMID]:27199397
[Au] Autor:Underwood E
[Ti] Título:NEUROSCIENCE. Can brain scans reveal concussion-linked disease?
[So] Source:Science;352(6288):881, 2016 May 20.
[Is] ISSN:1095-9203
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Concussão Encefálica/complicações
Lesão Encefálica Crônica/diagnóstico
Lesão Encefálica Crônica/etiologia
Neuroimagem/métodos
Tomografia por Emissão de Pósitrons/métodos
Proteínas tau/análise
[Mh] Termos MeSH secundário: Adulto
Carbolinas/farmacocinética
Seres Humanos
[Pt] Tipo de publicação:NEWS
[Nm] Nome de substância:
0 (7-(6-fluoropyridin-3-yl)-5H-pyrido(4,3-b)indole); 0 (Carbolines); 0 (tau Proteins)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:160520
[Lr] Data última revisão:
160520
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160521
[St] Status:MEDLINE
[do] DOI:10.1126/science.352.6288.881



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