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Articoli di riviste sul tema "Brain injury"

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Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 11 marzo 2023

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1

Adelson, P. David. "Pediatric Traumatic Brain Injury : Present and Future Considerations in Management(Traumatic Brain Injury: Recent Advances)". Japanese Journal of Neurosurgery 19, n. 3 (2010): 196–201. http://dx.doi.org/10.7887/jcns.19.196.

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2

Kamalifar, Amir, Firooz Salehpoor, Farhad Mirzaii e Samar Kamalifar. "Stab Brain Injury: A Case Report". Journal of Surgical Case Reports and Images 4, n. 6 (30 agosto 2021): 01–03. http://dx.doi.org/10.31579/2690-1897/086.

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Penetrating foreign object rare cause of brain injury, and have high mortality and morbidity rate among traumatic brain injury, surgery and management of this patient challenged and need high experience health care system, we introduced 29 years old man admitted with stab brain injury to emergency department

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3

Volovitzr, Ilan. "Neuropsychological Assessment of Traumatic Brain Injury". Neuroscience and Neurological Surgery 2, n. 2 (20 aprile 2018): 01–02. http://dx.doi.org/10.31579/2578-8868/028.

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4

van den Pol, Anthony N. "Brain Trauma Enhances Transient Cytomegalovirus Invasion of the Brain Only in Mice That Are Immunodeficient". Journal of Virology 83, n. 1 (22 ottobre 2008): 420–27. http://dx.doi.org/10.1128/jvi.01728-08.

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ABSTRACT Cytomegalovirus (CMV) is one of the most common viral pathogens leading to neurological dysfunction in individuals with depressed immune systems. How CMV enters the brain remains an open question. The hypothesis that brain injury may enhance the entrance of CMV into the brain was tested. Insertion of a sterile needle into the brain caused a dramatic increase in mouse CMV in the brains of immunodeficient SCID mice inoculated peripherally within an hour of injury and examined 1 week later; peripheral inoculation 48 h after injury and a 1-week survival resulted in only a modest infection at the site of injury. In contrast, uninjured SCID mice, as well as injured immunocompetent control mice, showed little sign of viral infection at the same time intervals. Direct inoculation of the brain resulted in widespread dispersal and enhanced replication of mCMV in SCID brains tested 1 week later but not in parallel control brains. Differential viremia was unlikely to account for the greater viral load in the SCID brain, since increased mCMV in the blood of SCID compared to controls was not detected until a longer interval. These data suggest that brain injury enhances CMV invasion of the brain, but only when the adaptive immune system is compromised, and that the brain's ability to resist viral infection recovers rapidly after injury.

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5

Dries, David J. "Brain Injury". Shock 18, n. 1 (luglio 2002): 98. http://dx.doi.org/10.1097/00024382-200207000-00020.

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6

Perna, Robert. "Brain Injury". Journal of Head Trauma Rehabilitation 21, n. 1 (gennaio 2006): 82–84. http://dx.doi.org/10.1097/00001199-200601000-00009.

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7

Garber, James C., e Carl R. Boyd. "Brain injury". Current Surgery 57, n. 2 (marzo 2000): 126–30. http://dx.doi.org/10.1016/s0149-7944(00)00160-4.

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8

Olver, John H. "Brain injury". Current Opinion in Neurology 8, n. 6 (dicembre 1995): 443–46. http://dx.doi.org/10.1097/00019052-199512000-00008.

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9

Soares, Holly, e Tracy K. McIntosh. "Fetal Cortical Transplants in Adult Rats Subjected to Experimental Brain Injury". Journal of Neural Transplantation and Plasticity 2, n. 3-4 (1991): 207–20. http://dx.doi.org/10.1155/np.1991.207.

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Fetal cortical tissue was injected into injured adult rat brains following concussive fluid percussion (FP) brain injury. Rats subjected to moderate FP injury received E16 cortex transplant injections into lesioned motor cortex 2 days, 1 week, 2 weeks, and 4 weeks post injury. Histological assessment of transplant survival and integration was based upon Nissl staining, glial fibrillary acidic protein (GFAP) immunocytochemistry, and staining for acetylcholinesterase. In addition to histological analysis, the ability of the transplants to attenuate neurological motor deficits associated with concussive FP brain injury was also tested. Three subgroups of rats receiving transplant 1 week, 2 weeks, and 4 weeks post injury Were chosen for evaluation of neurological motor function. Fetal cortical tissue injected into the injury site 4 weeks post injury failed to incorporate with injured host brain, did not affect glial scar formation, and exhibited extensive GFAP immunoreactivity. No improvement in neurological motor function was observed in animals receiving transplants 4 weeks post injury. Conversely, transplants injected 2 days, 1 week, or 2 weeks post injury survived, incorporated with host brain, exhibited little GFAP immunoreactivity, and successfully attenuated glial scarring. However, no significant improvement in motor function was observed at the one week or two week time points. The inability of the transplants to attenuate motor function may indicate inappropriate host/transplant interaction. Our results demonstrate that there exists a temporal window in which fetal cortical transplants can attenuate glial scarring as well as be successfully incorporated into host brains following FP injury.

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10

Maria, Dalamagka. "Mild Brain Injury". Journal of Anesthesia and Anesthetic Drugs 2, n. 1 (2 marzo 2022): 1–2. http://dx.doi.org/10.54289/jaad2200103.

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The risk of developing an addiction to alcohol, tobacco, or drugs increases in the period immediately following mild traumatic brain injury (mTBI) but decreases over time, new research shows. The historical prospective study showed that in the short-term, individuals with mTBI had a significantly increased risk for alcohol dependence, nicotine dependence, and nondependent abuse of drugs or alcohol compared with a similarly injured non-mTBI comparison group. "Our findings suggest an increased risk for incidence of alcohol dependence, nondependent abuse of drugs or alcohol, and nicotine dependence during the first 30 days following mild TBI and a risk thereafter for alcohol dependence for at least 6 months after injury," the authors, led by Shannon C. Miller, MD, from the Veterans Affairs Medical Centre, Cincinnati, Ohio, write.

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11

Griffin, Allison D., L. Christine Turtzo, Gunjan Y. Parikh, Alexander Tolpygo, Zachary Lodato, Anita D. Moses, Govind Nair et al. "Traumatic microbleeds suggest vascular injury and predict disability in traumatic brain injury". Brain 142, n. 11 (14 ottobre 2019): 3550–64. http://dx.doi.org/10.1093/brain/awz290.

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Abstract Traumatic microbleeds are small foci of hypointensity seen on T2*-weighted MRI in patients following head trauma that have previously been considered a marker of axonal injury. The linear appearance and location of some traumatic microbleeds suggests a vascular origin. The aims of this study were to: (i) identify and characterize traumatic microbleeds in patients with acute traumatic brain injury; (ii) determine whether appearance of traumatic microbleeds predict clinical outcome; and (iii) describe the pathology underlying traumatic microbleeds in an index patient. Patients presenting to the emergency department following acute head trauma who received a head CT were enrolled within 48 h of injury and received a research MRI. Disability was defined using Glasgow Outcome Scale-Extended ≤6 at follow-up. All magnetic resonance images were interpreted prospectively and were used for subsequent analysis of traumatic microbleeds. Lesions on T2* MRI were stratified based on ‘linear’ streak-like or ‘punctate’ petechial-appearing traumatic microbleeds. The brain of an enrolled subject imaged acutely was procured following death for evaluation of traumatic microbleeds using MRI targeted pathology methods. Of the 439 patients enrolled over 78 months, 31% (134/439) had evidence of punctate and/or linear traumatic microbleeds on MRI. Severity of injury, mechanism of injury, and CT findings were associated with traumatic microbleeds on MRI. The presence of traumatic microbleeds was an independent predictor of disability (P < 0.05; odds ratio = 2.5). No differences were found between patients with punctate versus linear appearing microbleeds. Post-mortem imaging and histology revealed traumatic microbleed co-localization with iron-laden macrophages, predominately seen in perivascular space. Evidence of axonal injury was not observed in co-localized histopathological sections. Traumatic microbleeds were prevalent in the population studied and predictive of worse outcome. The source of traumatic microbleed signal on MRI appeared to be iron-laden macrophages in the perivascular space tracking a network of injured vessels. While axonal injury in association with traumatic microbleeds cannot be excluded, recognizing traumatic microbleeds as a form of traumatic vascular injury may aid in identifying patients who could benefit from new therapies targeting the injured vasculature and secondary injury to parenchyma.

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12

Willinger, R., e C. Deck. "K02200 History and Prospect of Traumatic Brain Injury Research". Proceedings of Mechanical Engineering Congress, Japan 2015 (2015): _K02200–1_—_K02200–8_. http://dx.doi.org/10.1299/jsmemecj.2015._k02200-1_.

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13

Sahoo, Debasis, Caroline Deck e Remy Willinger. "OS7-3 BRAIN INJURY CRITERIA EXPRESSED IN TERMS OF AXONS STRAINS(OS7: Injury Biomechanics I)". Proceedings of the Asian Pacific Conference on Biomechanics : emerging science and technology in biomechanics 2015.8 (2015): 103. http://dx.doi.org/10.1299/jsmeapbio.2015.8.103.

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14

Orita, Tetsuji, Takafumi Nishizaki, Toshifumi Kamiryo, Kunihiko Harada e Hideo Aoki. "Cerebral microvascular architecture following experimental cold injury". Journal of Neurosurgery 68, n. 4 (aprile 1988): 608–12. http://dx.doi.org/10.3171/jns.1988.68.4.0608.

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✓ The sequential changes in microvascular architecture following local cold injury in rat brains were studied post mortem by scanning electron microscopy and the vascular casting method. The findings were compared with the results of immunohistochemical studies of injured endothelial cells using the bromodeoxyuridine (BUdR) and anti-BUdR monoclonal antibody technique. Repair of the microvascular architecture had begun by the 3rd day after injury, with hematogenous cells and reactive astrocytes present in the edematous brain participating in the regenerative process. The normal microvascular architecture was reconstructed starting from the edge of the lesion nearest to the brain surface. On the other hand, in the most severely injured part of the brain surface, newly formed microvascular architecture appeared, resembling that of the developing fetal and newborn rat cortex. Seven days after injury, the entire microvascular architecture in the region of the lesion had been reconstructed.

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15

Pumiglia, Luke, Aaron M. Williams, Michael T. Kemp, Glenn K. Wakam, Hasan B. Alam e Ben E. Biesterveld. "Brain proteomic changes by histone deacetylase inhibition after traumatic brain injury". Trauma Surgery & Acute Care Open 6, n. 1 (marzo 2021): e000682. http://dx.doi.org/10.1136/tsaco-2021-000682.

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BackgroundTraumatic brain injury (TBI) is a leading cause of morbidity and mortality. There are currently no cytoprotective treatments for TBI. There is growing evidence that the histone deacetylase inhibitor valproic acid (VPA) may be beneficial in the treatment of TBI associated with hemorrhagic shock and in isolation. We sought to further evaluate the mechanistic underpinnings of this demonstrated efficacy via proteomic analysis of injured brain tissue.MethodsSwine were subjected to TBI via controlled cortical impact, randomized to treatment with VPA or control and observed for 6 hours. The brains of the pigs were then sectioned, and tissue was prepared and analyzed for proteomic data, including gene ontology (GO), gene-set enrichment analysis and enrichment mapping, and network mapping.ResultsProteomic analysis demonstrated differential expression of hundreds of proteins in injured brain tissue after treatment with VPA. GO analysis and network analyses revealed groups of proteins and processes that are known to modulate injury response after TBI and impact cell fate. Processes affected included protein targeting and transport, cation and G-protein signaling, metabolic response, neurotransmitter response and immune function.DiscussionThis proteomic analysis provides initial mechanistic insight into the observed rescue of injured brain tissue after VPA administration in isolated TBI.Level of evidenceNot applicable (animal study).

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16

Iskandarovich, Iskandarov Alisher, Yakubov Khayot Hamidullaevich e Ismatov Abrorkhon Askarovich. "FORENSIC EVALUATION OF DIFFUSE AXONAL INJURY". American Journal of Medical Sciences and Pharmaceutical Research 04, n. 04 (1 aprile 2022): 16–18. http://dx.doi.org/10.37547/tajmspr/volume04issue04-04.

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Traumatic brain injury is a sudden damage to the bones of the skull and brain by various mechanical agents. Diffuse axonal injury is a type of traumatic brain injury resulting from a closed brain injury. Traumatic brain injury is the leading cause of death and disability worldwide.

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17

Jiang, Ji Y., Bruce G. Lyeth, Guy L. Clifton, Larry W. Jenkins, Robert J. Hamm e Ronald L. Hayes. "Relationship between body and brain temperature in traumatically brain-injured rodents". Journal of Neurosurgery 74, n. 3 (marzo 1991): 492–96. http://dx.doi.org/10.3171/jns.1991.74.3.0492.

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✓ Recent work has shown that mild to moderate levels of hypothermia may profoundly reduce the histological and biochemical sequelae of cerebral ischemic injury. In the present study, the authors examined the effect of fluid-percussion injury on brain temperature in anesthetized rats and the effect of anesthesia on brain temperature in uninjured rats. The relationship between the brain, rectal, and temporalis muscle temperatures during normothermia, hypothermia, and hyperthermia was studied following a moderate magnitude of fluid-percussion brain injury (2.10 to 2.25 atmospheres) in rats. The results showed that mean brain temperature in 10 anesthetized injured rats, in 21 anesthetized uninjured rats, and in 10 unanesthetized uninjured rats was a mean (± standard error of the mean) of 36.04° ± 0.20°C, 36.30° ± 0.08°C, and 37.95° ± 0.09°C, respectively. There was no significant difference in temperature under general anesthesia between injured and uninjured rats (p > 0.05). In the absence of brain injury, mean brain temperature was significantly lower in anesthetized rats than in unanesthetized rats (p < 0.001). In anesthetized brain-injured rats, temporalis muscle temperature correlated well with brain temperature over a 30° to 40°C range, even when brain temperature was rapidly changed during induction of hypothermia or hyperthermia (r = 0.9986, p < 0.0001). In contrast, rectal temperature varied inconsistently from brain temperature. These observations indicated that: 1) brain injury itself does not influence brain temperature in this model; 2) anesthesia alone decreases brain temperature to levels producing cerebral protection in this model; and 3) external monitoring of temporalis muscle temperature can provide a reliable indirect measure of brain temperature in the course of experimental brain injury. The authors believe that it is essential to monitor or control brain temperature in studies of experimental brain injury.

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18

Scafidi, Susanna, Jennifer Jernberg, Gary Fiskum e Mary C. McKenna. "Metabolism of Exogenous [2,4-13C]β-Hydroxybutyrate Following Traumatic Brain Injury in 21-22-Day-Old Rats: An Ex Vivo NMR Study". Metabolites 12, n. 8 (29 luglio 2022): 710. http://dx.doi.org/10.3390/metabo12080710.

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Traumatic brain injury (TBI) is the leading cause of morbidity in young children. Acute dysregulation of oxidative glucose metabolism within the first hours after injury is a hallmark of TBI. The developing brain relies on ketones as well as glucose for energy. Thus, the aim of this study was to determine the metabolism of ketones early after TBI injury in the developing brain. Following the controlled cortical impact injury model of TBI, 21–22-day-old rats were infused with [2,4-13C]β-hydroxybutyrate during the acute (4 h) period after injury. Using ex vivo 13C-NMR spectroscopy, we determined that 13C-β-hydroxybutyrate (13C-BHB) metabolism was increased in both the ipsilateral and contralateral sides of the brain after TBI. Incorporation of the label was significantly higher in glutamate than glutamine, indicating that 13C-BHB metabolism was higher in neurons than astrocytes in both sham and injured brains. Our results show that (i) ketone metabolism was significantly higher in both the ipsilateral and contralateral sides of the injured brain after TBI; (ii) ketones were extensively metabolized by both astrocytes and neurons, albeit higher in neurons; (iii) the pyruvate recycling pathway determined by incorporation of the label from the metabolism of 13C-BHB into lactate was upregulated in the immature brain after TBI.

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19

Savelieff, Masha G., e Eva L. Feldman. "Traumatic Brain Injury". Neurology 96, n. 8 (6 gennaio 2021): 357–58. http://dx.doi.org/10.1212/wnl.0000000000011455.

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20

Kumar, Sailesh, Lisa Story e Mellisa Damodaram. "Perinatal Brain Injury". Current Pediatric Reviews 4, n. 2 (1 maggio 2008): 71–79. http://dx.doi.org/10.2174/157339608784461981.

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21

McNair, Norma D. "TRAUMATIC BRAIN INJURY". Nursing Clinics of North America 34, n. 3 (settembre 1999): 637–59. http://dx.doi.org/10.1016/s0029-6465(22)02411-2.

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Fernoagă, Cristina, e Mihai Cătălin Cereaciuchin. "Traumatic brain injury". Practica Veterinara.ro 2, n. 36 (2022): 22. http://dx.doi.org/10.26416/pv.36.2.2022.6432.

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23

Nelasari, Diamond, Astri Sumandari e Ridha Sasmitha Ajiningrum. "Traumatic Brain Injury". KESANS : International Journal of Health and Science 1, n. 4 (21 gennaio 2022): 357–67. http://dx.doi.org/10.54543/kesans.v1i4.34.

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Traumatic brain injury (TBI) is an injury to the brain that is non-degenerative and non-congenital but is caused by external mechanical forces that can cause a decrease in consciousness and temporary or permanent disturbances in cognitive, physical, and psychosocial functions. The latest data from the CDC in 2014 there were as many as 2.87 million people in the world suffered head injuries. Certain segments of society that are at high risk for TBI include young people, low-income individuals, unmarried individuals, members of ethnic minority groups, male gender, urban dwellers, substance abusers, and people with previous TBI. Keywords: Head Trauma, Traumatic Brain Injury, Radiology

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24

Polunina, N. A., D. E. Semenov, E. A. Orlov, A. A. Veselkov, E. V. Galitskiy, E. D. Grigorievskiy e A. Yu Kudashev. "Brain retraction injury". Voprosy neirokhirurgii imeni N.N. Burdenko 85, n. 4 (2021): 103. http://dx.doi.org/10.17116/neiro202185041103.

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Ferriero, Donna M. "Neonatal Brain Injury". New England Journal of Medicine 351, n. 19 (4 novembre 2004): 1985–95. http://dx.doi.org/10.1056/nejmra041996.

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26

Ling, Geoffrey. "Traumatic Brain Injury". Seminars in Neurology 35, n. 01 (25 febbraio 2015): 003–4. http://dx.doi.org/10.1055/s-0035-1544236.

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Potter, R. J., e L. J. Potter. "Severe brain injury". Medical Journal of Australia 154, n. 5 (marzo 1991): 367–68. http://dx.doi.org/10.5694/j.1326-5377.1991.tb112908.x.

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&NA;. "Traumatic Brain Injury". Neurosurgery 62, n. 6 (giugno 2008): 1386. http://dx.doi.org/10.1227/01.neu.0000333346.16264.57.

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&NA;. "Traumatic Brain Injury". Neurosurgery 62, n. 6 (giugno 2008): 1393. http://dx.doi.org/10.1227/01.neu.0000333411.47445.c5.

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Hooper, Stephen R. "Traumatic Brain Injury". Exceptionality 14, n. 3 (9 gennaio 2006): 121–23. http://dx.doi.org/10.1207/s15327035ex1403_1.

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Parikh, Samir, Marcella Koch e Raj K. Narayan. "Traumatic Brain Injury". International Anesthesiology Clinics 45, n. 3 (2007): 119–35. http://dx.doi.org/10.1097/aia.0b013e318078cfe7.

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Rao, Prakash J. "Traumatic Brain Injury". Critical Care Medicine 27, n. 7 (luglio 1999): 1404. http://dx.doi.org/10.1097/00003246-199907000-00057.

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Galgano, Michael, Gentian Toshkezi, Xuecheng Qiu, Thomas Russell, Lawrence Chin e Li-Ru Zhao. "Traumatic Brain Injury". Cell Transplantation 26, n. 7 (30 giugno 2017): 1118–30. http://dx.doi.org/10.1177/0963689717714102.

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Finnie, J. W., e P. C. Blumbergs. "Traumatic Brain Injury". Veterinary Pathology 39, n. 6 (novembre 2002): 679–89. http://dx.doi.org/10.1354/vp.39-6-679.

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Animal models have played a critical role in elucidating the complex pathogenesis of traumatic brain injury, the major cause of death and disability in young adults in Western countries. This review discusses how different types of animal models are useful for the study of neuropathologic processes in traumatic, blunt, nonmissile head injury.

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Sumners, David. "Traumatic brain injury". Current Opinion in Psychiatry 7, n. 1 (gennaio 1994): 83–86. http://dx.doi.org/10.1097/00001504-199401000-00021.

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Eames, Peter. "Traumatic brain injury". Current Opinion in Psychiatry 10, n. 1 (gennaio 1997): 49–52. http://dx.doi.org/10.1097/00001504-199701000-00011.

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Griffin, Leslie C. "Conquering Brain Injury". Journal of Head Trauma Rehabilitation 34, n. 5 (2019): 366–70. http://dx.doi.org/10.1097/htr.0000000000000518.

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Sena, A. "Postischemic brain injury". Neurology 44, n. 9 (1 settembre 1994): 1767. http://dx.doi.org/10.1212/wnl.44.9.1767.

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White, B. C. "Postischemic brain injury". Neurology 44, n. 9 (1 settembre 1994): 1767. http://dx.doi.org/10.1212/wnl.44.9.1767-a.

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Youse, Kathleen M., Karen N. Le, Michael S. Cannizzaro e Carl A. Coelho. "Traumatic Brain Injury". ASHA Leader 7, n. 12 (dicembre 2002): 4–7. http://dx.doi.org/10.1044/leader.ftr1.07122002.4.

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Ripley, David L., e Kristine Pacheco. "Brain Injury Medicine". Journal of Head Trauma Rehabilitation 22, n. 6 (novembre 2007): 413. http://dx.doi.org/10.1097/01.htr.0000300238.28737.54.

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Niedzwecki, Christian M., Jennifer H. Marwitz, Jessica M. Ketchum, David X. Cifu, Charles M. Dillard e Eugenio A. Monasterio. "Traumatic Brain Injury". Journal of Head Trauma Rehabilitation 23, n. 4 (luglio 2008): 209–19. http://dx.doi.org/10.1097/01.htr.0000327253.61751.29.

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&NA;. "BRAIN INJURY SYMPOSIUM". Critical Care Nursing Quarterly 9, n. 4 (marzo 1987): 83. http://dx.doi.org/10.1097/00002727-198703000-00012.

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Nolan, Scot. "Traumatic Brain Injury". Critical Care Nursing Quarterly 28, n. 2 (aprile 2005): 188–94. http://dx.doi.org/10.1097/00002727-200504000-00010.

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Wintersgill, Joanne. "Traumatic Brain Injury". Neurology Now 10, n. 1 (2014): 7. http://dx.doi.org/10.1097/01.nnn.0000444207.06267.f6.

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&NA;. "Traumatic Brain Injury". Neurology Now 10, n. 1 (2014): 7. http://dx.doi.org/10.1097/01.nnn.0000444208.06267.12.

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Bernie. "Traumatic Brain Injury". Neurology Now 10, n. 1 (2014): 7. http://dx.doi.org/10.1097/01.nnn.0000444209.83395.be.

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Hux, Karen, Mary Walker e Dixie D. Sanger. "Traumatic Brain Injury". Language, Speech, and Hearing Services in Schools 27, n. 2 (aprile 1996): 171–84. http://dx.doi.org/10.1044/0161-1461.2702.171.

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Abstract (sommario):

School-based speech-language pathologists from 10 states responded to a survey concerning their readiness to provide services to students with traumatic brain injuries (TBIs). Survey responses provided a means of exploring speech-language pathologists’ knowledge of TBI and facilitated recognition of accurate and inaccurate conceptions held by school-based speech-language pathologists concerning the characteristics and behaviors, criteria for identification and verification, and procedures for the assessment, treatment, and reintegration of students with TBI. Findings indicated that training had a positive effect on speech-language pathologists’ knowledge of assessment, treatment, and overall management of students with TBI; however, a large percentage of school-based speech-language pathologists remain uncertain about providing services to students with TBI even after receiving specific TBI training. Furthermore, school-based speech-language pathologists continue to hold many misconceptions concerning TBI and its consequences.

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Guluma, Kama, e Brian Zink. "Traumatic Brain Injury". Seminars in Respiratory and Critical Care Medicine 23, n. 01 (7 marzo 2002): 037–46. http://dx.doi.org/10.1055/s-2002-20587.

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Middleton, Judith A. "Acquired brain injury". Psychiatry 4, n. 7 (luglio 2005): 61–64. http://dx.doi.org/10.1383/psyt.2005.4.7.61.

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