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Journal articles on the topic 'Brain injury'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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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, no. 3 (2010): 196–201. http://dx.doi.org/10.7887/jcns.19.196.

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Kamalifar, Amir, Firooz Salehpoor, Farhad Mirzaii, and Samar Kamalifar. "Stab Brain Injury: A Case Report." Journal of Surgical Case Reports and Images 4, no. 6 (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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Volovitzr, Ilan. "Neuropsychological Assessment of Traumatic Brain Injury." Neuroscience and Neurological Surgery 2, no. 2 (2018): 01–02. http://dx.doi.org/10.31579/2578-8868/028.

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4

Kocamer Şahin, Şengül, Ufuk Gönültaş, and Bahadır Demir. "TRICOTILLLOMANIA SECONDARY TO TRAUMATIC BRAIN INJURY." PSYCHIATRIA DANUBINA 35, no. 3 (2023): 430–32. http://dx.doi.org/10.24869/psyd.2023.430.

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5

Pal, Urvashi. "TRAUMATIC BRAIN INJURY AND ITS MANAGEMENT." Indian Journal of Health Care Medical & Pharmacy Practice 5, no. 1 (2024): 134–43. http://dx.doi.org/10.59551/ijhmp/25832069/2024.5.1.170.

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A prevalent illness with a high morbidity and death rate is head injuries. Early detection and evacuation are crucial for serious cerebral hemorrhages in order to optimize the likelihood of independent recovery. It isthe primary cause of death for children and young people and a significant medical and socioeconomic issue. The Brain Trauma Foundation’s “Guidelines for the Management of this disease” are a major source of inspiration for critical care management of this injury. The primary goals are to maintain cerebral perfusion pressure (CPP), optimize cerebral oxygenation, and prevent and cu

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Bhatia, Avi, Deepti Nandakumar, Jagannath Ravindran, and Jillian F. Turner. "Seconds Save Lives: Prehospital Strategies for Managing Traumatic Brain Injuries." Journal of Neurophysiological Monitoring 2, no. 3 (2024): 67–75. https://doi.org/10.5281/zenodo.14503352.

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Henry VIII of England is one of the most notorious rulers of the 15th century, primarily recognized for the execution of several of his wives. Initially, he was a beloved and intellectual figure. Still, his personality underwent a dramatic change after he sustained a severe head injury during a jousting match when he fell from his horse. Many researchers today believe that this traumatic brain injury (TBI) played a significant role in his subsequent violent and erratic behavior. Traumatic brain injury affects millions of people globally, with studies indicating that the prevalence is substanti

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van den Pol, Anthony N. "Brain Trauma Enhances Transient Cytomegalovirus Invasion of the Brain Only in Mice That Are Immunodeficient." Journal of Virology 83, no. 1 (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

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Kokolakis, Michail, and Ioannis Koutelekos. "PEDIATRIC TRAUMATIC BRAIN INJURY." PERIOPERATIVE NURSING (GORNA) E-ISSN:2241-3634 5, no. 3 (2016): 130–53. https://doi.org/10.5281/zenodo.232941.

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Traumatic brain injury is a major cause of serious harm and death in children under the age of 15. The injury affects not only the patient, but also impacts heavily on close relatives. Caring for victims with traumatic brain injury is perhaps the most difficult of many professional challenges for nursing staff, requiring both technical and skills and sensitivity to the needs of the relatives. The <strong>aim </strong>of this study was to present a review of recent publications specifically addressing nursing intervention in the care of children with traumatic brain injury. <strong>Methodolog

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Kayabaş, Murat. "Experimental traumatic brain injury models in rats." RATS 1, no. 1 (2023): 15–19. https://doi.org/10.5281/zenodo.8143363.

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Head traumas are high-mortality pathologies that can disable. Traumatic brain injury (TBI) is a heterogeneous disease containing brain damage caused by external effects. In the human brain injury after trauma, examinations cannot be made at histopathological and molecular levels, and the effect of a new drug on a head -trauma person cannot be examined. Human models are required to experimentally reveal the similarities of human TBI’s biomechanical, cellular, and molecular events and to develop new treatments and show their effectiveness. Today, the most commonly used animals in TBI exper

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10

Soares, Holly, and Tracy K. McIntosh. "Fetal Cortical Transplants in Adult Rats Subjected to Experimental Brain Injury." Journal of Neural Transplantation and Plasticity 2, no. 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 con

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11

Andrianov, Viacheslav V., Vladimir A. Kulchitsky, Guzel G. Yafarova, et al. "Investigation of NO Role in Neural Tissue in Brain and Spinal Cord Injury." Molecules 28, no. 21 (2023): 7359. http://dx.doi.org/10.3390/molecules28217359.

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Nitric oxide (NO) production in injured and intact brain regions was compared by EPR spectroscopy in a model of brain and spinal cord injury in Wistar rats. The precentral gyrus of the brain was injured, followed by the spinal cord at the level of the first lumbar vertebra. Seven days after brain injury, a reduction in NO content of 84% in injured brain regions and 66% in intact brain regions was found. The difference in NO production in injured and uninjured brain regions persisted 7 days after injury. The copper content in the brain remained unchanged one week after modeling of brain and spi

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12

Dries, David J. "Brain Injury." Shock 18, no. 1 (2002): 98. http://dx.doi.org/10.1097/00024382-200207000-00020.

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13

Perna, Robert. "Brain Injury." Journal of Head Trauma Rehabilitation 21, no. 1 (2006): 82–84. http://dx.doi.org/10.1097/00001199-200601000-00009.

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14

Garber, James C., and Carl R. Boyd. "Brain injury." Current Surgery 57, no. 2 (2000): 126–30. http://dx.doi.org/10.1016/s0149-7944(00)00160-4.

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15

Olver, John H. "Brain injury." Current Opinion in Neurology 8, no. 6 (1995): 443–46. http://dx.doi.org/10.1097/00019052-199512000-00008.

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Setkowicz, Zuzanna, and Rafał Guzik. "Injections of vehicle, but not cyclosporin A or tacrolimus (FK506), afford neuroprotection following injury in the developing rat brain." Acta Neurobiologiae Experimentalis 67, no. 4 (2007): 399–409. http://dx.doi.org/10.55782/ane-2007-1657.

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Susceptibility of the injured rat brain to seizures depends on the developmental stage at which the injury had been inflicted. Our previous study shows that tacrolimus (FK506) and cyclosporin A (CsA) applied following the injury can also decrease or increase the seizure susceptibility in an age-dependent way. To find possible neuronal substrates of the effects, we examined influences of the agents on the injured brain and on its neuronal population. Rat brains were mechanically injured on postnatal days 6 (P6) or 30 (P30). Twenty minutes and 24 hours following the injury, FK506 or CsA were inj

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Scafidi, Susanna, Jennifer Jernberg, Gary Fiskum та 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, № 8 (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

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Shibata, Masaaki, Stephanie Einhaus, John B. Schweitzer, Samuel Zuckerman, and Charles W. Leffler. "Cerebral blood flow decreased by adrenergic stimulation of cerebral vessels in anesthetized newborn pigs with traumatic brain injury." Journal of Neurosurgery 79, no. 5 (1993): 696–704. http://dx.doi.org/10.3171/jns.1993.79.5.0696.

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✓ Changes in cerebral blood flow (CBF), pial arteriolar diameter, and arterial blood pressure, gases, and pH were examined before and for 3 hours after fluid-percussion brain injury in α-chloralose-anesthetized piglets. The brain injury was induced by a percussion of 2.28 ± 0.06 atm applied for 23.7 ± 0.5 msec to the right parietal cortex. Regional CBF was measured with radiolabeled microspheres, and changes in pial arteriolar diameter were monitored in the left parietal cortex using closed cranial windows. Immediately following brain injury, mean blood pressure transiently (for approximately

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Orita, Tetsuji, Takafumi Nishizaki, Toshifumi Kamiryo, Kunihiko Harada, and Hideo Aoki. "Cerebral microvascular architecture following experimental cold injury." Journal of Neurosurgery 68, no. 4 (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 ar

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Fatima, Tahreem, Muhammad Irshad, Muhammad Rizwan Sarwar, Rahmatullah Salah, Abdul Ghaffoor, and Freshta Asekzai. "Effect of Traumatic Brain Injury on Serum Magnesium." International Journal of Science and Research (IJSR) 11, no. 8 (2022): 266–69. http://dx.doi.org/10.21275/sr22801002707.

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21

Maria, Dalamagka. "Mild Brain Injury." Journal of Anesthesia and Anesthetic Drugs 2, no. 1 (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 dependen

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Shah, Ekta J., Katherine Gurdziel, and Douglas M. Ruden. "Sex-Differences in Traumatic Brain Injury in the Absence of Tau in Drosophila." Genes 12, no. 6 (2021): 917. http://dx.doi.org/10.3390/genes12060917.

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Traumatic brain injuries, a leading cause of death and disability worldwide, are caused by a severe impact to the head that impairs physiological and psychological function. In addition to severity, type and brain area affected, brain injury outcome is also influenced by the biological sex of the patient. Traumatic brain injury triggers accumulation of Tau protein and the subsequent development of Tauopathies, including Alzheimer’s disease and Chronic traumatic encephalopathy. Recent studies report differences in Tau network connections between healthy males and females, but the possible role

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Jiang, Ji Y., Bruce G. Lyeth, Guy L. Clifton, Larry W. Jenkins, Robert J. Hamm, and Ronald L. Hayes. "Relationship between body and brain temperature in traumatically brain-injured rodents." Journal of Neurosurgery 74, no. 3 (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 r

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Alam, Sayed, Shafiq Ur Rehman та Myeong Ok Kim. "Nicotinamide Improves Functional Recovery via Regulation of the RAGE/JNK/NF-κB Signaling Pathway after Brain Injury". Journal of Clinical Medicine 8, № 2 (2019): 271. http://dx.doi.org/10.3390/jcm8020271.

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Brain injuries are a serious global health issue and are the leading cause of neurodegeneration. To date, there is no proper cure and treatment for brain-injury-induced neuropathological conditions because of a lack of sufficient knowledge and the failure to develop a drug due to the multi-pathological conditions in the brain. Herein, we explored the neurotherapeutic effects of Nicotinamide (NAM), against brain injury-induced neurodegeneration and behavioral problems. Treating injured mouse brains with NAM, for 7 days, significantly ameliorated several pathological events. Interestingly, NAM t

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HUNEA, Iuliana, ILIESCU Diana BULGARU, Simona Irina DAMIAN, et al. "Chemical Biomarkers of Diffusse Axonal Injury." BRAIN. Broad Research in Artificial Intelligence and Neuroscience 11, no. 2 (2020): 18–32. https://doi.org/10.18662/brain/11.2/72.

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Craniocerebral trauma is the most common cause of deathand post-traumatic disability in people under 45 years of age. InRomania, the annual incidence shows, that for every 100,000inhabitants, there are 300 cases of craniocerebral trauma that requirespecialized medical assistance. Craniocerebral traumas are the mostcommon types of traumas encountered in current forensic practice.Research on the mechanisms of injury, the timing of head trauma and theestablishment of causes of death remain relevant. Establishing thetraumatic moment implies both the distinction between pre-mortem andpost-mortem in

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Griffin, Allison D., L. Christine Turtzo, Gunjan Y. Parikh, et al. "Traumatic microbleeds suggest vascular injury and predict disability in traumatic brain injury." Brain 142, no. 11 (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 presentin

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Iskandarovich, Iskandarov Alisher, Yakubov Khayot Hamidullaevich, and Ismatov Abrorkhon Askarovich. "FORENSIC EVALUATION OF DIFFUSE AXONAL INJURY." American Journal of Medical Sciences and Pharmaceutical Research 04, no. 04 (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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McIntosh, Tracy K., and Donna Ferriero. "Changes in Neuropeptide Y after Experimental Traumatic Brain Injury in the Rat." Journal of Cerebral Blood Flow & Metabolism 12, no. 4 (1992): 697–702. http://dx.doi.org/10.1038/jcbfm.1992.95.

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We utilized a model of fluid percussion (FP) brain injury in the rat to examine the hypothesis that alterations in brain neuropeptide Y (NPY) concentrations occur following brain injury. Male rats (n = 44) were subjected to FP traumatic brain injury. One group of animals (n = 38) was killed at 1 min, 15 min, 1 h, or 24 h after brain injury, and regional brain homogenates were analyzed for NPY concentrations using radioimmunoassay. A second group of animals (n = 6) was killed for NPY immunocytochemistry. Concentrations of NPY in the injured left parietal cortex were significantly elevated at 15

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Grant, P. Ellen, Nadege Roche-Labarbe, Andrea Surova, et al. "Increased Cerebral Blood Volume and Oxygen Consumption in Neonatal Brain Injury." Journal of Cerebral Blood Flow & Metabolism 29, no. 10 (2009): 1704–13. http://dx.doi.org/10.1038/jcbfm.2009.90.

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With the increasing interest in treatments for neonatal brain injury, bedside methods for detecting and assessing injury status and evolution are needed. We aimed to determine whether cerebral tissue oxygenation (StO2), cerebral blood volume (CBV), and estimates of relative cerebral oxygen consumption (rCMRO2) determined by bedside frequency-domain near-infrared spectroscopy (FD-NIRS) have the potential to distinguish neonates with brain injury from those with non-brain issues and healthy controls. We recruited 43 neonates ≤15 days old and >33 weeks gestational age (GA): 14 with imaging evi

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Marklund, Niklas, Carrie Keck, Rachel Hoover, et al. "Administration of monoclonal antibodies neutralizing the inflammatory mediators tumor necrosis factor alpha and interleukin -6 does not attenuate acute behavioral deficits following experimental traumatic brain injury in the rat." Restorative Neurology and Neuroscience 23, no. 1 (2005): 31–42. https://doi.org/10.3233/rnn-2005-00287.

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Purpose: Although many previous studies have indicated that the acute inflammatory response following traumatic brain injury (TBI) is detrimental, inflammation may also positively influence outcome in the more chronic post-injury recovery period. We evaluated the effects of monoclonal antibodies (mAB), neutralizing either IL-6 (IL-6 mAB) or TNF-α (TNF mAB), administered intracerebroventricularly (i.c.v) on acute neurobehavioral outcome following TBI. Methods: Male Sprague-Dawley rats (n = 173) were anesthetized (sodium pentobarbital, 60 mg/kg) and subjected to lateral fluid percussion (FP) bra

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Pumiglia, Luke, Aaron M. Williams, Michael T. Kemp, Glenn K. Wakam, Hasan B. Alam, and Ben E. Biesterveld. "Brain proteomic changes by histone deacetylase inhibition after traumatic brain injury." Trauma Surgery & Acute Care Open 6, no. 1 (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

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Barrett, Ken. "Psychiatric sequelae of acquired brain injury." Advances in Psychiatric Treatment 5, no. 4 (1999): 250–58. http://dx.doi.org/10.1192/apt.5.4.250.

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Improvements over recent decades in acute care of the brain-injured now ensure that all but the most severely injured survive. The legacy of that survival is an increasing number of people with enduring organic mental disorders. Here, I will focus upon the psychiatric sequelae of five types of severe single-insult brain injury: head trauma, subarachnoid haemorrhage, and hypoxic, hypoglycaemic and postencephalitic injury. Thrombotic stroke is a common and important cause of brain injury but the psychiatric consequences have been more extensively studied and are fairly well-known (Robinson &

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Taiwo, Akhigbe, Damilola Tope Akinrinsola, and Anakwenze Ahusimere. "Role of Corticosteroids in the Management of Acute Traumatic Brain Injury: Literature Review and Critical Appraisal of Evidence." International Journal of Medical Reviews and Case Reports 2, no. 2 (2018): 22–28. https://doi.org/10.5455/IJMRCR.acute-traumatic-brain-injury-corticosteroids.

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Background Traumatic brain injury is a prominent and leading cause of premature mortality and disability. Corticosteroids were widely used in the clinical management of traumatic brain injury but their benefit has been challenged in so many studies and their efficacy but their use in TBI still remains unclear. The aim of this review is to evaluate the effectiveness and efficacy of corticosteroids in reducing mortality or morbidity in people with acute traumatic brain injury. Methods A systematic literature searches as enabled a thorough and robust process of rigorous critical appraisal in orde

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Keck, Carrie A., Hilaire J. Thompson, Asla Pitkänen, et al. "The novel antiepileptic agent RWJ-333369-A, but not its analog RWJ-333369, reduces regional cerebral edema without affecting neurobehavioral outcome or cell death following experimental traumatic brain injury." Restorative Neurology and Neuroscience 25, no. 2 (2007): 77–90. https://doi.org/10.3233/rnn-2007-00370.

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Purpose: To evaluate the therapeutic efficacy of two antiepileptic compounds, RWJ-333369 and RWJ-333369-A in a well-established experimental model of lateral fluid percussion (FP) traumatic brain injury (TBI) in the rat. Methods: Anethestized Male Sprague-Dawley rats (n=227) were subjected to lateral FP brain injury or sham-injury. Animals were randomized to receive treatment with RWJ-333369 (60 mg/kg, p.o.) or its analog RWJ-333369-A (60 mg/kg, p.o.), or vehicle (equal volume) at 15 minutes, 4, 8, and 24 hours post-injury. In Study I, animals were assessed at 48 hours for acute motor and cogn

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Raghupathi, Ramesh, Seamus C. Fernandez, Hisayuki Murai, et al. "BCL-2 Overexpression Attenuates Cortical Cell Loss after Traumatic Brain Injury in Transgenic Mice." Journal of Cerebral Blood Flow & Metabolism 18, no. 11 (1998): 1259–69. http://dx.doi.org/10.1097/00004647-199811000-00013.

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The proto-oncogene, BCL-2, has been suggested to participate in cell survival during development of, and after injury to, the CNS. Transgenic (TG) mice overexpressing human Bcl-2 (n = 21) and their wild-type (WT) littermates (n = 18) were subjected to lateral controlled cortical impact brain injury. Lateral controlled cortical impact brain injury resulted in the formation of a contusion in the injured cortex at 2 days, which developed into a well-defined cavity by 7 days in both WT and TG mice. At 7 days after injury, brain-injured TG mice had a significantly reduced cortical lesion (volume =

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Başkaya, Mustafa K., Aclan Doğan, A. Muralikrishna Rao, and Robert J. Dempsey. "Neuroprotective effects of citicoline on brain edema and blood—brain barrier breakdown after traumatic brain injury." Journal of Neurosurgery 92, no. 3 (2000): 448–52. http://dx.doi.org/10.3171/jns.2000.92.3.0448.

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Object. Cytidine 5′-diphosphocholine (CDPC), or citicoline, is a naturally occurring endogenous compound that has been reported to provide neuroprotective effects after experimental cerebral ischemia. However, in no study has such protection been shown after traumatic brain injury (TBI). In this study the authors examined the effect of CDPC on secondary injury factors, brain edema and blood-brain barrier (BBB) breakdown, after TBI.Methods. After anesthesia had been induced in Sprague—Dawley rats by using 1.5% halothane, an experimental TBI was created using a controlled cortical impact (CCI) d

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Willinger, R., and 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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Kumar, Akhilesh, Bhal Singh, Sandeep Kundal, and Sunil Garg. "Traumatic Brain Injury in Geriatric Population: Epidemiology and Outcomes." International Journal of Science and Research (IJSR) 11, no. 7 (2022): 1533–38. http://dx.doi.org/10.21275/sr22722225252.

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Hossain, Md Monir, Nahid Parvez, and Ershad Ali. "Swallowing difficulties among traumatic brain injury patients in Bangladesh." Edorium Journal of Disability and Rehabilitation 9, no. 2 (2023): 8–14. http://dx.doi.org/10.5348/100055d05mh2023ra.

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Aim: To determine the number of people having swallowing difficulties among traumatic brain injury patient. Methods: This is a quantitative type of cross-sectional survey study where 117 samples were assigned purposively from Dhaka Medical College Hospital (DMCH). The Swallowing Disturbance Questionnaire (SDQ) was used for the study. Data were analyzed by using descriptive statistical analysis (SPSS = Statistics package for social science) method. Results: On an average, most of the participants 90.60% (106) were males and other participants 9.40% (11) were females. The maximum numbers of part

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Dr., Mian Awais1* Prof. Muhammad Akmal Hussain2 Dr. Inam Ullah Asgher3 Dr. Jahanzab Aslam4 Dr. Mian Abubakr5. "Frequency of Cervical spine injuries in moderate to severe Head Injuries at Allied Hospital Faisalabad." Singapore Journal of Neurosciences 1, no. 1 (2020): 4. https://doi.org/10.5281/zenodo.4023873.

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<strong><em>ABSTRACT</em></strong> <strong>Objective: </strong>Traumatic brain injury, often referred to as TBI, is considered as acute event similar to other injuries. After sustaining the head injury One moment the person is normal and the minutes after life has changed suddenly. Trauma team mostly miss the diagnosis of cervical spine injury (CSI) due to  altered level of consciousness as a result of a traumatic brain injury (TBI).The objective  of this study was to determine the frequency of cervical spine injury in patients having moderate to severe head injury due to different t

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Nakamura, Michio, Kathryn E. Saatman, James E. Galvin, et al. "Increased Vulnerability of NFH-LacZ Transgenic Mouse to Traumatic Brain Injury-Induced Behavioral Deficits and Cortical Damage." Journal of Cerebral Blood Flow & Metabolism 19, no. 7 (1999): 762–70. http://dx.doi.org/10.1097/00004647-199907000-00006.

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The authors evaluated the neurobehavioral and neuropathologic sequelae after traumatic brain injury (TBI) in transgenic (TG) mice expressing truncated high molecular weight neurofilament (NF) protein fused to beta-galactosidase (NFH-LacZ), which develop Lewy body-like NF-rich inclusions throughout the CNS. TG mice and their wild-type (WT) littermates were subjected to controlled cortical impact brain injury (TG, n=19; WT, n=17) or served as uninjured controls (TG, n =11; WT, n =11). During a 3-week period, mice were evaluated with an array of neuromotor function tests including neuroscore, bea

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Savelieff, Masha G., and Eva L. Feldman. "Traumatic Brain Injury." Neurology 96, no. 8 (2021): 357–58. http://dx.doi.org/10.1212/wnl.0000000000011455.

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Kumar, Sailesh, Lisa Story, and Mellisa Damodaram. "Perinatal Brain Injury." Current Pediatric Reviews 4, no. 2 (2008): 71–79. http://dx.doi.org/10.2174/157339608784461981.

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McNair, Norma D. "TRAUMATIC BRAIN INJURY." Nursing Clinics of North America 34, no. 3 (1999): 637–59. http://dx.doi.org/10.1016/s0029-6465(22)02411-2.

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Fernoagă, Cristina, and Mihai Cătălin Cereaciuchin. "Traumatic brain injury." Practica Veterinara.ro 2, no. 36 (2022): 22. http://dx.doi.org/10.26416/pv.36.2.2022.6432.

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Nelasari, Diamond, Astri Sumandari, and Ridha Sasmitha Ajiningrum. "Traumatic Brain Injury." KESANS : International Journal of Health and Science 1, no. 4 (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 abuse

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Polunina, N. A., D. E. Semenov, E. A. Orlov, et al. "Brain retraction injury." Voprosy neirokhirurgii imeni N.N. Burdenko 85, no. 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, no. 19 (2004): 1985–95. http://dx.doi.org/10.1056/nejmra041996.

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Ling, Geoffrey. "Traumatic Brain Injury." Seminars in Neurology 35, no. 01 (2015): 003–4. http://dx.doi.org/10.1055/s-0035-1544236.

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Potter, R. J., and L. J. Potter. "Severe brain injury." Medical Journal of Australia 154, no. 5 (1991): 367–68. http://dx.doi.org/10.5694/j.1326-5377.1991.tb112908.x.

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