共查询到20条相似文献,搜索用时 15 毫秒
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《Neurosurgery Clinics of North America》2016,27(4):489-497
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Traumatic brain injury (TBI) is a complex disease process that requires constant attention as one manages the associated body
systems. Even though an “isolated” brain injury may be the cause for admission to the hospital, the injured brain cannot be
thought of in isolation from the remainder of the body. All body systems, from cardiac to pulmonary, need to be addressed
as one moves from the initial to the long-term management of the TBI. The multiple issues are best addressed with a dedicated
neurocritical care team that is in continuous communication with the neurosurgical team throughout the course of treatment.
To date, no pharmacologic treatment has led to improved outcomes after TBI, but it is becoming increasingly clear that advances
in the critical care of TBI patients are contributing to better results. 相似文献
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《The Surgical clinics of North America》2017,97(6):1237-1253
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Models of Traumatic Brain Injury 总被引:2,自引:0,他引:2
Helmut L. Laurer Philipp M. Lenzlinger Tracy K. McIntosh 《European Journal of Trauma》2000,26(3):95-110
We present a review of the currently popular preclinical models of non-penetrating traumatic brain injury (TBI). This article focuses on animal models that cause TBI by applying mechanical energy to the head, skull or dura. It attempts to provide a compendium of the main characteristics of each of these experimental models of TBI in respect to acute and chronic histological findings and behavioral impairment in neurologic motor and cognitive function. Finally, several limitations of the described models are discussed briefly. 相似文献
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Global cognitive impairment following traumatic brain injury (TBI) is common, with some abilities more significantly affected than others. However, due to difficulties in estimating premorbid intelligence, there has been no systematic evaluation of the extent of decline in different cognitive abilities following TBI. Recent studies indicate that the Wide Range Achievement Test-Revised (WRAT-R) Reading subtest is an accurate estimate of premorbid intelligence, suggesting that post-TBI cognitive test scores can be compared to the WRAT-R to estimate the extent of decline that occurs in specific cognitive abilities. The current study estimated the extent of deficit in intelligence, memory, attention, speed of processing, and cognitive flexibility for 97 outpatients with TBI. Extent of decline was calculated by subtracting WRAT-R z-scores from cognitive test 2-scores to determine a z-difference score (ZDiff) for each cognitive ability. The results suggest that intelligence is least declined following TBI (WAIS-R 3-4-point decline; VIQ ZDiff = -0.23: FIQ ZDiff = -0.27), followed by attention (WMS-R 5-point decline; ZDiff = -0.31), memory (WMS-R 6-9-point decline; Verbal Memory ZDiff = -0.41; General Memory ZDiff = -0.51; Delay Memory ZDiff = -0.57), speed of processing (Trails A 15-16 second decline; ZDiff = -1.90) and cognitive flexibility (Trails B 35-52 second decline; ZDiff = -2.65). Implications for provision of feedback to individuals with TBI and their families are discussed. 相似文献
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《The Surgical clinics of North America》2017,97(5):1015-1030
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Opinion statement
相似文献
– | Vision disturbances following traumatic brain injury (TBI) include anomalies of accommodation, version, vergence (nonstrabismic, as well as strabismic), photosensitivity, visual field integrity, and ocular health. |
– | Traumatic brain injury patients with complex diplopia patterns, noncomitant strabismic anomalies, and advanced ocular health anomalies are either monitored by or referred to neuro-ophthalmologists and ophthalmologists for evaluation and possible surgical or medical intervention, as needed. |
– | Anomalies of accommodation, vergence, version, photosensitivity, and field of vision are amenable to noninvasive, rehabilitative interventions, such as vision therapy, which is rendered by optometrists and is described in this article. Further, vision therapy may be performed in isolation or in conjunction with the application of the following: Fusional prism spectacles (for diplopia) Tinted spectacles (for photosensitivity) Yoked prism spectacles (for visual-spatial hemispheric inattention, with or without a manifest visual field defect), as appropriate |
– | Dependent on the severity of vision impairment post-TBI, other types of rehabilitation, such as vestibular, physical, cognitive, and occupational rehabilitation, are deferred pending the stabilization of vision function to an appropriate level. |
– | Rehabilitative optometric intervention is appropriate and beneficial for many TBI patients. Therefore, it should be offered as a possible evaluation and treatment option to investigate the patient’s symptoms and determine the prognosis for treatment, as would be done with any other therapeutic modality. |
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The Role of Neuroinflammation in Traumatic Brain Injury 总被引:1,自引:0,他引:1
Oliver I. Schmidt Manfred Infanger Christoph E. Heyde Wolfgang Ertel Philip F. Stahel 《European Journal of Trauma》2004,30(3):135-149
Abstract
In industrialized countries, traumatic brain injury (TBI) still represents the leading cause of death and persisting neurologic impairment among young individuals < 45 years of age. Patients who survive the initial injury are susceptible to sustaining secondary cerebral insults which are initiated by the release of neurotoxic and inflammatory endogenous mediators by resident cells of the central nervous system (CNS). The presence of hypoxia and hypotension in the early resuscitative period further aggravates the inflammatory response due to ischemia/reperfusion-mediated injuries. These are induced by the intrathecal generation of free radicals and activation of the complement cascade. Posttraumatic neuroinflammation is further exacerbated by the subsequent intracranial recruitment of blood-derived immunocompetent cells, leading to secondary cerebral edema and increased intracranial pressure. The profound endogenous neuroinflammatory response after TBI, which is phylogenetically aimed at defending the CNS from invading pathogens and repairing lesioned tissue, is, in large part, responsible for the development of secondary brain damage and adverse outcome. However, aside from these deleterious effects, posttraumatic inflammation mediates neuroreparative mechanisms after TBI as well. This dual effect of neuroinflammation has been the focus of extensive experimental and clinical research in the past years and has led to an expanded basic knowledge on the cellular and molecular mechanisms which regulate the intracranial inflammatory response after trauma. The present article provides an up-to-date overview on the pathophysiological mechanisms of neuroinflammation after TBI. New potential therapeutic strategies for reducing the extent of secondary brain damage after neurotrauma are discussed. 相似文献
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《Transplantation proceedings》2019,51(7):2186-2188
In addition to primary injury in severe head trauma, secondary systemic insults that aggravate the brain injury may result in fatal neurologic outcome. We aim to evaluate the correlation between brain death and secondary systemic insults in 100 patients with severe traumatic brain injury (TBI) admitted to the intensive care unit. We collected data on hypotension and hypoxemia at the time of admission to intensive care unit and data on hypotension, hypoxemia, hypocarbia, hypercarbia, shock, anemia, hyperglycemia, and hyperthermia within the first 24 hours. In addition, we recorded the category of TBI according to computed tomography findings. Twenty-six patients (26%) who developed brain death were significantly younger than survivors. Early hypotension (odds ratio [OR], 10.24; 95% confidence interval [CI], 3.64–28.78; P = .000) and early shock (OR, 8.31; 95% CI, 2.65–26.01; P = .000) were significantly more frequent among brain-death patients. The most featured factor that independently predicted the development of brain death in patients with severe TBI was the existence of hypotension (B–2.74; 95% CI, 0.016–0.252; P = .000). The most common type of injury among brain death patients was a surgically evacuated mass lesion. Although all critical care principles are applied to prevent secondary systemic brain insults, when brain death occurs, the prevention of hypotension will become significant in preserving organs in better condition for procurement. 相似文献
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Gupta AK Zygun DA Johnston AJ Steiner LA Al-Rawi PG Chatfield D Shepherd E Kirkpatrick PJ Hutchinson PJ Menon DK 《Journal of neurotrauma》2004,21(6):678-684
The ability to measure brain tissue chemistry has led to valuable information regarding pathophysiological changes in patients with traumatic brain injury (TBI). Over the last few years, the focus has been on monitoring changes in brain tissue oxygen to determine thresholds of ischemia that affect outcome. However, the variability of this measurement suggests that it may not be a robust method. We have therefore investigated the relationship of brain tissue pH (pH(b)) and outcome in patients with TBI. We retrospectively analyzed prospectively collected data of 38 patients admitted to the Neurosciences Critical Care Unit with TBI between 1998 and 2003, and who had a multiparameter tissue gas sensor inserted into the brain. All patients were managed using an evidence-based protocol targeting CPP > 70 mm Hg. Physiological variables were averaged over 4 min and analyzed using a generalized least squares random effects model to determine the temporal profile of pH(b) and its association with outcome. Median (IQR) minimum pH(b) was 7.00 (6.89, 7.08), median (IQR) maximum pH(b) was 7.25 (7.18, 7.33), and median (IQR) patient averaged pH(b) was 7.13 (7.07, 7.17). pH(b) was significantly lower in those who did not survive their hospital stay compared to those that survived. In addition, those with unfavorable neurological outcome had lower pH(b) values than those with favorable neurological outcome. pH(b) differentiated between survivors and non-survivors. Measurement of pH(b) may be a useful indicator of outcome in patients with TBI. 相似文献