高压氧治疗提高重型脑外伤患者的认知能力;前瞻性研究

S. R
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摘要

创伤性脑损伤(TBI)是发病率的重要原因。在美国,严重TBI患者的平均终身护理费用从600000美元到1875000美元不等[1]。在印度,每年有160万人患有脑脊髓炎。这20万人中会有人死亡[2]。幸存者面临一系列挑战,最常见的是认知或皮质脊髓束功能障碍。脑损伤相关的神经心理障碍影响生活质量[3]。这种情况的常见表现是:注意力不集中、注意力下降、容易分心、视觉空间概念化受损、言语/视觉刺激处理缓慢、记忆力受损、沟通障碍、判断力差、执行功能差[4]。参与是不同能力人群生活满意度的有力预测因素。当这些问题导致人格解体时,会导致ADL依赖[5]。标准治疗包括药物和治疗练习。所用的药物从Citocholine到Amantadine不等[6]。心理干预是:针对注意力缺陷的注意力过程训练和任务,针对记忆缺陷的补偿策略和无错误学习训练,针对认知交际障碍的语用语言技能和社会行为指导,元认知策略,针对执行障碍的解决问题训练是治疗TBI患者认知缺陷的主要方法[7]。这些都没有直接解决皮层基础设施的损伤。通常,他们处理的是保存下来的东西。摘要
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hyperbaric Oxygen Therapy Improves Cognition in Patients Severe TBI; A Prospective Study
Traumatic brain injury (TBI) is a significant cause of morbidity. In the USA the average lifetime cost of care for a severe TBI patient ranges from $600,000 to $1,875,000 [1]. In India 1.6 million persons sustain TBI annually. Of those 200,000 will die [2]. The survivors face a spectrum of challenges most commonly related to cognitive or corticospinal tract dysfunction. Brain injury related neuropsychological impairment affects quality of life (QoL) [3]. The common presentations of this are: impaired concentration, decreased attention, easy distractibility, impaired visuo-spatial conceptualization, slow verbal/ visual stimulus processing, impaired memory, communication disorder, poor judgment, poor executive function [4]. Participation is a strong predictor of life satisfaction in the differently-abled. These issues lead to ADL dependence when they result in depersonalization [5]. The standard treatment consists of pharmacological agents and therapeutic exercises. Pharmacological agents used vary from agents like Citocholine to Amantadine [6]. Psychological intervention is: Attention process training and tasks for attention deficits, compensatory strategies and errorless learning training for memory deficits, pragmatic language skills and social behavior guidance for cognitive-communication disorder, meta-cognitive strategy, and problem-solving training for executive disorder are the mainstay of therapy for cognitive deficits in persons with TBI [7]. None of these directly address the cortical infrastructure damage. Often, they work with what is preserved. Abstract
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