卒中偏瘫患者出院后习得性废用发展情况的调查研究

目的 调查卒中亚急性期偏瘫患者出院后习得性废用发展情况，分析习得性废用与患者人口学因素、 临床特点及功能恢复的相关性。 方法 前瞻性连续纳入2018年7月-2019年12月期间南方医科大学深圳医院预备出院的卒中偏瘫患 者。收集患者一般资料和临床特点，并在出院后4周、8周和12周用运动活动记录表（motor activity log， MAL）评估患者的习得性废用情况，在出院前3 d，出院后4周、8周和12周用改良Ashworth指数测试肘 腕屈肌群肌张力，偏瘫上肢功能测试香港版、Fugl-Meyer评定量表上肢部分和箱块测试评价上肢功 能，功能独立性评定评价日常生活能力。对各随访时间点MAL与其他评估量表、人口学因素和临床特 点进行相关性分析。 结果 研究完成随访患者47例，男性36例（76.6%），平均年龄58.74±11.08岁，平均发病时间 48.00±28.38 d，其中缺血性卒中32例（68.1%），出血性卒中15例（31.9%）。MAL的患手使用频率/ 患者活动质量在出院后4周、8周和12周时分别为2.66（1.38～4.03）分/2.87（1.03～3.56）分、3.30 （1.93～4.41）分/3.17（1.55～3.77）分和3.59（2.00～4.33）分/3.28（2.00～3.96）分，除8周与12周 之间的患手使用频率差异无统计学意义之外，其他时间点之间差异均具有统计学意义。各随访时间 点患者肘屈肌群张力变化差异无统计学意义（P =0.076），其余功能表现均显著恢复（均P <0.05）。出 院后4周、8周和12周各时间点，MAL与年龄呈一般正相关（ρ=0.33～0.39），与发病时间呈一般负相关 （ρ=-0.49～-0.33），与肘腕部屈肌张力呈一般至中等负相关（ρ=-0.58～-0.38），与日常生活能力 呈一般至中等正相关（ρ=0.30～0.60），与上肢运动功能呈一般至强正相关（ρ=0.49～0.76）。 结论 卒中亚急性期偏瘫患者出院后患肢仍然可以保持显著的功能恢复，但依然面临习得性废用 的挑战，且习得性废用与年龄、发病时间、腕肘屈肌群张力、日常生活生活能力和上肢功能相关。     

卒中气管切开患者拔管的康复治疗研究进展

气管切开是临床抢救重症卒中患者的一种重要手段，但长期气管切开套管留置易造成多 种并发症，及早康复介入可促进患者早期拔管。本文从呼吸功能康复、吞咽康复、说话瓣膜的使用、 气道及套管的循证护理管理和一般支持治疗方面对促进卒中气管切开患者拔管的康复治疗进展进 行了归纳总结，为提高临床卒中患者拔管率提供参考。气道廓清技术、呼吸肌训练、运动训练和体位 管理可改善患者呼吸功能；直接与间接吞咽功能训练、唾液的管理和咽腔电刺激可改善患者吞咽功 能；说话瓣膜的合理使用可促进患者早日拔管；对气道进行气道湿化、气囊管理和吸痰护理，对套管 进行合理的固定与清洁消毒等，可减少并发症，防止感染；稳定患者病情，给予良好的营养支持和心 理康复等一般支持治疗，可提高拔管成功率。虽然目前对卒中气管切开患者拔管的康复治疗并无统一 标准，但是多学科合作的综合性康复治疗可提高患者拔管率，促进患者早日康复。     

The gait profile score characterises walking performance impairments in young stroke survivors

BackgroundThe Gait Profile Score (GPS) provides a composite measure of the quality of joint movement during walking, but the relationship between this measure and metabolic cost, temporal (e.g. walking speed) and spatial (e.g. stride length) parameters in stroke survivors has not been reported.Research Question: The aims of this study were to compare the GPS (paretic, non-paretic, and overall score) of young stroke survivors to the healthy able-bodied control and determine the relationship between the GPS and metabolic cost, temporal (walking speed, stance time asymmetry) and spatial (stride length, stride width, step length asymmetry) parameters in young stroke survivors to understand whether the quality of walking affects walking performance in stroke survivors.MethodsThirty-nine young stroke survivors aged between 18 and 65years and 15 healthy age-matched able-bodied controls were recruited from six hospital sites in Wales, UK. Joint range of motion at the pelvis, hip, knee and ankle, and temporal and spatial parameters were measured during walking on level ground at self-selected speed with calculation of the Gait Variable Score and then the GPS.ResultsGPS for the paretic leg (9.40° (8.60–10.21) p < 0.001), non-paretic leg (11.42° (10.20–12.63) p < 0.001) and overall score (11.18° (10.26–12.09) p < 0.001)) for stroke survivors were significantly higher than the control (4.25° (3.40–5.10), 5.92° (5.11 (6.73)). All parameters with the exception of step length symmetry ratio correlated moderate to highly with the GPS for the paretic, non-paretic, and/or overall score (ρ = <−0.732 (p < 0.001)).SignificanceThe quality of joint movement during walking measured via the GPS is directly related to the speed and efficiency of walking, temporal (stance time symmetry) and spatial (stride length, stride width) parameters in young stroke survivors.     

Simvastatin Reduces Lipopolysaccharides-Accelerated Cerebral Ischemic Injury via Inhibition of Nuclear Factor-kappa B Activity

Preceding infection or inflammation such as bacterial meningitis has been associated with poor outcomes after stroke. Previously, we reported that intracorpus callosum microinjection of lipopolysaccharides (LPS) strongly accelerated the ischemia/reperfusion-evoked brain tissue damage via recruiting inflammatory cells into the ischemic lesion. Simvastatin, 3-hydroxy-3-methylgultaryl (HMG)-CoA reductase inhibitor, has been shown to reduce inflammatory responses in vascular diseases. Thus, we investigated whether simvastatin could reduce the LPS-accelerated ischemic injury. Simvastatin (20 mg/kg) was orally administered to rats prior to cerebral ischemic insults (4 times at 72, 48, 25, and 1-h pre-ischemia). LPS was microinjected into rat corpus callosum 1 day before the ischemic injury. Treatment of simvastatin reduced the LPS-accelerated infarct size by 73%, and decreased the ischemia/reperfusion-induced expressions of pro-inflammatory mediators such as iNOS, COX-2 and IL-1β in LPS-injected rat brains. However, simvastatin did not reduce the infiltration of microglial/macrophageal cells into the LPS-pretreated brain lesion. In vitro migration assay also showed that simvastatin did not inhibit the monocyte chemoattractant protein-1-evoked migration of microglial/macrophageal cells. Instead, simvastatin inhibited the nuclear translocation of NF-κB, a key signaling event in expressions of various proinflammatory mediators, by decreasing the degradation of IκB. The present results indicate that simvastatin may be beneficial particularly to the accelerated cerebral ischemic injury under inflammatory or infectious conditions.     

Physical exercise prevents motor disorders and striatal oxidative imbalance after cerebral ischemia-reperfusion

Stroke is the third most common cause of death worldwide, and most stroke survivors present some functional impairment. We assessed the striatal oxidative balance and motor alterations resulting from stroke in a rat model to investigate the neuroprotective role of physical exercise. Forty male Wistar rats were assigned to 4 groups: a) control, b) ischemia, c) physical exercise, and d) physical exercise and ischemia. Physical exercise was conducted using a treadmill for 8 weeks. Ischemia-reperfusion surgery involved transient bilateral occlusion of the common carotid arteries for 30 min. Neuromotor performance (open-field and rotarod performance tests) and pain sensitivity were evaluated beginning at 24 h after the surgery. Rats were euthanized and the corpora striata was removed for assay of reactive oxygen species, lipoperoxidation activity, and antioxidant markers. Ischemia-reperfusion caused changes in motor activity. The ischemia-induced alterations observed in the open-field test were fully reversed, and those observed in the rotarod test were partially reversed, by physical exercise. Pain sensitivity was similar among all groups. Levels of reactive oxygen species and lipoperoxidation increased after ischemia; physical exercise decreased reactive oxygen species levels. None of the treatments altered the levels of antioxidant markers. In summary, ischemia-reperfusion resulted in motor impairment and altered striatal oxidative balance in this animal model, but those changes were moderated by physical exercise.