- 作者列表："Deng, Yan","Shi, Jin","Zhang, Ming","Qi, Xueliang
Objective To summarize and analyze the clinical data of 12 Chinese patients of cerebral hemorrhage with bilateral sudden deafness as the first symptom and to explore the relationship between cerebral hemorrhage and bilateral sudden deafness. Methods Retrospective analysis of clinical data of patients, including age, clinical manifestations, location of cerebral hemorrhage, hearing loss, and recovery. Results The average age of onset in 12 patients was 53.92 years, 9 had a history of hypertension, 7 had a history of stroke, and 6 had typical stroke symptoms. There were 7 cases of basal ganglia hemorrhage; 2 cases of cerebellum hemorrhage; and 1 case of pontine hemorrhage, temporal lobe hemorrhage, and thalamus infarction. The auditory brainstem evoked potential test results of 3 patients were normal, and 5 of 6 patients who completed pure tone audiometry had hearing impairment. Five out of 9 patients had basically or completely recovered hearing. Conclusion The results showed that patients were mostly middle-aged and elderly with no typical stroke symptoms, and a history of stroke and hypertension increased the risk of hearing loss. The cause of hearing loss in patients with cerebral hemorrhage may be related to the damage of the hearing conduction pathway or (and) the lack of blood supply to the central auditory nervous system. Detecting hearing impairment in time and actively intervening can help most patients to improve their hearing significantly. The degree of hearing damage and recovery is related to the bleeding site, the amount of bleeding, and the timely treatment.
目的总结分析 12 例以双侧突发性耳聋为首发症状的中国脑出血患者的临床资料，探讨脑出血与双侧突发性耳聋的关系。方法回顾性分析患者的临床资料，包括年龄、临床表现、脑出血部位、听力损失及恢复情况。结果 12 例患者平均发病年龄 53.92 岁，9 例有高血压病史，7 例有脑卒中病史，6 例有典型脑卒中症状。基底节区出血 7 例，小脑出血 2 例，脑桥出血、颞叶出血、丘脑梗死各 1 例。3 例患者听性脑干诱发电位检测结果正常，6 例完成纯音测听的患者中有 5 例听力受损。9 例患者中有 5 例听力基本或完全恢复。结论研究结果显示，患者多为中老年，无典型脑卒中症状，脑卒中和高血压病史增加了听力损失的风险。脑出血患者听力损失的原因可能与听力传导通路受损或 (和) 中枢听觉神经系统供血不足有关。及时发现听力障碍，积极干预，可帮助大多数患者听力明显改善。听力损伤和恢复的程度与出血部位、出血量、治疗及时有关。
METHODS:BACKGROUND:People with stroke are not meeting recommended levels of physical activity. The modifiable factors associated with post-stroke physical activity levels need to be identified to develop targeted interventions. OBJECTIVE:The objective of this study was to investigate the factors at discharge from inpatient rehabilitation that are associated with physical activity levels at 3 months following discharge. DESIGN:This was a prospective cohort study. METHODS:Sixty-four people with stroke completed baseline assessments at discharge from inpatient rehabilitation and 55 completed the follow-up 3 months later. The candidate factors (i.e. gait speed, balance, strength, cognition, mood and motivation) were measured at discharge. The primary outcome measure at follow-up was walking related activity (measured by wrist-worn accelerometer). Secondary outcome measures were physical activity participation (Activity Card Sort) and intensity of physical activity (International Physical Activity Questionnaire - Short 7 days). Adjusted separate multivariable linear regression models or proportional odds regression models were used to evaluate the associations between candidate factors and physical activity. RESULTS:Gait speed and balance were associated with all aspects of physical activity. Higher level of intrinsic motivation was also associated with higher physical activity participation. Anxiety demonstrated a significant non-linear relationship with physical activity participation. LIMITATIONS:Inclusion of fatigue and individual muscle strength could have provided further insights into associations with steps per day. CONCLUSION:The results demonstrated that better physical function at discharge from inpatient rehabilitation was associated with future increased levels of physical activity. Additionally, higher levels of motivation impacted on increased physical activity participation. The influence of anxiety on physical activity participation requires further exploration. Mixed-method study designs can be utilized to further understand the factors associated with post-stroke physical activity.
METHODS:Cerebral ischemia-reperfusion (I/R) is characterized by initial transient cerebral ischemia followed by reperfusion. Various pathophysiological processes are involved in brain injury and functional recovery during cerebral I/R. There are few studies on dynamic metabolic process after cerebral I/R. The present study was to observe dynamic alteration of brain injury, functional recovery, and metabolites after cerebral I/R in rats and discover potential metabolic markers. The cerebral I/R model was established by middle cerebral artery occlusion (MCAO) for 90 min, following reperfusion in rats. The results of cerebral infarction area, cerebral edema, and behavior test showed that there were dynamic changes in brain injury and functional recovery at different periods after cerebral I/R. Further analysis showed that the brain injury was severe on the first day of cerebral I/R, and there was a significant functional recovery from the 7th day of cerebral I/R, followed by an aggravation trend of brain injury from the days 7 to 28. Furthermore, Matrix-assisted laser desorption ionization mass spectrometry imaging analysis showed that the expression of ATP, glucose, and citric acid on 7th day was the highest during cerebral I/R, which indicated that energy metabolism and oxidative phosphorylation played important roles during cerebral I/R. In addition, the untargeted metabolomic results showed that the level of isocitric acid, the ratio of oxyglutaric acid/glutamic acid, and the level of pyruvic acid associated with the TCA cycle were also the highest on the 7th day during cerebral I/R, which indicated that the transient spontaneous recovery of ischemic brain on the 7th day after ischemia-reperfusion might be related to oxidative phosphorylation and energy metabolism in the brain in this period. In conclusion, the results suggest that some small molecule metabolites participate in the brain injury and functional recovery during cerebral I/R, which is of great significance to the development of therapeutic drugs and diagnostic markers.
METHODS:The aims of this study were to study the effects of miR-2 on cerebral ischemia–reperfusion rats and to explore its further mechanism. Rats were assigned into sham, model, miR-22 control and miR-22 groups. Observation of neurological behaviors at 24 h after operation found that neurological functions were severely damaged in the model and miR-22 control groups and these damages were improved by miR-22. RT-PCR indicated that miR-22 mRNA level in the brain tissue was significantly decreased in the model and miR-22 control groups, but increased in the miR-22 group. TTC staining showed increased percentage of cerebral infarction volume in the model and miR-22 control groups and this increase was reduced by miR-22. Immunohistochemistry showed increased densities of CD34^+ and VEGF^+ microvessels in the cortex in the model and miR-22 control groups, which were further increased in the miR-22 group. ELISA showed increased serum VEGF and Ang-1 levels in the model and miR-22 control groups, which were also further increased in the miR-22 group. Western blot analysis showed increased phosphorylation level of PI3K and Akt in brain tissue in the model and miR-22 control groups, which were further increased in the miR-22 group. Administration of LY294002, a specific PI3K pathway inhibitor, significantly reversed all the effects of miR-22 on rats in the model group. miR-22 exerts its neuroprotective and angiogenic functions via the PI3K/Akt signaling pathway, at least partly, in rats under cerebral ischemia–reperfusion.