Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 6 uppsatser.

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Ke Changshu. / "March 2001." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (p. 142-174). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

痴呆是导致中风后存活人群自理能力降低的重要因素。中风后痴呆（PSD）包括发生在中风后的所有类型的痴呆，不论其痴呆的原因为何，如血管性痴呆(VD)，阿尔茨海默氏症(AD)以及混合型痴呆。由于中风致死率的降低和人口老龄化的到来，有可能在未来几十年，全世界范围内中风后痴呆的发病率将大幅增加。在此，我们将报告中风后早期出现的痴呆及长期的认知功能下降的发病率和危险因素，并通过使用PIB正电子扫描确定中风后痴呆中合并脑部淀粉样变的发病率。了解中风后痴呆的发病机制和危险因素，将有利于我们寻求治疗和预防措施，从而减低中风后痴呆的发生。 / 研究目的 / 研究1：中风后早期痴呆的发病率及危险因素 / 早期PSD及长期认知功能下降的发病机制甚为复杂。我们在中国中风存活者中建立了名为 STroke Registry IVEstigating COGnitive decline (STRIVE-COG) 的研究。此研究将报告早期PSD的危险因素。 / 研究2：中风后长期（15-18个月）认知功能下降的发病率及预测因素中风会增加远期痴呆的发生。但是，中风后远期认知功能下降的发病机制还未确定。我们的研究旨在观察中风后远期认知功能下降的危险因素。 / 研究方法 / 研究1：我们连续纳入一年的在我院中风中心留院的中风及短暂性缺血发作病人。在病人中风发生后的3-6个月后，对其进行多个认知领域的神经心理学检查。我们观察了患者的临床特征及结构影像学改变与早期PSD的相关性。我们还对部分早期PSD的病人进行了PIB正电子发射扫描（PIB-PET）检查。 / 研究2：在完成中风后3-6个月认知检查后的1年，即中风后的15-18个月，我们完成了认知心理学的随访检查。我们将认知功能下降定义为简易精神状态评分降低3分及以上，或者临床痴呆评分增加1分及以上。我们观察了认知功能下降和基线期临床、认知心理学和影像学特征（包括白质病变严重程度、陈旧性腔梗、全脑萎缩、额叶萎缩、顶叶萎缩、中颞叶萎缩）。在一组（n=18）早期PSD患者中，我们观察了脑部有类似阿尔茨海默氏病变表现的患者的认知功能下降的发病率。 / 结果 / 研究1：在所有入组的患者中（n=549），早期PSD的发病率为15.3%（n=84）。多因素回归分析显示，除了年龄和性别，早期PSD的危险因素包括急性腔隙性梗死灶(危险比[OR] 2.725, 95% 可信区间[CI] 1.364-5.434, P=0.004)及急性非腔隙性梗死灶(OR 2.809, 95%CI 1.124-6.410, P=0.014)比上无急性梗死灶的病人，还包括白质病变严重度（OR 1.120, 95% CI 1.037-1.210, p=0.004），额叶萎缩（OR 2.596, 95% CI 1.080-6.241, p=0.033），由脑室-大脑比表示的全脑萎缩（4th 四分卫区间 vs 1st区间, OR 3.096, 95% CI 1.374-6.993, p=0.006）。在19个完成了PIB-PET扫描的病人中，6人（31.6%）具有类似AD的脑部淀粉样物聚集的表现。 / 研究2：在452（82.3%）个完成了中风后15-18个月随访检查的病人中，认知功能下降的患者有73个（16.2%）。而年龄、受教育年限、多发陈旧性腔隙性梗死是其独立性预测因素。随访过程中中风复发的患者只有5.1%并且与认知功能下降无相关性。进展性的认知功能下降在PIB阴性（n=12）和PIB阳性（n=6）的患者中分别为41.7%和33.3%，而两者之间显著差别（p=0.731）。 / 结论 / 研究 1: 早期PSD的危险因素除了包括年龄、性别及脑部急性梗死灶之外，还包括脑部的慢性改变，包括白质病变、全脑萎缩、额叶萎缩及合并AD样病变特征。 / 研究 2: 年龄、受教育水平和多发陈旧性腔隙梗死是中风后15-18个月认知功能下降的独立危险因素。而合并AD样病变并不是导致中风后远期认知功能下降的必要因素。 / Dementia is a main cause of dependency in stroke survivors. Poststroke dementia (PSD) includes any dementia after a stroke, irrespective of its causes, e.g. vascular dementia (VD), Alzheimer’s disease (AD) or mixed dementia. A huge increase in prevalence and burden of PSD is likely to happen because of the decline in mortality after stroke and ageing of populations in the coming decades worldwide. In this thesis, we reported the risk factors for early PSD and delayed poststroke cognitive decline, and the prevalence of concurrent amyloid pathology as identified by Pittsburgh compound B (PIB) positron emission tomography (PET) in PSD. Understanding the risk factors of PSD will help to devise preventive and treatment strategies that may reduce the burden of PSD. / Objectives / Study1: Risk factors of early PSD / Mechanisms explaining poststroke early and delayed cognitive decline are complex. We set up a STroke Registry IVEstigating COGnitive decline (STRIVE-COG) among Chinese stroke survivors. Study 1 reported the findings on risk factors for early PSD. / Study 2: Prevalence and predictors for delayed (15-18 months) cognitive decline after stroke / Having a stroke increases the risk of delayed dementia. However, mechanisms accounting for the cognitive decline are uncertain. We investigated the predictors for delayed poststroke cognitive decline. / Subjects and Methods / Study 1：We recruited consecutive stroke or transient ischemic attack (TIA) patients admitted to our acute stroke unit over 1 year. We performed neuropsychological assessment 3-6 months poststroke. We investigated the association between clinical and structural neuroimaging features with early PSD. We performed PIB positron PET among a subset of subjects with early PSD. / Study 2: We performed neuropsychological assessment at baseline (i.e. 3-6 months poststroke) and at 15-18 months poststroke. We defined cognitive decline as a drop of ≥ 3 points in the mini-mental state examination and/or increment in ≥ 1 grading of the clinical dementia rating scale. We investigated the association between cognitive decline with baseline clinical, neuropsychological, and neuroimaging features (white matter changes [WMC] severity, old lacunar infarct, global atrophy, frontal lobe atrophy [FLA], parietal lobe atrophy, medial temporal lobe atrophy). Among a subset of subjects (n=18) with PSD at baseline, we investigated the influence of AD-like PIB retention upon the rate of cognitive decline. / Results / Study 1: Prevalence of early PSD among all recruited subjects (n=549) was 15.3% (n=84). Apart from age and female gender, multivariate regression analyses showed that risk factors for early PSD were presence of acute lacunar (odds ratio [OR] 2.725, 95% confidence interval [CI] 1.364-5.434, P=0.004) or non-lacunar infarct (OR 2.809, 95%CI 1.124-6.410,P=0.014) over no acute infarct apparent on neuroimaging, WMC severity (OR 1.120, 95% CI 1.037-1.210, p=0.004), FLA (OR 2.596, 95% CI 1.080-6.241, p=0.033), and global brain atrophy (4th quartile vs 1st quartile, OR 3.096, 95% CI 1.374-6.993, p=0.006). Among 19 subjects with early PSD who had PIB PET, 6 (31.6%) had AD-like PIB retention. / Study 2: Among 452(82.3%) subjects who had completed the study, cognitive decline occurred in 73 (16.2%) subjects. Age, education, and multiple old lacunar infarcts independenty predicted cognitive decline. Recurrent stroke occurred only in 5.1% and was not associated with cognitive decline. Progressive cognitive decline occurred in 41.7% and 33.3% of PIB negative (n=12) and PIB positive (n=6) PSD patients, respectively (p=0.731). / Conclusion / Study 1: Apart from age, female gender, and presence of acute infarct evident in neuroimaging, chronic brain changes (WMC, global brain atrophy, FLA, and concurrent AD pathology) are associated with early PSD. / Study 2: Age, education, and multiple old lacunar infarcts predicted cognitive decline at 15-18 months poststroke. Concurrent AD-like lesion is not necessary associated with a rapid cognitive decline. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Yang, Jie. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2012. / Includes bibliographical references (leaves 93-109). / Abstract also in Chinese. / Chapter PART I --- LITERATURE REVIEW --- p.1 / Chapter Chapter 1 --- Introduction --- p.2 / Chapter 1.1 --- An overview of stroke --- p.2 / Chapter 1.2 --- Introduction of poststroke dementia --- p.5 / Chapter Chapter 2 --- Poststroke Dementia --- p.6 / Chapter 2.1 --- Defining poststroke dementia --- p.6 / Chapter 2.2 --- Classification of poststroke dementia --- p.7 / Chapter 2.3 --- Frequency, incidence, and clinical determinants of poststroke dementia --- p.20 / Chapter 2.4 --- Imaging methods and imaging features in poststroke dementia --- p.22 / Chapter 2.5 --- Mechanisms of stroke-associated dementia --- p.24 / Chapter 2.6 --- Influence of poststroke dementia on stroke outcome --- p.28 / Chapter PART II --- STUDIES ON EARLY POSTSTROKE DEMENTIA AND DELAYED COGNITIVE DECLINE --- p.31 / Chapter Chapter 3: --- Stroke Registry Investigating Cognitive decline (STRIVE-COG): Risk Factors for Early Poststroke Dementia (Study 1) --- p.32 / Chapter 3.1 --- Abstract --- p.32 / Chapter 3.2 --- Introduction --- p.33 / Chapter 3.3 --- Methods --- p.35 / Chapter 3.4 --- Results --- p.45 / Chapter 3.5 --- Discussion --- p.48 / Chapter Chapter 4 --- Stroke Registry Investigating Cognitive decline (STRIVE-COG): Predictors for Delayed Poststroke Cognitive decline (Study 2) --- p.63 / Chapter 4.1 --- Abstract --- p.63 / Chapter 4.2 --- Introduction --- p.64 / Chapter 4.3 --- Methods --- p.66 / Chapter 4.4 --- Results --- p.76 / Chapter 4.5 --- Discussion --- p.78 / Chapter PART III --- CONCLUSION --- p.88 / Chapter Chapter 5 --- Strengths and Limitations --- p.89 / Chapter Chapter 6 --- Summary and Future Directions --- p.91 / References --- p.93

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 7 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 5 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 5 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 5 uppsatser.

Studies have shown that the alignment of the knee in the coronal plane has a significant effect on the joint contact stress. However, gait analysis demonstrated that factors other than alignment contributed significantly to the outcome of corrective surgery. It was therefore hypothesized that muscle contraction can alter the stress distribution within the knee joint and that overloading can occur in the absence of a deformity. Six normal knees were harvested from different donors. The exact orientation of all muscle groups was recorded and their tendinous insertions carefully preserved. Custom built pressure transducers (6 per compartment, 0.5 mm thick, 10 mm diameter) were inserted through 2 small, posterior, capsular incisions and placed on the tibial surface and the menisci. The knees were mounted in a loading system which allowed free self-alignment of the joint under load. All muscles were replaced by wire cables instrumented with force transducer, tensioner and grip. Several alignment models (5, 10 degree varus, neutral, 5 degree valgus and 15 degree of flexion) as well as the effect of contraction of all major muscles crossing the knee joint were tested. An even pressure distribution was seen in neutral alignment. In a varus deformity the peak pressure shifted medially and laterally in valgus. Unloading of the opposite compartment was seen for deformities as small as 5 degrees. A flexion deformity produced a postero-lateral shift of the peak pressure area. Muscle contraction increased the pressure significantly in a region next to the muscle. Generally, unloading - though less significant - was seen in a region diagonally across the joint. These results suggest that muscular hyperactivity may considerable increase the contact stresses. However, muscle weakness or lack of muscular contraction may indirectly play a significant role in affecting the contact pressure distribution. If the muscle force is insufficient to counterbalance the external moment condylar lift-off occurs. This increases the angulation between femur and tibia thereby overloading the compartment where contact takes place; One can therefore conclude that abnormal gait patterns or neuromuscular control mechanisms may result in unphysiologically high contact stresses which may cause the development of unicompartmental osteoarthritis and subsequently, a deformity.

The management of acute myocardial infarction (AMI) has been improved by the realisation that the size of infarction can influence mortality (Sobel et al, 1972) and that the infarct size can be altered by subsequent therapy (Maroko et al, 1972). The identification of any factor which may have adverse effects on the ischaemic myocardium and which is amenable to treatment would therefore have important prognostic implications. Elevation of circulating free fatty acid (FFA) concentrations is a consistent feature (Kurien and Oliver, 1966; Oliver et al, 1968) of the profound, non-specific metabolic reaction associated with the onset of AMI (Opie, 1975). The FFA rise has been correlated with the development of arrhythmias (Oliver et al, 1968) after AMI, and with the severity of ischaemic damage (Oliver et al, 1968; Gupta et al, 1969; Russell & Oliver, 1978) on clinical grounds. The method of quantifying infarct size developed by Shell et al (1972) has provided a means of correlating the degree of metabolic disturbance with extent of myocardial damage, and of assessing the benefits of metabolic interventions. The purpose of the studies reported in this thesis was to examine in detail the FFA rise in the early phase of AMI and to correlate this rise with the development of arrhythmias and other complications of AMI and with enzymatically estimated infarct size, thus leading to a more rational approach to therapeutic interventions.