A total of 188 patients completed data at twelve months (attrition rate: 29% over 12 months). The path coefficients show low functional ability (beta=0.51), more depressive symptoms (beta=-0.27), low state self-esteem (beta3=0.20), female gender (beta=0.13), older age (beta=-0.11) and living in a residential care facility (beta=-0.12) have a direct effect on participation restriction, and these variables accounted for 71% of the variance in explaining participation restrictions at 12 months. Repeated measures revealed significant decreases in overall levels of participation restriction and depressive symptoms from baseline to one year. However, no significant early changes in the levels of state self-esteem and depressive symptoms (from baseline to six months) and no significant late changes in both depressive symptoms and LHS scores were found (between six months and 12 months). / A total of 210 stroke survivors completed data at six months. Functional ability, state self-esteem, and number of strokes significantly accounted for 57% of the variance in participation restriction. Lower levels of functional ability, state self-esteem and social support satisfaction were associated with an increased likelihood of having depressive symptoms (z = 5.30, 34.12, and 5.51). / Aims. To gain understanding about the social, psychological and physical outcomes following inpatient stroke rehabilitation; to determine the variables predicting the level of participation and depressive symptoms of stroke survivors at baseline, six and 12 months following discharge from a rehabilitation hospital; to test a theoretical model of predictors of participation restriction at 12 months; and to determine the level over time for each of the outcomes. / Conclusion and implications. The findings in this study indicate that identification of stroke survivors at risk of high levels of participation restriction and low self-esteem will assist health professionals to devise appropriate interventions that target improving the psychological well being amongst person with stroke. Rehabilitation services need to continue to focus on restoring functional independence but also need to diagnose and treat depressive symptoms in order to minimise the restriction to participation in society. Assisting stroke survivors in redefining their identity after stroke could be an important aspect in stroke rehabilitation. (Abstract shortened by UMI.) / Chau, Pak Chun Janita. / Adviser: Shelia Twinn. / Source: Dissertation Abstracts International, Volume: 70-06, Section: B, page: 3426. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2008. / Includes bibliographical references (leaves 237-276). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstracts in English and Chinese. / School code: 1307.

Wong, Adrian. / "August 2007." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (p. 183-221). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstracts in English and Chinese.

Chan, Chun Kit. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2008. / Includes bibliographical references (leaves 147-161). / Abstracts in English and Chinese. / Chapter Chaper 1 --- Introduction --- p.1 / Chapter 1.1 --- General introduction to cerebral stroke --- p.1 / Chapter 1.2 --- Different types of cerebral stroke --- p.2 / Chapter 1.3 --- Statistics --- p.3 / Chapter 1.4 --- Symptoms of cerebral stroke --- p.4 / Chapter 1.5 --- Complications of cerebral stroke --- p.5 / Chapter 1.6 --- Risks and preventions of cerebral stroke --- p.6 / Chapter 1.7 --- Cerebral stroke treatment --- p.8 / Chapter 1.8 --- Post stroke rehabilitation --- p.11 / Chapter 1.9 --- Mechanisms of stroke --- p.15 / Chapter 1.9.1 --- Energy production failure and loss of ionic homeostasis --- p.15 / Chapter 1.9.2 --- Excitotoxicity --- p.16 / Chapter 1.9.3 --- Calcium ions mediated toxicity --- p.17 / Chapter 1.9.4 --- Passive neuronal cell death --- p.18 / Chapter 1.9.5 --- Oxidative stress --- p.19 / Chapter 1.9.6 --- Inflammation --- p.22 / Chapter 1.9.7 --- Apoptosis --- p.25 / Chapter 1.10 --- Potential therapeutic agents for cerebral stroke --- p.24 / Chapter 1.10.1 --- Anti-oxidative enzyme and free radical scavengers --- p.24 / Chapter 1.10.2 --- Ions channel blockers and glutamate antagonists --- p.26 / Chapter 1.10.3 --- Anti-inflammatory agent --- p.28 / Chapter 1.10.4 --- Anti-apoptotic agent --- p.28 / Chapter 1.11 --- Experimental model of cerebral ischemia-reperfusion --- p.29 / Chapter 1.11.1 --- In vitro model (oxygen and glucose deprivation model) --- p.29 / Chapter 1.11.2 --- In vivo model (Middle cerebral artery occlusion) --- p.31 / Chapter 1.12 --- Traditional Chinese Medicine (TCM) --- p.32 / Chapter 1.12.1 --- General Introduction to Traditional Chinese Medicine --- p.32 / Chapter 1.12.2 --- TCM and cerebral stroke --- p.33 / Chapter 1.12.3 --- Chinese compound formula --- p.34 / Chapter 1.12.4 --- Introduction to individual herb --- p.34 / Chapter 1.12.4.1 --- Astragali Radix (Pinyin name: Huangqi) --- p.34 / Chapter 1.12.4.2 --- Rhizoma Chuanxiong (Pinyin name: Chuanxiong) --- p.35 / Chapter 1.12.4.3 --- Radix Salviae Miltorrhizae (Pinyin name: Danshen) --- p.35 / Chapter 1.12.4.4 --- Cassia Obtusifolia Linne (Pinyin name: Jue Ming Zi) --- p.36 / Chapter 1.12.4.5 --- Radix Glycyrrhizae (Pinyin name: Gancao) --- p.37 / Chapter 1.12.4.6 --- Radix Angelicae Sinensis (Pinyin name: Dongquai) --- p.37 / Chapter 1.12.4.7 --- Paeoniae Veitchii Radix (Pinyin name: Chi Shao) --- p.38 / Chapter 1.12.5 --- Salvianolic acid B --- p.39 / Chapter 1.13 --- Aim of study --- p.40 / Chapter Chapter 2 --- Materials and Methods --- p.41 / Chapter 2.1 --- Materials --- p.41 / Chapter 2.1.1 --- Drug --- p.41 / Chapter 2.1.1.1 --- Herbal Medicine --- p.41 / Chapter 2.1.1.2 --- Herbal extraction of PSR --- p.42 / Chapter 2.1.1.3 --- Herbal extraction of individual herb --- p.43 / Chapter 2.1.1.4 --- Salvianolic acid B --- p.43 / Chapter 2.1.2 --- Chemical --- p.44 / Chapter 2.1.3 --- Animal --- p.48 / Chapter 2.2 --- Methods --- p.49 / Chapter 2.2.1 --- (AAPH)- induced erythrocyte hemolysis --- p.49 / Chapter 2.2.2 --- Cell Culture study --- p.51 / Chapter 2.2.2.1 --- Cell Line --- p.51 / Chapter 2.2.2.2 --- Cell differentiation --- p.52 / Chapter 2.2.2.3 --- In vitro model of ischemia - Oxygen glucose deprivation (OGD) experiment --- p.53 / Chapter 2.2.2.4 --- Cell viability assay --- p.54 / Chapter 2.2.3 --- In vivo Study --- p.54 / Chapter 2.2.3.1 --- Cerebral blood flow (CBF) measurement --- p.54 / Chapter 2.2.3.2 --- In vivo transient focal cerebral ischemia model - Middle cerebral artery occlusion (MCAo) --- p.55 / Chapter 2.2.3.3 --- Administration of PSR --- p.57 / Chapter 2.2.3.4 --- Administration of salvianolic acid B (SAB) --- p.59 / Chapter 2.2.3.5 --- Measurement of brain infarct volume --- p.60 / Chapter 2.2.3.6 --- In vivo anti-oxidative enzyme activity determination in the brain --- p.61 / Chapter 2.2.3.6.1 --- Brain tissue preparation --- p.61 / Chapter 2.2.3.6.2 --- Tissue homogenization and protein extraction --- p.61 / Chapter 2.2.3.6.3 --- Protein concentration determination --- p.63 / Chapter 2.2.3.6.4 --- Catalase activity determination in the brain --- p.63 / Chapter 2.2.3.6.5 --- Glutathione Peroxidase (GPx) activity determination in the brain --- p.64 / Chapter 2.2.3.6.6 --- The Superoxide Dismutase (SOD) activity determination in the brain --- p.65 / Chapter 2.2.3.7 --- Behavioral Evaluation --- p.66 / Chapter 2.2.3.7.1 --- Neurological behavioural test --- p.66 / Chapter 2.2.3.7.2 --- Shuttle box escape experiment --- p.67 / Chapter 2.3 --- Statistical analyses --- p.71 / Chapter Chapter 3 --- Results --- p.72 / Chapter 3.1 --- In vitro model of ischemia - Oxygen glucose and deprivation (OGD) experiment --- p.72 / Chapter 3.2 --- AAPH assay of PSR --- p.75 / Chapter 3.3 --- AAPH assay of individual herb --- p.77 / Chapter 3.4 --- Brain slices after middle cerebral artery occlusion (MCAo) experiment --- p.81 / Chapter 3.5 --- Brain infarct volume of single dose protocol --- p.83 / Chapter 3.6 --- Neurological behavioural test of single dose protocol --- p.85 / Chapter 3.7 --- Brain infarct volume of double doses protocol --- p.87 / Chapter 3.8 --- Neurological behavioural test of double doses protocol --- p.89 / Chapter 3.9 --- Determination of superoxide dismutase (SOD) activity in the brain --- p.91 / Chapter 3.10 --- Determination of glutathione peroxidase (GPx) activity in the brain --- p.93 / Chapter 3.11 --- Determination of catalase activity in the brain --- p.95 / Chapter 3.12 --- Brain infarction volume of Salvianolic acid B (SAB) treatment --- p.98 / Chapter 3.13 --- Neurological behavioural test of SAB treatment --- p.100 / Chapter 3.14 --- Shuttle box performance in training and testing series --- p.102 / Chapter 3.15 --- Change in shuttle box performance (% avoidance c.f. last day of training) in testing series --- p.104 / Chapter 3.16 --- Escape latency in testing and training series --- p.107 / Chapter 3.17 --- Change in escape latency (c.f. last day of training) in testing series --- p.109 / Chapter 3.18 --- Brain infarct volume of shuttle box escape experiment --- p.112 / Chapter 3.19 --- Neurological score in shuttle box escape experiment --- p.114 / Chapter Chapter 4 --- Discussion --- p.117 / Chapter 4.1 --- The protective effect of PSR in in vitro oxygen and glucose deprivation (OGD) on human neuroblastoma SH-SY5Y cell line --- p.117 / Chapter 4.1.1 --- OGD model and cell line --- p.117 / Chapter 4.1.2 --- Protective effect of PSR in OGD experiment --- p.118 / Chapter 4.1.3 --- Free radical scavenging property of PSR --- p.120 / Chapter 4.2 --- The protective effects of PSR in in vivo middle cerebral artery (MCAo) model --- p.121 / Chapter 4.2.1 --- The shortcomings of in vitro OGD model --- p.121 / Chapter 4.2.2 --- Development of in vivo MCAo model and TTC staining --- p.122 / Chapter 4.2.3 --- Protective effect of PSR in MCAo experiment (single dose protocol) --- p.124 / Chapter 4.2.4 --- Protective effect of PSR in MCAo experiment (double doses protocol) --- p.125 / Chapter 4.2.5 --- The effect of PSR toward neurological deficits --- p.127 / Chapter 4.2.6 --- Anti-oxidative effects of PSR in MCAo model --- p.128 / Chapter 4.3 --- The protective effects of SAB in in vivo middle cerebral artery (MCAo) model --- p.130 / Chapter 4.3.1 --- Free radical scavenging property of different herbs --- p.130 / Chapter 4.3.2 --- Selection of pure compound that used to treat stroke --- p.131 / Chapter 4.3.3 --- Protective effect of Salvianolic B in MCAo experiment --- p.132 / Chapter 4.3.4 --- The effect of SAB toward neurological deficits --- p.133 / Chapter 4.4 --- The effects of PSR and SAB on stroked rats' performance in shuttle box escape experiment --- p.134 / Chapter 4.4.1 --- Establishment of shuttle box escape experiment --- p.134 / Chapter 4.4.2 --- Effects of PSR and SAB on avoidance performance --- p.135 / Chapter 4.4.3 --- Effects of PSR and SAB on escape latency --- p.138 / Chapter 4.5 --- Assessment on the contribution of SAB to the protective effect of PSR --- p.140 / Chapter 4.6 --- Comparison of acute and chronic testing --- p.140 / Chapter 4.6.1 --- The protective effect of the drugs (Histopathological examination) --- p.140 / Chapter 4.6.2 --- The severity of motor deficit (Neurological score) --- p.141 / Chapter Chapter 5 --- Conclusion and Future prospect --- p.143 / Chapter 5.1 --- Conclusion --- p.143 / Chapter 5.2 --- Future prospect --- p.144 / References --- p.147

Thesis (Ph. D.)--University of Washington, 2003. / Vita. Includes bibliographical references (leaves 73-82).

Thesis (M.S.W.)--University of Hong Kong, 1985.

published_or_final_version / Medical Sciences / Master / Master of Medical Sciences

published_or_final_version / Medical Sciences / Master / Master of Medical Sciences

This thesis investigates the behavioural and anatomical correlates of recovery from motor cortex damage in rats. The effectiveness of behavioural, pharmacological, and regenerative treatments was investigated using models of focal stroke. Chronic bilateral motor deficits were found after motor cortex damage induced by various methods. These behavioural deficits were similar in severity and duration although they were correlated with different patterns of reorganization seen in Golgi-stained tissue. Animals with motor cortex injury benefited from postinjury olfactory stimulation, chronic administration of nicotine, and infusions of epidermal growth factor followed by erythroprotein. Different mechanisms of plasticity in remaining cortical circuits are discussed as possible candidates responsible for the behavioural improvement. The current thesis expands the current knowledge of the effects of adult cortical damage to ares critical to motor control. It may also stimulate research on therapies and possible mechanisms that might enhance recovery after stroke. / xviii, 299 leaves : ill. (some col.) ; 29 cm.

The effects of pre-stroke exercise and levesl of brain-derived neurotrophic factor (BDNF) on behavioural and functional recovery were examined following focal cortical ischemic infarct. Intracortical microstimulation (ICMS) was used to derive topographical maps of forelimb representations within the motor cortex and ischemia was induced via bipolar coagulation of surface vasculature. One month of excerise prior to ischemia significantly increased the amount of peri-infarct movement represnetations and initiates vascular changes within motor cortex. Further, this exercise-induced preservation of peri-infarct movement representations is associated with behavioural recovery and is dependent on BDNF levels in the motor cortex. These results provide further support for the idea that endurance exercise prior to stroke may enhance functional and behavioural recovery. / 140 leaves : ill. (some col.) ; 29 cm.

Stroke is a preventable disease. Minor stroke and transient ischaemic attack (TIA) are important warning signs of the possibility of a major stroke. Worldwide, stroke is the third most common killer and the largest cause of disability. The incidence of stroke is predicted to increase with the predominance of unhealthy lifestyles and the aging population. The adoption of a healthy lifestyle can reduce many of the risk factors. This descriptive study was designed to explore patients’ understanding of modifiable risk factors of cerebrovascular disease. It investigated lifestyle changes actually made, as well as the factors affecting patients’ decisions about whether to make lifestyle changes. The two major factors considered were patients’ sources and level of knowledge and their attitudes and beliefs around making changes. A convenience sample of patients who had suffered a minor stroke or TIA was recruited through a major metropolitan hospital. Thirty-five subjects responded to a postal questionnaire. The mean age was 68 years and 37% of the subjects had sustained some disability as a result of the TIA or minor stroke. The results demonstrated that many subjects had a poor understanding of risk factors of stroke. While smoking was well recognised as a risk factor, subjects showed less awareness of other risk factors, such as excessive alcohol consumption and obesity. Subjects also reported significant confusion regarding diet. Sixty-six percent of subjects depended on doctors as their main source of health information. This may be problematic as the current shortages of General Practitioners has put pressure on doctors to keep appointment times short and reduce the time available for health education. The main barriers to lifestyle change, were lack of motivation, and inadequate, knowledge, guidance, and support and the inability to access good information. Although 83% of subjects suffered from hypertension, medication was the accepted method of control, few subjects realised the significance of lifestyle factors. Nine percent of subjects were only diagnosed with hypertension after their stroke or TIA and few monitor their own blood pressure, despite the wide availability of home monitoring devices. From the findings of this study it is concluded that health promotion and education are very important strategies in the prevention of stroke and it is recommended that this kind of education begins in childhood with tailored, age-specific programs delivered to the public over the lifespan. The role of health screening cannot be underestimated in the detection of risk factors such as hypertension and obesity. Early detection makes effective treatment possible and helps prevent the occurrence of strokes, thus reducing the cost to the community. Long-term health strategies such as improving health resource distribution and enhancing health education are needed where patients and their families participate together in comprehensive education programs. It is hoped that this may lead to a shared understanding, which may translate to patients being more supported, and therefore more able, to make the necessary lifestyle changes. Dysphagia is a common complication following stroke, which can result in significant morbidity and mortality. Multidisciplinary collaboration facilitates management strategies, decision-making and the efficiency of rehabilitation. Nurses are responsible for coordination of management and in particular for continuous monitoring, assessment of swallowing and nutritional state, maintaining safety and preventing complications. An understanding of the issues and strategies relating to management may provide valuable information to enhance the safety, cost-effectiveness and quality of care. A retrospective review of patients’ medical records was used to collect data. A sample of ninety-five adults who were admitted to an Australian public hospital between January 2003 and April 2006, with a diagnosis of dysphagic stroke were recruited. Statistical Package for Social Sciences (SPSS) was used to analyse the quantitative data, while content analysis was used to analyse the qualitative data. All subjects were assessed by a speech pathologist, the mean age was 75 years and 50.5% were male. Except for critically ill subjects, almost all were assessed within three days. Ninety-six percent of subjects had communication problems and 81% had upper limb motor impairment. During hospitalisation almost 60% of subjects had an improvement in their oral intake including 8% resuming their premorbid diet. Eighteen percent were on enteral tube feeding upon discharge, 4% deteriorated and 16% died. It appears that oral intake of most subjects was unsatisfactory. When recorded the mean body weight lost was 2.3kg. At least 22% had malnutrition or dehydration. Forty-five percent aspirated and 22% had respiratory infection. Almost half of the subjects (48%) were discharged to aged care facilities. Eighty percent had no documented follow-up scheduled for management of their dysphagia. Early identification of dysphagia, prudent supervising of appropriate oral intake and mouth care may help to maintain safe swallowing, preventing aspiration and chest infection. Regular checks of body weight, serum albumin level, oral intake and early enteral feeding are essential to guide nutritional support, minimise malnutrition and problematic medication administration. Encouraging oral intake and providing families with support could promote recovery of swallowing skills and help patients to regain the ability to eat independently. Providing helpful information on the care options available may allay patient and family anxiety. A qualified nurse practitioner could assess patients and ensure that a tailored care plan was designed to meet patients’ needs and this may improve the outcomes considerably. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1320650 / Thesis (D.Nurs.) - University of Adelaide, School of Population Health and Clinical Practice, 2008