ABSTRACT
[Purpose] This study aimed to explore whether trunk kinesiology taping (KT) can improve trunk function, mobility, and balance in post-stroke patients with hemiparesis. [Participants and Methods] We conducted a single-group pre-post design pilot feasibility study. Thirteen individuals with post-stroke hemiplegia were recruited for this study. All patients received therapeutic trunk KT on the skin, representing the direction of fibres of the trunk muscles underneath. We used the Trunk Impairment Scale (TIS) and Trunk Control Test (TCT) to measure trunk function, Fugl-Meyer assessment (FMA) for balance, limits of stability (LOS) to evaluate balance, and the modified Rivermead mobility index (MRMI) to assess mobility in post-stroke patients. All measures were assessed before and immediately after the intervention. [Results] No adverse effects were found and all patients completed the trial. Compared to the baseline, TIS scores were significantly increased after KT, whereas no changes in TCT score were detected. The directional control of LOS was significantly improved, while no significant changes were seen in the other parameters of LOS, FMA-balance, and MRMI scores. [Conclusion] The results of this investigation show that trunk KT has immediate effects that improve certain trunk functional and balance parameters in stroke patients.
ABSTRACT
Obstructive sleep apnea syndrome (OSAS), characterized by intermittent hypoxia/reoxygenation, may impair the cerebral system. Although mitogenactivated protein kinase (MAPK) signaling was observed to have a key role in hypoxiainduced brain injury, the intracellular events and their underlying mechanisms for intermittent hypoxia/reoxygenation-associated damage to hippocamal MAPKs, including extracellular signalregulated kinase (ERK)1/2, P38MAPK and cJun Nterminal kinase (JNK) remain to be elucidated and require further investigation. A total of five rats in each subgroup were exposed to intermittent hypoxia or continued hypoxia for 2, 4, 6 or 8 weeks. Histological, immunohistochemical and biological analyses were performed to assess nerve cell injury in the hippocampus. Surviving CA1 pyramidal cells were identified by hematoxylin and eosin staining. The levels of phosphorylated ERK1/2, P38MAPK and JNK were detected by western blotting. Bcell lymphoma 2 (Bcl2) and Bcl2associated X protein (Bax) in neural cells were examined by immunohistochemistry. The malondialdehyde (MDA) contents and superoxide dismutase (SOD) activities were measured by thiobarbituric acid and xanthine oxidation methods, respectively. Under continued hypoxia, the levels of phosphoERK1/2 peaked at the fourth week and then declined, whereas phosphoP38MAPK and JNK were detected only in the late stages. By contrast, under intermittent hypoxia, ERK1/2, P38MAPK and JNK were activated at all time-points assessed (2, 4, 6 and 8 weeks). The levels of phosphoERK1/2, P38MAPK and JNK were all higher in the intermittent hypoxia groups than those in the corresponding continued hypoxia groups. Bcl2 was mainly increased and reached the highest level at six weeks in the continued hypoxia group. Of note, Bcl2 rapidly increased to the peak level at four weeks, followed by a decrease to the lowest level at the eighth week in the intermittent hypoxia group. Bax was generally increased at the late stages under continued hypoxia, but increased at all time-points under the intermittent hypoxia conditions. The two types of hypoxia induced an increase in the MDA content, but a decrease in SOD activity. Marked changes in these two parameters coupled with markedly reduced surviving cells in the hippocampus in a timedependent manner were observed in the intermittent hypoxia group in comparison with the continued hypoxia group. OSASinduced intermittent hypoxia markedly activated the MAPK signaling pathways, which were triggered by oxidative stress, leading to abnormal expression of downstream Bcl2 and Bax, and a severe loss of neural cells in the hippocampus.
