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OBJECTIVE: To explore the effects of trunk training using motor imagery on trunk control and balance function in patients with stroke. METHODS: One hundred eligible stroke patients were randomly divided into a control group and trial group. The control group was given routine rehabilitation therapy, while the trial group was given routine rehabilitation therapy and trunk training using motor imagery. RESULTS: Prior to treatment, there was no significant difference between the two groups (P > 0.05) in Sheikh's trunk control ability, Berg rating scale (BBS), Fugl-Meyer assessment (FMA), movement length, movement area, average front-rear movement speed, average left-right movement speed, and surface electromyography (sEMG) signal of the bilateral erector spinae and rectus abdominis. After treatment, Sheikh's trunk control ability, FMA, and BBS in the two groups were significantly higher than those before treatment (P < 0.05). The movement length, movement area, the average front-rear movement speed, and the average left-right movement speed in the two groups decreased significantly (P < 0.05). The differences of these indicators between the two groups were statistically significant (P < 0.05). After treatment, the rectus abdominis and erector spinae on the affected side of the two groups improved when compared with those before treatment (P < 0.05). The rectus abdominis and erector spinae on the healthy side of the trial group descended after treatment (P < 0.05), while little changes were observed on the healthy side of the control group after treatment (P > 0.05). The rectus abdominis and erector spinae on the affected side of the trial group improved when compared with those in the control group (P < 0.05). There was no significant difference between the two groups in the decline of abdominalis rectus and erector spinal muscle on the healthy side. CONCLUSION: Trunk training using motor imagery can significantly improve the trunk control ability and balance function of stroke patients and is conducive to promoting the recovery of motor function.
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Objective: To underscore the paramount significance of incorporating comprehensive rehabilitation therapy as a crucial aspect of managing lymphedema caused by breast cancer surgery, and to illuminate our first-hand experience and insights gained in utilizing this approach. Methods: We present a case report of a breast cancer survivor who had been suffering from persistent left upper-limb edema for over 15 years, who was effectively treated with a combination of conventional rehabilitation (seven-step decongestion therapy) and a comprehensive rehabilitation program (seven-step decongestion therapy, along with core and respiratory function training, as well as functional brace wearing). The efficacy of the rehabilitation therapy was evaluated through a comprehensive assessment. Results: Although the patient underwent the conventional rehabilitation program for one month, only limited improvement was observed. However, after an additional month of comprehensive rehabilitation treatment, the patient exhibited significant improvement in both lymphedema and the overall function of the left upper limb. The patient's progress was quantified by measuring the reduction in arm circumference, which demonstrated a notable decrease. Furthermore, improvements in joint range of motion were observed, with forward flexion of the shoulder enhancing by 10°, forward flexion improving by 15°, and elbow flexion increasing by 10°. In addition, manual muscular strength tests revealed an increase in strength from Grade 4 to Grade 5. The patient's quality of life was also significantly improved, as evidenced by the increase in the Activities of Daily Living score from 95 to 100 points, the increase in the the Functional Assessment of Cancer Therapy: Breast score from 53 to 79 points, and the decrease in the Kessler Psychological Distress Scale score from 24 to 17 points. Conclusion: While seven-step decongestion therapy has been shown to be effective in reducing upper-limb lymphedema caused by breast cancer surgery, it has limitations in treating more chronic cases of the condition. However, when combined with core and respiratory function training and functional brace wearing, seven-step decongestion therapy has been shown to be even more effective in reducing lymphedema and improving limb function, ultimately leading to significant improvements in quality of life.
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Background: Acetylcholinesterase (AChE) and choline acetyltransferase (ChAT) are closely related to the regulation of learning and memory. Nevertheless, whether sevoflurane has influence on cognition through regulating the expression of AChE and ChAT remains unclear. Methods: Aging rat model was established by subcutaneously injection of D-galactose for 6 consecutive weeks. To determine the role of AChE and ChAT in sevoflurane-induced cognitive impairment, the Morris water maze (MWM) was used to assess the cognitive and memory function after sevoflurane exposure. Then, the variations of AChE and ChAT was detected by western blotting analysis and quantitative real-time polymerase chain reaction (qRT-PCR) respectively. Results: Our result indicated that aging model rats had showed cognition decline at 2 hours and 1week after exposure to sevoflurane. Moreover, the expression of AChE and ChAT enhanced in rats that had inhaled sevoflurane. Interestingly, our study also found that the increase of oxygen concentration had a positive impact on the gene expression of ChAT. Conclusion: We have identified that the overexpression of AChE and ChAT improved significantly cognitive function after sevoflurane exposure.
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OBJECTIVE: To assess changes in the cognitive function and hippocampal ultrastructure of elderly rats exposed to sevoflurane. METHODS: Ault male Sprague-Dawley rats were given subcutaneous injection of D-galactose on the neck for 40 d to establish elderly models, after 9-day behavioral training. The model rats were divided into 3 groups randomly: control group with natural air, A/O group with 6 h exposure to carrier gas (2 L/min Air+2 L/min O2), and Sev group with 6 h exposure to 3.2% sevoflurane through carrier gas. Morris Water Maze and balance beam experiment were conducted on 6 rats in each group 2 h, 1 week and 4 weeks after treatments, respectively. The hippocampal tissues of the rats were rapidly dissected and prepared by glutaraldehyde fixation, ethanol dehydration, infiltration, embedding polymerization, semimembrane section localization and staining for examinations under transmission electron microscopy. The hippocampal ultrastructure such as nucleus, cytoplasm, mitochondria, endoplasmic reticulum, medullary nerve fiber, synapse and apoptotic corpuscle were observed. RESULTS: Ethology: compared with the control and A/O groups, significant reductions in the probe trial capability were found in the rats after 2 h exposure to sevoflurane, which recovered at 1 week and 4 weeks. Sevoflurane also increased the working memory escape latency 2 h and 1 week after exposure. The balance beam experiment showed that sevoflurane prolonged the staring time of rats after 2 h exposure, which recovered at 1 week and 4 weeks. Prolonged length for going through the balance beam was found consistently in the rats exposed to sevoflurane. Transmission electron microscopy: rats in the control group were found to have clear hippocampal ultrastructure, intact nuclear membrane, no edema fluid in the cytoplasm, intact mitochondria and endoplasmic reticulum, normal medullary nerve fibers, intact synaptic structure, and no apoptotic bodies in the cells. But a small amount of edema were observed in the cytoplasm of hippocampal cells in the rats exposed to sevoflurane and A/O at 2 h, which increased at 1 week. The cytoplasmic morphology of rats in the A/O group returned to normal at 4 weeks. But further increase of edema was observed in the rats 4 weeks after exposure to sevoflurane. No abnormal morphological structures or apoptotic bodies in other organelles were found. CONCLUSIONS: Sevoflurane can induce early neurocognitive impairments in elderly rats, which may be related with changes in the hippocampus ultrastructure.
