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Objective: We investigated the effects of a computer-generated interactive visual feedback training program on the recovery from pusher syndrome in stroke patients. Design: Assessor-blinded, pilot randomized controlled study. Participants: A total of 12 stroke patients with pusher syndrome were randomly assigned to either the experimental group (N = 7, computer-generated interactive visual feedback training) or control group (N = 5, mirror visual feedback training). Main outcome measures: The scale for contraversive pushing for severity of pusher syndrome, the Berg Balance Scale for balance performance, and the Fugl-Meyer assessment scale for motor control were the outcome measures. Patients were assessed pre- and posttraining. Results: A comparison of pre- and posttraining assessment results revealed that both training programs led to the following significant changes: decreased severity of pusher syndrome scores (decreases of 4.0 ±1.1 and 1.4 ±1.0 in the experimental and control groups, respectively); improved balance scores (increases of 14.7 ±4.3 and 7.2 ±1.6 in the experimental and control groups, respectively); and higher scores for lower extremity motor control (increases of 8.4 ±2.2 and 5.6 ±3.3 in the experimental and control groups, respectively). Furthermore, the computer-generated interactive visual feedback training program produced significantly better outcomes in the improvement of pusher syndrome (p < 0.01) and balance (p < 0.05) compared with the mirror visual feedback training program. Conclusions: Although both training programs were beneficial, the computer-generated interactive visual feedback training program more effectively aided recovery from pusher syndrome compared with mirror visual feedback training. [ABSTRACT FROM AUTHOR]

Neurogenesis is a physiological response after cerebral ischemic injury to possibly repair the damaged neural network. Therefore, promoting neurogenesis is very important for functional recovery after cerebral ischemic injury. Our previous research indicated that hyperbaric oxygen therapy (HBOT) exerted neuroprotective effects, such as reducing cerebral infarction volume. The purposes of this study were to further explore the effects of HBOT on the neurogenesis and the expressions of cell migration factors, including the stromal cell-derived factor 1 (SDF1) and its target receptor, the CXC chemokine receptor 4 (CXCR4). Thirty-two Sprague–Dawley rats were divided into the control or HBO group after receiving transient middle cerebral artery occlusion (MCAO). HBOT began to intervene 24 h after MCAO under the pressure of 3 atmospheres for one hour per day for 21 days. Rats in the control group were placed in the same acrylic box without HBOT during the experiment. After the final intervention, half of the rats in each group were cardio-perfused with ice-cold saline followed by 4% paraformaldehyde under anesthesia. The brains were removed, dehydrated and cut into serial 20μm coronal sections for immunofluorescence staining to detect the markers of newborn cell (BrdU+), mature neuron cell (NeuN+), SDF1, and CXCR4. The affected motor cortex of the other half rats in each group was separated under anesthesia and used to detect the expressions of brain-derived neurotrophic factor (BDNF), SDF1, and CXCR4. Motor function was tested by a ladder-climbing test before and after the experiment. HBOT significantly enhanced neurogenesis in the penumbra area and promoted the expressions of SDF1 and CXCR4. The numbers of BrdU+/SDF1+, BrdU+/CXCR4+, and BrdU+/NeuN+ cells and BDNF concentrations in the penumbra were all significantly increased in the HBO group when compared with the control group. The motor functions were improved in both groups, but there was a significant difference between groups in the post-test. Our results indicated that HBOT for 21 days enhanced neurogenesis and promoted cell migration toward the penumbra area in transient brain ischemic rats. HBOT also increased BDNF expression, which might further promote the reconstructions of the impaired neural networks and restore motor function. [ABSTRACT FROM AUTHOR]

Brain ischemia leads to muscle inactivity-induced atrophy and may exacerbate motor function deficits. Intramuscular insulin-like growth factor I (IGF-I) injection has been shown to alleviate the brain ischemia-induced muscle atrophy and thus improve the motor function. Motor function is normally gauged by the integrity and coordination of the central nervous system and peripheral muscles. Whether brain ischemic regions are adaptively changed by the intramuscular IGF-I injection is not well understood. In this study, the effect of intramuscular IGF-I injection was examined on the central nervous system of brain ischemic rats. Rats were divided into 4 groups: sham control, brain ischemia control, brain ischemia with IGF-I treatment, and brain ischemia with IGF-I plus IGF-I receptor inhibitor treatment. Brain ischemia was induced by right middle cerebral artery occlusion. IGF-I and an IGF-1 receptor inhibitor were injected into the affected calf and anterior tibialis muscles of the treated rats for 4 times. There was an interval of 2 days between each injection. Motor function was examined and measured at the 24 hours and 7 days following a brain ischemia. The affected hind-limb muscles, sciatic nerve, lumbar spinal cord, and motor cortex were collected for examination after euthanizing the rats. IGF-I expression in the central nervous system and affected muscles were significantly decreased after brain ischemia. Intramuscular IGF-I injection increased the IGF-I expression in the affected muscles, sciatic nerve, lumbar spinal cord, and motor cortex. It also increased the p-Akt expression in the affected motor cortex. Furthermore, intramuscular IGF-I injection decreased the neuronal apoptosis and improved the motor function. However, co-administration of the IGF-I receptor inhibitor eliminated these effects. Intramuscular IGF-I injection after brain ischemia attenuated or reversed the decrease of IGF-I in both central and peripheral tissues, and these effects could contribute to neuroprotection and improve motor function. [ABSTRACT FROM AUTHOR]

Physical exercise may induce neuroprotective effects against brain damage after stroke. The authors aimed to investigate the effects of various exercises on motor function, striatal angiogenesis, and infarct volume in cerebral ischemic rats. Adult male Sprague Dawley rats were subjected to middle cerebral artery occlusion and randomly assigned to 1 of the 4 groups: Rota-rod training, lower speed treadmill training, higher speed treadmill training, or no exercise control. Motor function, striatal angiogenesis, and infarct volume were evaluated before or after motor training. After training, motor function and striatal angiogenesis changed significantly in Rota-rod and higher speed treadmill training groups as compared with the control group. Improvement in motor function significantly correlated with striatal angiogenesis after motor training. Infarct volumes were significantly decreased in lower and higher speed treadmill training groups. The results indicated that both motor training procedures can be used as effective training programs in stroke rehabilitation. [ABSTRACT FROM AUTHOR]

• Oxidative stress leads to secondary brain injury after brain ischemia. • Hyperbaric oxygen (HBO) enhances anti-oxidant system and reduces brain injury. • Glutathione is involved in the protective effects of HBO. Hyperbaric oxygen (HBO) has been suggested as a possible therapy for brain injury. However, the effects of HBO after transient brain ischemia are inconsistent and the underlying mechanisms are not fully known. The present study aimed to investigate the effects of repetitive HBO intervention in a transient middle cerebral artery occlusion (MCAO) animal model. Seventy-two Sprague-Dawley rats received MCAO and were randomly assigned to normal air control or HBO intervention groups. Each group was divided into 3 subgroups according to the intervention time period (7, 14, and 21 days). HBO was started 24 h post-MCAO for 1 h/day at 3.0 ATA with no-air breaks. After the final intervention, half of the rats in each subgroup were sacrificed and the right motor cortex was removed to examine levels of Akt phosphorylation and glutathione (GSH), as well as glutathione peroxidase (GPx) and reductase (GR) activity. The other half of the rats were used to examine infarct volume. At 24 h post-MCAO and the end of the final intervention, rats underwent tests to examine motor performance. We noted that 14- and 21-day HBO interventions significantly reduced infarct volume and increased Akt phosphorylation and GSH levels and GPx and GR activity. Motor performance was also significantly improved after 14- and 21-day interventions. No significant differences were observed between the controls and 7-day intervention groups. Repetitive HBO intervention starting 24 h post-MCAO and applied for at least 14 days, provided neuroprotective effects through modulating the cell survival pathway and antioxidative defense system. [ABSTRACT FROM AUTHOR]

Although insulin-like growth factor 1 (IGF 1) has been used in immobilizated muscles to prevent muscle atrophy, its effects on muscle atrophy after brain ischemia are not known. This study aimed to determine the effects of IGF 1 on preventing muscle atrophy in rats with brain ischemia. Middle cerebral artery occlusion (MCAO) was used to induce the brain ischemia. In the first part of the study, rats were assigned to sham control, ischemic control, and ischemia with different dosages of IGF 1 injection groups to determine the optimal dosage of IGF 1 on preventing muscle atrophy after brain ischemia. In the second part of the study, rats were assigned to sham control, ischemic control, ischemia with IGF 1, or with IGF 1 receptor inhibitor (AG1024) injection groups to determine the specificity of IGF 1 on preventing muscle atrophy after brain ischemia. IGF 1 or AG1024 was injected locally to calf muscles and anterior tibialis (TA) starting from one day after brain ischemia and injections were carried out every other day for 4 times. Muscle weight and myosin heavy chain (MHC) expression in both red (red gastrocnemius and soleus) and white (white gastrocnemius and TA) muscles were significantly decreased after brain ischemia. With at least moderate-dosage (200 ng/100 microl PBS) IGF 1 injection, the muscle weight and MHC protein could be restored in both red and white muscles resulting in better motor performance. However, the high-dose injection of IGF 1 (400 ng/100 microl PBS) did not result in further effects. IGF 1 increased the expression of p-Akt, but such effects were prevented by AG1024 resulting in muscle atrophy and poor motor function. In conclusion, peripheral application of IGF 1 not only prevented muscle atrophy but also enhanced motor function in rats with brain ischemia. The IGF 1-induced PI3K/Akt pathways are important for preventing muscle atrophy induced by brain ischemia.