Paraplegic gait orthosis has been shown to help paraplegic patients stand and walk, although this method cannot be individualized for patients with different spinal cord injuries and functional recovery of the lower e...Paraplegic gait orthosis has been shown to help paraplegic patients stand and walk, although this method cannot be individualized for patients with different spinal cord injuries and functional recovery of the lower extremities. There is, however, a great need to develop individualized paraplegic orthosis to improve overall quality of life for paraplegic patients. In the present study, 36 spinal cord(below T4) injury patients were equally and randomly divided into control and observation groups. The control group received systematic rehabilitation training, including maintenance of joint range of motion, residual muscle strength training, standing training, balance training, and functional electrical stimulation. The observation group received an individualized paraplegic locomotion brace and functional training according to the various spinal cord injury levels and muscle strength based on comprehensive systematic rehabilitation training. After 3 months of rehabilitation training, the observation group achieved therapeutic locomotion in 8 cases, family-based locomotion in 7 cases, and community-based locomotion in 3 cases. However, locomotion was not achieved in any of the control group patients. These findings suggest that individualized paraplegic braces significantly improve activity of daily living and locomotion in patients with thoracolumbar spinal cord injury.展开更多
Long-term potentiation (LTP) at synapses between primary afferents and spinal dorsal horn neurons induced by noxious electrical stimulation or injury of peripheral nerve is con- sidered to underlie chronic pain [1]....Long-term potentiation (LTP) at synapses between primary afferents and spinal dorsal horn neurons induced by noxious electrical stimulation or injury of peripheral nerve is con- sidered to underlie chronic pain [1]. The mechanisms of the spinal LTP have been intensively investigated, since it was discovered in 1995 [2]. In recent years, spinal application of ATP [3], brain-derived neurotrophic factor (BDNF) [4] and opioid [5] has been shown to induce spinal LTP at C-fiber synapses in the absence of conditioning activation of primary afferents. This is contrary to the general belief that coinci- dent pre- and postsynaptic activity is needed for LTP induction. Recently, Sandkiihler and his co-workers reported in Science that combined activation of microglia and astro- cytes by P2X7 receptor agonist BzATP induces LTP at synapses between afferent C-fibers and spinal lamina I neurons in the absence of presynaptic activation, which is termed gliogenic LTP [6] (Fig. 1C). To determine the rela- tionship between the gliogenic LTP and high frequency stimulation (HFS)-indueed LTP, they used transverse lum- bar spinal cord slices with long dorsal roots which were separated into halves. Twenty two lamina I neurons that received independent monosynaptic C-fiber inputs from each dorsal root half were recorded. Homosynaptic LTP is recorded in 12 neurons, among them 6 neurons also show heterosynaptic LTP (Fig. 1A). Interestingly, heterosynaptic LTP is also induced in 5 neurons in which HFS fails to induce homosynaptic LTP (Fig. 1B).展开更多
文摘Paraplegic gait orthosis has been shown to help paraplegic patients stand and walk, although this method cannot be individualized for patients with different spinal cord injuries and functional recovery of the lower extremities. There is, however, a great need to develop individualized paraplegic orthosis to improve overall quality of life for paraplegic patients. In the present study, 36 spinal cord(below T4) injury patients were equally and randomly divided into control and observation groups. The control group received systematic rehabilitation training, including maintenance of joint range of motion, residual muscle strength training, standing training, balance training, and functional electrical stimulation. The observation group received an individualized paraplegic locomotion brace and functional training according to the various spinal cord injury levels and muscle strength based on comprehensive systematic rehabilitation training. After 3 months of rehabilitation training, the observation group achieved therapeutic locomotion in 8 cases, family-based locomotion in 7 cases, and community-based locomotion in 3 cases. However, locomotion was not achieved in any of the control group patients. These findings suggest that individualized paraplegic braces significantly improve activity of daily living and locomotion in patients with thoracolumbar spinal cord injury.
文摘Long-term potentiation (LTP) at synapses between primary afferents and spinal dorsal horn neurons induced by noxious electrical stimulation or injury of peripheral nerve is con- sidered to underlie chronic pain [1]. The mechanisms of the spinal LTP have been intensively investigated, since it was discovered in 1995 [2]. In recent years, spinal application of ATP [3], brain-derived neurotrophic factor (BDNF) [4] and opioid [5] has been shown to induce spinal LTP at C-fiber synapses in the absence of conditioning activation of primary afferents. This is contrary to the general belief that coinci- dent pre- and postsynaptic activity is needed for LTP induction. Recently, Sandkiihler and his co-workers reported in Science that combined activation of microglia and astro- cytes by P2X7 receptor agonist BzATP induces LTP at synapses between afferent C-fibers and spinal lamina I neurons in the absence of presynaptic activation, which is termed gliogenic LTP [6] (Fig. 1C). To determine the rela- tionship between the gliogenic LTP and high frequency stimulation (HFS)-indueed LTP, they used transverse lum- bar spinal cord slices with long dorsal roots which were separated into halves. Twenty two lamina I neurons that received independent monosynaptic C-fiber inputs from each dorsal root half were recorded. Homosynaptic LTP is recorded in 12 neurons, among them 6 neurons also show heterosynaptic LTP (Fig. 1A). Interestingly, heterosynaptic LTP is also induced in 5 neurons in which HFS fails to induce homosynaptic LTP (Fig. 1B).