Both sensorimotor and autonomic dysfunctions often occur after spinal cord injury（SCI）. Particularly, a high thoracic or cervical SCI interrupts supraspinal vasomotor pathways and results in disordered hemodynamics ...Both sensorimotor and autonomic dysfunctions often occur after spinal cord injury（SCI）. Particularly, a high thoracic or cervical SCI interrupts supraspinal vasomotor pathways and results in disordered hemodynamics due to deregulated sympathetic outflow. As a result of the reduced sympathetic activity, patients with SCI may experience hypotension, cardiac dysrhythmias, and hypothermia post-injury. In the chronic phase, changes within the CNS and blood vessels lead to orthostatic hypotension and life-threatening autonomic dysreflexia（AD）. AD is characterized by an episodic, massive sympathetic discharge that causes severe hypertension associated with bradycardia. The syndrome is often triggered by unpleasant visceral or sensory stimuli below the injury level. Currently the only treatments are palliative - once a stimulus elicits AD, pharmacological vasodilators are administered to help reduce the spike in arterial blood pressure. However, a more effective means would be to mitigate AD development by attenuating contributing mechanisms, such as the reorganization of intraspinal circuits below the level of injury. A better understanding of the neuropathophysiology underlying cardiovascular dysfunction after SCI is essential to better develop novel therapeutic approaches to restore hemodynamic performance.展开更多
Spinal cord injury（SCI）is a traumatic event that can lead to permanent motor and sensory deficits.After the initial trauma,axons of surviving neurons rapidly retract.While there may be a small degree of abortive spr...Spinal cord injury（SCI）is a traumatic event that can lead to permanent motor and sensory deficits.After the initial trauma,axons of surviving neurons rapidly retract.While there may be a small degree of abortive sprouting,virtually all attempts at robust regrowth across the lesion site ultimately fail.Thus,neurons below the level of the injury are permanently disconnected from their normal input,resulting in persistent loss of function.展开更多
基金supported by research grants to VJT from the National Institutes of Health(R01 NS085426)the Department of Defense(W81XWH-14-1-060)
文摘Both sensorimotor and autonomic dysfunctions often occur after spinal cord injury（SCI）. Particularly, a high thoracic or cervical SCI interrupts supraspinal vasomotor pathways and results in disordered hemodynamics due to deregulated sympathetic outflow. As a result of the reduced sympathetic activity, patients with SCI may experience hypotension, cardiac dysrhythmias, and hypothermia post-injury. In the chronic phase, changes within the CNS and blood vessels lead to orthostatic hypotension and life-threatening autonomic dysreflexia（AD）. AD is characterized by an episodic, massive sympathetic discharge that causes severe hypertension associated with bradycardia. The syndrome is often triggered by unpleasant visceral or sensory stimuli below the injury level. Currently the only treatments are palliative - once a stimulus elicits AD, pharmacological vasodilators are administered to help reduce the spike in arterial blood pressure. However, a more effective means would be to mitigate AD development by attenuating contributing mechanisms, such as the reorganization of intraspinal circuits below the level of injury. A better understanding of the neuropathophysiology underlying cardiovascular dysfunction after SCI is essential to better develop novel therapeutic approaches to restore hemodynamic performance.
基金funded by NIH R01 NS085426(VJT)the Craig H.Neilsen Foundation(DW)
文摘Spinal cord injury（SCI）is a traumatic event that can lead to permanent motor and sensory deficits.After the initial trauma,axons of surviving neurons rapidly retract.While there may be a small degree of abortive sprouting,virtually all attempts at robust regrowth across the lesion site ultimately fail.Thus,neurons below the level of the injury are permanently disconnected from their normal input,resulting in persistent loss of function.
