Autonomic dysreflexia （AD） is a serious cardiovascular disorder in patients with spinal cord injury （SCI）. The primary underlying cause of AD is loss of supraspinal control over sympathetic preganglionic neurons ...Autonomic dysreflexia （AD） is a serious cardiovascular disorder in patients with spinal cord injury （SCI）. The primary underlying cause of AD is loss of supraspinal control over sympathetic preganglionic neurons （SPNs） caudal to the injury, which renders the SPNs hyper-responsive to stimulation. Central maladaptive plasticity, including C-fiber sprouting and propriospinal fiber proliferation exaggerates noxious afferent transmission to the SPNs, causing them to release massive sympathetic discharges that result in severe hypertensive episodes. In parallel, upregulated peripheral vascular sensitivity following SCI exacerbates the hypertensive response by augmenting gastric and pelvic vasoconstriction. Currently, the majority of clinically employed treatments for AD involve anti-hypertensive medications and Botox injections to the bladder. Although these approaches mitigate the severity of AD, they only yield transient effects and target the effector organs, rather than addressing the primary issue of central sympathetic dysregulation. As such, strategies that aim to restore supraspinal reinnervation of SPNs to improve cardiovascular sympathetic regulation are likely more effective for AD. Recent pre-clinical investigations show that cell transplantation therapy is efficacious in reestablishing spinal sympathetic connections and improving hemodynamic per- formance, which holds promise as a potential therapeutic approach.展开更多
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
BACKGROUNDAutonomic dysreflexia (AD) can be a life-threatening condition in patients withspinal cord injury. It is important to prevent bladder overdistension in thesepatients as it may trigger AD. Sensation-dependent...BACKGROUNDAutonomic dysreflexia (AD) can be a life-threatening condition in patients withspinal cord injury. It is important to prevent bladder overdistension in thesepatients as it may trigger AD. Sensation-dependent bladder emptying (SDBE), asa method of bladder management, improves the quality of life and allowsphysiologic voiding. In this study, we report disruption of the SDBE habit afterbladder overdistension leading to AD with chest pain.CASE SUMMARYA 47-year-old male with a diagnosis of C4 American Spinal Cord InjuryAssociation impairment scale A had been emptying his bladder using the cleanintermittent catheterization method with an itchy sensation in the nose as asensory indication for a full bladder for 23 years, and the usual urine volume wasabout 300-400 mL. At the time of this study, the patient had delayed catheterizationfor approximately five hours. He developed severe abdominal pain andheadache and had to visit the emergency room for bladder overdistension (800mL) and a high systolic blood pressure (205 mmHg). After control of AD, ahypersensitive bladder was observed despite using anticholinergic agents. Thesensation indicating bladder fullness changed from nose itching to pain in theabdomen and precordial area. Moreover, the volume of the painful bladder fillingsensation became highly variable and was noted when the bladder urine volumeexceeded only 100 mL. The patient refused intermittent clean catheterization Finally, a cystostomy was performed, which relieved the symptoms.CONCLUSIONPatients using physiologic feedback, such as SDBE, for bladder management arerecommended to avoid bladder overdistension.展开更多
基金supported by NIH NINDS R01NS099076,Morton Cure Paralysis Funds(MCPF)
文摘Autonomic dysreflexia （AD） is a serious cardiovascular disorder in patients with spinal cord injury （SCI）. The primary underlying cause of AD is loss of supraspinal control over sympathetic preganglionic neurons （SPNs） caudal to the injury, which renders the SPNs hyper-responsive to stimulation. Central maladaptive plasticity, including C-fiber sprouting and propriospinal fiber proliferation exaggerates noxious afferent transmission to the SPNs, causing them to release massive sympathetic discharges that result in severe hypertensive episodes. In parallel, upregulated peripheral vascular sensitivity following SCI exacerbates the hypertensive response by augmenting gastric and pelvic vasoconstriction. Currently, the majority of clinically employed treatments for AD involve anti-hypertensive medications and Botox injections to the bladder. Although these approaches mitigate the severity of AD, they only yield transient effects and target the effector organs, rather than addressing the primary issue of central sympathetic dysregulation. As such, strategies that aim to restore supraspinal reinnervation of SPNs to improve cardiovascular sympathetic regulation are likely more effective for AD. Recent pre-clinical investigations show that cell transplantation therapy is efficacious in reestablishing spinal sympathetic connections and improving hemodynamic per- formance, which holds promise as a potential therapeutic approach.
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.
文摘BACKGROUNDAutonomic dysreflexia (AD) can be a life-threatening condition in patients withspinal cord injury. It is important to prevent bladder overdistension in thesepatients as it may trigger AD. Sensation-dependent bladder emptying (SDBE), asa method of bladder management, improves the quality of life and allowsphysiologic voiding. In this study, we report disruption of the SDBE habit afterbladder overdistension leading to AD with chest pain.CASE SUMMARYA 47-year-old male with a diagnosis of C4 American Spinal Cord InjuryAssociation impairment scale A had been emptying his bladder using the cleanintermittent catheterization method with an itchy sensation in the nose as asensory indication for a full bladder for 23 years, and the usual urine volume wasabout 300-400 mL. At the time of this study, the patient had delayed catheterizationfor approximately five hours. He developed severe abdominal pain andheadache and had to visit the emergency room for bladder overdistension (800mL) and a high systolic blood pressure (205 mmHg). After control of AD, ahypersensitive bladder was observed despite using anticholinergic agents. Thesensation indicating bladder fullness changed from nose itching to pain in theabdomen and precordial area. Moreover, the volume of the painful bladder fillingsensation became highly variable and was noted when the bladder urine volumeexceeded only 100 mL. The patient refused intermittent clean catheterization Finally, a cystostomy was performed, which relieved the symptoms.CONCLUSIONPatients using physiologic feedback, such as SDBE, for bladder management arerecommended to avoid bladder overdistension.
