Key result
Transient hypertension secondary to autonomic dysreflexia caused acute cerebral hyperperfusion in patients with spinal cord injury and led to cerebrovascular endothelial dysfunction in a rat model.
Why the study?
Does transient hypertension secondary to autonomic dysreflexia after spinal cord injury cause cerebrovascular endothelial dysfunction and fibrosis?
Population
Patients with spinal cord injury and a rat model of spinal cord injury
Design
Preclinical
Follow-up
4 weeks (in rat model)
Authors
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Highlights potential cerebrovascular risk from transient hypertension in SCI; hypothesis-generating and requires prospective validation.
Does transient hypertension secondary to autonomic dysreflexia after spinal cord injury cause cerebrovascular endothelial dysfunction and fibrosis?
p-value: p=<0.0001
Transient hypertension from autonomic dysreflexia after spinal cord injury causes unique cerebrovascular impairment characterized by endothelial dysfunction and profibrotic stiffening.
Phillips et al. (2017) studied Spinal cord injury with autonomic dysreflexia (n=62). Transient hypertension (autonomic dysreflexia) vs. Baseline/Unexposed was evaluated on Cerebral blood flow (CBF) response to transient hypertension (p=<0.0001). Transient hypertension secondary to autonomic dysreflexia caused acute cerebral hyperperfusion in patients with spinal cord injury and led to cerebrovascular endothelial dysfunction in a rat model.
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