The effect of concurrent neural injuries on hemorrhage

Spinal cord injury (SCI) is often accompanied by additional tissue damage (polytrauma) that amplifies inflammation and activates pain pathways. The latter has been studied by engaging nociceptive fibers using electrical stimulation or capsaicin caudal to a thoracic SCI. Nociceptive stimulation 1 day after SCI increases hemorrhage, amplifying secondary tissue loss. Noxious stimulation also promotes hemorrhage after a traumatic brain injury (TBI). A common form of polytrauma after SCI involves a TBI. The current study examines whether a concurrent TBI promotes hemorrhage after SCI. This also allowed us to evaluate whether a concurrent SCI promotes brain hemorrhage after TBI.

Animals received a thoracic SCI and a concurrent brain surgery (anesthesia alone, craniectomy, or TBI). Other animals received a TBI to the frontal region and a concurrent spinal surgery (anesthesia alone, laminectomy, or SCI). Tissue was collected 24 h later, sectioned, and the extent of brain/spinal cord hemorrhage was quantified. Sham controls were included to verify a remote injury (SCI/TBI) does not induce hemorrhage in the absence of local neural damage.

A concurrent TBI with a SCI amplified hemorrhage in the spinal cord. A craniectomy had an intermediate effect on hemorrhage. Additionally, concurrent SCI with a TBI increased hemorrhage in the brain with a more modest effect.

The results provide a link between hemorrhage development and concurrent neural injuries, with greater hemorrhage observed after SCI in animals with a concurrent TBI. SCI modestly impacted hemorrhage after TBI. These results provide a basis to further investigate the mechanisms responsible for interactions between multiple neurotraumatic injuries.