ArticleFrontiers in systems neuroscience2019
Brain-Dependent Processes Fuel Pain-Induced Hemorrhage After Spinal Cord Injury.
Article in Frontiers in systems neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Review
- Regional anesthesia after spinal cord injury attenuates behavioral loss, hemorrhage, and cell death.Frontiers in neurology · 2026Article
- Updating perspectives on spinal cord function: motor coordination, timing, relational processing, and memory below the brain.Frontiers in systems neuroscience · 2024Review
- General Anesthesia Blocks Pain-Induced Hemorrhage and Locomotor Deficits After Spinal Cord Injury in Rats.Journal of neurotrauma · 2023Article
- A modified impactor for establishing a graded contusion spinal cord injury model in rats.Annals of translational medicine · 2022Article
- Noxious Stimulation Induces Acute Hemorrhage and Impairs Long-Term Recovery after Spinal Cord Injury (SCI) in Female Rats: Evidence Estrous Cycle May Have a Modulatory Effect.Neurotrauma reports · 2022Article
- Hemorrhage and Locomotor Deficits Induced by Pain Input after Spinal Cord Injury Are Partially Mediated by Changes in Hemodynamics.Journal of neurotrauma · 2021Article
- Contribution of Brain Processes to Tissue Loss After Spinal Cord Injury: Does a Pain-Induced Rise in Blood Pressure Fuel Hemorrhage?Frontiers in systems neuroscience · 2021Article
- Learning to promote recovery after spinal cord injury.Experimental neurology · 2020Review
- Pharmacological Transection of Brain-Spinal Cord Communication Blocks Pain-Induced Hemorrhage and Locomotor Deficits after Spinal Cord Injury in Rats.Journal of neurotrauma · 2020Article
- The effect of concurrent neural injuries on hemorrhage.Frontiers in neurologyArticle
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Pain (nociceptive) input caudal to a spinal contusion injury can undermine long-term recovery and increase tissue loss (secondary injury). Prior work suggests that nociceptive stimulation has this effect because it fosters the breakdown of the blood-spinal cord barrier (BSCB) at the site of injury, allowing blood to infiltrate the tissue. The present study examined whether these effects impact tissue rostral and caudal to the site of injury. In addition, the study evaluated whether cutting communication with the brain, by means of a rostral transection, affects the development of hemorrhage. Eighteen hours after rats received a lower thoracic (T11-12) contusion injury, half underwent a spinal transection at T2. Noxious electrical stimulation (shock) was applied 6 h later. Cellular assays showed that, in non-transected rats, nociceptive stimulation increased hemoglobin content, activated pro-inflammatory cytokines and engaged signals related to cell death at the site of injury. These effects were not observed in transected animals. In the next experiment, the spinal transection was performed at the time of contusion injury. Nociceptive stimulation was applied 24 h later and tissue was sectioned for microscopy. In non-transected rats, nociceptive stimulation increased the area of hemorrhage and this effect was blocked by spinal transection. These findings imply that the adverse effect of noxious stimulation depends upon spared ascending fibers and the activation of rostral (brain) systems. If true, stimulation should induce less hemorrhage after a severe contusion injury that blocks transmission to the brain. To test this, rats were given a mild, moderate, or severe, injury and electrical stimulation was applied 24 h later. Histological analyses of longitudinal sections showed that nociceptive stimulation triggered less hemorrhage after a severe contusion injury. The results suggest that brain-dependent processes drive pain-induced hemorrhage after spinal cord injury (SCI).
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