ReviewCurrent neuropharmacology2021
The Role of Astrogliosis in Formation of the Syrinx in Spinal Cord Injury.
Review in Current neuropharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- Hypoxia Upregulates RIPK1 via the HIF-1α-JAK-STAT Pathway Leading to Astrocyte Necroptosis to Promote Cavitation After Spinal Cord Injury.CNS neuroscience & therapeutics · 2026Article
- Exosomal miR-149 from human umbilical cord mesenchymal stem cells attenuates spinal cord injury-induced blood-spinal cord barrier disruption by suppressing the ET-1/PI3K/Akt signaling pathway.Stem cell research & therapy · 2025Article
- Holocord syringomyelia caused by tethered cord syndrome: case report and literature review.BMC neurology · 2024Review
- Effects of CFTR-ENaC on spinal cord edema after spinal cord injury.Open medicine (Warsaw, Poland) · 2024Article
- Spinal cord tethering and syringomyelia after trauma: impact of age and surgical outcome.Scientific reports · 2023Article
- MiR-155-5p Aggravated Astrocyte Activation and Glial Scarring in a Spinal Cord Injury Model by Inhibiting Ndfip1 Expression and PTEN Nuclear Translocation.Neurochemical research · 2023Article
- Neural Stem Cells Overexpressing Arginine Decarboxylase Improve Functional Recovery from Spinal Cord Injury in a Mouse Model.International journal of molecular sciences · 2022Article
- Pathophysiology and Therapeutic Approaches for Spinal Cord Injury.International journal of molecular sciences · 2022Review
- Early mobilization in spinal cord injury promotes changes in microglial dynamics and recovery of motor function.IBRO neuroscience reports · 2022Article
- Barriers to axonal regeneration after spinal cord injury: a current perspective.Neural regeneration research · 2022Article
- Challenges of Delirium Management in Patients with Traumatic Brain Injury: From Pathophysiology to Clinical Practice.Current neuropharmacology · 2021Review
- The Pathogenesis of Neurotrauma Indicates Targets for Neuroprotective Therapies.Current neuropharmacology · 2021Article
- Imaging of Neurotrauma in Acute and Chronic Settings.Current neuropharmacology · 2021Review
- Roadmap for Stroke: Challenging the Role of the Neuronal Extracellular Matrix.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A massive localized trauma to the spinal cord results in complex pathologic events driven by necrosis and vascular damage which in turn leads to hemorrhage and edema. Severe, destructive and very protracted inflammatory response is characterized by infiltration by phagocytic macrophages of a site of injury which is converted into a cavity of injury (COI) surrounded by astroglial reaction mounted by the spinal cord. The tissue response to the spinal cord injury (SCI) has been poorly understood but the final outcome appears to be a mature syrinx filled with the cerebrospinal fluid with related neural tissue loss and permanent neurologic deficits. This paper reviews known pathologic mechanisms involved in the formation of the COI after SCI and discusses the integrative role of reactive astrogliosis in mechanisms involved in the removal of edema after the injury. A large proportion of edema fluid originating from the trauma and then from vasogenic edema related to persistent severe inflammation, may be moved into the COI in an active process involving astrogliosis and specifically over-expressed aquaporins.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.