Abstract
BackgroundYears after a traumatic spinal cord injury (SCI), a subset of patients may develop progressive clinical deterioration due to intradural scar formation and spinal cord tethering, with or without an associated syringomyelia. Meningitis, intradural hemorrhages, or intradural tumor surgery may also trigger glial scar formation and spinal cord tethering, leading to neurological worsening. Surgery is the treatment of choice in these chronic SCI patients.ObjectiveWe hypothesized that cerebrospinal fluid (CSF) and plasma biomarkers could track ongoing neuronal loss and scar formation in patients with spinal cord tethering and are associated with clinical symptoms.MethodsWe prospectively enrolled 12 patients with spinal cord tethering and measured glial fibrillary acidic protein (GFAP), ubiquitin C-terminal hydrolase L1 (UCH-L1), and phosphorylated Neurofilament-heavy (pNF-H) in CSF and blood. Seven patients with benign lumbar intradural tumors and 7 patients with cervical radiculopathy without spinal cord involvement served as controls.ResultsAll evaluated biomarker levels were markedly higher in CSF than in plasma, without any correlation between the two compartments. When compared with radiculopathy controls, CSF GFAP and pNF-H levels were higher in patients with spinal cord tethering (p ≤ 0.05). In contrast, CSF UCH-L1 levels were not altered in chronic SCI patients when compared with either control groups.ConclusionsThe present findings suggest that in patients with spinal cord tethering, CSF GFAP and pNF-H levels might reflect ongoing scar formation and neuronal injury potentially responsible for progressive neurological deterioration.
Highlights
Glial scar formation, resulting in spinal cord tethering, may become clinically evident many years following spinal cord injury (SCI), irrespective of the initial injury mechanism or severity [11, 12, 14, 24]
When the spinal cord is tethered to the surrounding dura, impaired cord pulsations, reduced flow of the cerebrospinal fluid, and/or spinal cord traction can lead to neurological dysfunction and/or spinal cord cyst formation [18, 33, 52]
Most symptomatic spinal cord tethering occurs secondary to traumatic SCI where up to 5% of patients develop progressive neurological deterioration after a few months up to many years following the initial injury [11, 14, 24, 43]
Summary
Glial scar formation, resulting in spinal cord tethering, may become clinically evident many years following spinal cord injury (SCI), irrespective of the initial injury mechanism or severity [11, 12, 14, 24]. Most symptomatic spinal cord tethering occurs secondary to traumatic SCI where up to 5% of patients develop progressive neurological deterioration after a few months up to many years following the initial injury [11, 14, 24, 43]. This clinical entity is named post-traumatic myelopathy. Years after a traumatic spinal cord injury (SCI), a subset of patients may develop progressive clinical deterioration due to intradural scar formation and spinal cord tethering, with or without an associated syringomyelia. Surgery is the treatment of choice in these chronic SCI patients
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