Spinal Obstruction-Related vs. Craniocervical Junction-Related Syringomyelia: A Comparative Study

Abstract

BackgroundNo prior reports have focused on spinal cord injury (SCI) characteristics or inflammation after destruction of the blood–spinal cord barrier by syringomyelia. This study aimed to determine the differences in syringomyelia-related central SCI between craniocervical junction (CCJ) syringomyelia and post-traumatic syringomyelia (PTS) before and after decompression.MethodsIn all, 106 CCJ, 26 CCJ revision and 15 PTS patients (mean history of symptoms, 71.5 ± 94.3, 88.9 ± 85.5, and 32.3 ± 48.9 months) between 2015 and 2019 were included. The symptom course was analyzed with the American Spinal Injury Association ASIA and Klekamp–Samii scoring systems, and neurological changes were analyzed by the Kaplan–Meier statistics. The mean follow-up was 20.7 ± 6.2, 21.7 ± 8.8, and 34.8 ± 19.4 months.ResultsThe interval after injury was longer in the PTS group, but the natural history of syringomyelia was shorter (p = 0.0004 and 0.0173, respectively). The initial symptom was usually paraesthesia (p = 0.258), and the other main symptoms were hypoesthesia (p = 0.006) and abnormal muscle strength (p = 0.004), gait (p < 0.0001), and urination (p < 0.0001). SCI associated with PTS was more severe than that associated with the CCJ (p = 0.003). The cavities in the PTS group were primarily located at the thoracolumbar level, while those in the CCJ group were located at the cervical-thoracic segment at the CCJ. The syrinx/cord ratio of the PTS group was more than 75% (p = 0.009), and the intradural adhesions tended to be more severe (p < 0.0001). However, there were no significant differences in long-term clinical efficacy or peripheral blood inflammation markers (PBIMs) except for the red blood cell (RBC) count (p = 0.042).ConclusionPTS tends to progress faster than CCJ-related syringomyelia. Except for the RBC count, PBIMs showed no value in distinguishing the two forms of syringomyelia. The predictive value of the neutrophil-to-lymphocyte ratio for syringomyelia-related inflammation was negative except in the acute phase.

Long-Term Impairment of the Blood-Spinal Cord Barrier in Patients With Post-Traumatic Syringomyelia and its Effect on Prognosis

“…In recent decades, the therapeutic effect of arachnoid adhesion lysis on syringomyelia has been fully confirmed in PTS or CM-syringomyelia patients 2,12,13 . Most PTS patients in our cohort had unfavorable outcomes after successful arachnoid adhesion lysis compared with a previous CM-syringomyelia report, 2 which is positively related to severe BSCB damage. We speculated that fluid crossing a deficient BSCB may contribute to the accumulation of syrinx fluid 29 .…”

“…Its goals are to expand the intradural space, restore the unimpeded flow of CSF through the spine, end syrinx distension, and arrest progressive myelopathy 1,5,27,28 . In recent decades, the therapeutic effect of arachnoid adhesion lysis on syringomyelia has been fully confirmed in PTS or CM-syringomyelia patients 2,12,13 . Most PTS patients in our cohort had unfavorable outcomes after successful arachnoid adhesion lysis compared with a previous CM-syringomyelia report, 2 which is positively related to severe BSCB damage.…”

“…In addition, intradural decompression often only improves myelopathy in 50% of PTS patients 2,4,[13][14][15] but improves Chiari-associated syringomyelia in 80% of patients. 2,13 We speculated that the BSCB is still severely damaged and that fluid crossing a deficient BSCB in PTS patients may contribute to the accumulation of syrinx fluid in addition to the development of arachnoid adhesions.…”

“…Post-traumatic syringomyelia (PTS) is a disorder characterized by progressive neurological deterioration as a result of the expansion of a cerebrospinal fluid (CSF)-filled cyst that develops following a spinal cord injury (SCI) over several years. Approximately 20% of patients with a traumatic SCI have secondary PTS 1–5 . The pathophysiological mechanism of PTS is generally attributed to the transparenchymal flow of CSF from the subarachnoid space to the syrinx 4 .…”

Neurological deterioration after posterior fossa decompression for adult syringomyelia: Proposal for a summarized treatment algorithm

“…Conditions such as CMI, trauma, arachnoiditis, spinal degenerative diseases, and epidural and extramedullary tumors often lead to occlusion of the subarachnoid space followed by disturbances in CSF flow resulting in syringomyelia ( 25 – 27 ). However, for intramedullary tumors or vascular lesions, transudation and tumor cell secretion are responsible for syrinx progression ( 28 ).…”