The inflammatory response and blood-spinal cord barrier integrity in traumatic spinal cord injury: a prospective pilot study

• Published in: Acta neurochirurgica Vol. 164; no. 12; pp. 3143 - 3153
• Main Authors: Wichmann, Thea Overgaard, Kasch, Helge, Dyrskog, Stig, Høy, Kristian, Møller, Bjarne Kuno, Krog, Jan, Hviid, Claus Vinter Bødker, Hoffmann, Hans Jürgen, Rasmussen, Mikkel Mylius
• Format: Journal Article
• Language: English
• Published: Vienna Springer Vienna 01-12-2022; Springer Nature B.V
• Subjects: Cerebrospinal fluid; Cytokines; Flow cytometry; Humans; Immunoglobulin G; Inflammation; Interleukin 10; Interleukin 6; Interleukin 8; Interventional Radiology; Medicine; Medicine & Public Health; Minimally Invasive Surgery; Neurology; Neuroradiology; Neurosurgery; Original Article - Spine trauma; Patients; Peripheral blood; Pilot Projects; Prospective Studies; Spinal Cord Injuries; Spine trauma; Surgical Orthopedics; Tumor necrosis factor-α; γ-Interferon; Traumatic spinal cord injury; Blood-spinal cord barrier; Flow cytometry; Multiplex immunoassay; Inflammation; Imaging flow cytometry
• ISSN: 0942-0940; 0001-6268; 0942-0940
• DOI: 10.1007/s00701-022-05369-6

Purpose
Triggering of inflammatory responses and disruption of blood-spinal cord barrier (BSCB) integrity are considered pivotal events in the pathophysiology of traumatic spinal cord injury (TSCI). Yet, these events are poorly understood and described in humans. This study aims to describe inflammatory responses and BSCB integrity in human TSCI.
Methods
Fifteen TSCI patients and fifteen non-TSCI patients were prospectively recruited from Aarhus University Hospital, Denmark. Peripheral blood (PB) and cerebrospinal fluid (CSF) were collected at median day 0 [IQR: 1], median day 9 [IQR: 2], and median day 148 [IQR: 49] after injury. PB and CSF were analyzed for immune cells by flow cytometry, cytokines by multiplex immunoassay, and BSCB integrity by IgG Index.
Results
Eleven TSCI patients completed follow-up. Results showed alterations in innate and adaptive immune cell counts over time. TSCI patients had significantly increased cytokine concentrations in CSF at the first and second follow-up, while only concentrations of interleukin (IL)-4, IL-8, and tumor necrosis factor-α remained significantly increased at the third follow-up. In PB, TSCI patients had significantly increased IL-6, IL-8, and IL-10 concentrations and significantly decreased interferon-γ concentrations at the first follow-up. Results further showed increased IgG Index indicative of BSCB disruption in seven TSCI patients at the first follow-up, five TSCI patients at the second follow-up, and two patients at the third follow-up.
Conclusions
Our results suggest that TSCI mainly triggers innate inflammatory responses that resolves over time, although with some degree of non-resolving inflammation, particularly in CSF. Our results cannot confirm BSCB disruption in all TSCI patients.