J Neurosurg Spine. 2015 Jun;22(6):611-21.

Predictors of intramedullary lesion expansion rate on MR images of patients with subaxial spinal cord injury.

Le E1, Aarabi B1,2, Hersh DS1, Shanmuganathan K2, Diaz C2, Massetti J2, Akhtar-Danesh N3.
  • 11Department of Neurosurgery and.
  • 22R Adams Cowley Shock Trauma Center, University of Maryland School of Medicine, Baltimore, Maryland; and.
  • 33School of Nursing and Department of Clinical Epidemiology and Biostatistics, McMaster University, Hamilton, Ontario, Canada.

 

Abstract

OBJECT Studies of preclinical spinal cord injury (SCI) in rodents indicate that expansion of intramedullary lesions (IMLs) seen on MR images may be amenable to neuroprotection. In patients with subaxial SCI and motor-complete American Spinal Injury Association (ASIA) Impairment Scale (AIS) Grade A or B, IML expansion has been shown to be approximately 900 μm/hour. In this study, the authors investigated IML expansion in a cohort of patients with subaxial SCI and AIS Grade A, B, C, or D. METHODS Seventy-eight patients who had at least 2 MRI scans within 6 days of SCI were enrolled. Data were analyzed by regression analysis. RESULTS In this cohort, the mean age was 45.3 years (SD 18.3 years), 73 patients were injured in a motor vehicle crash, from a fall, or in sport activities, and 77% of them were men. The mean Injury Severity Score (ISS) was 26.7 (SD 16.7), and the AIS grade was A in 23 patients, B in 7, C in 7, and D in 41. The mechanism of injury was distraction in 26 patients, compression in 22, disc/osteophyte complex in 29, and Chance fracture in 1. The mean time between injury onset and the first MRI scan (Interval 1) was 10 hours (SD 8.7 hours), and the mean time to the second MRI scan (Interval 2) was 60 hours (SD 29.6 hours). The mean IML lengths of the first and second MR images were 38.8 mm (SD 20.4 mm) and 51 mm (SD 36.5 mm), respectively. The mean time from the first to the second MRI scan (Interval 3) was 49.9 hours (SD 28.4 hours), and the difference in IML lengths was 12.6 mm (SD 20.7 mm), reflecting an expansion rate of 366 μm/ hour (SD 710 μm/hour). IML expansion in patients with AIS Grades A and B was 918 μm/hour (SD 828 μm/hour), and for those with AIS Grades C and D, it was 21 μm/hour (SD 304 μm/hour). Univariate analysis indicated that AIS Grade A or B versus Grades C or D (p < 0.0001), traction (p= 0.0005), injury morphology (p < 0.005), the surgical approach (p= 0.009), vertebral artery injury (p= 0.02), age (p < 0.05), ISS (p < 0.05), ASIA motor score (p < 0.05), and time to decompression (p < 0.05) were all predictors of lesion expansion. In multiple regression analysis, however, the sole determinant of IML expansion was AIS grade (p < 0.005). CONCLUSIONS After traumatic subaxial cervical spine or spinal cord injury, patients with motor-complete injury (AIS Grade A or B) had a significantly higher rate of IML expansion than those with motor-incomplete injury (AIS Grade C or D).

KEYWORDS: AIS= American Spinal Injury Association (ASIA) Impairment Scale; AMS= ASIA motor score; IML= intramedullary lesion; ISS= Injury Severity Score; MABP= mean arterial blood pressure; MCC= maximum canal compromise; MRI; MSCC= maximum spinal cord compression; SCI= spinal cord injury; cervical spine; spinal cord injury; trauma

PMID: 25746115

 

SUPPLEMENT

Each year nearly 15,000 new cases of spinal cord injury (SCI) are seen on the North American continent, and globally more than 2.5 million people live with SCI, enduring an immense personal, social, financial, and psychological burden.1-4 SCI is one of the greatest unsolved medical problems. While SCI has no simple cure, new advances in molecular biology may help us better understand its pathophysiology, thereby introducing novel medical or surgical management.5-12 Traumatic SCI is abrupt and usually incomplete, leaving behind minute amounts of viable tissue at the injury epicenter.8 Evidence indicates that spontaneous regeneration of interrupted spinal cord fiber tracts and cytoskeleton does not happen easily, and the remaining viable tissue at the injury epicenter and beyond might be engulfed coagulative necrosis and edema as a consequence of secondary injury triggered by ischemia, molecular cascades, excitotoxicity, and progressive hemorrhagic necrosis (PHN) (Figure 1).13-19 Over-activation of α-amino-3-hydroxy-5-methyl-e-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) cationic channel receptors and upregulation of endothelial sulfonylurea receptor 1-regulated NC Ca-ATP channels contributing to PHN result in cytotoxic and vasogenic edema that spreads beyond the injury epicenter for several motion segments.8, 10, 20, 21 Preclinical light and electron microscopic studies of the 1970s indicated that within 5 minutes of a blunt trauma there was congestion of the central graymater at the epicenter of injury followed by extravasation of red blood cells. Collection of blood in the gray matter gave rise to a hemorrhagic lesion surrounded by coagulative necrosis (myelomalacia) and edema, which spread rostrally and caudally above and below the injury epicenter.22-25 It was not until the late 1980s and later that in-vivo MRI studies visualized the true face of SCI. Different MRI sequences revealed the hemorrhagic injury epicenter, myelomalacia, and spinal cord edema and swelling (Figure 2).26-31 In-vivo MRI studies of rodent models of SCI indicates that one could see signal changes compatible with SCI within 34 minutes following trauma.32, 33 In our clinical studies we have been able to visualize MRI evidence of SCI within 3 hours of trauma.34-36 Results from clinical and preclinical research indicate that intramedullary lesion length (IMLL) relates to neurological outcome and injury severity.32, 33 Decompressive studies in the 1990s clearly stressed the importance of preoperative MRI as a proof of spinal cord compression due to fracture dislocations and spinal cord swelling.37-39 Studies from our center have indicated that intramedullary lesion length (IMLL) predicted neurological outcome in acute traumatic central cord syndrome.34 Patients with longer IMLL had less hand dexterity and more neuropathic pain. Comparing the pre- and post-operative MRI images of 42 AIS grades A and B patients, we discovered that the IMLL increased over time, being longer in patients with more severe traumatic injury. IMLL on MRI images taken at the time of admission 6.8 hours following trauma was 59.2 millimeters. The lesion length increased to 88.5 millimeters when MRI was obtained 54.5 hours following trauma. The IML rate of expansion was 900 µmeters/hour.35, 36, 40 The expansion rate of the intramedullary lesion was most intense during the early hours of SCI (Figure 3). In-vivo MRI studies of rodent models of SCI have confirmed the relationship between IMLL and the injury severity. In addition, the IMLL decreased with hypertonic saline, glibenclamide, and N-nitrosoglutathion treatment. 10, 41, 42 Our findings in the present investigation support the concept that IMLL or IML rate of expansion might be used as a biological marker in order to determine effect size of therapeutic trials before the end of 6 to 12 months of clinical follow-up, when neurological recovery reaches its maximum.  

 

 

Figure 1Figure 1: Midsagittal T2 weighted MRI image of a young man following an AIS grade A SCI and a comparable sketch of a rodent model of SCI indicating fusiform extension of brain edema from the injury epicenter. Please see Ref 19.

 

 

Figure 2

Figure 2: Midsagittal T2 W post-operative MRI image of a young male patient following motor vehicle accident and AIS grade A SCI indicating hemorrhage at the injury epicenter surrounded by myelomalacia and intramedullary edema spreading rostrally and caudally.

 

 

 

Figure 3

Figure 3: IML expansion in relationship with timing of spinal cord injury.

 

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