Contusion, dislocation, and distraction: primary hemorrhage and membrane permeability in distinct mechanisms of spinal cord injury

Abstract

<jats:sec> <jats:title>Object</jats:title> <jats:p>In experimental models of spinal cord injury (SCI) researchers have typically focused on contusion and transection injuries. Clinically, however, other injury mechanisms such as fracture–dislocation and distraction also frequently occur. The objective of the present study was to compare the primary damage in three clinically relevant animal models of SCI.</jats:p></jats:sec> <jats:sec> <jats:title>Methods</jats:title> <jats:p>Contusion, fracture–dislocation, and flexion–distraction animal models of SCI were developed. To visualize traumatic increases in cellular membrane permeability, fluorescein–dextran was infused into the cerebrospi-nal fluid prior to injury. High-speed injuries (approaching 100 cm/second) were produced in the cervical spine of deeply anesthetized Sprague–Dawley rats (28 SCI and eight sham treated) with a novel multimechanism SCI test system. The animals were killed immediately thereafter so that the authors could characterize the primary injury in the gray and white matter.</jats:p> <jats:p>Sections stained with H &amp; E showed that contusion and dislocation injuries resulted in similar central damage to the gray matter vasculature whereas no overt hemorrhage was detected following distraction. Contusion resulted in membrane disruption of neuronal somata and axons localized within 1 mm of the lesion epicenter. In contrast, membrane compromise in the dislocation and distraction models was observed to extend rostrally up to 5 mm, particularly in the ventral and lateral white matter tracts.</jats:p></jats:sec> <jats:sec> <jats:title>Conclusions</jats:title> <jats:p>Given the pivotal nature of hemorrhagic necrosis and plasma membrane compromise in the initiation of downstream SCI pathomechanisms, the aforementioned differences suggest the presence of mechanism-specific injury regions, which may alter future clinical treatment paradigms.</jats:p></jats:sec>

Increased Intracranial Pressure after Diffuse Traumatic Brain Injury Exacerbates Neuronal Somatic Membrane Poration but not Axonal Injury: Evidence for Primary Intracranial Pressure-Induced Neuronal Perturbation

“…This study is also in agreement with previous data reporting that mechanical force associated with traumatic spinal cord or brain injury (Singleton and Povlishock, 2004;Farkas et al, 2006;Choo et al, 2007;Whalen et al, 2008) as well as the induction of mechanical insults in vitro (Geddes et al, 2003b;Kilinc et al, 2008;LaPlaca et al, 2009;Cullen et al, 2011) precipitate plasmalemmal mechanoporation visualized using cell impermeable dyes. This membrane poration can be initiated at the onset of injury and precipitated at more chronic time points after injury (Singleton and Povlishock, 2004;Farkas et al, 2006;Cullen et al, 2011).…”

Effects of Advanced Age on the Morphometry and Degenerative State of the Cervical Spine in a Rat Model

“…Vertebral fracture-dislocation has been cited as the most common mechanism of cervical SCI in humans (Sekhon and Fehlings, 2001), is associated with ''complete'' SCI in humans (Pickett et al, 2006), and in rats causes more severe histological indices of damage compared to contusion and flexion-distraction injury mechanisms (Choo et al, 2007;. Despite this, fracture-dislocation is relatively understudied injury mechanism in experimental SCI research.…”

“…Although age-related changes in vertebral column morphology may have little influence on spinal cord tissue damage during injury mechanisms such as clip compression, hemisection, or crush, they could potentially play a substantial role during more clinically relevant injury mechanisms including contusion (simulating a burst fracture) (Scheff et al, 2003) or fracture-dislocation (caused by relative shearing of two adjacent vertebral bodies) (Choo et al, 2007;. For example, if the vertebral canal is significantly larger in older rats, a given vertebral dislocation displacement would cause less relative shearing of the spinal cord than in young animals.…”

Assessment of efficiency of early decompression of the spinal cord in spinal injury based on morphological and statistical analysis

“…Generally, the progression of the second phase takes place during the first 24-48 hours. Vascular dysfunction, ischemia, glutamatergic excitotoxicity, inflammation and apoptosis are progressed in this period [1][2][3][4][5][6][7][8][9][10][11][12].…”