Neuronal and Vascular Biomarkers in Syringomyelia: Investigations Using Longitudinal Mri

Abstract

Syringomyelia is a formation of fluid-filled cavities in the spinal cord, caused by a number of situations including trauma. To understand the origin and progression of syringomyelia, animal models were developed to mimick the condition and computer models were implemented for performing numerical analysis. This article characterizes the neuropathological stages of a contused spinal cord before and after the syringomyelia formation using longitudinal in vivo MRI. Rat was subject to a contusion-type spinal cord injury (SCI) at the T12 level. MRI data were gathered on post-injury days 3, 14, 28, 72, 94 and 404 using a 9.4 T scanner. In addition, neurobehavioral tests were performed prior to the scans on these days. Pathological consequences of SCI included significant edema and, to a lesser degree, hemorrhage in the acute phase, followed by neuronal loss, tissue alterations and vascular changes in the late stages. The images from the post-injury day 14 indicated shrinkage of the injured tissue and occlusion of the central canal. Subsequently, syringomyelia was initiated cranial to the occlusion and the fluid-filled cavities enlarged with time. The neurologic deficits of the injured rat also worsened over time. The inflammatory, but not the hemostatic, component seems to be a prerequisite for syringomyelia proceeding contusive SCI and abnormal flow of the cerebrospinal fluid (CSF) is likely the main factor. Bioimaging markers from high-resolution MRI sensitized to inflammation and CSF flow may be used for early detection of syringomyelia and assessing its prognosis.