Experimental Syringohydromyelia Induced by Adhesive Arachnoiditis in the Rabbit: Changes in the Blood–Spinal Cord Barrier, Neuroinflammatory Foci, and Syrinx Formation

Abstract

There are many histological examinations of syringohydromyelia in the literature. However, there has been very little experimental work on blood permeability in the spinal cord vessels and ultrastructural changes. We prepared an animal model of spinal adhesive arachnoiditis by injecting kaolin into the subarachnoid space at the eighth thoracic vertebra of rabbits. The animals were evaluated 4 months later. Of the 30 rabbits given kaolin injection into the cerebrospinal fluid, 23 showed complete circumferential obstruction. In the 7 animals with partial obstruction of the subarachnoid space, intramedullary changes were not observed. However, among the 23 animals showing complete obstruction of the subarachnoid space, dilatation of the central canal (hydromyelia) occurred in 21, and intramedullary syrinx (syringomyelia) was observed in 11. In animals with complete obstruction, fluorescence microscopy revealed intramedullary edema around the central canal, extending to the posterior columns. Electron microscopy of hydromyelia revealed a marked reduction of villi on the ependymal cells, separation of the ependymal cells, and cavitation of the subependymal layer. The dilated perivascular spaces indicate alterations of fluid exchange between the subarachnoid and extracellular spaces. Syringomyelia revealed that nerve fibers and nerve cells were exposed on the surface of the syrinx, and necrotic tissue was removed by macrophages to leave a syrinx. Both pathologies differ in their mechanism of development: hydromyelia is attributed to disturbed reflux of cerebrospinal fluid, while tissue necrosis due to disturbed intramedullary blood flow is considered to be involved in formation of the syrinx in syringomyelia.

Abnormalities in spinal cord ultrastructure in a rat model of post-traumatic syringomyelia

“…3) and enlarged perivascular spaces (Fig. 2) reported in this study are consistent with earlier reports on the ultrastructure of human and rabbit syrinx cavities [14,15,32,33]. Interestingly, enlarged perivascular spaces were also reported in hydrocephalus [34][35][36] and a number of cerebrovascular and systemic pathologies including small vessel disease [37,38], moyamoya disease [39], ischemic and lacunar stroke [40], lupus erythematosus [41], and arteriosclerosis [42].…”

“…This is supported by previous findings using an excitotoxic model of PTS, which demonstrated that the BSCB is permeable to vascular tracers surrounding a syrinx [31]. Further, this is consistent with findings of increased vesicular transport and endothelial tight junctional opening adjacent to syrinxes in a leporine model of adhesive arachnoiditis [32]. Overall, these studies support the hypothesis that perivascular spaces play an important role in facilitating fluid flow in the spinal cord tissue, and their integrity is compromised in PTS.…”

Syringomyelia

“…20 In an experiment with rabbits, 21 kaolin was injected into the spinal subarachnoid space to induce adhesive arachnoiditis. 20 In an experiment with rabbits, 21 kaolin was injected into the spinal subarachnoid space to induce adhesive arachnoiditis.…”

Clinical Reasoning: A 39-year-old man with abdominal cramps

“…By contrast, syringomyelia is a progressive condition associated with intramedullary ischemia and tissue necrosis causing cavitation. 3 A filiform, or slitlike, appearance on MRI is said to distinguish hydromyelia from syringomyelia, but in some series 20% of patients with filiform dilations of the central spinal cord canal show progression consistent with syringomyelia. 4 The presence of objective neurologic deficits and certain features on MRI (spinal cavity .6 mm in diameter and .5 segments in length; abnormal contrast enhancement; spinal cord expansion; cavity enlargement over time) or electrophysiologic testing (abnormalities on EMG, somatosensory evoked potentials [SSEPs], or motor evoked potentials [MEPs]) allows patients with syringomyelia to be distinguished more reliably from those with hydromyelia.…”

“…These result in macrocystic or microcystic changes. 3 Where an obvious structural cause cannot be identified, the term idiopathic syringomyelia is applied.…”