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  • Author or Editor: Marcus A. Stoodley x
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Jason Sheehan

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Marcus A. Stoodley, Cornelia Hermann and Bryce Weir

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Lynne E. Bilston, Marcus A. Stoodley and David F. Fletcher

Object

The mechanisms of syringomyelia have long puzzled neurosurgeons and researchers alike due to difficulties in identifying the driving forces behind fluid flow into a syrinx, apparently against a pressure gradient between the spinal cord and the subarachnoid space (SAS). Recently, the synchronization between CSF flow and the cardiac cycle has been postulated to affect fluid flow in the spinal cord. This study aims to determine the effect of changes in the timing of SAS pressure on perivascular flow into the spinal cord.

Methods

This study uses a computational fluid dynamics model to investigate whether the relative timing of a spinal artery cardiovascular pulse wave and fluid pressure in the spinal SAS can influence CSF flow in the perivascular spaces.

Results

The results show that the mass flow rate of CSF through a model periarterial space is strongly influenced by the relative timing of the arterial pulse wave and the SAS pressure.

Conclusions

These findings suggest that factors that might alter the timing of the pulse wave or the fluid flow in the SAS could potentially affect fluid flow into a syrinx.

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Marcus A. Stoodley, Jason D. Warren and Peter E. Oatey

✓ A case is reported of a 63-year-old woman with thalamic syndrome as the presenting feature of an unruptured cerebral aneurysm. Unruptured aneurysm is a rare cause of thalamic syndrome; the possible mechanisms of production of the sensory disturbance are discussed.

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Perry P. Ng, Brendan Steinfort and Marcus A. Stoodley

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Elizabeth C. Clarke, Marcus A. Stoodley and Lynne E. Bilston

Object

The pathogenesis of syringomyelia in association with Chiari malformation Type I (CM-I) is unclear. Studies of patients with CM-I have shown alterations in the CSF velocity profile using cardiac-gated cine phase-contrast MRI, and computational simulations have demonstrated that temporal features of the CSF pulse could contribute to syrinx development or enlargement. Few studies have reported temporal characteristics of the CSF profile, and few studies have reported on CM-I patients with and without syringomyelia separately. This study was performed to determine whether specific temporal features of the CSF flow profile may underlie the development or enlargement of a syrinx in patients with CM-I.

Methods

Ten healthy volunteers and 18 patients with CM-I with (8 patients) and without (10 patients) syringomyelia were studied using cardiac-gated cine phase-contrast MRI, measuring the maximum CSF velocities in the cranial and caudal directions, the timing of these maximums relative to the cardiac cycle time, the timing of caudal flow onset, timing of cranial flow onset, and the duration of caudal flow.

Results

The caudal CSF flow was significantly faster (p ≤ 0.01) and earlier (p < 0.02) in patients without syringomyelia than in healthy volunteers and patients with syringomyelia. There were no significant differences in the CSF velocities between patients with syringomyelia and healthy volunteers. Patients with CM-I who had syringomyelia had a significantly later start of caudal CSF flow (p < 0.01) and earlier maximum cranial velocity (p = 0.03) than healthy volunteers, but the relative durations of caudal and cranial flow were not significantly different between any of the groups.

Conclusions

The significantly earlier arrival and earlier peak velocity of caudal CSF flow may underlie the development of syringomyelia in patients with CM-I, and after a syrinx develops the CSF flow profile appears to stabilize.

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Jian Tu, Jinxin Liao, Marcus A. Stoodley and Anne M. Cunningham

Object

Endogenous stem cells theoretically could replace lost tissue and repair deficits caused by syringes. In this study the authors quantitatively examined 1) whether neural progenitor cells exist in an adult rat model of posttraumatic syringomyelia (PTS); 2) and if so, how long an active population of progenitor cells can persist; 3) whether the cell population's location is associated with the syrinx; 4) the degree of differentiation of the progenitor cells; and 5) the phenotypic fate of the progenitor cells.

Methods

Wistar rats were divided into intact, sham-operated, and experimental syrinx groups. Animals in each group were equally subdivided according to 4 time points: 7, 14, 28, and 56 days post–syrinx induction. Rats in the experimental syrinx group underwent a C-7 and T-1 laminectomy and then received 0.5 μl of a 24-mg/ml quisqualic acid spinal cord injection at the C-8 level to mimic an excitotoxic injury with an initial cyst, and 10 μl of a 250-mg/ml kaolin injection into the subarachnoid space at the C-8 level to create arachnoiditis. The proliferation, distribution, and differentiation of endogenous progenitor cells were identified immunocytochemically.

Results

The authors observed a 20-fold increase in progenitor cells excluding inflammatory cells in the 1st 2 weeks post–syrinx induction. The cells persisted for at least 56 days, and 80% of them were located in the gray matter along the border of cysts. They included neural multipotential progenitor cells, oligodendroglial progenitor cells, and astrocytes.

Conclusions

Data in this study provide evidence for proliferation, distribution, and differentiation of endogenous progenitor cells in a model of PTS in adult rats. These progenitor cells proliferate rapidly, extend for long periods, and are mainly located in the gray matter along the border of syringes. Neural multipotential progenitor cells are expected to be associated with reparative and regenerative mechanisms of PTS. Glial cells are involved in the formation of a glial scar barrier that surrounds the syrinx and may prevent cyst enlargement. The authors' findings suggest that neural progenitor cells play a protective role in PTS.

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Sarah J. Hemley, B. Biotech, Jian Tu and Marcus A. Stoodley

Object

Posttraumatic syringomyelia produces a significant burden of pain and neurological deficits in patients with spinal cord injury. The mechanism of syrinx formation is unknown and treatment is often ineffective. A possible explanation for syrinx formation is fluid leakage from the microcirculation in the presence of a compromised blood-spinal cord barrier (BSCB). The aim of this study was to investigate the structural and functional integrity of the BSCB in a model of posttraumatic syringomyelia.

Methods

The excitotoxic amino acid and arachnoiditis model of syringomyelia was used in 27 Sprague-Dawley rats. Structural integrity of the BSCB was assessed using immunoreactivity to endothelial barrier antigen (EBA), and loss of functional integrity was assessed by extravasation of intravascular horseradish peroxidase. Animals were studied after 3 days, or at 1, 3, 6, or 12 weeks after surgery. There were laminectomy-only and saline injection control animals for comparison at each time point.

Results

Syrinxes formed in 16 of the 17 animals injected with excitotoxic amino acid. Loss of structural and functional integrity of the BSCB in syrinx animals was noted at all time points. Disruption of the BSCB was most dramatic in tissue adjacent to the syrinx, and in the central and dorsal gray matter. Changes in EBA expression generally corresponded with altered vascular permeability, although in the acute stages, widespread vascular permeability occurred without a corresponding decrease in EBA expression. At the later time points (3–12 weeks) EBA expression was often absent, although no vascular leakage was observed.

Conclusions

This study demonstrated a prolonged structural and functional disruption of the BSCB in this model of posttraumatic syringomyelia. Loss of functional integrity of the BSCB, with fluid entering the interstitial space of the spinal cord, may contribute to initial cyst formation after spinal cord injury and subsequent enlargement of the cyst, to produce posttraumatic syringomyelia.

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Michael G. Fehlings and James W. Austin