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arachnoiditis/peroxidase
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6 resultados
Altered subarachnoid space compliance and fluid flow in an animal model of posttraumatic syringomyelia.
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METHODS
A histologic study of cerebrospinal fluid tracers in Sprague-Dawley rats undergoing lumboperitoneal shunt insertion in the excitotoxic animal model of posttraumatic syringomyelia (PTS).
OBJECTIVE
To determine the effects of cerebrospinal fluid (CSF) diversion from the subarachnoid space on
Fluid outflow in a large-animal model of posttraumatic syringomyelia.
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BACKGROUND
Posttraumatic syringomyelia affects approximately 28% of spinal cord injury patients, and current treatments are often ineffective. The pathogenesis of this condition remains poorly understood. Previous reports have focused on pathways and mechanisms of fluid inflow; however, disturbances
Postlaminectomy adhesion of the cauda equina. Changes of postoperative vascular permeability of the equina in rats.
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METHODS
The authors evaluated the vascular permeability changes of the cauda equina after lumbar laminectomy in rats.
OBJECTIVE
To clarify the early vascular responses in postlaminectomy adhesive arachnoiditis.
BACKGROUND
Laminectomy-induced cauda equina adhesion has been visualized by postoperative
Role of the blood-spinal cord barrier in posttraumatic syringomyelia.
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OBJECTIVE
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
Fluid flow in an animal model of post-traumatic syringomyelia.
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More than a quarter of patients with spinal cord injury develop syringomyelia, often with progressive neurological deficit. Treatment options remain limited and long-term failure rates are high. The current poor understanding is impeding development of improved therapies. The source and route of
Mechanisms underlying the formation and enlargement of noncommunicating syringomyelia: experimental studies.
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The pathogenesis of noncommunicating syringomyelia is unknown, and none of the existing theories adequately explains the production of cysts that occur in association with conditions other than Chiari malformation. The authors' hypothesis is that an arterial pulsation-driven perivascular flow of
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