PubMed · 12650411
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Harold A Wilkinson. 2003. Arachnoiditis ossificans.. https://doi.org/10.3171/spi.2003.98.2.0226
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BACKGROUND: Enlarging fluid filled cystic cavitations form within the spinal cord in up to 28% of spinal cord injured patients. These post-traumatic syrinxes can cause neurological deterioration and current treatment results are unsatisfactory. Localized scar tissue (arachnoiditis) within the subarachnoid space at the level of injury has been suggested to be involved in the pathogenesis of syrinx formation. This study tests the hypothesis that pressure pulses in the subarachnoid space are accentuated adjacent to regions of arachnoiditis, which may drive fluid into the spinal cord and contribute to syrinx formation. METHODS: An axisymmetric, cylindrical computational fluid dynamics model was developed to represent the subarachnoid space under normal physiological conditions and in the presence of arachnoiditis. Cerebrospinal fluid flow into the model was estimated from magnetic resonance imaging flow studies. Arachnoiditis was modelled as a porous obstruction in the subarachnoid space. FINDINGS: Peak fluid pressures were higher above the obstruction than in the absence of obstruction. The peak pressures were strongly dependent on the permeability of the obstruction. INTERPRETATION: Elevations in subarachnoid space pressures due to arachnoiditis may facilitate fluid flow into the spinal cord, enhancing syrinx formation. This suggests that it may be worthwhile to investigate strategies that inhibit arachnoiditis or minimize systolic pressure peaks for treating or preventing syringomyelia.
Paradoxical enlargement and development of new intracranial tuberculomas and tuberculous brain abscesses on adequate antituberculosis treatment are well recognized and supposedly cytokine mediated. These lesions are often unresponsive to conventional antituberculosis treatment, corticosteroids, and surgery. We therefore assessed the effect of adjunctive thalidomide, a tumor necrosis factor alpha-modulating drug, in intractable intracranial tuberculosis that did not respond to standard medical and surgical therapy. Four consecutive children (three children with bacteriologic proof and one child with clinical evidence of intracranial tuberculosis) were studied. Three patients each had a giant tuberculous abscess, and the fourth had chronic basal arachnoiditis with progressive loss of vision. Three of the four patients had relentless neurologic deterioration, and all showed disease progression on neuroimaging despite full medical and appropriate surgical treatment. Marked clinical and neuroradiologic improvement occurred after thalidomide was added to the antituberculosis treatment regimen of these four patients. Adjunctive thalidomide might have a role in the management of intractable intracranial tuberculosis and needs further investigation in this regard.
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