Most spinal arachnoid cysts are asymptomatic and detected incidentally during magnetic resonance imaging or myelography. The etiology of intraspinal arachnoid cyst is not yet clear. We present two children with three spinal extradural arachnoid cysts and each cyst protruded from a separate dura defect. In both patients, plain radiographs demonstrated widening of the interpedicular distance, which suggested progressive widening of the spinal bony canal. Limited laminectomy was performed to remove the intraspinal cysts. Separate dura defects, the apparent predisposing factors, were also found and repaired. The patients completely recovered neurologically. Radical cyst removal and dura defect closure are the surgical intervention of choice in patients with symptomatic extradural arachnoid cyst.
We hypothesized that more gelatinases appear in effusions of septic arthritis than aseptic arthritis. This study examined the laboratory variables of inflammation and the levels of gelatinase A and B (matrix metalloproteinases-2 and -9) in 75 effusions from the knees of 37 patients with inflammatory arthritis and compared them with effusions of septic and aseptic arthritis. Gelatin zymography revealed that the levels of the latent matrix metalloproteinase-9 were higher in 24 effusions of septic arthritis than in 51 effusions of aseptic arthritis. The latent matrix metalloproteinase-9 levels of septic arthritis also correlated with the neutrophil counts in effusions. Significantly more activated matrix metalloproteinases-2 and -9 appeared in effusions of septic arthritis in native and replaced knees than in effusions of aseptic arthritis. A high matrix metalloproteinase-9 level and the appearance of activated matrix metalloproteinases-2 and -9 may distinguish septic from aseptic arthritis, even in cases with a low neutrophil count in the replaced knee. Joint aspiration may not only reduce the bacteria counts, endotoxins, and proinflammatory cytokines, but also decrease the amount of matrix metalloproteinases in effusions that attack the extracellular matrix of native and artificial joints.
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