Clinicopathologic features of spinal arachnoiditis in patients with surgically treated syringomyelia: A retrospective study of 60 cases.

Arachnoiditis develops from inflammatory processes in the intrathecal space and can cause syringomyelia, myelopathy, radiculopathy, and chronic pain. Understanding inflammatory and fibrotic mechanisms may identify therapeutic targets. We performed a retrospective study of 60 adults who had undergone surgery for arachnoiditis-associated syringomyelia. Clinical status was assessed preoperatively and at 3 to 4 months post-surgery. Cerebrospinal fluid (CSF) was obtained preoperatively, 1-week post-operatively, and at 3 to 4 months. Operative arachnoid adhesion specimens underwent histopathologic review and immunofluorescence staining with quantitative assessment of fibrosis, inflammation, and human endogenous retrovirus group K (HERV-K) antigens. Lesions had mid-thoracic predominance and heterogeneous etiologies. Median CSF white cell counts were low preoperatively (1 cell/µL, range: 0 to 11 cells/µL). Tissue profiling supported a fibroblast-associated, scar-forming lesion (mean density of CRABP2 = 434 cells/mm2, ER-TR7 = 430 cells/mm2) with moderate collagen I deposition (8.1% of specimens), less adaptive immune signals (9 to 180 cells/mm2), and minimal HERV-K staining (1.1% of tissue). In arachnoiditis-associated syringomyelia, preoperative CSF had few white blood cells; 1-week postoperative CSF had RBC and WBC counts consistent with postoperative meningeal irritation. Chronic fibrosis characterized arachnoid tissue removed at surgery. Histology and immunohistochemical staining suggested that arachnoiditis manifested as a fibroproliferative, adhesive phenotype within the subarachnoid space.