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Adhesive arachnoiditis (AA) is a rare form of chronic degenerative pathology associated with persistent inflammation in the arachnoid matter of the spinal cord. Despite the existing knowledge, the detailed pathological mechanisms underlying AA are not fully understood. This study aimed to elucidate through comprehensive single nuclei RNA sequencing (snRNA-seq) to delineate the transcriptomic landscape of AA. From six arachnoid membrane samples, a total of 52,886 cells met the quality control standards for analysis. The main cell populations identified with specific gene markers were as follows: fibroblasts, glial cells, microglial cells, endothelial cells, mural cells, plasma cells, and T cells. Downstream analysis of fibroblasts, glial cells, and microglial cells was performed. Notably, fibroblast subsets 1 and 3 demonstrated a strong association with AA. Among them, subcluster 3 demonstrated elevated expression of genes COL1A1, COL3A1, and FN1, indicative of enhanced Wnt/β-catenin and extracellular matrix (ECM) synthesis pathways. Subcluster 3 was predicted to progressively transform into subcluster 1. In subcluster 1, there was a significant upregulation of genes such as BMP and ALPL, signaling enhanced activation of calcification-related pathways. This was highly relevant to end-stage arachnoid ossification formation. After being activated, microglial cells transformed into inflammatory disease-associated microglial cells and continued to express high levels of chemokines CCL2, CCL4, IL-1β, and other inflammatory factors NAMPT, INPP5D and NLRP3. This might be the main reason why AA recurrence is frequently observed in patients. These insights enhance our understanding of the pathological progression of AA and may contribute to the identification of novel therapeutic targets., Competing Interests: Declaration of competing interest All authors report no competing interests., (Copyright © 2025 The Authors. Published by Elsevier B.V. All rights reserved.)

The pathophysiological mechanism of adhesive arachnoiditis (AA) is complex, involving the interaction of multiple proteins. In recent years, the development of quantitative proteomics technology has provided a new perspective to reveal its pathological mechanism. The main objective of this study was to reveal the changes of protein expression profiles in arachnoid tissue of patients with AA. Proteomic analysis of arachnoid tissue samples was performed by high-throughput mass spectrometry. Bioinformatics tools were used to process and analyze the data and screen out 712 differentially expressed proteins (DEPs). Specially, 2 hub DEPs (TNC and RANBP1) were found as potential diagnostic markers. The expression levels of TNC and RANBP1 proteins were significantly up-regulated in patients with AA. TNC protein played a key role in inflammation and extracellular matrix remodeling, while RANBP1 was involved in cytoplasmic transport and cell cycle regulation. The abnormal expression and modification of these two proteins were closely related to the pathophysiological process of the disease. Immunoinfiltration analysis found the pathological process of AA were related to the infiltration of memory B cells, activated NK cells and CD8(+) T cells. Additonally, weighted gene co-expression network analysis (WGCNA) showed the organization of the arachnoid proteome into a network of 28 biologically meaningful modules of co-expressed proteins. Of these, 2 modules were positively correlated to AA phenotypes. This study shows a distinct proteomic landscape of AA and non-adhesive arachnoiditis (nAA). These findings also provide valuable insights into the molecular changes associated with potential mechanisms underlying AA., Competing Interests: Declaration of competing interest The authors declare no competing interests., (Copyright © 2024 Elsevier B.V. All rights reserved.)

The authors report that Leber's optic atrophy is a familial hereditary optochiasmatic arachnoiditis: 70 patients from 44 families are analysed. In 17 families a medicogenetic analysis was conducted at least in three generations and a recessive type of heredity was determined in most cases. Fifty-five patients underwent operation after ineffective nonoperative treatment. Optochiasmatic arachnoiditis was found in all patients during surgery. Visual functions improved six months after the operation in half the patients. The similarity of the clinical picture of familial hereditary optochiasmatic arachnoiditis with that of infectious-allergic meningitis dictates the need for studying the familial medical history of all patients with retrobulbar neuritis.

We describe a brother and sister with microcephaly and mental retardation who were shown by cranial CT scan to have almost identical unilateral arachnoid cysts. The occurrence in sibs suggests the possibility of a genetic basis for at least some cases of arachnoid cysts.

Six patients (3 couples of brothers) with adhesive arachnoiditis of the opto-chiasmatic cistern, surgically verified, are presented. Only one couple of brothers offered a possible family history of a similar condition in one maternal uncle. The visual damage had almost constantly a sudden onset and was predominantly of the axial type. No gross pathology, other than the arachnoiditic involvement of the chiasmal cistern and alterations of the anterior optic pathways, was found at surgery. Pneumocisternoencephalographic findings did not prove constantly reliable for a preoperative diagnosis of the condition when compared with surgical pathology. The overall results of the neurosurgical operations (exploration of the chiasm and removal of the adhesions) can be considered as favorable and this type of treatment is once again recommended as the therapy of choice without undue delay when general or local medical treatment proves of no avail after a reasonable length of time.