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. 2025 Apr 11:16:1536649.
doi: 10.3389/fneur.2025.1536649. eCollection 2025.

Arachnoid fibrosis in the cerebellopontine angle of primary trigeminal neuralgia: a histopathological study

Affiliations

Arachnoid fibrosis in the cerebellopontine angle of primary trigeminal neuralgia: a histopathological study

Siqiang Tang et al. Front Neurol. .

Abstract

Objective: This study aimed to evaluate differences in the arachnoid membrane of the cerebellopontine angle (CPA) cistern between patients with trigeminal neuralgia (TN) and trauma patients without TN, providing novel insights into the pathogenesis of TN.

Methods: Arachnoid specimens were collected from patients with primary TN undergoing their first microvascular decompression at the Neurosurgery Department of Shaoyang Central Hospital between January 2021 and September 2024 (study group) and from patients with posterior cranial fossa trauma undergoing surgery during the same period (normal control group). Specimens from both groups were subjected to hematoxylin-eosin (HE) staining and picric acid-Sirius red staining. Morphological thickness and collagen fiber thickness in the arachnoid membrane were measured under polarized light microscopy and then compared and statistically analyzed.

Results: The study included 41 patients with primary TN and 38 normal control subjects. In the TN group, the mean thickness of the entire arachnoid layer in the CPA cistern was 87.86 ± 9.34 μm, and the mean thickness of collagen fibers was 53.95 ± 8.90 μm. In the control group, these values were 62.55 ± 1.55 μm and 33.50 ± 3.60 μm, respectively. The differences in both arachnoid thickness (p < 0.001) and collagen fiber thickness (p < 0.001) between the groups were statistically significant.

Conclusion: Patients with TN exhibited significant arachnoid fibrosis and thickening in the CPA cistern, primarily due to an increase in collagen fibers. These findings suggested a potential pathological mechanism underlying TN.

Keywords: Sirius red staining; arachnoid fibrosis; cerebellar pontine horn cisterna; microvascular decompression; primary trigeminal neuralgia.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Flow chart of patient inclusion and exclusion. TN, trigeminal neuralgia; MVD, microvascular decompression.
Figure 2
Figure 2
Histological analysis of the arachnoid membrane in patients with trigeminal neuralgia compared to normal controls, utilizing HE and Sirius red staining. The images demonstrate that the thickening of the arachnoid membrane in the trigeminal neuralgia group, compared to the normal control group, is primarily attributed to an increase in collagen fibers. (A) HE staining of the arachnoid membrane in trigeminal neuralgia patients, magnification ×400. (B) HE staining of the arachnoid membrane in the normal group, magnification ×400. (C) Polarized light imaging of collagen fibers in the arachnoid membrane of trigeminal neuralgia patients, stained with Sirius red staining, magnification ×400. (D) Polarized light imaging of collagen fibers in the normal group, stained with Sirius red staining, magnification ×400.
Figure 3
Figure 3
Statistical comparison of the thickness of arachnoid and collagen fibers between the two patient groups. (A) Comparison of full thickness between the normal and trigeminal neuralgia groups. (B) Comparison of thickness with collagen fiber of arachnoids between the normal and trigeminal neuralgia groups.

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