Trapezius fascia reveals mechanosensory capacity and predominance of nociceptive axons in occipital neuralgia. Academic Article uri icon

Overview

abstract

  • UNLABELLED: Occipital neuralgia (ON) is a complex and painful condition that presents significant clinical challenges, often resistant to conventional treatments. This study focuses on the trapezius fascia’s role in ON, exploring its neural and mechanosensitive properties. We conducted a detailed analysis of the trapezius fascia in 18 patients with ON and ten control patients using specific molecular markers (PGP9.5, S100, CGRP, TH and Piezo2). Our findings reveal a rich neural composition within the fascia, characterized by heterogenous tissues that include abundant collagen, vasculature, and diverse neural components. Notably, both myelinated and non-myelinated axonal populations were identified, with a significant presence of sympathetic nerve fibers (tyrosine hydroxylase-positive) in ON patients but absent in controls. Mechanosensitive entities resembling cutaneous mechanoreceptors such as Pacinian- and Ruffini-like corpuscles were also observed, highlighting the fascia’s capacity for mechanosensation, which could contribute to pain perception in ON. Crucially, we observed a 71% increase in the nociceptive axonal population in ON patients compared to controls, suggesting a profound alteration in nociceptive signaling pathways and peripheral sensitization. This alteration was underscored by the marked upregulation of Calcitonin Gene-Related Peptide (CGRP) specifically within neural components of the fascia, indicating a potential mechanism for the observed pain sensitization. These alterations were not significantly influenced by the presence of neck injuries, indicating other underlying pathophysiological mechanisms at play. The study underscores the trapezius fascia’s critical role not only in biomechanical support but also in neuromuscular communication and pathological pain processing in occipital neuralgia. These insights provide a deeper understanding of the neurobiology of ON and may guide future therapeutic strategies targeting these underlying mechanisms for more effective management of the condition. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1038/s41598-026-42746-y.

publication date

  • March 10, 2026

Identity

PubMed Central ID

  • PMC13103052

Scopus Document Identifier

  • 105036715257

Digital Object Identifier (DOI)

  • 10.1038/s41598-026-42746-y

PubMed ID

  • 41807486

Additional Document Info

volume

  • 16

issue

  • 1