末梢神経圧迫障害後の早期虚血誘発性神経炎症を高周波超音波で検出する

Peripheral compressive neuropathy involves complex ischemic and inflammatory responses, yet early diagnostic tools remain limited. This study evaluated the utility of high-frequency ultrasound (HFUS) for detecting ischemia-induced neuroinflammation and microvascular alterations following sciatic nerve compression.

A chronic constriction injury (CCI) model was established in Sprague-Dawley rats. Intraneural perfusion and vascular density were assessed longitudinally using a 40 MHz HFUS imaging. Immunofluorescence and Western blotting were employed to quantify temporal expression of hypoxia (HIF-1α), inflammation (IL-1β, TNF-α), and angiogenic (VEGF, vWF) markers in sciatic nerve tissue across multiple timepoints post-injury.

HFUS detected an immediate reduction in blood flow velocity and vessel density within 30 min of nerve compression. While velocity normalized by Day 7, structural vascular density remained reduced through Day 14. HIF-1α peaked within 2 h, returning to baseline by Day 14. IL-1β and TNF-α were upregulated by Day 1 and persisted for 2 wk. VEGF showed early upregulation peaking at Day 1, while vWF exhibited delayed, prolonged expression, peaking between Days 3-7. Axonal demyelination and Schwann cell remodeling were observed, with partial recovery noted at Day 14.

HFUS enables sensitive, non-invasive visualization of acute vascular and inflammatory responses to peripheral nerve compression. These results support its potential in early diagnosis and monitoring of compressive neuropathies, offering insights into the pathophysiological timeline of ischemia, neuroinflammation, and vascular remodeling.