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Purpose <p>To characterize longitudinal changes in axillary-pouch capsular thickness and clinical outcomes after ultrasound-guided hydrodilation with corticosteroid injection in patients with post-stroke adhesive capsulitis, and to examine associations between structural and clinical changes.</p> Methods <p>In this longitudinal observational study, 20 patients underwent clinical and ultrasonographic assessment before the first procedure (T0) and at follow-up (T1), separated by a median of 5.7&#xa0;months. All participants also received conventional neurorehabilitation. Paired changes in pain measured using the Numeric Rating Scale (NRS), range of motion (ROM), strength, muscle tone, disability, quality of life, and capsular thickness were assessed using Wilcoxon signed-rank or exact McNemar tests. Associations between within-participant changes were explored using Spearman correlations.</p> Results <p>Median movement-evoked pain decreased by 4 NRS points during flexion and abduction and by 5 points during external rotation (all <i>p</i> &lt; 0.001). Active and passive ROM improved across all assessed movements (all <i>p</i> ≤ 0.001). Median affected-side capsular thickness decreased from 3.7 to 2.45&#xa0;mm, with a median within-participant reduction of 1.4&#xa0;mm (<i>p</i> &lt; 0.001). The proportion meeting the ultrasonographic criteria for adhesive capsulitis decreased from 20/20 at T0 to 4/20 at T1. Capsular-thickness changes were not significantly associated with changes in any clinical outcome (all |ρ|≤ 0.35; all <i>p</i> ≥ 0.13).</p> Conclusion <p>In this uncontrolled cohort, hydrodilation with corticosteroid injection, delivered alongside neurorehabilitation, was followed by reduced movement-evoked pain, improved shoulder mobility, and axillary-pouch capsular thinning. Capsular thickness should be interpreted as a complementary structural marker rather than a surrogate for clinical recovery.</p>

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Axillary-pouch capsular thinning after ultrasound-guided hydrodilation in post-stroke adhesive capsulitis: a longitudinal observational study

  • 期刊论文

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  • 发表日期：

    2026年8月5日

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  • Filippo Cotellessa,
  • Luca Puce,
  • Salvatore Massimo Stella,
  • Riccardo Picasso,
  • Vittorio Anfossi,
  • Laura Mori,
  • Maria Cesarina May,
  • Matteo Formica,
  • Carlo Trompetto,
  • William Campanella

摘要

Purpose

To characterize longitudinal changes in axillary-pouch capsular thickness and clinical outcomes after ultrasound-guided hydrodilation with corticosteroid injection in patients with post-stroke adhesive capsulitis, and to examine associations between structural and clinical changes.

Methods

In this longitudinal observational study, 20 patients underwent clinical and ultrasonographic assessment before the first procedure (T0) and at follow-up (T1), separated by a median of 5.7 months. All participants also received conventional neurorehabilitation. Paired changes in pain measured using the Numeric Rating Scale (NRS), range of motion (ROM), strength, muscle tone, disability, quality of life, and capsular thickness were assessed using Wilcoxon signed-rank or exact McNemar tests. Associations between within-participant changes were explored using Spearman correlations.

Results

Median movement-evoked pain decreased by 4 NRS points during flexion and abduction and by 5 points during external rotation (all p < 0.001). Active and passive ROM improved across all assessed movements (all p ≤ 0.001). Median affected-side capsular thickness decreased from 3.7 to 2.45 mm, with a median within-participant reduction of 1.4 mm (p < 0.001). The proportion meeting the ultrasonographic criteria for adhesive capsulitis decreased from 20/20 at T0 to 4/20 at T1. Capsular-thickness changes were not significantly associated with changes in any clinical outcome (all |ρ|≤ 0.35; all p ≥ 0.13).

Conclusion

In this uncontrolled cohort, hydrodilation with corticosteroid injection, delivered alongside neurorehabilitation, was followed by reduced movement-evoked pain, improved shoulder mobility, and axillary-pouch capsular thinning. Capsular thickness should be interpreted as a complementary structural marker rather than a surrogate for clinical recovery.