# Quantifying and Treating Myofascial Dysfunction in Post Stroke Shoulder Pain

> **NIH NIH R33** · JOHNS HOPKINS UNIVERSITY · 2024 · $3,086,679

## Abstract

PROJECT SUMMARY
Shoulder pain is extremely common after stroke and occurs in 30-70% of patients. Chronic post stroke
shoulder pain (PSSP) contributes to depression, interferes with motor recovery, and decreases quality of life.
Although PSSP is thought to be caused by damage to the myofascial tissues around the shoulder joint, the
pathophysiology of myofascial dysfunction and pain in PSSP has not been elucidated, leading to missed
opportunities for early diagnosis and variable success with pain management. The accumulation of hyaluronic
acid (HA) in muscle and its fascia can cause myofascial dysfunction. HA is a glycosaminoglycan (GAG) and a
chief constituent of the extracellular matrix of muscle. In physiologic quantities, it functions as a lubricant and a
viscoelastic shock absorber, enabling force transmission during muscle contraction and stretch. Reduced joint
mobility and spasticity can result in focal accumulation and alteration of HA in muscle, leading to the
development of taut bands, dysfunctional gliding of deep fascia and muscle layers, reduced range of motion
(ROM), and pain. Muscle HA concentrations can be imaged using T1rho (T1ρ) MRI, and myofascial
dysfunction can be assessed using echo texture analysis and shear strain mapping on quantitative ultrasound
(US), which may serve as useful biomarkers to elucidate the pathophysiology of myofascial dysfunction in
PSSP. Hence, in the R61 phase we will: (1) Quantify the extent of GAG/HA accumulation using T1ρ MRI in the
paretic versus non-paretic shoulder rotator muscles, and correlate the T1ρ MRI measurements with US echo
texture measurements to develop a clinic-friendly tool to infer the extent of HA accumulation; and (2)
Distinguish between latent versus active PSSP using US shear strain mapping of the same muscles on the
paretic side compared with the non-paretic side during passive shoulder external rotation (ER), which is
strongly associated with PSSP. To proceed to the R33 phase, we will demonstrate a statistically significant
difference in (1) GAG/HA accumulation using T1ρ MRI, and (2) shear strain mapping for latent and active
PSSP using quantitative US. In the R33 phase, we will use the imaging metrics identified in the R61 phase to
monitor treatment response in a clinical trial of intramuscular (IM) hyaluronidase injections to increase pain-free
passive shoulder ER-ROM. We will administer human recombinant hyaluronidase or normal saline injections in
the dysfunctional shoulder girdle muscles, and measure pain-free shoulder ER-ROM (primary outcome) (1)
pre-injection, (2) 1–2 weeks post-injection (primary endpoint) and (3) 6-8 weeks post-injection. We expect that
local hyaluronidase injections will breakdown the accumulated HA leading to increased pain-free shoulder ER,
and that the improvement will correlate with quantitative MRI and US imaging metrics. At its conclusion, this
proposal will develop quantitative imaging biomarkers of myofascial dysfunction to monitor response to
...

## Key facts

- **NIH application ID:** 11170291
- **Project number:** 4R33AT012279-02
- **Recipient organization:** JOHNS HOPKINS UNIVERSITY
- **Principal Investigator:** PREETI RAGHAVAN
- **Activity code:** R33 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $3,086,679
- **Award type:** 4N
- **Project period:** 2022-09-21 → 2027-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/11170291

## Citation

> US National Institutes of Health, RePORTER application 11170291, Quantifying and Treating Myofascial Dysfunction in Post Stroke Shoulder Pain (4R33AT012279-02). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/11170291. Licensed CC0.

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