Quantifying Myofascial Dysfunction in Post-Stroke Pain

Johns Hopkins University

Status: Completed

Conditions: Myofascial Dysfunction

Treatments: Diagnostic Test: Imaging

Study type: Interventional

Funder types: Other; NIH

Identifiers

NCT05762679

1R61AT012279-01 (U.S. NIH Grant/Contract)

IRB00354876

Details and patient eligibility

About

The purpose of this study is to quantify the extent of GlycosAminoGlycan/Hyaluronic Acid (GAG/HA) accumulation using T1rho (T1ρ) MRI in the paretic versus non-paretic shoulder rotator muscles, and correlate the T1ρ Magnetic Resonance Imaging (MRI) measurements with US echo texture measurements to develop a clinic-friendly tool to infer the extent of HA accumulation; and to distinguish between latent versus active Post Stroke Shoulder Pain (PSSP) using ultrasound (US) shear strain mapping of the same muscles on the paretic side compared with the non-paretic side.

Full description

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 HA in muscle and its fascia can cause myofascial dysfunction. HA is a 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 T1ρ MRI, and myofascial dysfunction can be assessed using echo texture analysis and shear strain mapping on quantitative US, which may serve as useful biomarkers to elucidate the pathophysiology of myofascial dysfunction in PSSP.

Enrollment: 46 patients

Sex: All

Ages: 18+ years old

Volunteers: No Healthy Volunteers

Inclusion criteria

• 18 years or older
• Hemiparesis from Ischemic or Hemorrhagic Stroke
• 4-120 months post-stroke with Hemiparesis since the incidence and intensity of PSSP
• Show a difference of more than 10 degrees of passive ER-ROM between non-paretic and paretic shoulders with or without pain
• Able to provide informed consent and comply with testing protocols

Exclusion criteria

• Received treatment for spasticity with Botulinum Toxin or Intrathecal Baclofen within the past three months
• Have another neurologic condition that may affect motor response (e.g. Parkinson's disease, Amyotrophic Lateral Sclerosis (ALS), Multiple Sclerosis (MS))
• Have a contraindication to MRI (claustrophobia, magnetic pacemakers and clips)
• Have non-musculoskeletal PSSP such as only central pain or Chronic Regional Pain Syndrome (CRPS)
• Have a complicated medical condition, or significant injury to either upper limb.

Trial design

Primary purpose: Diagnostic

Allocation: Non-Randomized

Interventional model: Parallel Assignment

Masking: None (Open label)

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46 participants in 2 patient groups

Paretic

Experimental group

Description:

Subgroups: Low severity PSSP - defined as focal palpable nodules that may be tender on palpation with pain rating of \< 5/10 when combined with the hand-behind-neck (HBN) maneuver. High severity PSSP - defined as focal palpable nodules that are tender on palpation, reproducing the pain, and eliciting a pain rating of \>= 5/10 when combined with the hand-behind-neck (HBN) maneuver.

Treatment:

Diagnostic Test: Imaging

Non-Paretic

Other group

Description:

The non-paretic side of the same patients serves as the control.

Treatment:

Diagnostic Test: Imaging