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Does muscle guarding play a role in range of motion loss in patients with frozen shoulder?

PainSci » bibliography » Hollmann et al 2018

Two pages on PainSci cite Hollmann 2018: 1. Complete Guide to Frozen Shoulder2. Can the Mind Freeze Shoulders? Five Studies (Member Post)

PainSci notes on Hollmann 2018:

Five capsular release surgery patients with moderate to high levels of disability were checked before and after being put under general anaesthesia. All five of them had significantly more passive shoulder abduction and external rotation when they were knocked out … which would be impossible if their capsules were actually contractured or adhered or full of cement or any physical limitation. The improvement in abduction range was ranged from 60 to 223%, and from 18 to 156% (excluding one patient who already had normal external rotation, so she couldn't improve). The researchers reasonably concluded:

Passive range of motion loss in frozen shoulder is not fully explained by a true capsular contracture alone. Passive shoulder abduction ROM assessed in awake patients with frozen shoulder does not accurately reflect the true available ROM of the affected shoulder. It appears that active stiffness or muscle guarding is a major contributing factor to reduced ROM in patients with frozen shoulder.

Case closed? No, not yet. It’s really a shame it was such a small study. We really need someone to do the same thing with five times as many patients.

Note that this paper is a more polished re-publication of data originally reported in 2015.

original abstract Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.

STUDY DESIGN: Observational: cross-sectional study.

BACKGROUND: Idiopathic frozen shoulder is a common cause of severe and prolonged disability characterised by spontaneous onset of pain with progressive shoulder movement restriction. Although spontaneous recovery can be expected the average length of symptoms is 30 months. Chronic inflammation and various patterns of fibrosis and contracture of capsuloligamentous structures around the glenohumeral joint are considered to be responsible for the signs and symptoms associated with frozen shoulder, however, the pathoanatomy of this debilitating condition is not fully understood.

OBJECTIVES: To investigate the feasibility of a muscle guarding component to movement restriction in patients with idiopathic frozen shoulder.

METHODS: Passive shoulder abduction and external rotation range of motion (ROM) were measured in patients scheduled for capsular release surgery for frozen shoulder before and after the administration of general anaesthesia.

RESULTS: Five patients with painful, global restriction of passive shoulder movement volunteered for this study. Passive abduction ROM increased following anaesthesia in all participants, with increases ranging from approximately 55°-110° of pre-anaesthetic ROM. Three of these participants also demonstrated substantial increases in passive external rotation ROM following anaesthesia ranging from approximately 15°-40° of pre-anaesthetic ROM.

CONCLUSION: This case series of five patients with frozen shoulder demonstrates that active muscle guarding, and not capsular contracture, may be a major contributing factor to movement restriction in some patients who exhibit the classical clinical features of idiopathic frozen shoulder. These findings highlight the need to reconsider our understanding of the pathoanatomy of frozen shoulder.


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