Original article
Persistent Shoulder Pain in the First 6 Months After Stroke: Results of a Prospective Cohort Study

Presented in a poster session to the International Association for the Study of Pain, World Congress on Pain, September 2, 2010, Montreal, Canada.
https://doi.org/10.1016/j.apmr.2011.02.016Get rights and content

Abstract

Roosink M, Renzenbrink GJ, Buitenweg JR, Van Dongen RT, Geurts AC, IJzerman MJ. Persistent shoulder pain in the first 6 months after stroke: results of a prospective cohort study.

Objective

To identify factors associated with persistent poststroke shoulder pain (pPSSP) in the first 6 months after stroke.

Design

Prospective inception cohort study.

Setting

Stroke units of 2 teaching hospitals.

Participants

Patients (N=31) with a clinical diagnosis of stroke.

Interventions

Not applicable.

Main Outcome Measures

The development of pPSSP within the first 6 months after stroke. Clinical assessment of motor, somatosensory, cognitive, emotional, and autonomic functions, undertaken within 2 weeks (t0), at 3 months (t1), and at 6 months (t2) after stroke.

Results

Patients with pPSSP (n=9) were compared with patients without pPSSP (n=22). Bivariate logistic regression analyses showed that pPSSP was significantly associated with impaired voluntary motor control (t0, t1, t2), diminished proprioception (t0, t1), tactile extinction (t0), abnormal sensation (t1, t2), spasticity of the elbow flexor muscles (t1, t2), restricted range of motion (ROM) for both shoulder abduction (t2) and shoulder external rotation (t1, t2), trophic changes (t1), and type 2 diabetes mellitus (t0).

Conclusions

These findings suggest a multifactorial etiology of pPSSP. The association of pPSSP with restricted, passive, pain-free ROM and signs indicative of somatosensory sensitization may implicate a vicious cycle of repetitive (micro)trauma that can establish itself rapidly after stroke. Intervention should therefore be focused on maintaining and restoring joint ROM as well as preventing injury and somatosensory sensitization. In this perspective, strategies that aim to intervene simultaneously at various levels of function can be expected to be more effective than treatment directed at merely 1 level.

Section snippets

Participants

All consecutive stroke patients (age, ≥18y) admitted to the stroke units of 2 teaching hospitals in The Netherlands (Ziekenhuisgroep Twente and Medisch Spectrum Twente) with a clinical diagnosis of stroke were screened for participation between May and December 2009.

All stroke patients who had sustained a first-ever cortical or subcortical unilateral stroke (infarction or hemorrhage) resulting in somatosensory and/or motor symptoms or signs were deemed eligible. Based on the screening of

pPSSP Development

Thirty-seven patients entered the study (see fig 1). Three patients were lost to follow-up. PSSP was observed at all time points, with the highest frequency at t1 (n=11, 32%). Nine patients developed PSSP at both t1 and t2 and formed the pPSSP group. None of the patients with pPSSP could be classified as having SHS or CPSP. Patients who recovered from PSSP after t1 (n=2) or developed CPSP at another location (n=1) were excluded from the analysis. The remaining patients formed the NoPSSP group

Discussion

The aim of the present study was to identify factors associated with pPSSP in the first 6 months after stroke. pPSSP was associated with impaired voluntary motor control, diminished proprioception, tactile extinction, abnormal sensation, spasticity of the elbow flexor muscles, restricted ROM for both shoulder abduction and shoulder external rotation, trophic changes, and DM-2. The associations depended on the time after stroke, suggesting that different factors may be involved in the initiation

Conclusions

The findings suggest a multifactorial etiology of pPSSP and warrant a multifactorial approach to both prevention and treatment. The association of pPSSP with restricted passive pain-free joint ROM and with signs indicative of somatosensory sensitization may implicate a vicious cycle of pain, limited ROM, reinjury, and somatosensory sensitization that seems to establish itself quite rapidly (ie, within 3mo after PSSP onset). Prevention of (repetitive) (micro)trauma at the shoulder should

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  • Cited by (0)

    Supported by the AMPHoraest Foundation, Leusden, The Netherlands.

    Clinical Trial Registration Number: NTR1746.

    No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit on the authors or on any organization with which the authors are associated.

    Reprints are not available from the authors

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