Published online before print September 13, 2007, doi: 10.1161/STROKEAHA.107.492785
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(Stroke. 2007;38:e146.)
© 2007 American Heart Association, Inc.
Letters to the Editor |
Effect of Hand Splinting: Isn’t Temporality Crucial?
Department of Occupational Therapy, National University of Ireland Galway, Galway, Ireland
Department of Physiotherapy, Christian Medical College, Vellore, India
To the Editor:
The article by Lannin et al1 aimed at testing effect of hand splinting for patients with stroke is one of the few sufficiently powered randomized controlled trials. Findings of such studies are crucial for evidence-based clinical practice. However, certain conceptual concerns left unaddressed/unaccounted for need thought and consideration.
In attempts that study muscle contractures, their progressive worsening and/or measures to arrest or delay their susceptibility for progressive worsening, 3 temporal considerations are pivotal and warrant close inquiry.
What is the ‘Crucial Time’ for Initiation of Intervention (splinting)?
Muscle contractures are likely to develop both immediately (acute phase) and through several weeks, months poststroke (chronic phase). Acute phase contracture development cascade is triggered by immobilization of the muscle in the shortened position primarily due to paralysis and malpositioning. Reduction in protein systhesis, sarcomere disorganization, shortening of muscle fiber length and increase in connective tissue perimysium are changes that happen within hours to days.2 Therefore, delaying onset of intervention up to an average of 4 weeks and a maximum of 8 weeks may be a late start.
How Many ‘Intervention Sessions’ Are Ideal to Expect/Perceive Visible Macroscopic Changes (extensibility)?
The contracture cascade initiated in the acute phase continues to evolve into the chronic phase of spastic paresis, with the emergence of additional muscle overactivity, caused by both the lesion and the paresis related disuse, leading to further contractures.3 This observation continues to unfold over weeks, months and even after years. Because there is paucity of studies that explain the ‘time course’ of muscle contracture evolution and deterioration in stroke survivors, it is difficult for the clinician to decisively earmark the time to initiate intervention and sustain intervention, for a sufficiently optimal duration, to cause significant changes in muscle extensibility. Therefore, a 4-week/28-session intervention period, with a short duration 2-week follow-up, may or may not be sufficient to study muscle extensibility in totality.
Is There Consensus/Understanding on the ‘Optimal Duration’ of Splint-Wear During Each Session?
There is lack of unison in the understanding among experts on the optimal splint-wear (positioning) duration. It is evident from the current effort that immobilizing for 10 to 12 hours has no positive effect in contrast to the finding of Ada et al’s, two 30-minute sessions per day of positioning for the shoulder.4 The possibility of multiple short sessions of wrist positioning with splint, yielding positive results have not been ruled out entirely. Therefore, introspection and emphasis in future efforts on the importance attached to the time duration of splint wear per session before drawing premature conclusions is vital.
Other aspects of the study which need careful and close reflection are: lateral photographs: in the absence of proven validity and reliability, the use of lateral photographs in estimating the wrist angle, the primary outcome measure, cautions the reader on potential methodological errors or biases1; secondary outcome measures: the chosen secondary outcome measures are applaudable. However, acknowledging these subtle but definite changes between groups, at baseline, 4-weeks and 2-weeks of follow-up, as indirect reflectors of improved muscle extensibility would have appeared as a more balanced presentation to the reader (vide Table-II).1 The Tardieu spasticity angle has decreased in the extended splint group versus other groups, from 6.3 to 4.7, indicating a reduction in spasticity or an improvement in the mechanical restraint of the soft tissue.1 Pain, an established indicator of soft tissue tightness and spasticity has decreased again in the extended splint group against other groups, from 58.3 to 53.3. The DASH score too has marginally improved in both the splint groups compared with the control signifying reduction in disability.
In conclusion, we suggest developing a ‘rehabilitation protocol’ that titrates between activity and immobility, as opposed to simply discontinuing splinting completely as the authors very strongly assert. Intervention dosimetry pertaining to the time of initiation, number of interventional sessions and duration of each session, are to be meticulously considered within that ‘proposed protocol.’
Acknowledgments
Disclosures
None.
References
- Lannin NA, Cusick A, McCluskey A, Herbert RD. Effects of splinting on wrist contracture after stroke: a randomized controlled trial. Stroke. 2007; 38: 111–116.
[Abstract/Free Full Text] - Gracies JM. Pathophysiology of spastic paresis. I: Paresis and soft tissue changes. Muscle Nerve. 2005; 31: 535–551.[CrossRef][Medline] [Order article via Infotrieve]
- Gracies JM. Pathophysiology of spastic paresis. II: Emergence of muscle overactivity. Muscle Nerve. 2005; 31: 552–571.[CrossRef][Medline] [Order article via Infotrieve]
- Ada L, Goddard E, McCully J, Stavrinos T, Bampton J. Thirty minutes of positioning reduces the development of shoulder external rotation contracture after stroke: a randomized controlled trial. Arch Phys Med Rehabil. 2005; 86: 230–234.[CrossRef][Medline] [Order article via Infotrieve]
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