Department of Exercise Sciences

Bilateral priming accelerates recovery of upper limb function after stroke: a randomized controlled trial

Cathy M. Stinear, Matthew A. Petoe, Samir Anwar, Peter Alan Barber and Winston D. Byblow
Published in Stroke: online October 31, 2013


The ability to live independently after stroke depends on the recovery of motor function, particularly of the upper limb. The potential for recovery is related to the extent of cerebral damage that creates a ceiling effect, with a plateau usually reached within 6 months after stroke. With no treatment available for repairing the stroke lesion and raising the recovery ceiling, it is crucial to develop adjuvant techniques that accelerate recovery and help patients more efficiently reach a plateau of best possible function.

Techniques that prime the brain for a more plastic response to therapy may accelerate motor recovery after stroke. Increasing excitability and reducing inhibition are important precursors for neural plasticity, which may allow surviving neural elements to more easily reorganize in response to therapy. Active-passive bilateral priming (APBP) is a pattern of coordinated movement that disinhibits the M1 contralateral to the assisted (paretic) limb and facilitates its excitability for ≥ 30 minutes after a 15-minute session.

Stinear 2013 - Figure 2 (insert after results)


The aim of this study was to determine the immediate and longer term effects of bilateral priming with patients with stroke at the subacute stage.

We hypothesized that APBP before upper limb therapy would accelerate the recovery of hand and arm function, with a greater proportion of PRIMED participants reaching maximum recovery by 12 weeks.


A single-center randomized controlled trial of bilateral priming was conducted with 57 patients randomized at the subacute stage after first-ever ischemic stroke. The PRIMED group made device-assisted mirror symmetrical bimanual movements before upper limb physiotherapy, every weekday for 4 weeks. The CONTROL group was given intermittent cutaneous electric stimulation of the paretic forearm before physiotherapy. Assessments were made at baseline, 6, 12, and 26 weeks. The primary end point was the proportion of patients who reached their plateau for upper limb function at 12 weeks, measured with the Action Research Arm Test.


As shown in Figure 2A, a greater proportion of participants achieved a plateau of upper limb function by 12 weeks in the PRIMED group than the CONTROL group. PRIMED participants were around 3 times more likely to achieve their plateau within 12 weeks compared with CONTROL participants.

Neurophysiological measures revealed that bilateral priming promoted rebalancing of corticomotor excitability at 12 and 26 weeks (Figure 2B and 2C). Also, PRIMED participants had greater interhemispheric inhibition at 26 weeks than controls as increased excitability of transcallosal projections from the ipsilesional to contralesional M1 was observed.


This is the first study to show that bilateral priming before upper limb therapy accelerates the recovery of upper limb function after stroke and increases the odds of reaching the recovery plateau by 12 weeks for equivalent therapy dose.

The neurophysiological effects of APBP are the most likely mechanism underlying the observed acceleration of recovery. Excitability increased for both descending and transcallosal projections from the ipsilesional M1 in the PRIMED group but not in the CONTROL group. These effects were evident 12 and 26 weeks after stroke, indicating long-term benefits for the motor system, which may overcome a progressive neurophysiological decline.


We thank Suzanne Ackerley, Yvette Baker, Claudia Barclay, Patricia Bennett, Jemma Crowe, Alison Elston, Marie-Claire Smith, Anne Ronaldson, and Anna Vette for their assistance with patient recruitment and study coordination. We thank the Centre for Advanced MRI and LabPlus for assistance with imaging and genotyping.