Strategies for stroke rehabilitation

Abstract

Rehabilitation after hemiplegic stroke has typically relied on the training of patients in compensatory strategies. The translation of neuroscientific research into care has led to new approaches and renewed promise for better outcomes. Improved motor control can progress with task-specific training incorporating increased use of proximal and distal movements during intensive practice of real-world activities. Functional gains are incorrectly said to plateau by 3-6 months. Many patients retain latent sensorimotor function that can be realised any time after stroke with a pulse of goal-directed therapy. The amount of practice probably best determines gains for a given level of residual movement ability. Clinicians should encourage patients to build greater strength, speed, endurance, and precision of multijoint movements on tasks that increase independence and enrich daily activity. Imaging tools may help clinicians determine the capacity of residual networks to respond to a therapeutic approach and help establish optimal dose-response curves for training. Promising adjunct approaches include practice with robotic devices or in a virtual environment, electrical stimulation to increase cortical excitability during training, and drugs to optimise molecular mechanisms for learning. Biological strategies for neural repair may augment rehabilitation in the next decade.

Conflict of interest statement

Conflict of interest: I have no conflicts of interest.

Figures

Figure

Functional MRI series with the blood-oxygen-level dependent signal and analysis of regions of interest during voluntary ankle dorsiflexion. The patient had chronic hemiparesis after a subcortical stroke 14 months earlier and still walked at less than 65 cm/s. The behavioural changes from baseline to the end of the first 12 training sessions were significant, so further therapy would probably not have been offered. The increase in fMRI activity, however, suggested ongoing recruitment within primary sensorimotor cortex (S1M1). Therapy was extended another six sessions in 2 weeks to see if gains in walking and recruitment had reached a plateau. There was a 20% increase in walking speed and improved motor control. The fMRI study at 6 weeks revealed an expansion of the foot representation medially into the representation for the back and hip muscles. Also, greater cerebellar and cingulate motor cortex activity developed. Two additional bouts of therapy led to greater motor control of the ankle during walking and focusing, rather than expanding fMRI activity within M1, consistent with greater synaptic efficacy (not shown).