Spasticity and orthotic intervention: A neurophysiological approach

The neurophysiology of spasticity is complex but involves abnormalities in proprioceptive, cutaneous and nociceptive reflexes. Orthoses are often prescribed for patients with neuromuscular disease, including patients with stroke, to prevent or correct deformities, alleviate symptoms and improve function. However, the role of these orthoses is an area of controversy and confusion. Orthotic devices have been designed routinely to optimize the biomechanics and their design for neurological conditions has rarely considered neuromuscular impairments from a neurophysiological point of view such as hyperexcitability of stretch reflexes. Clinical evidence suggests neuromuscular responses, improvement or further complications, to the modifications of biomechanics due to orthoses in people with upper motor neuron syndrome. Previous studies have demonstrated that orthoses can influence electromyographic (EMG) activity of muscles in the normal population. Therefore, there is the potential that an orthosis could affect the neuromuscular function of patients with neuromuscular disease, specifically spasticity, after stroke. Spasticity is a velocity dependent increase in muscle tone and it has been reported that muscles activity increased at a much lower lengthening velocity for stroke subjects than controls. If an orthosis could change the pattern of muscle lengthening, therefore it could affect the velocity of lengthening and thus spasticity. The main purpose of this presentation is to discuss the effect of orthoses on the muscle-tendon complex length and lengthening velocity of muscles, with a view to informing orthotic prescription for patients with upper motor neuron syndrome.