Rehabilitation medicine: 3. Management of adult spasticity

Abstract

Spasticity refers to an abnormal, velocity-dependent (i.e., how fast the joint is moved through its range) increase in muscle tone resulting from interruption of the neural circuitry regulating the muscles and is a common complication of cerebral palsy, brain injuries, spinal cord injuries, multiple sclerosis and stroke. The muscle stretch reflex is thought to play an important role in spasticity generation. Spasticity can have a significant detrimental effect on daily functions, such as feeding, dressing, hygiene, bladder and bowel control, and mobility; patients' need for support can also influence the cost of care. Thus, managing these patients appropriately or referring them to those with expertise in this area is important. In this article, I review the pathophysiology of spasticity and the evaluation and management of adult patients with the condition. Two hypothetical cases are presented to illustrate the management of spasticity.

Fig. 1: The stretch reflex arc. When a muscle is stretched, an impulse is generated in the muscle spindle and is transmitted via the sensory neuron to the grey matter of the spinal cord. Here the sensory neuron synapses with the motor neuron, and the transmitted impulse results in muscle contraction. While agonist muscles contract in response to stretching, antagonist muscles must relax. Their relaxation is brought about via an inhibitory neuron within the spinal cord. Photo: Christine Kenney

Fig. 2: Potential spinal mechanisms of suppression of hyperactivity in the final common pathway (alpha motor neuron and muscle). There are numerous excitatory and inhibitory modulatory synaptic influences on this pathway. An imbalance in these influences results in hyperexcitability of the stretch reflex arc, which is thought to be the basis for spasticity. Factors that play a role in suppressing hyperactivity of the final common pathway at the spinal cord level include nonreciprocal Ib inhibition (from golgi tendon organ receptors in tendons), presynaptic inhibition of the Ia terminal (at the axoaxonic synapse between 2 axons), reciprocal Ia inhibition by the inhibitory interneuron (inhibition of antagonistic muscles [see Fig. 1]) and recurrent Renshaw inhibition (inhibitory feedback of the alpha motor neuron cell body by the inhibitory interneuron). Photo: Christine Kenney

Fig. 3: Treatment planning for patients with spasticity.

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