Management of Spasticity Revisited

Laura A. Graham


Age Ageing. 2013;42(4):435-441. 

In This Article


The neural mechanisms underlying normal muscle tone are complex and the contribution of nervous system components to the development of spasticity remains ill-understood.[6] Spasticity can be thought of as a breakdown in control of the spinal stretch reflex mechanisms (involving Ia and II sensory afferents and alpha motor neurones) that cause inappropriate muscle over-activity, limiting the movement of the joints and limbs through a full range of movement. Interactions between the 'neural' components of these mechanisms which cause potentially reversible muscle tightness and fixed 'non-neuronal' stiffening and shortening of muscle fibres and supporting soft tissues form the basis of resistance to movement. When an UMN lesion occurs, the balance between these two components changes, disturbing normal resting tone and preventing muscle lengthening causing loss of joint range. The ageing process produces changes in muscle bulk (sarcopenia), strength and architecture, as well as increased tendon and soft tissue stiffening, meaning older people may be more susceptible to the shortening process and subsequent contracture.