The pathophysiology of spasticity is a complex subject and one frequently avoided by clinicians. Spasticity and the other features, positive and negative, of the upper motor neurone (UMN) syndrome arise from disruption of certain descending pathways involved in motor control. Hyperexcitability of spinal reflexes forms the basis of most of the positive clinical signs of the UMN syndrome, which have in common excessive muscle activity. These spinal reflexes may be divided into two groups, proprioceptive reflexes and nociceptive/cutaneous reflexes. The clasp-knife phenomenon combines features of both groups, at least in the lower limbs. Contractures are a well known and feared complication of the UMN syndrome, reducing the range of motion of a joint. There has been a recent investigation of the relationship between the stretch reflex hyper excitability of spasticity and contractures. Spasticity does not appear to exist in contracting agonists and would not really interfere with movement.

This introduction provides an overview of spasticity management. Spasticity can cause problems with activity and participation in people with a variety of neurological disorders. It is only one of the many different features of the upper motor neurone (UMN) syndrome. The clinical features of the UMN syndrome can be divided into two broad groups such as negative phenomena and positive phenomena. A characteristic feature of spasticity is that the hypertonia is dependent upon the velocity of the muscle stretch, in other words, greater resistance is felt with faster stretches. Thus, spasticity resists muscle stretch and lengthening. Severe muscle spasms are often found in UMN syndrome. These can be in either a flexor pattern or an extensor pattern. The description of the different patterns of the UMN syndrome makes it clear that there is a potentially wide range of functional problems.