Alternatively, rehabilitation robotics can be used to provide high volumes of passive or assisted movement, depending on the individuals requirements; this form of therapy can be useful if therapists are at a premium, and has been found effective at reducing spasticity in patients with strokes. For muscles that lack any volitional control, such as after complete spinal cord injury, exercise may be assisted, and may require equipment, such as using a standing frame to sustain a standing position. A general treatment guideline can be followed that involves:

The initial focus on first activating contraction of antagonist muscles to provide reciprocal inhibition and lengthen spastic muscles
Reciprocal actions are attempted. Agonist contractions are performed first in small ranges progressing to larger arcs of movement
Highly stressful activities be minimized early in training
Functional skills are targeted for training
Patients and family/caregivers should be educated about the importance of maintaining range of motion and doing daily exercisesMedical interventions may include such medications as baclofen, diazepam, dantrolene, or clonazepam. Phenol injections can be used, or botulinum toxin injections into the muscle belly, to attempt to dampen the signals between nerve and muscle. The effectiveness of medications vary between individuals, and vary based on location of the upper motor neuron lesion (in the brain or the spinal cord). Medications are commonly used for spastic movement disorders, but research has not shown functional benefit for some drugs. Some studies have shown that medications have been effective in decreasing spasticity, but that this has not been accompanied by functional benefits.
This is common in people who have cerebral palsy, brain injuries or a spinal cord injury, but it can happen to anybody e.g. having a stroke.One factor that is thought to be related to spasticity is the stretch reflex. This reflex is important in coordinating normal movements in which muscles are contracted and relaxed and in keeping the muscle from stretching too far. Although the result of spasticity is problems with the muscles, spasticity is actually caused by an injury to a part of the central nervous system (the brain or spinal cord) that controls voluntary movements. The damage causes a change in the balance of signals between the nervous system and the muscles. This imbalance leads to increased activity (excitability) in the muscles. Receptors in the muscles receive messages from the nervous system, which sense the amount of stretch in the muscle and sends that signal to the brain. The brain responds by sending a message back to reverse the stretch by contracting or shortening.Overall, a defining feature of spasticity is that the increased resistance to passive stretch is velocity-dependent. Lance (1980) describes it this way:  "...a motor disorder, characterised by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyper-excitability of the stretch reflex as one component of the upper motor neurone (UMN) syndrome".Spasticity is found in conditions where the brain and/or spinal cord are damaged or fail to develop normally; these include cerebral palsy, multiple sclerosis, spinal cord injury and acquired brain injury including stroke.