Abstract
Paresis is one of the three main clinical symptoms of the upper motor neuron lesion. Other symptoms, which could worsen central palsy, are muscle shortening and increased muscle activity.
Besides motor inactivity, muscle shortening is caused by the atrophy of the muscle, tendon and surrounding soft tissues and is accompanied by decreased contractility, elasticity and loss of muscle volume, all of which leads to a fixed contracture in later stages. Increased muscle activity emerges a couple of weeks or months after the central lesion and is responsible for further deterioration of the paresis.
It manifests with spasticity - a sudden increase in muscle tone during a fast muscle stretch; spastic dystonia - spontaneous involuntary muscle contraction of paretic limbs under resting condition with no apparent provoking factor; spastic co-contractions - involuntary contraction of antagonist muscle during volitional contraction of the agonists in the same segment; and spastic synkinesias - aberrant motor activity in the distant segments accompanying the active movement of the paretic limb. The spastic dystonia and co-contractions are notably the most disabling signs of increased muscular activity.
They belong to critical limiting factors of neurorehabilitation as they contribute to further muscle shortening. Treatment of spastic paresis is successful if simultaneously focused on the three domains of spastic paresis - stretching the muscle (for prevention of shortening), strengthening the agonists (for improvement of paresis) and weakening the antagonists (for reduction of increased muscle activity).