**2. Spasticity: pathophysiology and classification**

#### **2.1 Pathophysiology of spasticity**

Muscle tone depends on the intrinsic elasticity/stiffness of the muscle, and this in turn is modulated by the nervous system. In physiological conditions, the neural circuits in the spinal cord mediate muscle stretch reflexes. These local circuits also provide a mechanism to adjust muscle tone from supraspinal structures according to physiological requirements. Due to this configuration, lesions in these supraspinal structures or in the descending motor pathways are frequently associated with alterations in muscle tone. These alterations may involve an abnormal increase or decrease in tone. The most common form of hypertonia is spasticity, which is characterized by a velocity-dependent resistance to passive movement of a joint and its associated musculature. A slowly applied stretch in a patient with spasticity causes little resistance, but as the speed of the stretch increases, the stretch resistance also increases progressively. Thus, spasticity is primarily a phasic phenomenon. An active reflex contraction that occurs only during a rapid stretch; when the muscle is held in an elongated position, the reflex contraction decreases. However, in some cases hypertonia also has a tonic component, for example if reflex contractions persist even after the muscle is no longer stretched [5].

In the last years, the pathophysiology of spasticity has been increasingly understood. Stretch reflex hyperactivity was long thought to be caused by overactive gamma motor neurons. However, although gamma motor neurons may be overactive in some cases, changes in the background activity of alpha motor neurons and interneurons are probably more important. Particularly relevant seem to be modifications in the intrinsic properties of motor neurons that generate a sustained firing in response to a brief excitatory input. Another mechanism that produces spasticity is the strong facilitation of synaptic transmission in the sensory fiber of the monosynaptic reflex pathway. In fact, this provides a mechanism for treating this disorder. Currently, a relatively common therapeutic procedure favors presynaptic inhibition in the *Ia* fiber terminals by the intrathecal infusion of baclofen, a GABA-B receptor agonist, that blocks neurotransmitter release [5, 6].

#### **2.2 Classification of spasticity**

Classifying the severity and distribution of spasticity in each patient is an essential element to achieve effective treatment and to observe its response over time. The severity of this disorder can range from a focal problem with mild muscle stiffness to a severe and painful diffuse spasticity.

Based on its location, spasticity can be classified into Focal, Regional, and Generalized. In the first case, a single muscle group or part of the body is affected, in regional spasticity, adjacent muscle groups are affected in a region of the body. In the patients with generalized spasticity, all or almost all areas of the body are affected [6]. *Neurosurgical Spasticity Treatment: From Lesion to Neuromodulation Procedures DOI: http://dx.doi.org/10.5772/intechopen.96054*
