**1.1 Pathophysiology of spasticity and dystonia syndromes**

Typically, spasticity is considered as a specific "pyramidal" sign; nevertheless, selective lesions of the primary motor cortex or corticospinal tract often induce hypotonia, deficit, or weakness in distal movements, without inducing spasticity [4]. Only the involvement of non-primary motor areas (premotor and supplementary areas) and the corticoreticulospinal fibres together with cortical lesions may induce spasticity. Corticoreticulospinal fibres sends through the dorsolateral reticulospinal tract descending just anteriorly to the corticospinal tract, a massive bilateral inhibitory projection to spinal motor neurons, which are located in the lateral funiculus of the spinal cord. So the fact that a selective lesion of the anterior limb or the genu of the internal capsula predominantly induces spasticity without an evident motor deficit and vice versa can be explained by the different courses of corticoreticular and corticospinal fibres in the internal capsula. Hence, a lesion involving the corticoreticulospinal fibres will lead to a decreased inhibition (or to an increased facilitation) of the spinal cord and ultimately to spasticity [13, 14]. Three fundamental phenomena occur after a lesion to the central motor pathways assigned to motor command execution:

