[Pyramidal syndrome: its physiopathology and treatment]

Is characterized by several various signs. One of these, spasticity, involves a velocity dependent increase in muscle stiffness during stretch and by hyperactive tendon jerks. When intense, spasticity impedes residual strength in antagonistic muscles and interferes with attempts to move, especially if complicated by clonus and/or spasms. Assessment of spasticity is multifactorial and implies clinical as well as instrumental methods. The pathophysiological mechanisms responsive for the hyperexcitability of the myotatic reflex can be studied by methods of clinical neurophysiology. It appears that there are various factors involved at the spinal level, involving reduction in both pre- and post-synaptic inhibitions. Although spasticity is not responsible for the major part of the disability imposed by upper motor neurone syndrome, it should be reduced. The therapeutic methods are medical, surgical or from physical medicine. In many cases, the results have been validated by blind studies. As paresis is the most disabling effect, it would be worthwhile to develop drugs able to reduce spasticity and increase muscle strength at the same time. Recent trials suggest than TRH-T may be effective in this regard.