The first part of this review deals with arguments that the essential properties and organization of spinal interneuronal systems in the cat and in man are similar. The second part is concerned with the possibility that some interneuronal systems may be responsible for motor disturbances caused by spinal cord injuries and that these interneurones may be defined. This possibility is discussed with respect to the hyperexcitability of alpha-motoneurones and the exaggeration of stretch reflexes in spastic patients. To this end, what is known about cat spinal interneurones and about the neuronal basis and pharmacological treatment of spasticity, is put together. Interneurones in di- and trisynaptic reflex pathways from group II muscle afferents are singled out, since they are depressed by the alpha(2) noradrenaline receptor agonists clonidine and tizanidine, which is a critical feature of interneurones expected to contribute to exaggerated stretch reflexes which are reduced by alpha(2) noradrenaline receptor agonists. Recent observations that reflex excitation of extensor motoneurones from group II afferents is enhanced in spastic patients and that the pathologically strong reflex actions of group II afferents are reduced by clonidine and tizanidine support this proposal. On the other hand, a lack of effect of clonidine and tizanidine upon other types of excitatory or inhibitory interneurones argues against any major contribution of such interneurones to the abnormally strong responses of alpha-motoneurones to muscle stretch.