THE HISTORY OF BASAL GANGLIA - THE SLOW D EVELOPMENT OF A MAJOR CEREBRAL SYSTEM

Initially basal ganglia was a descriptive term for onto- and phylogene tic or topographic classifications. A variable list of structures were included as basal ganglia. A major step,vas made,when the thalamus wa s separated from the ''striated bodies'' (Vie d'Azyr, 1786) which was sometimes taken into account in the French description of the noyaux g ris centraux. Even if the term is not perfect, it is preferable to ''t he system of basal ganglia''. The subdivisions of the putamen, the dis tinction between the striatum and the pallidum were not really made un til the beginning of the twentieth century. Modern tracing methods wer e needed to demonstrate the main connections. It was not until the end of the 1960s that the importance of the striato-pallido-nigral networ k within the basal ganglia and the cortico-striatal connections, the m ain afferent system, were recognized. With the description of the the cortico-striatal connections, the sub-cortical system with multiple co mplex ''loops'' was questioned. The term ''extra-pyramidal system'' ha d an exagerated success. Initially, if designated descending non-pyram idal afferents (some which do not exist) and their source. In 1992, Sp atz based his separation of this heterogeneous group on the iron conte nt. The terms of extra-pyramidal ''system'' and ''syndrome'' should be abandonned by clinicians. Physiological interpretations have varied. The role of automatic a habitual motricity, derived from a concept of hierarchic, Jacksonian cerebral organization, was questioned when the pyramidal network was described. Clinico-pathological analysis (hemiba llism, Parkinson's disease...) has placed new emphasis on the motor ro le, for a time the only role accepted as real. More recently, debate h as centred on other roles, particularly in cognition and motivation. A n illustration of functions other than purely motor functions of the b asal ganglia is given by the syndromes of loss of psychic auto-activat ion secondary to bilateral lesions.