Sixteen unpublished observations of Benign intracranial hypertension were reviewed from a clinical, aetiological and prognostic standpoint. The hypothesis that this affection could be caused by some disturbance of the C.S.F. resorption was assessed using an experimental tests battery allowing the measurement of the main factors involved in C.S.F. resorption. Our patients presented with a pure, solitary state of intra-cranial hypertension, of variable duration, capable of returning. The vital outcome was always favourable, but several severe and protracted cases were marked by a definitive visual damage. The visual risk, often underlined in the literature, requires a careful attention and eventually needs some effective treatment including C.S.F. diversion. A disorder of C.S.F. absorption could be demonstrated in most of our observations and appears to account for the principal features of Benign intracranial hypertension, including the lack of ventricular enlargement. The absorption disorder resulted either from the reversion of the pressure gradient between the C.S.F. and the venous sinuses when a dural sinus was obstructed, - or from an elevation of the resistance to flow when the sinuses were patent, thus suggesting some structural alteration of the arachnoid villi. However, for lack of histological control, such an alteration remains hypothetical, and a primary brain edema probably yield a similar a pathophysiological pattern. Finally, an attempt is made to classify the various aetiological factors encountered in Benign intracranial hypertension according to the previous pathogenic discussion.