Janny P, Chazal J, Colnet G, Devoize J L, Barretto L C
Neurochirurgie. 1981;27(2):79-88.
Sixteen unpublished observations of Benign intracranial hypertension were reviewed from a clinical, aetiological and prognostic standpoint.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.
从临床、病因学和预后的角度对16例未发表的良性颅内高压观察病例进行了回顾。使用一组实验测试评估了这种疾病可能由脑脊液吸收的某些紊乱引起的假设,这些测试能够测量脑脊液吸收中涉及的主要因素。我们的患者表现为单纯的、孤立的颅内高压状态,持续时间可变,能够恢复。生命预后总是良好的,但有几例严重且病程迁延的病例出现了永久性视力损害。文献中经常强调的视力风险需要密切关注,最终可能需要一些有效的治疗,包括脑脊液分流。在我们的大多数观察中都可以证明脑脊液吸收紊乱,这似乎可以解释良性颅内高压的主要特征,包括脑室无扩大。吸收紊乱要么是由于硬脑膜窦阻塞时脑脊液与静脉窦之间压力梯度的逆转,要么是由于窦开放时血流阻力的升高,从而提示蛛网膜绒毛存在一些结构改变。然而,由于缺乏组织学对照,这种改变仍然是假设性的,原发性脑水肿可能产生类似的病理生理模式。最后,根据之前的病因学讨论,尝试对良性颅内高压中遇到的各种病因因素进行分类。