The limitation of pulsatile flow through the aqueduct of Sylvius as a cause of hydrocephalus.
The concept is advanced that hydrocephalus results from limitation in the pulsatile flow of CSF downwards through the aqueduct of Sylvius during systole which is necessary to accommodate for the pulsatile pressure and volume increase that accompanies the propagation of the arterial pulse through the brain. Evidence is given to show that flow through the fixed human aqueduct is disturbed and not laminar. Further, with the pressures availalbe, the aqueduct is only just large enough to pass the quantity of fluid which must be vented extracranially during systole. Should the capacity of this systolic venting mechanism be exceeded, physical strain will cause cellular damage in the periventricular and periaqueductal regions which, if prolonged, will lead to tissue destruction and hydrocephalus. There appear to be two main causes for hydrocephalus resulting from this mechanism. Firstly, structural lesions, restricting the lumina of the CSF-venting pathways, especially the aqueduct, will reduce the volume of CSF that can flow through these pathways during systole. The hydrocephalic process will then be continuous and only limited when tissue destruction reduces the systolic volume expansion of the brain such that it can be accomodated by the restricted CSF venting pathways. Secondly, conditions which may increase the amount of the systolic volume expansion of the brain beyond the capacity of the CSF venting pathways. Raised mean intracranial pressure is the most important of these conditions. In such cases the hydrocephalus will be limited by the duration of the causal process and possibly also by the enlargement of the venting pathways, as a result of tissue destruction. This hypothesis also accounts for hydrocephalus resulting from obliteration of the cortical subarachnoid space, obstruction to the cranial venous drainage, deformities in the region of the foramen magnum and arterial encroachment upon the ventricular system.
D000138:Acidosis / Q000150:complications; D001696:Biomechanical Phenomena; D001794:Blood Pressure; D001921:Brain / Q000098:blood supply / Q000503:physiopathology; D001929:Brain Edema / Q000150:complications; D002245:Carbon Dioxide; D002535:Cerebral Aqueduct / Q000503:physiopathology*; D002555:Cerebrospinal Fluid / Q000502:physiology; D006801:Humans; D006849:Hydrocephalus / Q000134:cerebrospinal fluid / Q000209:etiology* / Q000503:physiopathology; D006850:Hydrocephalus, Normal Pressure / Q000209:etiology; D066298:In Vitro Techniques; D007427:Intracranial Pressure; D011674:Pulse; D012119:Respiration; D013595:Syringomyelia / Q000209:etiology; D013599:Systole; D014664:Vasodilation
D002245:Carbon Dioxide