Object: Findings in animal models of noncommunicating hydrocephalus have suggested that a reduction in compliance of the superior sagittal sinus, an elevation in venous outflow pressure, and the development of venous collateral flow may be associated with this condition. Although elevated venous pressure is known to cause hydrocephalus in children, this mechanism has fallen out of favor as a theory in adults.
Methods: Twenty-one patients with late-onset idiopathic aqueductal stenosis (LIAS) underwent magnetic resonance imaging with flow quantification measuring the degree of ventricular enlargement, sulcal compression, total blood inflow, superior sagittal/straight sinus outflow, aqueduct flow, arteriovenous delay (AVD), and the extent of collateral venous flow. Data obtained in these patients were compared with those obtained in 21 age-matched control individuals.
Results: There was a reduction in compliance in the patients with LIAS in whom the AVD decreased by 50% (p = 0.01). The arterial inflow and the straight sinus outflow were normal, but the sagittal sinus outflow was reduced by 23% (p = 0.001). This indicated that significant collateral venous outflow pathways were draining blood away from the superficial but not the deep drainage system.
Conclusions: Similar to the animal models, patients with LIAS exhibit a reduced venous compliance and an elevation in venous collateral flow. Together, these findings suggest that an elevation in venous pressure may be associated with this disease process. A review of the literature has indicated that only subtle differences may exist in the pathophysiology among patients with LIAS, normal-pressure hydrocephalus, and idiopathic intracranial hypertension.