Pulse-wave encephalopathy: a comparative study of the hydrodynamics of leukoaraiosis and normal-pressure hydrocephalus

There is a strong association between the occurrence of leukoaraiosis and normal-pressure hydrocephalus (NPH). Venous compression secondary to alterations in craniospinal compliance is implicated in the pathogenesis of NPH, and venous pathology has also been implicated in leukoaraiosis. The purpose of this paper is to compare and contrast the bloodflow and fluid-pulsatility characteristics of these conditions. I initially studied 18 subjects without pathology, with MRI flow-quantification studies of the cerebral arteries and veins, to define the range of normality. The main study involved 10 patients with idiopathic dementia but no leukoaraiosis who served as controls, 50 with idiopathic dementia with varying degrees of leukoaraiosis and IS with NPH. I compared blood-flow volumes, vascular pulse-wave amplitudes and velocities. There was no significant difference in blood flow across the dementia patients. In patients with moderate leukoaraiosis, arterial pulsatility was 69%, cerebrospinal fluid (CSF) pulsation 104%, sagittal sinus pulsatility 48% and cortical vein pulsatility 34% higher than in demented patients without leukoaraiosis. Patients with NPH showed similar results with arterial pulsatility increased by 56% and sagittal sinus pulsatility by 70%. By contrast, the NPH patients' CSF pulse was 42% and the pulse wave delay at the sagittal sinus 50% less than in moderate leukoaraiosis. Thus, leukoaraiosis and NPH share increased arterial and sinus pulsatility. In leukoaraiosis cortical vein compliance is initially increased but in severe leukoaraiosis and NPH it is reduced.