, Volume 47, Issue 10, pp 741–748 | Cite as

The pathophysiology of the aqueduct stroke volume in normal pressure hydrocephalus: can co-morbidity with other forms of dementia be excluded?

  • Grant A. BatemanEmail author
  • Christopher R. Levi
  • Peter Schofield
  • Yang Wang
  • Elizabeth C. Lovett
Diagnostic Neuroradiology


Variable results are obtained from the treatment of normal pressure hydrocephalus (NPH) by shunt insertion. There is a high correlation between NPH and the pathology of Alzheimer’s disease (AD) on brain biopsy. There is an overlap between AD and vascular dementia (VaD), suggesting that a correlation exists between NPH and other forms of dementia. This study seeks to (1) understand the physiological factors behind, and (2) define the ability of, the aqueduct stroke volume to exclude dementia co-morbidity. Twenty-four patients from a dementia clinic were classified as having either early AD or VaD on the basis of clinical features, Hachinski score and neuropsychological testing. They were compared with 16 subjects with classical clinical findings of NPH and 12 aged-matched non-cognitively impaired subjects. MRI flow quantification was used to measure aqueduct stroke volume and arterial pulse volume. An arterio-cerebral compliance ratio was calculated from the two volumes in each patient. The aqueduct stroke volume was elevated in all three forms of dementia, with no significant difference noted between the groups. The arterial pulse volume was elevated by 24% in VaD and reduced by 35% in NPH, compared to normal (P=0.05 and P=0.002, respectively), and was normal in AD. There was a spectrum of relative compliance with normal compliance in VaD and reduced compliance in AD and NPH. The aqueduct stroke volume depends on the arterial pulse volume and the relative compliance between the arterial tree and brain. The aqueduct stroke volume cannot exclude significant co-morbidity in NPH.


Normal pressure hydrocephalus Vascular dementia Alzheimer’s disease Aqueduct stroke volume Compliance 



We thank the Australian Brain Foundation and the John Hunter Hospital Research Committee for granting funding for this research.


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Copyright information

© Springer-Verlag 2005

Authors and Affiliations

  • Grant A. Bateman
    • 1
    Email author
  • Christopher R. Levi
    • 2
  • Peter Schofield
    • 3
  • Yang Wang
    • 2
  • Elizabeth C. Lovett
    • 2
  1. 1.Department of Medical ImagingJohn Hunter HospitalNewcastleAustralia
  2. 2.Clinical Neurosciences ProgramHunter Medical Research InstituteNewcastleAustralia
  3. 3.Neuropsychiatry UnitJames Fletcher HospitalNewcastleAustralia

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