Intracranial venous haemodynamics in multiple sclerosis

Paolo Zamboni1, Erica Menegatti, Ilaria Bartolomei

  • 1Vascular Diseases Center, University of Ferrara, Ferrara, Italy. zmp@unife.it

Insights

Multiple sclerosis patients exhibit altered intracranial venous blood flow, with increased reflux and impaired drainage. These hemodynamic changes correlate with disease severity and may impact MS progression.

Area of Science:

  • Neurology
  • Vascular Biology
  • Medical Imaging

Background:

  • Multiple sclerosis (MS) lesions are venocentric, sharing features with peripheral venous disorders.
  • Despite anatomical links, intracranial venous hemodynamics in MS remain unexplored.
  • Understanding venous involvement is crucial for MS pathogenesis.

Purpose of the Study:

  • To investigate intracranial venous hemodynamics in multiple sclerosis patients.
  • To assess the relationship between altered venous flow and MS disability.
  • To explore the role of venous drainage in MS pathology.

Main Methods:

  • Eighty-nine MS patients and 60 controls underwent transcranial color-coded duplex sonography (TCCS).
  • Venous flow direction and velocity were measured in deep middle cerebral veins (dMCVs) and transverse sinuses (TS) in supine and sitting positions.
  • Peak systolic velocity (PSV), peak diastolic velocity (PDV), and resistance index (RI) were assessed.

Main Results:

  • MS patients showed significantly higher reflux/bidirectional flow rates in dMCVs compared to controls.
  • PDV was significantly lower in MS patients, with negative values indicating abnormal flow.
  • RI was dramatically increased in MS patients, indicating impaired cerebral venous drainage.
  • Reflux toward subcortical grey matter strongly correlated with higher disability scores.

Conclusions:

  • Significant hemodynamic alterations exist in cerebral veins of MS patients.
  • Impaired venous drainage and increased reflux may contribute to MS inflammation and neurodegeneration.
  • These findings highlight the potential role of venous dysfunction in MS pathogenesis.

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