Original Article

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No evidence of chronic cerebrospinal venous insufficiency at multiple sclerosis onset

  1. Claudio Baracchini MD1,*,
  2. Paola Perini MD1,2,
  3. Massimiliano Calabrese MD1,2,
  4. Francesco Causin MD3,
  5. Francesca Rinaldi MD1,2,
  6. Paolo Gallo MD, PhD1,2

Article first published online: 28 JAN 2011

DOI: 10.1002/ana.22228

Issue

Annals of Neurology

Annals of Neurology

Volume 69, Issue 1, pages 90–99, January 2011

Additional Information

How to Cite

Baracchini, C., Perini, P., Calabrese, M., Causin, F., Rinaldi, F. and Gallo, P. (2011), No evidence of chronic cerebrospinal venous insufficiency at multiple sclerosis onset. Ann Neurol., 69: 90–99. doi: 10.1002/ana.22228

Author Information

  1. 1

    From the First Neurology Clinic, University Hospital, Padova, Italy

  2. 2

    Multiple Sclerosis Centre of the Veneto Region, University Hospital, Padova, Italy

  3. 3

    Neuroradiology Unit, Department of Neurosciences, University Hospital, Padova, Italy

*Department of Neuroscience, University of Padua School of Medicine, Via Giustiniani, 5, 35128 - Padova, Italy

Publication History

  1. Issue published online: 28 JAN 2011
  2. Article first published online: 28 JAN 2011
  3. Manuscript Accepted: 13 AUG 2010
  4. Manuscript Revised: 2 AUG 2010
  5. Manuscript Received: 27 JUN 2010

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Abstract

Objective

An impaired cerebrospinal venous drainage, defined as chronic cerebrospinal venous insufficiency (CCSVI), has been recently hypothesized to be the possible cause of multiple sclerosis (MS). We investigated this hypothesis by studying the occurrence of CCSVI in clinically isolated syndromes (CISs) suggestive of MS.

Methods

Fifty consecutive patients presenting with a CIS and evidence of dissemination in space of the inflammatory lesions (ie, possible MS [pMS]) underwent a detailed diagnostic workup, including extracranial and transcranial venous echo-color Doppler sonography (ECDS-TCDS). Those with CCSVI underwent selective venography. Fifty healthy subjects (HCs) age-matched and gender-matched with pMS patients (HC1); 60 patients with transient global amnesia (TGA); and 60 healthy subjects age-matched and gender-matched with TGA patients (HC2) constituted the control groups and underwent ECDS-TCDS.

Results

Mean age of pMS patients was 33.0 ± 8.5 years (range, 14–50); 35 (70%) were female (female:male ratio, 2.3). TCDS was normal in all pMS patients. One or more abnormal ECDS findings were observed in 26 of 50 (52.0%) pMS patients, in 35 of 110 (31·8%) HCs (HC1+HC2), and in 41 of 60 (68.3%) TGA patients. Eight (16%) pMS patients fulfilled the diagnosis of CCSVI. Selective phlebography performed in 7 of these patients (1 denied consent) did not show venous anomalies.

Interpretation

Our findings do not support a cause-effect relationship between CCSVI and pMS. Further studies are warranted to clarify whether CCSVI is associated with later disease stages and characterizes the progressive forms of MS. Ann Neurol 2011;69:90–99.

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