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cheerleader wrote:Dr. Zivadinov and Dr. Zamboni collaborated on a study of slowed cerebral bloodflow in pwMS, also known as hypoperfusion. They tested 16 pwMS and 8 healthy controls.

All of the pwMS had CCSVI, as noted by doppler ultrasound. All of the healthy controls did not.

They found slowed bloodflow in all of the people with MS...it especially affected cerebral blood flow in the gray matter.

The worse the venous obstructions, the less cerebral bloodflow. Severity of CCSVI was directly related to severity of hypoperfusion in CBF.

This paper will never be published in a neurological journal....so, the doctors kindly published it on an open access site. This research was also presented at ECTRIMS, where it received little fanfare and no press.
Here's the pdf. Enjoy!
http://www.biomedcentral.com/content/pd ... 5-9-22.pdf
cheer

marcstck wrote:Unless I'm reading it completely wrong, this study used 3T MRV imaging, not Doppler Ultrasound.

Cerebral venous return was examined using echo-color Doppler equipped with 2.5 and7.5 to 10 MHz transducers (Esaote-Biosound My Lab 25, Genoa, Italy), with the subject positioned on a bed tilted at 90° and 0° as previously described [2]. All subjects were scanned in a blinded manner following the established protocol for diagnosis of CCSVI [2], consisting of transcranial and extracranial echocolor Doppler to measure the following five venous hemodynamic (VH) parameters indicative of CCSVI: (1) reflux in the IJVs and/or in the vertebral veins (VVs) in sitting and in supine positions (90° and 0°), with reflux defined as flow directed toward the brain for a duration of >0.88 seconds; (2) reflux in the intracranial veins with reflux defined as reverse flow for a duration of 0.5 seconds in one of the insonated veins (superior and inferior petrosus sinus, and/or Rosenthal vein); (3) B-mode abnormalities causing absence of flow or significant flow disturbances (vestigial valves, septum, immobile valve leaflets, see Figure 2), or stenoses in IJVs. IJV stenosis was defined as a cross-sectional area of this vein ≤0.3 cm2 ; (4) flow that is not Doppler-detectable in IJVs and/or VVs despite multiple deep breaths; and (5) a wider cross-sectional area of the IJVs in the upright positions respect to supine. A subject was considered CCSVIpositive if at least two VH criteria were fulfilled as previously proposed [2].

Also, looked at the whole paper, and it was originally present]ed at the AAN convention in April 2010. So it's about one year old.

This paper was presented in the poster session of
the American Academy of Neurology annual meeting, Toronto, ON, Canada, 10 to 17 April 2010.

cheerleader wrote:

marcstck wrote:Unless I'm reading it completely wrong, this study used 3T MRV imaging, not Doppler Ultrasound.

CCSVI was established using blinded doppler ultrasound on 16 pwMS and 8 controls with the Zamboni criteria.

Cerebral venous return was examined using echo-color Doppler equipped with 2.5 and7.5 to 10 MHz transducers (Esaote-Biosound My Lab 25, Genoa, Italy), with the subject positioned on a bed tilted at 90° and 0° as previously described [2]. All subjects were scanned in a blinded manner following the established protocol for diagnosis of CCSVI [2], consisting of transcranial and extracranial echocolor Doppler to measure the following five venous hemodynamic (VH) parameters indicative of CCSVI: (1) reflux in the IJVs and/or in the vertebral veins (VVs) in sitting and in supine positions (90° and 0°), with reflux defined as flow directed toward the brain for a duration of >0.88 seconds; (2) reflux in the intracranial veins with reflux defined as reverse flow for a duration of 0.5 seconds in one of the insonated veins (superior and inferior petrosus sinus, and/or Rosenthal vein); (3) B-mode abnormalities causing absence of flow or significant flow disturbances (vestigial valves, septum, immobile valve leaflets, see Figure 2), or stenoses in IJVs. IJV stenosis was defined as a cross-sectional area of this vein ≤0.3 cm2 ; (4) flow that is not Doppler-detectable in IJVs and/or VVs despite multiple deep breaths; and (5) a wider cross-sectional area of the IJVs in the upright positions respect to supine. A subject was considered CCSVIpositive if at least two VH criteria were fulfilled as previously proposed [2].

Cerebral perfusion was measured by MRI ---since that's the only way to measure blood flow inside the gray matter.

Also, looked at the whole paper, and it was originally present]ed at the AAN convention in April 2010. So it's about one year old.

This paper was presented in the poster session of
the American Academy of Neurology annual meeting, Toronto, ON, Canada, 10 to 17 April 2010.

Correction...you're right, Marc, it wasn't ECTRIMS. It was presented as a poster at the AAN meeting.
It is published in an open access journal today. And that is the full paper I linked, for the first time available. Many papers take a year or more to go from poster/abstract to publication...although you wouldn't know that reading the CCSVI studies in the Annals of Neurology
cheer

All subjects were examined on a 3-T GE Signa Excite scanner (General Electric,Milwaukee, WI, USA). The following sequences were acquired: two-dimensional (2-D)multiplanar dual fast spin-echo proton density and T2-weighted images, fluid-attenuatedinversion recovery (FLAIR) images, a 3-D high-resolution (HIRES) fast spoiledgradient echo (FSPGR) with magnetization-prepared inversion recovery (IR) pulse- and
perfusion-weighted imaging (PWI).

There was a significant association between increased VHISS and decreased CBF in the majority of examined regions of the brain parenchyma in MS patients (Figures 3 to 5 and Table 2). The most robust correlations were observed for GM (Figure 3) and WM (Figure 4) (r = -0.70 to -0.71, P < 0.002, Q = 0.022) and for the putamen, thalamus, pulvinar nucleus of thalamus, globus pallidus and hippocampus (r = -0.59 to -0.71, P < 0.01, Q < 0.05). No results for correlation between VHISS and CBVor MTT survived multiple comparison correction (Figures 3 and 4 and Table 2). No significant relationship was observed between VHISS and PWI outcomes in HC.

This pilot study demonstrates that the presence and severity of CCSVI are associated with hypoperfusion of the brain parenchyma in patients with MS. In particular, a strong relationship was found between increased VHISS and decreased CBF in the GM, SGM and WM regions of the brain. No significant association was found in HC.

It has previously been demonstrated that MS patients show abnormal blood flow PWI patterns. These include increased MTT and decreased CBF and CBV within normal appearing WM and GM [4, 11-15]. Perfusion abnormalities in the normal appearing WM are present from the earliest stages of the disease. The GM perfusion changes seem to appear somewhat later in the disease [4, 13] and involve the thalamus,
putamen and other SGM structures. PWI indices are also altered in both enhancing and nonenhancing lesions [12]. The severity of the perfusion changes is more pronounced in progressive MS compared to relapsing forms of the disease [11, 13, 15].

Rokkit wrote:Can anyone help me understand the significance of this form of publishing? Does it go through a peer review process? Does it have the cache of something published in a journal or would it be panned by the medical community?