This Is MS Multiple Sclerosis Knowledge & Support Community

Differences Between Internal Jugular Vein and Vertebral Vein Flow Examined in Real Time With the Use of Multigate Ultrasound Color Doppler

G. Ciuti, D. Righi, L. Forzoni, A. Fabbri and A. Moggi Pignone


Abstract


BACKGROUND AND PURPOSE: The hypothesis that MS could be provoked by a derangement of the blood outflow from the brain has been largely discredited. In part, it was because data on the normal pattern of outflow are scarce and obtained with different methods. The aim of this study was to evaluate the normal pattern of outflow for the vertebral and internal jugular veins in healthy subjects with multigate color Doppler.


MATERIALS AND METHODS: Twenty-five volunteers were studied to assess vessel area, mean velocity, and flow for the vertebral and internal jugular veins in the supine and sitting positions.


RESULTS: In the sitting position, flow decreases, both in vertebral veins and internal jugular veins, as the total vessel area decreases (from 0.46 ± 0.57 to 0.09 ± 0.08 cm2), even if the mean velocity increases (from 12.58 ± 10.19 to 24.14 ± 17.60 cm/s). Contrary to what happens to the blood inflow, outflow in the supine position, through vertebral and internal jugular veins, is more than twice the outflow in the sitting position (739.80 ± 326.32 versus 278.24 ± 207.94 mL/min). In the sitting position, on application of very low pressure to the skin with the sonography probe, internal jugular veins rarely appear to occlude. A pronounced difference of diameter between internal jugular veins was present in approximately one-third of subjects.


CONCLUSIONS: Our results support the view that other outflow pathways, like the vertebral plexus, play a major role in the normal physiology of brain circulation and must be assessed to obtain a complete picture of blood outflow.

Largely discredited, hmpfrgh. But I appreciate that they're looking at outflow in healthy patients.

http://www.ajnr.org/content/early/2013/ ... 2.abstract

Intracranial Nonjugular Venous Pathways: a Possible Compensatory Drainage Mechanism

M. Kopelman,
A. Glik,
S. Greenberg and
I. Shelef

+ Author Affiliations

From the Departments of Biomedicine Engineering (M.K.), and Electrical and Computer Engineering (S.G.), Ben-Gurion University of the Negev, Beer Sheva, Israel; Neuroradiology Unit (I.S.), Soroka University Medical Center, Beer Sheva and Ben-Gurion University of the Negev, Beer Sheva, Israel; and Department of Neurology (A.G.), Sheba Medical Center, Tel Hashomer, Israel.


Abstract


BACKGROUND AND PURPOSE: The IJVs are considered to be the main pathway draining the intracranial venous system. There is increasing evidence for the existence of alternative venous pathways. Studies using extracranial sonography techniques have demonstrated a nonjugular venous system. In the current study, we used MR images to investigate the NJV drainage system and its components (vertebral plexus, pterygopalatine plexus). The exact visualization and measurement of the intracranial NJVs could be of diagnostic importance and may have clinical importance.


MATERIALS AND METHODS: A total of 64 participants with no history of neurologic disease were included in the study. All participants underwent scanning with a 2D time-of-flight, multisection sequence in the supine position. Image processing software was developed to identify and quantify the size of the IJVs and NJVs in the plane of the internal JF. For evaluation of software accuracy, all images were reviewed by a neuroradiologist experienced in neurovascular imaging preprocessing and postprocessing.


RESULTS: The CSA of the NJVs correlated inversely with the CSA of the IJVs (r2 = 0.25; P < .0001). An inverse correlation was also significant when comparing IJV with NJV components (vertebral plexus: r2 = 0.19; P = .0004; pterygopalatine plexus: r2 = 0.11; P = .0069). Furthermore, only NJV cumulative CSA correlated inversely with participant age (r2 = 0.2; P = .0002).


CONCLUSIONS: Our study indicates that the NJVs might serve as a compensatory drainage mechanism in the intracranial compartment. This mechanism appears less significant as the age of the patient progresses.

Why the correlation with age? Is the compensatory drainage less effective with age?

Sir,

Catheterisation of the internal jugular vein (IJV) is commonly practiced for central venous access in intensive care unit (ICU); however, may cause significant complications such as internal carotid artery puncture, pneumothorax, vessel erosion, thrombosis, airway obstruction and infection. Here, we have reported an unusual; however, dreaded complication of IJV cannulation.

A 45-year-old male patient admitted to ICU with burn over chest (20%) and bilateral lower limb crush injury with cellulitis. Patient was haemodynamically stable and maintained oxygen saturation (SpO 2 >95%) on the face mask. In view of poor venous access, the central venous cannulation in right IJV was planned. Under full aseptic precaution, right IJV was cannulated in 2 nd attempt, triple lumen was inserted using seldinger technique and fixed at 12 cm after confirming backflow. A check X-ray chest was carried out, which showed tip of central venous (CV) line in 2 nd intercostal (IC) space. Four hours after CV line placement, the patient complained of difficulty in breathing, chest pain, falling oxygen saturation and became haemodynamically unstable (BP <90/50 mm Hg). To rule out pneumothorax, repeat X-ray chest was carried out and it showed right haemothorax. The patient condition further deteriorated and was intubated and put on ventilatory support. Even with ventilator support, he was not maintaining saturation (SpO 2 <92%) and blood pressure continued to fall and inotropic support was started (Dopamine infusion 6-10 mcg/kg/min). A diagnostic tap was carried out, 200 ml of hemorrhagic fluid was aspirated and intercostal drain (ICD) was put in the 5 th IC space. ICD drained 1200 ml of hemorrhagic fluid within 30 min. Patient was transfused two packed red cells. Haemodynamic parameters improved (BP = 100/60 mm Hg and SpO 2 >95%). Six hours after ICD placement his haemodynamic again became unstable. ICD repositioning was carried out, a contrast enhanced computed tomogram (CECT) chest was carried out, which showed a right hemothorax with mediastinal shift. Thoracic team decided to do an emergency video assisted thoracic surgery (VATS). During the VATS, 2.5 l of collected blood was evacuated and a puncture in the azygous vein was visualised. Bleeding point in the azygous vein was repaired and the patient was shifted to ICU [Figure 1]. Patient condition improved, haemodynamics stabilised and was extubated on the 2 nd post-operative day. ICD was removed on 4 th post-operative day.

Unrelated to the above two articles. But yikes! Azygous vein rupture led to serious downgrade in patient's condition until the puncture was found and treated.
In CCSVI, if an azygous vein happened to rupture during balloon angioplasty, it could be treated with a stent. I did not realize azygous vein rupture could be as serious as this particular case appeared to be. Maybe it was a very big puncture in the vein.

http://www.sciencedirect.com/science/ar ... 0612009094

Effects of Jugular Vein Occlusion on Cardiovascular Parameters in Horses During Exercise on a Treadmill

Abstract

The purpose of the present investigation was to examine the effects of unilateral and bilateral jugular vein occlusion by temporary surgical ligature on the heart rate and arterial and venous blood pressure in sedentary horses during progressive treadmill exercise. Six horses performed three exercise tests (ET). ET1, considered the control, was performed in horses without jugular occlusions. ET2 and ET3 were performed with unilateral and bilateral occlusion by temporary surgical ligature of the jugular veins, respectively. Heart rate, arterial pressure, and pressure of the occluded jugular vein were evaluated. Clinically, the horses presented apathy, head edema, congested mucous membranes, increased capillary refill time, and dysphagia. These signs were observed with the unilateral jugular vein occlusion and became more evident with the bilateral occlusion. Comparing ETs, no differences were observed in heart rate. However, jugular occlusions promoted a decrease in the mean arterial pressure and a severe increase in jugular pressure. Head edema caused by the jugular vein occlusion in the horses could interfere with the autonomic cardiovascular regulation of arterial blood pressure during exercise, likely leading to an impairment of tissue perfusion. Jugular occlusion, even unilateral, also causes severe head venous congestion, leading to venous hypertension that was aggravated by exercise, which could risk development of cerebral edema and neurological damage. The present results obtained from sedentary horses are preliminary data that lead us to suggest that sport horses presenting jugular occlusive thrombophlebitis, even unilateral, may be prevented from performing athletic activities.

Instead of studying jugular vein occlusion in mice, maybe it should be studied in horses? This study showed an effect in the short term. If exercise aggravates the cerebral congestion and hypertension, then in the previous ccsvi mice studies, maybe the mice needed to be active instead of sedentary to show effect.

To me this is the most interesting of the articles I've posted so far today.

http://www.jvascsurg.org/article/S0741- ... 0/abstract

Journal of Vascular Surgery
Volume 57, Issue 5, Supplement , Pages 100S-101S, May 2013.

Internal Jugular Vein Stenosis in Patients With Thoracic Outlet Symptoms

Samuel S. Ahn, Travis J. Miller, Julia F. Chen, Sheena W. Chen, Robert Feldtman, William Hwang

No abstract available unfortunately.

http://synapse.koreamed.org/search.php? ... vmode=FULL

An MEV is an embryonic residual venous tract that connects the sigmoid sinus and extracranial venous system, and may serve as an exit route for diploic venous blood (6). An MEV can become dilated by high-flow vascular malformations or when associated with severely hypoplastic jugular veins (7). In our case, however, we observed only a dilated MEV, with no other vascular abnormality seen in the posterior fossa or jugular venous system.

Large mastoid emissary vein associated with severely hypoplastic jugular veins? I followed the reference but didn't find any more information.
(7) http://www.ncbi.nlm.nih.gov/pubmed?cmd= ... s=11901009

SHORT REPORT

Stenting venous outflow gives symptomatic improvement in a patient with an inoperable brainstem arteriovenous malformation

Posted online on May 16, 2013. (doi:10.3109/02688697.2013.795524)

J. Nicholas P. Higgins 1 & Peter J. Kirkpatrick 2
1Department of Radiology, Addenbrooke's Hospital,
Cambridge, UK
2Academic Neurosurgical Unit, Addenbrooke's Hospital,
Cambridge, UK

The extent to which arterial steal or venous hypertension contributes to symptoms in patients with high flow brain arteriovenous malformations (AVMs) is not always clear. We describe a patient with an inoperable AVM of the pons, presenting with headache and neurological deficit where improving venous outflow by stenting produced substantial clinical benefit.



Read More: http://informahealthcare.com/doi/abs/10 ... alCode=bjn

they suggested that stenting the venous outflow (which I'm guessing is the jugulars but not sure) reduced the pressure, and that reduction in pressure improved the neurological condition

http://link.springer.com/article/10.100 ... 013-0917-1
Apparently during surgery for esophageal atresia, they commonly ligate the azygous vein. This article found that preserving it was probably a good modification of the technique. CCSVI is mentioned in passing. I am as always against the ligation of any of our major ccsvi veins.

http://link.springer.com/article/10.100 ... 012-1110-6
Interesting article on how valves form. Some diagrams too. The whole article is available as a pdf.

Flow control in our vessels: vascular valves make sure there is no way back

Eleni Bazigou, Taija Makinen

Evidence that venous valves can thicken over time and go from being invisible to being visible.
That's relevant to ccsvi.

A unique stenosis in saphenous vein graft visualized by optical coherence tomography

http://link.springer.com/article/10.100 ... 013-0362-x

Surgeons put in a graft upside down. Angiography showed no suspicion of any venous valve. Twelve years later, there was a thickened venous valve causing stenosis.

Compared with venous valves of normal SVGs [6], the valve in this case was clearly thickened. Venous valves
differ in size or thickness depending on several factors, such as position, vessel diameter, and dynamic stress caused by blood. Thickening of the venous valve in an upside-down SVG might be due to its position, which is against the direction of the blood flow, leading to thrombus formation.

Ok I vote for this as the most interesting article turned up tonight. Let me know if you agree?

OK. Back to IJVs and collaterals. This study seems to be a duplication of Dr. Zamboni's paper with the venous outflow model. It seems to me, though they may have used a new instrument. Dr. Zamboni brings to bear a much more useful picture of what is going on. If you analyze it, it is clear, since the numbers must in general, add up. Also he has used several indexes which describe outflow relative to inflow, and ratio of collateral to vertebral and jugular circulation. I am not aware, having not read the paper, of how the G. Ciuti et. al. study measured the total venous versus arterial flows, but the conclusions they came to are very similar.

However, seems they are missing a piece of the picture.

I think in the MRV paper they concluded jugular and non-jugular are reciprocals (the sum being equal to the total inflow).

I do not quite understand the following:

Contrary to what happens to the blood inflow, outflow in the supine position, through vertebral and internal jugular veins, is more than twice the outflow in the sitting position (739.80 ± 326.32 versus 278.24 ± 207.94 mL/min).

I can't see how total outflow can ever be different from the inflow. What goes in must come out. Perhaps it is contrary considering carotid vs non-carotid.

They seem though to have missed out on the fact that a significant portion of the outflow is neither jugular nor vertebral. Equal, in total, perhaps, to the jugular flow.

The normal subject, as shown in the Multigate Ultrasound Colour Doppler paper, has some amount of venous outflow by non-jugular veins. Dr. Zamboni goes farther, and measures flow in vertebrals, jugulars, and collaterals as three separate sets of veins. One interesting result in the Zamboni paper is the zero flow value in the vertebrals. I don't know how typical this patient was, but it seems to me, the vertebral flow may be important. I am unsure why a vein draining the head is even called vertebral. If it is bacause there are vertebrae in the neck being drained separately, then a condition of zero flow does not sound good at all to me. When we are concerned with degradation of the upper spine, and can see why it is crucial they remain in good condition, because of its function in supporting and balancing the head, a condition of zero flow sounds pathological to me.

We have discussed how failure to allow good blood-flow through a vein must eventually be bad for the vein's health. Perhaps this is a case where the problem is that, say, there is only zero flow when the subject is prone. We lie down an average time somewhere in the vicinity of one third of our lives. If this zero-flow condition only happens in a certain type of "MS", that might arguably be causative.

So it can be seen why good data of this kind on a large number of normals might be valuable. Perhaps a combination of Dr. Zamboni's methods and those of the "Multigate" paper would be appropriate. His model seems to be very useful. If everybody who has "MS" would do those measurements, and were held up against an equal number of normals, I think a lot of unassailable statements might result.

We are bound to find what is wrong versus normals if we measure enough stuff.

Agreed 1eye, we must keep on measuring...we must keep searching for answers.
I found the abstract for the citation you provided earlier CeCe.

http://universityvascular.com/tag/thora ... -syndrome/

We have dedicated a number of recent posts to the discussion of thoracic outlets syndrome (TOS), a condition which causes compression of the blood vessels and nerves at the top of the chest. Dr. Sam Ahn of University Vascular Associates, along with other colleagues, study this condition and recently found that compression (stenosis) of the internal jugular vein is found in patients with TOS.

This finding represents a new concept in the diagnosis of this often debilitating condition. Furthermore, the authors reported that using a balloon on the tip of a catheter to expand the compression or blockage in the jugular and/or subclavian veins can relieve symptoms of TOS. This new concept will be presented to other surgeons at the Fall semi-annual meeting of The Texas Surgical Society to be held this September in Houston (http://txsurgicalsociety.com/UpcomingMeeting.aspx).
Below is the abstract of the scientific paper to be presented at the meeting.

RR32. Internal Jugular Vein Stenosis in Patients with Thoracic Outlet Symptoms
Samuel S. Ahn2, Travis J. Miller3, Julia F. Chen3, Sheena W. Chen3, Robert Feldtman1, William Hwang4
1DFW Vascular Group, Dallas, TX; 2University Vascular Associates, Los Angeles, CA; 3UTSW Medical School, Dallas, TX; 4Neurologist, Dallas, TX.

OBJECTIVES: Traditionally, thoracic outlet syndrome (TOS) has been associated with axillo-subclavian vein stenosis without any mention of the internal jugular (IJ) vein. However, we recently reported a high prevalence of IJ stenosis in 109 patients with TOS in a limited study. To confirm this finding, we analyzed a bigger cohort of patients.

METHODS: We retrospectively analyzed 237 consecutive unique patients referred to our practice with thoracic outlet syndrome. From April 2008 to Dec 2012, all patients underwent diagnostic brachiocephalic venograms. Average age was 49.9 years (r:17 to 81), with 71.8% females and 28.2% male. We looked at the right and left internal jugular veins and the right and left subclavian veins. Stenoses were classified into high (>66%), medium (33%-66%) and low (<33%). We also looked for presence of collaterals around the obstructions. Venogram findings were confirmed by four investigators independently. For the purposes of this analysis, high stenosis was considered significant. Medium and low stenoses were considered significant only if there were visible collaterals.

RESULTS: Left internal jugular vein stenosis, left subclavian vein stenosis, right internal jugular vein stenosis, and right subclavian vein stenosis was seen in 67.5%, 57.6%, 62.7% and 61.6% of patients, respectively. Internal jugular vein stenosis was not present in 18.1% of patients, present unilaterally in 33.3% of patients and present bilaterally in 48.5% of patients. Subclavian vein stenosis was not present in 24.1% of patients, present unilaterally in 32.5% of patients and present bilaterally in 43.5% of patients. Significant collaterals were present in 26.80% of high stenosis, 21.5% of medium and 12.8% of low.

CONCLUSIONS: Internal jugular vein stenosis is common in patients with thoracic outlet symptoms. Treatment of internal jugular vein stenosis potentially could benefit these patients. These findings could fundamentally change the diagnosis and treatment of thoracic outlet syndrome. Further studies are warranted.

AUTHOR DISCLOSURES: S. S. Ahn: Nothing to disclose; J. F. Chen: Nothing to disclose; S. W. Chen: Nothing to disclose; R. Feldtman: Nothing to disclose; W. Hwang: Nothing to disclose; T. J. Miller: Nothing to disclose.

This is the actual abstract for the paper that will be presented to other surgeons at the Fall semi-annual meeting of The Texas Surgical Society to be held in Houston.

TITLE: Percutaneous Transluminal Angioplasty as Therapy for Thoracic Outlet Symptoms
AUTHORS: Ahn, Samuel S; Chen, Julia F; Miller, Travis J.; Chen, Sheena W.; Feldtman, Robert; Hwang, William

OBJECTIVES: Traditionally, thoracic outlet syndrome (TOS) has been associated with axillo-subclavian vein stenosis without any mention of the internal jugular (IJ) vein. However, we recently reported a high prevalence of IJ stenosis in 109 patients with TOS in a limited study. To further understand the clinical significance of this finding, we analyzed a larger cohort of patients and their subsequent follow-up.

METHODS: We retrospectively analyzed 237 consecutive unique patients referred to our practice with thoracic outlet syndrome. From April ’08 to Dec ’12, all patients underwent diagnostic brachiocephalic venograms. Average age was 49.9 years (r:17 to 81), with 71.8% females and 28.2% male. We looked at the right and left internal jugular veins and the right and left subclavian veins. Stenoses were classified into high (>66%), medium (33%-66%),and low (<33%). We also looked for presence of collaterals around the obstructions. Venogram findings were independently confirmed by four investigators. For the purposes of this analysis, high stenosis was considered significant. Medium and low stenoses were considered significant only if there were visible collaterals. Of this group, we then looked at all patients who received intervention via PTA at the stenosed IJ sites. Patients were categorized into Groups I or II. Group I: patients who received no immediate relief of symptoms after PTA; Group II: patients who did receive immediate relief of symptoms after PTA. Group II was further broken down into subgroups IIA, IIB, and IIC. Group IIA: those who required additional surgical intervention due to symptom recurrence; Group IIB: those who report sustained relief; Group IIC: those who were lost to follow-up.

RESULTS: Left internal jugular vein stenosis, left subclavian vein stenosis, right internal jugular vein stenosis, and right subclavian vein stenosis was seen in 67.5%, 57.6%, 62.7%, and 61.6% of patients, respectively. Internal jugular vein stenosis was not present in 18.1% of patients, present unilaterally in 33.3% of patients, and present bilaterally in 48.5% of patients. Subclavian vein stenosis was not present in 24.1% of patients, present unilaterally in 32.5% of patients, and present bilaterally in 43.5% of patients. Significant collaterals were present in 26.80% of high stenosis, 21.5% of medium and 12.8% of low. Of 237 patients, 67.7% (n=147) received PTA intervention. Of those who received intervention, 28.6% (n=42) were in Group I, 67.4% (n=99) were in Group II, and 4% (n=6) did not have available data. Of those in Group II, the breakdown was as follows: IIA (35%, n=34) with a median of less than 7 days (r: 2-210) of relief; IIB (31%, n=31) with 120 days (r: 5 to 406) of follow-up; IIIC (31%, n=31) with 93.5% (n=29) reporting sustained relief at 7-day follow-up and median follow-up of 7 days (avg: 25, r: 6-182).

CONCLUSIONS: Internal jugular vein stenosis is common in patients with thoracic outlet symptoms and percutaneous treatment provides benefit to some patients. These findings could fundamentally change the diagnosis and treatment of thoracic outlet syndrome. Further studies are warranted.

Ok that's a good abstract. "These findings could fundamentally change the diagnosis and treatment of thoracic outlet syndrome." Yup! I wonder if people with CCSVI could be diagnosed as people with thoracic outlet syndrome and treated for that without all the hoopla.

Cece wrote:Ok that's a good abstract. "These findings could fundamentally change the diagnosis and treatment of thoracic outlet syndrome." Yup! I wonder if people with CCSVI could be diagnosed as people with thoracic outlet syndrome and treated for that without all the hoopla.

The author of the book "Rise and Shine", Simon Lewis, was treated for Thoracic Outlet Syndrome. It consisted of removal of the first rib. I think PTA sounds easier.

CONCLUSIONS: Internal jugular vein stenosis is common in patients with thoracic outlet symptoms and percutaneous treatment provides benefit to some patients. These findings could fundamentally change the diagnosis and treatment of thoracic outlet syndrome. Further studies are warranted.

These guys should talk to Drs. Zamboni & Sclafani.