DrSclafani answers some questions

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Re: DrSclafani answers some questions

Postby drsclafani » Mon Nov 25, 2013 10:04 pm

MSandI wrote:Hi Dr Sclafani,
My mother have been discussing ccsvi, in in doing so a subject was brought up by my mom. She told me while she was pregnant with me she got sick and was put in the hospital for the last few months of pregnancy. She told me that the doctors told her she had toxemia (preeclampsia today). I started to google it and it seems that when the mother gets toxemia the is a shortned supply of blood flow to the baby via the placenta. Does that make someone like me (rrms), a good candidate for ccsvi?
Ann
http://www.hmhb.org/virtual-library/int ... eclampsia/


ann, i could not find any evidence that preeclampsia results in MS in offspring.

The college of phlebology believes that the vascular problem of CCSVI results most often from a developmental abnormality in the fetus during the maturation of the veins of the brain and spine. this should occur during the fifth month of fetal development. I cannot prove or disprove whether preeclampsia may incite that malformation.

It is my opinion that patients with RRMS are likely to have venous abnormalities of these veins and that angioplasty is effective in relieving those venous obstructions. How much benefit one derives from angioplasty is not predictable and often depends upon the degree and the nature of the symptoms of the patient.

I cannot advise you in your particular case because I have insufficient information and have not had an opportunity to assess you and examine you

DrS
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Re: DrSclafani answers some questions

Postby MSandI » Sun Dec 01, 2013 8:25 am

Thank you Dr Sclafani for answering my question.
Ann
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Re: DrSclafani answers some questions

Postby Cece » Wed Dec 11, 2013 6:52 am

drsclafani wrote:
pelopidas wrote:so, can you please describe what is the patient's profile and symptoms with renal vein compression?


There are several profiles of patients with renal compression (nutcracker)

1. no symptoms. 10-20% of humans have some degree of renal vein compression. The majority of them have no symptoms and renal vein compression is then called Nutcracker phenomenon.
2. symptoms related to renal vein compression in children: This is a common cause of chronic fatigue in childhood. These patients have symptoms of vascular congestion of the kidney manifested by protein in the urine and microscopic or gross hematuria. They may also have other symptoms listed below as seen in adults.
3. Symptoms related to reflux into the veins of the ovary or the testicle. In women this manifests as some of the following: chronic pelvic pain unrelated to menstrual cycle, pelvic floor fatigue and pain (especially on standing and relieved by lying down), frequent bouts of cystitis, hemorrhoids, rectal pain, varicose veins of the upper thigh and the external female genitalia. In men infertility with low sperm count and immobility of sperm, and varicose veins in the testicle are common.
4. Symptoms of the midline congestion syndrome described by Scholbach: a constellation of symptoms related to organs and structures that are located in the mid-line of the abdomen, including the spinal cord and vertebrae, the bowel, uterus, bladder, and genitalia. Symptoms include headaches (including migraine headaches), abdominal pain, back and flank pain, diarrhea, bloody bowel movements, painful sex, urinary pain and cystitis and rectal pain
5. In the 1970's Albouker reported on myelopathy resulting from renal vein compression. He stated that he found, among 60 patients treated for renal vein compression, that other venous obstructions, involving jugular, brachiocephalic, azygos and iliac veins were common. (sounds like CCSVI to me)

I contend that since jugular and azygos vein obstructions are so common in patients with MS, things are strongly affected by renal vein compression. When jugular veins are obstructed, epidural venous drainage provides an accessory collateral outflow draining into the superior vena cava through the azygos vein. When the azygos vein is also obstructed, azygos flow decompresses through the hemiazygo-left renal trunk into the renal vein and inferior vena cava. But if that renal vein is obstructed, it has a doubly negative effect. Not only is the collateral flow inhibited, but the flow from the renal vein is partially redirected INTO the hemiazygos vein back into the spine resulting in increased congestion of the spinal cord and worsening overload of the spinal circuits. The only remaining spinal vein is the ascending lumbar vein but we know that this vein is commonly hypoplastic in patients with MS. So that is not useful as a decompressing vein.

Scholbach thinks that congestion of the vertebral plexus of veins results in displacement of CSF upward and he suggests that resultant intracranial CSF overload can cause headaches. This may be compounded by the retardation of CSF outflow in the presence of jugular vein obstructions.

I must add that most IRs to do not focus on this at all.

I just noticed what you said about Scholbach. So if the jugular vein outflow obstructions lead to collateral flow through the vertebral plexus, and that leads to impairment of cerebrospinal fluid flow and congestion of cerebrospinal fluid flow, and that is exacerbated by the very jugular vein obstructions that initiated the sequence of events, then it is a vicious circle.

The following is from Scholbach's 2006 paper on midline congestion syndrome:
After a treatment with acetylsalicylic acid in doses from 15 to 200mg/d within 14–200 days a complete relief of so far long lasting therapy-resistant midline organ symptoms was achieved. Simultaneously the left/right renal perfusion ratio increased significantly to 1.24 (p=0.021). This improvement of left renal perfusion can be explained by a better drainage of collateral veins, diminution of their wall distension, thereby decline of their intramural inflammation, reduction of their mass effects (especially by the replaced spinal fluid inside the spinal canal and the skull), and altogether a reduction of pain and functional derangement in the affected midline organs.
http://www.medical-hypotheses.com/artic ... 1/abstract

All those results, from treatment with aspirin?
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Re: DrSclafani answers some questions

Postby Cece » Wed Dec 11, 2013 6:58 am

drsclafani wrote:preparing several documents for consideration
1. incidence of RVC in PwMS vs controls
2. IVUS in RVC
3. case reports
4. large case series

nothing completed yet

I think you are right about the importance of renal vein compression and the neglect of this currently. Urgent and important work, to get this into the literature.
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Re: DrSclafani answers some questions

Postby drsclafani » Wed Dec 11, 2013 7:42 am

Cece wrote:
drsclafani wrote:
pelopidas wrote:so, can you please describe what is the patient's profile and symptoms with renal vein compression?


There are several profiles of patients with renal compression (nutcracker)

1. no symptoms. 10-20% of humans have some degree of renal vein compression. The majority of them have no symptoms and renal vein compression is then called Nutcracker phenomenon.
2. symptoms related to renal vein compression in children: This is a common cause of chronic fatigue in childhood. These patients have symptoms of vascular congestion of the kidney manifested by protein in the urine and microscopic or gross hematuria. They may also have other symptoms listed below as seen in adults.
3. Symptoms related to reflux into the veins of the ovary or the testicle. In women this manifests as some of the following: chronic pelvic pain unrelated to menstrual cycle, pelvic floor fatigue and pain (especially on standing and relieved by lying down), frequent bouts of cystitis, hemorrhoids, rectal pain, varicose veins of the upper thigh and the external female genitalia. In men infertility with low sperm count and immobility of sperm, and varicose veins in the testicle are common.
4. Symptoms of the midline congestion syndrome described by Scholbach: a constellation of symptoms related to organs and structures that are located in the mid-line of the abdomen, including the spinal cord and vertebrae, the bowel, uterus, bladder, and genitalia. Symptoms include headaches (including migraine headaches), abdominal pain, back and flank pain, diarrhea, bloody bowel movements, painful sex, urinary pain and cystitis and rectal pain
5. In the 1970's Albouker reported on myelopathy resulting from renal vein compression. He stated that he found, among 60 patients treated for renal vein compression, that other venous obstructions, involving jugular, brachiocephalic, azygos and iliac veins were common. (sounds like CCSVI to me)

I contend that since jugular and azygos vein obstructions are so common in patients with MS, things are strongly affected by renal vein compression. When jugular veins are obstructed, epidural venous drainage provides an accessory collateral outflow draining into the superior vena cava through the azygos vein. When the azygos vein is also obstructed, azygos flow decompresses through the hemiazygo-left renal trunk into the renal vein and inferior vena cava. But if that renal vein is obstructed, it has a doubly negative effect. Not only is the collateral flow inhibited, but the flow from the renal vein is partially redirected INTO the hemiazygos vein back into the spine resulting in increased congestion of the spinal cord and worsening overload of the spinal circuits. The only remaining spinal vein is the ascending lumbar vein but we know that this vein is commonly hypoplastic in patients with MS. So that is not useful as a decompressing vein.

Scholbach thinks that congestion of the vertebral plexus of veins results in displacement of CSF upward and he suggests that resultant intracranial CSF overload can cause headaches. This may be compounded by the retardation of CSF outflow in the presence of jugular vein obstructions.

I must add that most IRs to do not focus on this at all.

I just noticed what you said about Scholbach. So if the jugular vein outflow obstructions lead to collateral flow through the vertebral plexus, and that leads to impairment of cerebrospinal fluid flow and congestion of cerebrospinal fluid flow, and that is exacerbated by the very jugular vein obstructions that initiated the sequence of events, then it is a vicious circle.

The following is from Scholbach's 2006 paper on midline congestion syndrome:
After a treatment with acetylsalicylic acid in doses from 15 to 200mg/d within 14–200 days a complete relief of so far long lasting therapy-resistant midline organ symptoms was achieved. Simultaneously the left/right renal perfusion ratio increased significantly to 1.24 (p=0.021). This improvement of left renal perfusion can be explained by a better drainage of collateral veins, diminution of their wall distension, thereby decline of their intramural inflammation, reduction of their mass effects (especially by the replaced spinal fluid inside the spinal canal and the skull), and altogether a reduction of pain and functional derangement in the affected midline organs.
http://www.medical-hypotheses.com/article/S0306-9877(06)00779-1/abstract [copy and paste for link to work]

All those results, from treatment with aspirin?


i am also surprised by his results. But remember his patients are predominantly (or completely) children and many symptoms of nutcracker, especially pelvic congestion, etc, may not be manifest until adulthood.

Reducing perivenous inflammation may be beneficial, however, even in adults. Based on his paper, I recommend low dose aspirin for at least 6 months after venoplasty for ccsvi. I have little objection to longer duration of aspirin therapy if tolerated.
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Re: DrSclafani answers some questions

Postby Rogan » Wed Dec 11, 2013 8:59 pm

Cece

You wrote
DrSclafani answers some questions
by Cece » Sat Feb 04, 2012 8:44 pm
Venous congestion, particularly when caused by tricuspid regurgitation, may produce venous pulsations which may produce low readings with ear probes.
http://www.nda.ox.ac.uk/wfsa/html/u05/u05_003.htm
http://www.oximeter.org/pulseox/lim_venous.htm
http://www.springerlink.com/content/q387524121462516/
Central venous pulsations associated with a falsely low oxygen saturation measured by pulse oximetry. But would the flow effects of CCSVI be comparable to that of central venous pulsations or tricuspid heart interfere wth an ear oximeter?




A company in Minnesota has invented a new noninvasive oximeter for the brain.

They should come to CCSVI meetings and give free screenings.

http://www.nonin.com/EquanoxTechnology
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Re: DrSclafani answers some questions

Postby dlynn » Wed Dec 18, 2013 3:03 pm

Dr. Sclafani,
Do any of your 50+ yr olds need a second (or third) CCSVI procedure?
What is the average length of time they benefit from the procedure?
Did any require stents?
Do you think bed-wetting as a child is a symptom of m.s., CCSVI, or NCS?

Thank you, I'm so very grateful for the time you give us
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Re: DrSclafani answers some questions

Postby drsclafani » Wed Dec 18, 2013 11:10 pm

dlynn wrote:Dr. Sclafani,
Do any of your 50+ yr olds need a second (or third) CCSVI procedure?
What is the average length of time they benefit from the procedure?
Did any require stents?
Do you think bed-wetting as a child is a symptom of m.s., CCSVI, or NCS?

Thank you, I'm so very grateful for the time you give us


actually, i havent had very many second or third treatments among people who have had a successful response to angioplasty. Reasons include cost, durability of the procedure, distance for travel, discouragement from short duration of response.

i think cost is an issue. If it were not, I would repeat venography at three months after the procedure to look for additional lesions or early restenosis. I think second treatments are often more durable and long lasting than second procedures.
Travel distance is also a real problem for many patients. I look forward when I can treat patients from new york city and advise local doctors of my out of town patients.
Discouragement of a short duration of response is justified. However that is not that common in my experience.

I like to think that high pressure large enough balloon angioplasty and detection of renal vein compression is leading to longer duration of effectiveness.

i do not think that age is a vital issue. I treat young patients just like i treat older patients. same disease just been there longer

i have no idea whether bed wetting is a manifestation of ms or ccsvi.

DrS
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Re: DrSclafani answers some questions

Postby Cece » Fri Dec 20, 2013 10:39 am

dlynn wrote:Dr. Sclafani,
Do any of your 50+ yr olds need a second (or third) CCSVI procedure?
What is the average length of time they benefit from the procedure?
Did any require stents?
Do you think bed-wetting as a child is a symptom of m.s., CCSVI, or NCS?

Thank you, I'm so very grateful for the time you give us

When it comes to age, the difference that I remember is that the obstructions may be more likely to be thickened, compared to the more subtle findings in a much younger patient. So the diagnosis part of the procedure could be easier in an older patient. I would think a more thickened valve might be more likely to recoil or leave residual valve material, so there might be a small difference in outcomes, but nothing that could be predicted in an individual case based solely on age?

Previous case study:
Cece wrote:May 29, 2012
chronic-cerebrospinal-venous-insufficiency-ccsvi-f40/topic10680-6885.html#p192606
A case study of a 20-year-old patient that illustrates the more subtle presentation of CCSVI in the younger patient.
drsclafani wrote:The case in point illustrates this point. I plan to go back and review the IVUS exams of the youngest patients and compare them to those who have had the disease for a considerable time.

A cliffhanger there: how do IVUS exams from the two different ages compare?
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Re: DrSclafani answers some questions

Postby NZer1 » Fri Dec 20, 2013 10:59 am

Cece wrote:
dlynn wrote:Dr. Sclafani,
Do any of your 50+ yr olds need a second (or third) CCSVI procedure?
What is the average length of time they benefit from the procedure?
Did any require stents?
Do you think bed-wetting as a child is a symptom of m.s., CCSVI, or NCS?

Thank you, I'm so very grateful for the time you give us

When it comes to age, the difference that I remember is that the obstructions may be more likely to be thickened, compared to the more subtle findings in a much younger patient. So the diagnosis part of the procedure could be easier in an older patient. I would think a more thickened valve might be more likely to recoil or leave residual valve material, so there might be a small difference in outcomes, but nothing that could be predicted in an individual case based solely on age?

Previous case study:
Cece wrote:May 29, 2012
chronic-cerebrospinal-venous-insufficiency-ccsvi-f40/topic10680-6885.html#p192606
A case study of a 20-year-old patient that illustrates the more subtle presentation of CCSVI in the younger patient.
drsclafani wrote:The case in point illustrates this point. I plan to go back and review the IVUS exams of the youngest patients and compare them to those who have had the disease for a considerable time.

A cliffhanger there: how do IVUS exams from the two different ages compare?


This aspect opens a whole can of worms due to the 'reason' why values would thicken?

Some people like me would suspect that there is a pathogen cause that is effecting a malformation or purely a pathogen effecting the internal linings and valves over the 'Life time'.

The tests/study from Dr Paul Thibault are finding that if there is an infection involved in MS such as the CPn infections, he has found in most patients with MS and CCSVI problems, that once the infection is being treated with a protocol approach over time the 'flow figures' improve. This will be published in the not too distant future.

So the age of PwMS is something for debate!

;)
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Re: DrSclafani answers some questions

Postby drsclafani » Fri Dec 20, 2013 12:44 pm

Cece wrote:
dlynn wrote:Dr. Sclafani,
Do any of your 50+ yr olds need a second (or third) CCSVI procedure?
What is the average length of time they benefit from the procedure?
Did any require stents?
Do you think bed-wetting as a child is a symptom of m.s., CCSVI, or NCS?

Thank you, I'm so very grateful for the time you give us

When it comes to age, the difference that I remember is that the obstructions may be more likely to be thickened, compared to the more subtle findings in a much younger patient. So the diagnosis part of the procedure could be easier in an older patient. I would think a more thickened valve might be more likely to recoil or leave residual valve material, so there might be a small difference in outcomes, but nothing that could be predicted in an individual case based solely on age?

Previous case study:
Cece wrote:May 29, 2012
chronic-cerebrospinal-venous-insufficiency-ccsvi-f40/topic10680-6885.html#p192606
A case study of a 20-year-old patient that illustrates the more subtle presentation of CCSVI in the younger patient.
drsclafani wrote:The case in point illustrates this point. I plan to go back and review the IVUS exams of the youngest patients and compare them to those who have had the disease for a considerable time.

A cliffhanger there: how do IVUS exams from the two different ages compare?


I havent noticed anything i could publish regarding age and thickness of valve
Outcome differences often depend more on degree of disability than age. Young people tend to have longer times between relapses and disability is often less when not actively in relapse or attack
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Re: DrSclafani answers some questions

Postby drsclafani » Fri Dec 20, 2013 12:46 pm

NZer1 wrote:
Cece wrote:
dlynn wrote:Dr. Sclafani,
Do any of your 50+ yr olds need a second (or third) CCSVI procedure?
What is the average length of time they benefit from the procedure?
Did any require stents?
Do you think bed-wetting as a child is a symptom of m.s., CCSVI, or NCS?

Thank you, I'm so very grateful for the time you give us

When it comes to age, the difference that I remember is that the obstructions may be more likely to be thickened, compared to the more subtle findings in a much younger patient. So the diagnosis part of the procedure could be easier in an older patient. I would think a more thickened valve might be more likely to recoil or leave residual valve material, so there might be a small difference in outcomes, but nothing that could be predicted in an individual case based solely on age?

Previous case study:
Cece wrote:May 29, 2012
chronic-cerebrospinal-venous-insufficiency-ccsvi-f40/topic10680-6885.html#p192606
A case study of a 20-year-old patient that illustrates the more subtle presentation of CCSVI in the younger patient.
drsclafani wrote:The case in point illustrates this point. I plan to go back and review the IVUS exams of the youngest patients and compare them to those who have had the disease for a considerable time.

A cliffhanger there: how do IVUS exams from the two different ages compare?


This aspect opens a whole can of worms due to the 'reason' why values would thicken?

Some people like me would suspect that there is a pathogen cause that is effecting a malformation or purely a pathogen effecting the internal linings and valves over the 'Life time'.

The tests/study from Dr Paul Thibault are finding that if there is an infection involved in MS such as the CPn infections, he has found in most patients with MS and CCSVI problems, that once the infection is being treated with a protocol approach over time the 'flow figures' improve. This will be published in the not too distant future.

So the age of PwMS is something for debate!

;)
Nigel


I would not disagree with you
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Re: DrSclafani answers some questions

Postby drsclafani » Fri Dec 20, 2013 12:49 pm


This aspect opens a whole can of worms due to the 'reason' why values would thicken?

Some people like me would suspect that there is a pathogen cause that is effecting a malformation or purely a pathogen effecting the internal linings and valves over the 'Life time'.

The tests/study from Dr Paul Thibault are finding that if there is an infection involved in MS such as the CPn infections, he has found in most patients with MS and CCSVI problems, that once the infection is being treated with a protocol approach over time the 'flow figures' improve. This will be published in the not too distant future.

So the age of PwMS is something for debate!

;)
Nigel




actually, one of the greatest thickenings I have seen is in a teenager with active neurological Lymes

DrS
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Re: DrSclafani answers some questions

Postby drsclafani » Fri Dec 20, 2013 1:19 pm

A commonly used MRI contrast agent has been associated with brain abnormalities, new research suggests.

A study conducted by investigators from the University School of Medicine in Tokyo and the Hyogo Cancer Center in Akashi, Japan, shows a link between the contrast medium gadolinium (Gd-CM) and hyperintensities in the dentate nucleus (DN) and globus pallidus (GP), independent of kidney function.

"Hyperintensity in the DN and GP on unenhanced MRI may be a consequence of the number of previous Gd-CM administrations," lead investigator Tomonori Kanda, MD, PhD, said in a statement.

These new findings, said Dr. Kanda, raise the possibility that a toxic component of the contrast agent may remain in the body long after administration.

"Because gadolinium has high signal intensity in the body, our data may suggest the fact that the toxic gadolinium remains in the body for a long time, even in the normal renal function patient," he said.

However, Dr. Kanda told Medscape Medical News that "more research is needed" before any change in practice should be considered. "My study was only [based on] image data and there is no risk for patients at present."

The study was published online December 7 in Radiology.

No Proof of Causation

Dr. Kanda and colleagues observed that patients with a history of multiple administrations of Gd-CM showed areas of hyperintensity on MRI in the DN and GP, in a dose-dependent manner, and that the signal intensity appeared higher with increasing number of exposures to Gd-CM.

To investigate further, they compared unenhanced T1-weighted MR images of 19 patients who had undergone 6 or more contrast-enhanced brain scans with 16 patients who had had 6 or fewer unenhanced scans.

They found a significant correlation between the number of previous Gd-CM administrations and hyperintensities in the DN (P < .001) and GP (P < .001), regardless of kidney function.

The investigators note these findings should be taken into account when MR images are interpreted.

"The present findings can be added to the differential diagnosis of a high-signal-intensity [DN] and [GP], and some differential diagnosis may be changed," they write.

Because patients with multiple sclerosis tend to undergo repeated contrast-enhanced brain MRI, the hyperintensity of the DN seen in these patients may have more to do with the large cumulative Gd-CM dose than the disease itself, the investigators suggest.

Learn more
The investigators also note the mechanisms by which Gd-CM administration causes hyperintensity of the DN and GP remain to be determined.

Dr. Kanda said there currently is no proof that Gd-CM is responsible for hyperintensity on brain MRI. A study is now underway to examine this hypothesis.

Further, he added, his team has recently completed a study looking at whether the macrocyclic type of Gd-CM (as opposed to the linear type) can prevent MRI hyperintensity.

"Our data suggested that macrocyclic type of gadolinium-based contrast media can prevent MRI hyperintensity," Dr. Kanda said.

It would also be worth studying whether patients who have hyperintensity on brain MRI have symptoms or not, he said.
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Re: DrSclafani answers some questions

Postby Squeakycat » Fri Dec 20, 2013 7:08 pm

A friend who is a neuroscientist told me a story of one case he was familiar with where a woman who had severe headache of unknown origin that resulted in 10 contrast enhanced MRIs in one year experienced considerable neurological degeneration to the point that she was diagnosed with ALS, but was then found to have renal problems that were preventing the clearance of gadolinium.

She was treated with fluids, bed rest and chelation therapy and all her neurological problems were resolved, though not the unexplained headaches that had led to all the MRIs in the first place.

Although N=1 and 10 contrast enhanced MRIs in one year is probably at the extreme, this would seem to indicate that accumulation of Gd in the CNS can have quite serious consequences.
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