NHE wrote:Amlodipine is a calcium channel blocker often prescribed to lower blood pressure since it causes arterial dilation by relaxing smooth muscle. Do you think that amlodipine could help MS patients with CCSVI by potentially increasing cerebral perfusion?
MarkW wrote:My limited understand is that veins do not have smooth muscle so calcium channel blockers would not work on veins, only arteries.
1. Why do ballooned veins sometimes get worse?
2. CCSVI: is age a problem, or length of time untreated?
3. If this thing some call MS is an invading creature, why does it leave its victims alive for so long, and not leave them altogether after a while, like other acute infections do? Is it really a chronic infection, or a symbiosis?enjoy the nightlife of New York City
I could use a good knight's sleep, that's for sure.
drsclafani wrote:1eye wrote:Questions:
1. Why do ballooned veins sometimes get worse? answered
2. CCSVI: is age a problem, or length of time untreated?
3. If this thing some call MS is an invading creature, why does it leave its victims alive for so long, and not leave them altogether after a while, like other acute infections do? Is it really a chronic infection, or a symbiosis? answeredenjoy the nightlife of New York City
I could use a good knight's sleep, that's for sure.
sorry for the delay. Again, i received no notifications that there were questions here. I do not know what i did to cause that. But i was preoccupied by the hockey in new york this late spring. The finals were really exciting. It really wasn't a typical 4games to one rout. Either team could have one it.
Some ballooned veins get worse for a couple of reasons.
1. intimal hyperplasia, or swelling and proliferation of the endothelium results in narrowing of the lumen of the vein
2. a microperforation has occured allowing some leakage of blood into the area surrounding the vein. When this undergoes inflammatory reaction, it is replaced by scar tissue that causes stricture of the vein
3. Some IRs perform prolonged balloon inflation. I do not, thinking that it might cause some ischemic changes in the vein wall that lead to stricture.
Since we really do not know what causes MS, it is difficult to ascribe it to an infectious agent.
the plasticity of the brain allows many patienst to adapt for quite some time before irreversible changes occur
NHE wrote:Hi Dr. Sclafani,
Amlodipine is a calcium channel blocker often prescribed to lower blood pressure since it causes arterial dilation by relaxing smooth muscle. Do you think that amlodipine could help MS patients with CCSVI by potentially increasing cerebral perfusion?
erinc14 wrote:I've had stents over 3 years and sometimes when I yawn or move my head I get a sharp pain on the left side of my neck . not always though . is this normal ?
Squeakycat wrote:Can we expect a critical examination of this recent paper soon: “Transvascular Autonomic Modulation: A Modified Balloon Angioplasty Technique for the Treatment of Autonomic Dysfunction in Multiple Sclerosis Patients” (Journal of Endovascular Therapy: June 2014, Vol. 21, No. 3, pp. 417-428)
drsclafani wrote:We have not had a case study in quite some time. This one was very interesting to me
The patient was a 37 year old woman with RRMS diagnosed in 2000. Symptoms at current time include fatigue, heat intolerance, head and neck pain, imbalance, numbness in both hands, weakness in both arms and legs with spasticity and requiring a wheelchair for long distance ambulation, urinary retention and constipation. She also complained of abdominal pain for many years. She had undergone extensive workup and diagnostic testing, including endoscopies, and imaging. She did not have any blood in the urine or history of kidney stones. It was thought by her neurologist that the pain might be caused by MS. Physical signs included spastic paresis of both upper and lower extremities, loss of vibratory sense in both feet, imbalance and cranial nerve deficits.
She had undergone treatment of CCSVI in 2011 at another institution which included angioplasty of both internal jugular veins with 10 mm and 12 mm balloons. She had symptomatic improvements that lasted for five months; then all symptoms came back and some were worse than before.
I thought that 12 mm balloons had been a bit small for both jugular veins. In my experience 14 mm is the average and 8mm to 26 mm is the range of balloons. Evaluation of the left renal vein, the left iliac vein and the left ascending lumbar vein were not imaged. IVUS was not used.
It seemed quite possible that inadequate treatment had been performed. I agreed to re-image and treat the patient.
The right internal jugular study was as follows:
The first two images (top row left) show the dural sinuses. There is reflux from the right transverse sinus into the left transverse sinus and then on into the left internal jugular vein. There seem to be stenoses of both internal jugular veins at the clavicles. The next four images in the top coolumn show evidence of high grade stenosis of the valvular segment with reflux under the valve into the valve sinus.
In the lower row first two images on left IVUS is shown. There is incomplete opening of a thickened valve. The IVUS on the right outlines the valve opening and compares it to the vein area itself. The numbers below show that this represents a 66.5% stsenosis. The cross sectional area of the vein (the blue circle) measures 92.5 square millimeters. A balloon of 12 millimeter diameter has a cross sectional area of 113 square millimeters. This balloon will barely stretch the vein at the area of the valve. Any of you who have seen the bulging neck veins of a weightlifter knows how much a vein can distend under normal circumstances. My general practice is to distend the vein to about 150% of its measured cross sectional area. In this case, that would be a 14 mm balloon (csa = 150 square millimeters)
The two images on the right show the constriction of the stenotic valve during balloon inflation and the venogram after angioplasty.
LEFT INTERNAL JUGULAR VEIN
A&B show the dural sinuses. There is no reflux. However at the bottom of B, there is a suggestion of narrowing. A selective study lower down in C clearly shows a significant stenosis (red arrows). The IVUS cross sectional views (E&F) and the composite coronal image (G) show thickened tissue that may represent a valve or a septum dividing the vein into two channels. While not shows, the cross sectional area of the vein in E measured about 160 square millimeters. Based upon my 150% balloon size algorithm, a balloon of about 250 square millimeters is necessary. That equates to an 18-millimeter diameter balloon. (figure D). After angioplasty (H) the vein diameter is much improved and flow was faster.
We have discussed many times how it is common to underestimate balloon size without IVUS and I am not showing this case for that reason. Rather I thought that the most interesting component was the renal vein imaging.
LEFT RENAL VEIN
The image on the left (A) is the venogram of vein of the left kidney. The darkness (density) of the contrast media is less in the circled area where the vein crosses between the aorta and the superior mesenteric artery as can be seen in Image C. The narrowed cross sectional area (in green on figure D) represents the renal vein at the area of narrowing. In Image D you can see that the vein is compressed between the SMA and the aorta. On the longitudinal vein (Image E) the narrowing in Green clearly indicates the stenosis. The calculations in image D show that this stenosis is greater that 95%. Images F and G faintly show the outline of the stents.
So why do I show this case? We have seen renal vein compressions in many other case studies. My recent analysis has shown that the incidence of renal vein compression stenosis is much more common and the degree of stenosis are much more severe in patients with MS when compared to healthy controls.
The patient's clinical symptoms included severe abdominal pain that was relieved only by lying down. She has underdone multiple endoscopies without detecting any abnormalities. In the absence of objective findings, some believed that the inflammatory brain and spine disease was the cause of it.
I will now quote the patient's subjective results of stenting:patient response five days after treatment wrote:I hope this email finds you well. I wanted to give an update on my situation, but before I do I wanted to reiterate how thankful I am for all that you have performed on me and on so many others. Again, thank you.
My parents and I left Brooklyn Saturday at 11:00 and drove back home. We stop every two hours of less so that I could stretch my leg and walk. I tried to walk as much as I could but the pain was very intense (pain from the stents in my back).
Since my intervention last Friday, I have notice improvements. My vertigo is almost gone, my balance is better, my foot drop is less, my bladder works better, so far no headaches, but the most amazing improvement is that my stomach pain is gone! I wasn't expecting for that and that was the worse of all of my issues. I can now eat without having to lie down immediately after, I am able to live in a more normal way. This is simply incredible!
The back pain from the stents is very slowly diminishing. I only take Tylenol.
Nutcracker syndrome, like CCSVI, is another entity that is not universally accepted as a clinical problem. Some say that it occurs in healthy patients. However it does cause pain and that pain may resolve after relieving the obstruction. This is not the first patienet who had pain relieved by stenting. In one patient that patient just expected to live with this pain, having never spoken to her doctor about it. This pain is often ascribed to ovarian pain, ovulation, muscle strain, and now even MS. I think that occlut abdominal pain without an explanation should be evaluated for nutcracker because of the high incidence. If one is not undergoing venography for ccsvi diagnosis and treatment, MRI or CT venography of the abdomen can pinpoint the compression. Venography is considered the Gold Standard for diagnosis but I believe that IVUS is by far superior to venography in assessing this compression stenosis.
So far, things are good since my intervention on may 9th. I was very tired when I came back from it but now I am ok. My stomach pain has not come back but I do have occasionnal pain in my abdomen. If I compare the two my stomach pain was inside my body where my stomach is while my abdomen pain is on the surface where my skin is and that pain moves around. It can be more to the left or to the right (up, down, etc) and I find it is slowly decreasing as time goes by.
My energy is good, but I do get tired easily when I am out doing things bbut a quick rest of 5-10 minutes and I am ready to go again so my recuperation is great.
My walking and balance have improved but they are not 100% but I can live with that. My bladder is working a lot better also.
I have seen both my gp and neurologist amd both have seen improvements. They were both very happy about it. They were thrilled when they heard my stomach pain was gone. I will see the physiatrist in August so he can run his tests (he was the one trying to help with my stomach pain since he thought it came from my spine).
I saw dre xxxx and too was happy to see my improvements. DrX prolonged the pradaxa for an additional three months, so six months in total. I will see the doctor again next year.
My physiotherapist was also very happy with my improvements. I can now work on getting better (rebuilding muscle strength and walking btter) since I am no longer in constant pain. was wondering if it was ok to use either heath or cold to reduce general pain?
Now, i am wondering about May-Thurner and what to do with this. I spoke to my doctors here and they are not familiar with it, most likely because it is called something else here or ... If I would go see you again to fix that, when could i do it (how long do I have to wait after my first intervention) How much would it be? I would love your input on the subject.
So, in summary, so far so good. I am very happy about the outcome of the precedure especially my stomach pain being gone!
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