Iron stores in cerebral veins

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

Iron stores in cerebral veins

Postby eric593 » Wed Mar 31, 2010 4:28 am

Iron stores and cerebral veins in MS studied by susceptibility weighted imaging.
Haacke EM, Garbern J, Miao Y, Habib C, Liu M.

Department of Radiology, Wayne State University, Detroit, MI, USA2 Department of Radiology, the First Affiliated Hospital, Dalian Medical University, Dalian, China - nmrimaging@aol.com.

AIM: In this paper, we seek to determine whether the iron deposition as seen by susceptibility weighted imaging (SWI) in the basal ganglia and thalamus of patients with multiple sclerosis is greater than the iron content measured in normal subjects (individuals unaffected by multiple sclerosis). As increased iron content may result from increased venous pressure, such information would add credence to the concept of Zamboni et al (1) that MS is caused by chronic cerebrospinal venous insufficiency. METHODS: Fourteen MS patients were recruited for this study with a mean age of 38 years ranging from 19 to 66 year-old. A velocity compensated 3D gradient echo sequence was used to generate SW images with a high sensitivity to iron content. We evaluated iron in the following structures: substantia nigra, red nucleus, globus pallidus, putamen, caudate nucleus, thalamus and pulvinar thalamus. Each structure was broken into two parts, a high iron content region and a low iron content region. The measured values were compared to previously established baseline iron content in these structures as a function of age. RESULTS: Twelve of fourteen patients had an increase in iron above normal levels and with a particular pattern of iron deposition in the medial venous drainage system that was associated with the confluence of the veins draining that structure. CONCLUSION: Iron may serve as a biomarker of venous vascular damage in multiple sclerosis. The backward iron accumulation pattern seen in the basal ganglia and thalamus of most MS patients is consistent with the hypothesis of venous hypertension.

PMID: 20351671 [PubMed - in process]

http://www.ncbi.nlm.nih.gov/pubmed/20351671
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Postby Merlyn » Wed Mar 31, 2010 12:09 pm

Problems Resulting From Iron Toxicity
There are many problems that may result from iron toxicity, these include: anorexia, oligura, diarrhea, hypothermia, diphasic shock, metabolic acidosis, and death. In addition to these, the patient may experience vascular congestion of the gastrointestinal tract, liver, kidneys, heart, brain, spleen, adrenals, and thymus.


http://www.ansci.cornell.edu/plants/tox ... /iron.html
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Postby cheerleader » Wed Mar 31, 2010 12:19 pm

RESULTS: Twelve of fourteen patients had an increase in iron above normal levels and with a particular pattern of iron deposition in the medial venous drainage system that was associated with the confluence of the veins draining that structure. CONCLUSION: Iron may serve as a biomarker of venous vascular damage in multiple sclerosis. The backward iron accumulation pattern seen in the basal ganglia and thalamus of most MS patients is consistent with the hypothesis of venous hypertension.


This study is stating that the venous congestion, created by CCSVI, might be depositing iron in the brain. It is related to the veins affected by blockage down river. Nothing about iron toxicity initiating these changes. This is about how blocked veins create reflux and microvascular deposits in brain tissue....don't want readers to be confused. Iron is essential for brain health. You cannot make myelin without iron. But iron deposited in brain tissue, caused by venous reflux, is not good. CCSVI is NOT due to iron overload.

I've just written to Dr. Haacke and asked him to explain..I'm sure he can clear this up, since it was his study.
cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby mangio » Wed Mar 31, 2010 1:47 pm

Venous Hypertension I read. Maybe this is why at Hamilton workshop this
was hinted at.
High blood meds, exercise anyone?
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Postby cheerleader » Wed Mar 31, 2010 3:28 pm

mangio wrote:Venous Hypertension I read. Maybe this is why at Hamilton workshop this
was hinted at.
High blood meds, exercise anyone?


Venous hypertension is different than simple hypertension, mangio. It isn't related to arterial output, but rather it is caused by slowed venous drainage creating a backflow and congestion. You can have low blood pressure and venous hypertension. Dr. Haacke has promised me he's going to write something up for all of us, explaining what this study means- and what it doesn't mean-
cheer
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http://ccsviinms.blogspot.com
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Postby mangio » Wed Mar 31, 2010 3:55 pm

okay look forward for that info
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Postby bretzke » Wed Mar 31, 2010 4:58 pm

cheerleader wrote:Venous hypertension is different than simple hypertension, mangio. It isn't related to arterial output, but rather it is caused by slowed venous drainage creating a backflow and congestion.


Cheer-
Do you need to have reflux to have venous hypertension?
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Postby cheerleader » Wed Mar 31, 2010 6:03 pm

OK...this is from Dr. Mark Haacke, one of the authors of the paper. He has taken the time to explain what "iron" means in his study-

Iron has been implicated in multiple sclerosis for many years. It has been observed by MRI and has been seen in vessel wall for small venules. More recent work has shown that there can be iron build up around MS lesions and inside the lesions although not all lesions show an increase in iron content. Further, different parts of the brain associated with the medial venous drainage system also can show increases in iron content that appear to be affiliated with the draining veins. This iron is often not present in MS lesions although in some cases it is and appears as either a uniform intensity or as a ring-like structure around the lesion. Iron in the pulvinar thalamus can increase and is seen in roughly 50% of MS cases especially for young people. It is quite possible these increases in iron are related to the chronic venous insufficiency and may represent iron in one of three forms: oligodendrocyte ferritin after macrophage activity, iron from blood products or iron in the vessel wall or some combination of these. The iron that is measured here may represent hemosiderin which comes from the breakdown of blood not from other sources of iron. There is no evidence at this time that there are stray sources of iron causing this problem, nor has that been proposed in this research. Further, it is unknown what role iron plays at this time and the main effect may remain the demyelinating inflammatory aspects of MS with iron representing either an outcome of endothelial damage or hemosiderin or as part of the inflammatory pathway. Much remains to be learned and it is possible that iron may serve as a biomarker for MS.


Thanks, Dr. Haacke- for taking time out to comment on this study. He says it this iron may represent 3 different types of iron in the brain.
1. "oligodendrocyte ferritin after macrophage activity"- oligos make up the myelin sheath, and when the macrophages are cleaning up foreign material in the brain (in this theory foreign material could include viral, bacterial, plasmic cells breaking thru the BBB- is deposited due to CCSVI reflux. This activates the macrophages) They errantly go after the oligos while they're cleaning up the other mess. The dying oligos leave a ferritin trail.

2. "iron from blood products"- iron is a natural part of our blood, and the CCSVI process may be breaking the blood brain barrier and leaving plasmic particles in brain tissue...kind of like footprints in the snow.

3. some combo of these...again, iron leaves a footprint, saying "heme was here!"

This is not about iron overload or stray sources of iron in the brain. An anemic person could have CCSVI and iron in their brains. Or someone with normal iron panels, like my husband, could still have CCSVI.

I hope this helps explain the situation.

Bretzke-In the legs, reflux tends to be from valves or clotting issues making reflux, also May Thurner, which is stenosis- this creates venous hypertension-
Venous hypertension
Affects 1-2% of population
Due to chronic venous insufficiency and distal vein hypertension
Usually due to post thrombotic syndrome
Can be due to primary valvular incompetence


cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby hope410 » Wed Mar 31, 2010 6:16 pm

That's great, cheer. Thanks for sharing that assessment from Dr. Haacke.
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Postby Cece » Thu Apr 01, 2010 6:57 pm

thanks for all the information on this...I am always straining my (iron-loaded?) brain trying to understand the finer details...
"However, the truth in science ultimately emerges, although sometimes it takes a very long time," Arthur Silverstein, Autoimmunity: A History of the Early Struggle for Recognition
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Postby bretzke » Fri Apr 02, 2010 7:49 am

Thanks Cheer. Great info...
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