Chronic hypoperfusion article - wonder if relevant?

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Chronic hypoperfusion article - wonder if relevant?

Postby eric593 » Thu Jul 29, 2010 12:43 am

J Cereb Blood Flow Metab. 2002 Jan;22(1):97-104.

Blood-brain barrier disruption in white matter lesions in a rat model of chronic cerebral hypoperfusion.

Ueno M, Tomimoto H, Akiguchi I, Wakita H, Sakamoto H.

Second Department of Pathology, Kagawa Medical University, Kita-gun, Kagawa, Japan.

Abstract
Blood-brain barrier damage has been implicated in the pathogenesis of cerebrovascular white matter lesions. This type of lesion is responsible for cognitive impairment in the elderly and can be induced by permanent ligation of the bilateral common carotid arteries in the rat. Because it is unclear whether the blood-brain barrier is impaired, we examined whether vascular permeability to horseradish peroxidase is altered using this model.

According to light microscopic results, the reaction product of horseradish peroxidase was most intensely localized to the paramedian part of the corpus callosum in the brain, occurring to a small degree at 3 hours, day 1, markedly on day 3, but reduced on days 7 and 14. By electron microscopic study of the same area, the reaction product of horseradish peroxidase was localized to the plasmalemmal vesicles in the endothelial cells 3 hours after ligation, but appeared in the cytoplasm on days 1 and 3, suggesting a diffuse leakage of horseradish peroxidase. I

n addition, the reaction product was dispersed into the cytoplasm of glial cells in the perivascular regions on day 3. The luminal surface of the endothelial cell cytoplasm appeared irregular on day 7, suggesting a conformational change of the endothelial cells.

Collagen fibrils proliferated in the thickened basal lamina and mitochondria degenerated in the pericyte on days 7 and 14. Perivascular glial endfeet were swollen throughout the survival period. In sham-operated rats, the reaction product of horseradish peroxidase was not observed at any time interval, except in vesicular structures.

These findings indicate that chronic cerebral hypoperfusion induces blood-brain barrier damage with subsequent morphologic changes of the vascular structures in the corpus callosum. An extravasation of macromolecules, such as proteases and immunoglobulins, may contribute to the pathogenesis of white matter lesions.

PMID: 11807399 [PubMed - indexed for MEDLINE]Free Article

http://www.ncbi.nlm.nih.gov/pubmed/11807399
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Postby gibbledygook » Fri Jul 30, 2010 8:30 am

Certainly. Herewith:
J Neurol Sci. 2009 Jul 15;282(1-2):28-33. Epub 2009 Jan 31.

White matter hemodynamic abnormalities precede sub-cortical gray matter changes in multiple sclerosis.
Varga AW, Johnson G, Babb JS, Herbert J, Grossman RI, Inglese M.

Department of Radiology, New York University, New York, NY, USA.

Abstract
BACKGROUND: Hypoperfusion has been reported in lesions, normal-appearing white (NAWM) and gray matter (NAGM) of patients with clinically definite multiple sclerosis (MS) by using perfusion MRI. However, it is still unknown how early such changes in perfusion occur. The aim of our study was to assess the presence of hemodynamic changes in the NAWM and subcortical NAGM of patients with clinically isolated syndrome (CIS) in comparison to healthy controls and to patients with early relapsing-remitting (RR) MS. METHODS: Absolute cerebral blood flow (CBF), blood volume (CBV) and mean transit time (MTT) were measured in the periventricular and frontal NAWM, thalamus and putamen nuclei of 12 patients with CIS, 12 with early RR-MS and 12 healthy controls using dynamic susceptibility contrast enhanced (DSC) T2*-weighted MRI. RESULTS: Compared to controls, CBF was significantly decreased in the periventricular NAWM of CIS patients and in the periventricular NAWM and putamen of RR-MS patients. Compared to CIS, RR-MS patients showed a significant CBF decrease in the putamen. CONCLUSIONS: CBF was decreased in the NAWM of both CIS and RR-MS patients and in the subcortical NAGM of RR-MS patients suggesting a continuum of tissue perfusion decreases beginning in white matter and spreading to gray matter, as the disease progresses.

PMID: 19181347 [PubMed - indexed for MEDLINE]PMCID: PMC2737614

http://www.ncbi.nlm.nih.gov/pubmed/19181347

it's not just Zamboni who has noted haemodynamic abnormalities...
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Postby eric593 » Fri Jul 30, 2010 11:49 pm

Thanks, GG!

MS demyelination seems to be attracted to the corpus callosum, and I have read that hypoperfusion is a part of CCSVI, so I wondered if the pieces might be coming together. This article seems to suggest that strangling the carotid and causing hypoperfusion creates BBB permeability, so it could support how our BBB becomes vulnerable if hypoperfusion also occurs with CCSVI, the strangling of the veins instead.

This article was just a little bit over my head, so I was wondering if I was on the right track or completely off base. 8O
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Postby gibbledygook » Tue Aug 03, 2010 1:09 am

Hi, I think that hypoperfusion does indeed increase blood brain barrier permeability and that hypoperfusion might be caused by a number of different things including a blocked venous outflow pathway as well as a blocked inflow via the artery. I think that low blood pressure would also tend to increase cerebral hypoperfusion. I am inferring this from my obstetrician's fear about placental hypoperfusion with very low blood pressure but I'm no medic and the article below discusses how hypertension (high blood pressure) would tend to cause vascular dementia. I love all the detail about the jugular veins below as they are quite clearly implicated in this dementia.

This article shows how hypoperfusion results from jugular vein reflux (JVR).

Med Hypotheses. 2010 Jul;75(1):85-90. Epub 2010 Feb 20.

Pathogenesis of leukoaraiosis: role of jugular venous reflux.
Chung CP, Hu HH.

Department of Neurology, Taipei Veterans General Hospital, Taipei, Taiwan.

Abstract
Leukoaraiosis (LA) is a major cause of vascular dementia and disability in the elderly. Age and hypertension are the most two important risk factors. Despite its clinical significance, the etiology is so far unclear. Chronic cerebral hypoperfusion associated with vasogenic edema, microbleeding or/and endothelial dysfunction found in LA favors venous ischemia, in stead of arterial ischemia, as its pathogenesis. The involved regions in LA, periventricular and subcortical regions, are the drainage territory of deep cerebral venous system and the watershed region between the superficial and deep cerebral venous system respectively. Adding the facts that periventricular venule collagenosis, and retinal and intraparenchymal venules dilatation are related to the severity of LA, cerebral venous hypertension caused by downstream venous outflow impairment might play a major role in the pathogenesis of LA. Internal jugular vein is the main venous outflow pathway for cerebral venous drainage. The frequency of jugular venous reflux (JVR) is increased with aging. Hypertension, which has a decreased venous distensibility, might further exacerbate the sustained or long-term repetitive retrograde-transmitted cerebral venous pressure and venous outflow insufficiency caused by JVR. Clinically, JVR caused by a dural AV fistula does lead to cerebral hypoperfusion, white matter abnormalities, vasogenic edema and cognitive impairment in several published reports. JVR is suggested to play a key role in the pathogenesis of LA through a sustained or long-term repetitive retrograde-transmitted cerebral venous pressure and venous outflow insufficiency, which might lead to chronic cerebral venous hypertensions, abnormal cerebral venules structural changes, decreased cerebral blood flow, endothelial dysfunction, and vasogenic edema in cerebral white matters. Copyright 2010 Elsevier Ltd. All rights reserved.

PMID: 20172657 [PubMed - in process]
http://www.ncbi.nlm.nih.gov/pubmed/20172657
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Postby Algis » Tue Aug 03, 2010 1:28 am

Drs Chung and Hu are the ones looking over my CCSVI here in Taiwan They "proceeded" 2 patients so far.

But it still in its infancy here; even if they studied reflux since a long while.
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Postby gibbledygook » Tue Aug 03, 2010 9:03 am

Looks like they've been pretty busy and helpful for those needing more support that jugular vein reflux is damaging to central nervous systems including eyesight:

Cerebrovasc Dis. 2010 Jan;29(2):122-9. Epub 2009 Dec 1.

Jugular venous reflux affects ocular venous system in transient monocular blindness.
Chung CP, Hsu HY, Chao AC, Cheng CY, Lin SJ, Hu HH.

Department of Neurology, Taipei Veterans General Hospital,Taipei, Taiwan.

Abstract
BACKGROUND: The frequency of jugular venous reflux (JVR) is higher in patients with transient monocular blindness (TMB). We hypothesize that JVR influences ocular venous outflow, and resulting disturbances in cerebral and ocular venous circulation might be a cause of TMB. To substantiate this hypothesis, we aimed to demonstrate that: (1) TMB patients have vasculature changes in their retinal venules, and (2) JVR could influence ocular venous outflow, as revealed by dilated retinal venules. METHODS: This study has 2 parts. The case-control study included 31 TMB patients and 31 age/gender-matched normal individuals, who all received fundus photography for retinal venule diameter comparisons. The Valsalva maneuver (VM) experiment included 30 healthy volunteers who received both color Doppler imaging of the internal jugular vein and fundus photography for retinal venule diameter measurement. RESULTS: In the case-control study, TMB patients had a wider retinal venule diameter (184.5 +/- 17.5 vs. 174.3 +/- 16.2 microm, right eye, p = 0.023; 194.20 +/- 24.6 vs. 176.6 +/- 19.5 microm, left eye, p = 0.017), especially TMB patients with JVR. The VM experiments showed that the presence of JVR was associated with a greater increase in retinal venule diameters during VM in the subjects' right eye (14.27 +/- 11.16 vs. 2.75 +/- 3.51%, JVR vs. non-JVR, p = 0.0002) and left eye (10.06 +/- 6.42 vs. 1.80 +/- 2.03%, p = 0.0003). CONCLUSIONS: These findings provide evidence that frequently occurring JVR associated with TMB impedes ocular venous outflow, and the subsequent disturbances in ocular venous circulation may be a cause of TMB. (c) 2009 S. Karger AG, Basel.

PMID: 19955735 [PubMed - indexed for MEDLINE
http://www.ncbi.nlm.nih.gov/pubmed/19955735

Ann Neurol. 2008 Feb;63(2):247-53.

Reflux of jugular and retrobulbar venous flow in transient monocular blindness.
Hsu HY, Chao AC, Chen YY, Yang FY, Chung CP, Sheng WY, Yen MY, Hu HH.

Section of Neurology, Taichung Veterans General Hospital, Taichung, Taiwan.

Abstract
OBJECTIVE: Transient monocular blindness (TMB) attacks may occur during straining activities that impede cerebral venous return. Disturbance of cerebral and orbital venous circulation may be involved in TMB. METHODS: Duplex ultrasonography and Doppler-flow measurement of jugular and retrobulbar veins were performed in 134 consecutive patients with TMB and 134 age- and sex-matched control subjects. All recruited patients received thorough examinations to screen for possible underlying causes. RESULTS: Of the 134 patients with TMB, 48 patients had ipsilateral carotid arterial lesion and 7 patients had TMB attack(s) caused by cardiac embolism. Of the remaining 79 patients with undetermined cause, 46 had 3 or more TMB attacks (undetermined-frequent group) and 33 had fewer than 3 attacks. In comparison with the control subjects, the TMB patients had greater frequencies of jugular venous reflux (57 vs 30%; p < 0.0001; odds ratio [OR]: 3.079, 95% confidence intervals [CI]: 1.861-5.096) and flow reversal in the superior ophthalmic vein (RSOV; 37 vs 9%; p < 0.0001; OR: 6.052, CI: 3.040-12.048). The undetermined-frequent group had the greatest frequencies of jugular venous reflux (74%, 34 patients; OR: 6.66, CI: 3.13-14.17) and RSOV (59%, 27 patients; OR: 6.51, CI: 3.12-13.58). Of the 50 patients with RSOV, 47 (94%) had RSOV on the side of the TMB attacks. INTERPRETATION: The increased incidences of jugular and orbital venous reflux in TMB patients suggest that disturbance of cerebral and orbital venous circulation is involved in the pathogenesis of TMB, especially among patients with frequent attacks of undetermined cause.

PMID: 18306412 [PubMed - indexed for MEDLINE
http://www.ncbi.nlm.nih.gov/pubmed/18306412

Ultrasound Med Biol. 2007 Apr;33(4):500-5.

Flow volume in the jugular vein and related hemodynamics in the branches of the jugular vein.
Chung CP, Hsu HY, Chao AC, Wong WJ, Sheng WY, Hu HH.

Section of Neurovascular Diseases, Neurological Institute, Veterans General Hospital-Taipei, Taipei, Taiwan.

Abstract
Venous reflux in the internal jugular vein branches (JB) was found frequently in patients of certain neurologic disorders. We hypothesized that the retrograde-flow in JB is associated with retrograde hypertension transmitted from the internal jugular vein (IJV), which presumably underlies those neurologic disorders. In this study, we used color-Doppler imaging to evaluate the dynamic venous flow patterns in the IJV and its branches in 50 normal individuals (21 men, 29 women; mean age: 40.9 +/- 14.9 y, range: 22 to 70 y). The flow-direction of all detected JB (n = 100) was flowing into the IJV at baseline. During the Valsalva maneuver (VM), 38 JB (38%) had a retrograde-flow. Retrograde-flow in JB was significantly associated with IJV valve incompetence (OR = 7.6; 95% CI = 2.6 to 21.8; p = 0.0002) and greater IJV blood flow volume (blood flow volume >670 mL/min) (OR = 6.6; 95% CI = 1.8 to 24.5; p = 0.0052), both of which may reflect higher IJV pressure transmission during VM. The sonographic findings can be used in the future studies of diseases that are suspected to be related with retrograde cerebral venous hypertension due to an elevated IJV venous pressure.

PMID: 17337108 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/17337108


I'd be very glad to be on their patient list!
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Postby sumsum » Tue Aug 03, 2010 12:09 pm

I don't understand how there can be literature out there on reflux and it's effect on body parts (in this case the eyes) - written by neurologists if I am not mistaken - and still there is such a hostile blockage from the neurological establishment...

This is really startling me (although I guess it's all about the "power of definition").

Gibbledygook, if I may ask: how are you doing now? Has your blood pressure come back to normal levels after pregnancy?

Anyways, I hope you are doing well.

Best wishes!
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Postby gibbledygook » Tue Aug 03, 2010 12:34 pm

Well, I guess also they are Taiwanese researchers and it's fairly recent research and neurologists are just not plugged in yet. But we'll just have to ligate one or two of their neck veins and I'm sure they'll come round...!

I am doing so much better since delivery. Thank goodness. my walking has been gradually getting steader and I've had virtually no myoclonus and the bladder is stronger though not as good as immediately after the stent operation. My c-section wound still hurts quite a bit so I've still got some healing to go there. I also don't know where my blood pressure is because I believe it takes 3 months for the veins/vasculature to resume it's normal shape and so my automated blood pressure reading will give false results. I'm going to see the doctor next week so I'll get an updated reading then.
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Postby ErikaSlovakia » Wed Aug 04, 2010 1:01 am

gibbledygook wrote:...
I am doing so much better since delivery. Thank goodness. my walking has been gradually getting steader and I've had virtually no myoclonus and the bladder is stronger though not as good as immediately after the stent operation. My c-section wound still hurts quite a bit so I've still got some healing to go there. I also don't know where my blood pressure is because I believe it takes 3 months for the veins/vasculature to resume it's normal shape and so my automated blood pressure reading will give false results. I'm going to see the doctor next week so I'll get an updated reading then.

I am very happy for you and your baby! :D
I wish you the best! You deserve it.
Erika
Aug. 7, 09 Doppler Ultras. in Poland, left Jugul. valve problem, RRMS since 1996, now SPMS,
- Nov.3,09: one stent in the left jug. vein in Katowice, Poland, LDN, never on DMDs
- Jan. 19, 11: control venography in Katowice - negative but I feel worse
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Postby sumsum » Wed Aug 04, 2010 1:26 am

:D

That sounds good gibbledygook! Keep on healing and all the best to you and your family.
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Postby eric593 » Wed Aug 04, 2010 12:45 pm

GG - so happy to hear about how well you're doing since the birth! That is such great news.

Thanks all for the input & further info. Algis, so cool that it's your docs that authored the articles on this!

Glad to see research on this has been going on so we may be further ahead than we know, doctors just weren't putting it all together yet before now.
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