dunkempt wrote:Interesting. And aren't many of the symptoms which seem to respond to treating CCSVI: cold extremities, weak voice, fatigue, etc., frequently associated with aging? In my case, for example, my voice had aged a lot faster than the rest of me: I sounded like my dad. This changed at once following procedure.
Our results mainly reveal the effect of age on the hemodynamics of the IJVs. We found an increase in the lumen area and a decrease in bilateral IJV ﬂow velocity with aging. Furthermore, although the total IJV blood ﬂow volume did not change, the distribution of venous drainage changed as the age of subjects increased (Fig. 2). The prevalence of left JVR also signiﬁcantly increased with increasing age. When impaired venous outﬂow results in venous pressure elevation, the upstream vein will dilate its lumen and its ﬂow velocity will be reduced (Attubato et al. 1994; Bousser et al. 1985; Donahue et al. 2009; Schaller and Graf 2004; Schaller 2004). If the extent of venous hypertension exceeds the ability of venous dilatation to compensate for it and compromises the competence of the jugular venous valve, the direction of venous ﬂow will be reversed[(Bousser et al. 1985; Schaller and Graf 2004; Schaller
2004). Therefore, a dilated lumen, reduced ﬂow velocity and increased prevalence of JVR in the left IJV, added to the fact that the proportion of blood ﬂow volume in the left IJV decreases with aging, suggests that left IJV venous outﬂow impedance may be associated with increasing age.
cheerleader wrote:This is very, very, very different than CCSVI in young people, where it is an occlusion in the jugular/azygos veins that is creating the slowed drainage and reflux. But the result of venous reflux is like the aging process....happening decades too soon.
Man, I wish the venous doctors would get together and do more research on the jugular veins in normal young people. What does "normal" jugular return look like? That's what we need to know.
Venous abnormalities contribute to the pathophysiology of several neurological conditions. This paper reviews the literature regarding venous abnormalities in multiple sclerosis (MS), leukoaraiosis, and normal-pressure hydrocephalus (NPH). The review is supplemented with hydrodynamic analysis to assess the effects on cerebrospinal fluid (CSF) dynamics and cerebral blood flow (CBF) of venous hypertension in general, and chronic cerebrospinal venous insufficiency (CCSVI) in particular.
CCSVI-like venous anomalies seem unlikely to account for reduced CBF in patients with MS, thus other mechanisms must be at work, which increase the hydraulic resistance of the cerebral vascular bed in MS. Similarly, hydrodynamic changes appear to be responsible for reduced CBF in leukoaraiosis. The hydrodynamic properties of the periventricular veins make these vessels particularly vulnerable to ischemia and plaque formation.
Venous hypertension in the dural sinuses can alter intracranial compliance. Consequently, venous hypertension may change the CSF dynamics, affecting the intracranial windkessel mechanism. MS and NPH appear to share some similar characteristics, with both conditions exhibiting increased CSF pulsatility in the aqueduct of Sylvius.
CCSVI appears to be a real phenomenon associated with MS, which causes venous hypertension in the dural sinuses. However, the role of CCSVI in the pathophysiology of MS remains unclear.
Sensitivity and specificity of SWI venography for detection of cerebral venous alterations in multiple sclerosis
Authors: Beggs, Clive B1; Shepherd, Simon J1; Dwyer, Michael G2; Polak, Paul2; Magnano, Christopher2; Carl, Ellen2; Poloni, Guy U2; Weinstock-Guttman, Bianca2; Zivadinov, Robert2
Source: Neurological Research, Volume 34, Number 8, October 2012 , pp. 793-801(9)
Publisher: Maney Publishing
Objectives: To determine the sensitivity and specificity of decreased venous vasculature visibility (VVV) on susceptibility-weighted imaging (SWI) venography in multiple sclerosis (MS) patients versus controls, and to compare this with assessment of whole brain atrophy.
Methods: Forty MS patients and 22 controls without known central nervous system (CNS) disease who had non-specific white-matter (WM) lesions were imaged on a 3T GE scanner using SWI venography. Apparent total venous volume (ATVV) and increased average distance from vein (DFV) were calculated for various vein mean diameter categories: <0·3, 0·3‐0·6, 0·6‐0·9, and >0·9 mm. Principal component analysis (PCA) was used to identify potential discriminatory metrics. Receiver operating characteristics (ROC) of these metrics, along with normalized brain volume (NBV), were calculated to determine sensitivity and specificity values between the groups. The efficacy of the metrics was validated against blinded data from 14 MS patients and 8 controls who had non-specific WM lesions.
Results: PCA identified 0·3‐0·6 mm venous relative fraction (VRF) and DFV as useful metrics. ROC analysis results in initial sample of 40 MS patients and 22 controls were (sensitivity, specificity): 0·3‐0·6 mm VRF (95·0%, 100·0%); DFV (100·0%, 100·0%); and NBV (82·5%, 68·2%). The results in validation sample were: 0·3‐0·6 mm VRF (92·9%, 75·0%); DFV (100·0%, 100·0%); and NBV (78·6%, 75·0%).
Discussion: Altered VVV indices on SWI venography showed high sensitivity and specificity for MS. The value of SWI venography for diagnosis of MS has to be further tested at early disease stages and against patients with other neurologic diseases.
1eye wrote:Just wanted to highlight that we have not heard the claim of 100% specificity in a long time... Thank you, Dr. Beggs.
1eye wrote:I don't know if I met the McDonald/CDMS criteria, but the time/space thing is only because they didn't have anything better, and it's unusually cruel for a sick person. Makes the work of diagnosis less stressful for the doctor.
From the first event I was not diagnosed for 15 years. OHIP (Ontario universal health insurance) paid for all the tests for all those years. A lot of space-time went by, and so did a lot of money.
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