ahhhh... don't get too impressed, I do not "KNOW" for certain. I simply chose a machine that seems to do it all, and is the latest machine / "top of the line" from a major producer (Phillips Medical). If this machine can not perform these tests, I can't see many alternative options to getting the tests performed on myself.mrhodes40 wrote:I'm impressed you are down to the level of knowing which ultrasound to use!
Has anyone got a date for a test organised yet?
By "Primary" i am guessing you mean my GP? as I do not see my neuro except yearly, if that.mrhodes40 wrote:Cur-o did you already see the vascular guy or are your tests being ordered by your primary?
BACKGROUND: Demyelinating events in relapsing-remitting multiple sclerosis (RRMS) can involve several locations in the central nervous system. We sought to determine if initial clinical demyelinating event (IDE) location predicts subsequent clinical relapse locations in early RRMS. METHODS: We identified all RRMS patients from two large MS clinics who were seen within one year of disease onset. Logistic regression was performed with the outcome defined as the second or third exacerbation location and the predictor defined as IDE +/- second event location. RESULTS: 195 patients with at least two clinical exacerbations were identified. There was an increased odds of a patient's second relapse occurring in the spinal cord if the IDE was in the spinal cord (OR=3.79, 95% CI [2.06, 7.00], p<0.001. There was more than a six-fold increase in the odds of a patient's second relapse occurring in the optic nerve if the IDE was in the optic nerve (OR=6.18, 95% CI [2.90, 13.18], p<0.001). These associations remained similar after adjusting for treatment and patient characteristics. If the IDE and second event were both in the same location (spinal cord, optic nerve, or brainstem/cerebellum), the third event was likely to remain in that location. CONCLUSION: Patients with RRMS have relatively localized clinical relapses. It remains to be determined if genetic or biologic processes are responsible for this pattern.
PMID: 19066192 [PubMed - as supplied by publisher]
The exact etiology of venous ulcers is not certain, but they are thought to arise when venous valves that exist to prevent backflow of blood do not function properly, causing the pressure in veins to increase. The body needs the pressure gradient between arteries and veins in order for the heart to pump blood forward through arteries and into veins. When venous hypertension exists, arteries no longer have significantly higher pressure than veins, blood is not pumped as effectively into or out of the area, and it pools.
Venous hypertension may also stretch veins and allow blood proteins to leak into the extravascular space, isolating extracellular matrix (ECM) molecules and growth factors, preventing them from helping to heal the wound. Leakage of fibrinogen from veins as well as deficiencies in fibrinolysis may also cause fibrin to build up around the vessels, preventing oxygen and nutrients from reaching cells. Venous insufficiency may also cause white blood cells (leukocytes) to accumulate in small blood vessels, releasing inflammatory factors and reactive oxygen species (ROS, free radicals) and further contributing to chronic wound formation. Buildup of white blood cells in small blood vessels may also plug the vessels, further contributing to ischemia. This blockage of blood vessels by leukocytes may be responsible for the "no reflow phenomenon," in which ischemic tissue is never fully reperfused. Allowing blood to flow back into the limb, for example by elevating it, is necessary but also contributes to reperfusion injury. Other comorbidities may also be the root cause of venous ulcers.
It is in the crus that the classic venous stasis ulcer occurs. Venous stasis results from damage to the vein valvular system in the lower extremity and in extreme cases allows the pressure in the veins to be higher than the pressure in the arteries. This pressure results in transudation of inflammatory mediators into the subcutaneous tissues of the lower extremity and subsequent breakdown of the tissue including the skin.
CONCLUSIONS: This report highlights a difference found in very long-term prognosis of surgical treatment of primary valve insufficiency as opposed to postthrombotic syndrome. Long-term elimination of symptoms of chronic venous insufficiency is achieved by valve repair for primary valve insufficiency beyond 10 years, whereas late results of treatment of postthrombotic syndrome in this study was accompanied by high recurrence rates and warrants further investigation.
The aim of this study was to define the underlying anatomical and pathophysiological conditions in limbs with venous ulcers in order to get information for the most appropriate treatment selection. Ninety-eight limbs (83 patients, 59 men), with active chronic venous ulcers, were analyzed retrospectively and classified according to the CEAP (clinical, etiological, anatomical, and pathophysiological) classification. Duplex-ultrasound was performed in all patients, while air-plethysmography and venography were performed selectively on potential candidates for deep venous reconstruction. Sixty-six ulcers were primary in origin and 32 were secondary. Reflux was present in all limbs except 1. Isolated reflux in 1 system (superficial = 3, deep = 4, perforator = 3) was seen in 10 legs (10%), while incompetence in all 3 systems was seen in 51 legs (52%). Superficial reflux with or without involvement of other systems was seen in 84 legs (86%), 72 legs (73%) had deep reflux with or without involvement of other systems, and incompetent perforator veins were identified in 79 limbs (81%). Axial reflux (continuous reverse flow from the groin region to below knee) was found in 77 limbs (79%). The femoral vein was the single most common deep venous segment in which either reflux or obstruction was found. Axial distribution of disease was found in the majority of cases and no patient had isolated deep venous incompetence below knee. Primary disease was the predominant etiologic cause and reflux was the main pathophysiological finding. Practically all patients were found to have 1 or more sites of reflux or obstruction that could benefit from operative treatment.
I think that the azygos vain has no valves, not sure about the jugular. Valves make backflow and reflux impossible. Their absence may very well mean that a blockade can affect microcirculation and gas/nutrient exchange with the cells themselves.
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