gibbledygook wrote:The Schelling paper seems fairly emphatic that the lesion results from mechanical injury and develops from the veins rather than the other way around.
Cerebral venous outflow impairment is known to produce cerebral dysfunction in many clinical and animal studies. However, knowledge and understanding of the cerebral venous system is far less than that of the arterial system. The internal jugular vein, which is easily
observed by color-coded Doppler sonography, is one of the main tracts for cerebral venous drainage. Recently, internal jugular venous reflux has been found to be related to several neurologic disorders. These associations suggest that the mechanism of these dis- orders is related to cerebral venous outflow impairment. In this article, we will briefly
introduce the cerebral venous system and extracranial venous drainage pathway, then specifically review the characteristics of the internal jugular vein, its branches, and the hemodynamic factors involved in internal jugular venous reflux.
Cerebral circulation encompasses both the arterial and venous system (CVS). The venous system con- tains approximately 70% of the blood volume, with approximately three-quarters contained within small veins and venules [1,2]. An alteration in cerebral venous volume would influence cerebral hydro- kinetics and intracranial pressure [2,3]. In addition to cerebral venous drainage impairment, an alteration in cerebral venous volume would produce brain edema and/or decreased cerebral perfusion, leading to cerebral dysfunction [3–8]. Despite its significance in cerebral circulation, in contrast to the cerebral arterial system, the CVS is far less described and studied.
Jean-Martin Charcot (1825–1893), a great teacher and physician, created the foundations for neurology as an independent discipline and has had a phenomenal influence on contemporary neu- rology [9–11].
Charcot proposed a topographic distribution of brain diseases according to the distribution of cerebral arteries, but paid little attention to the CVS. In the first half of the 20thcentury, his students, also very celebrated neurologists, established the principle of neuropathology. Since then, extensive studies and observations have been carried out on the cerebral arterial system compared with those on the CVS. Insufficient description makes for a poor understanding of the physiology and pathology of the CVS, which might lead to the underestimation of cerebral venous disorders .
Therefore, venous reflux overloads microcirculation (Bergan et
al., 2006) and increases trans-mural pressure (Zamboni et al.,
2007); in MS, changes of microcirculatory MRI perfusional parameters,
have been shown to precede plaque formation in a longitudinal
study (Wuerfel et al., 2004). Furthermore venous reflux,
with consequent microcirculatory overload and increased transmural
pressure, facilitates erytrocyte diapedesis (Zamboni, 2006;
Bergan et al., 2006; Zamboni et al., 2007) resulting in increased
perivenous iron deposits demonstrated histologically also in MS
lesions (Adams, 1989; Adams 1988) and confirmed by advanced
MRI techniques (Haacke et al., 2005; Tjoa et al., 2005; Brass et al.,
2006). Moreover, the excess of stored iron in the brain triggers a
series of deleterious events that lead to neurodegeneration, possibly
involving mechanisms of iron-driven free radicals generation and
oxidative stress (Ke et al., 2003,
Also Zamboni mentioned that treatment had no efect whatsoever on the vascular pproblem, you have the problem whether you are on treatment or not.
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