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PostPosted: Tue Mar 30, 2010 1:25 am 
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Here's an interesting paper which discusses internal jugular vein incompetence and it's potential role for contributing to the development of central nervous system diseases.

Internal jugular vein valve incompetence in COPD and primary pulmonary hypertension. J Clin Ultrasound. 2008 Oct;36(8):480-4.
    PURPOSE: Under physiologic conditions, intact internal jugular vein valves (IJVVs) efficiently prevent retrograde venous flow during intrathoracic pressure increase. Chronically elevated central venous pressure found in patients with chronic obstructive pulmonary disease (COPD) and primary pulmonary hypertension (PPH) might lead to IJVV incompetence (IJVVI). The aim of this study was to analyze the prevalence of IJVVI in patients with COPD and PPH using duplex sonography (DUS). METHOD: We included 30 COPD patients, 5 PPH patients, and 100 healthy controls in the study. IJVVI was diagnosed if retrograde jugular blood flow was seen on DUS during a Valsalva maneuver. Retrograde venous flow intensity was evaluated and graded according to extent and duration of reflux. RESULTS: IJVVI was found in 18 (60%) COPD patients and in all 5 (100%) PPH patients, which was significantly different from the controls (27%; p < 0.005). The intensity of venous retrograde flow correlated with the pulmonary artery pressure. CONCLUSION: Compared with healthy controls, COPDand PPH patients demonstrated a significantlygreater prevalence of IJVVI, which seems to be caused by the elevated central venous pressure. These patients may be at higher risk to develop central nervous system diseases related to cerebral outflow obstruction.


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PostPosted: Tue Mar 30, 2010 1:49 am 
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Here's another related paper. Internal jugular vein valve incompetence may be a contributuing factor in amnesia.


Increased incidence of jugular valve insufficiency in patients with transient global amnesia.
J Neurol. 2005 Dec;252(12):1482-6. Epub 2005 Jul 7.
    OBJECTIVE: While transient global amnesia (TGA) is a clinically well defined disorder, its etiology is poorly understood. Cerebral venous hypertension and subsequent damage to hippocampal and diencephalic structures are among the discussed hypothetical causes. Using a direct method for the study of retrograde flow during a Valsalva maneuver, we determined whether jugular valve insufficiency contributes to cerebral venous hypertension in patients with TGA. METHODS: Jugular valve closure was assessed by duplex sonography in 20 patients with TGA and 20 age and gender matched controls. The diagnosis of valvular insufficiency was made on the basis of recently established criteria. RESULTS: Valvular insufficiency (either left or right-sided, or bilateral) was identified in 85% of patients with TGA,and in 45% of controls (p = 0.008). All patients with involuntary Valsalva episodes immediately prior to TGA developed valvular insufficiency (n = 8; p = 0.13 compared with patients who did not recall such an event). The mean duration of the insufficiency jet did not differ significantly between patients with TGA (3.26 s) and controls (2.78 s; p = 0.315). However, patients with TGA who experienced a trigger event were characterized by significantly longer insufficiency reflux times (3.84 s) than those without (2.55 s; p = 0.03). CONCLUSIONS: TGA is associated with an increase in the prevalence of jugular insufficiency. Valvular insufficiency may lead to increased venous pressure transmission during a Valsalva maneuver and thus contribute to venous ischemia in TGA. The association of valvular insufficiency and longer reflux times with the occurrence of a trigger event further suggests that cerebral venous congestion is an important etiological factor in transient global amnesia.


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