Intracranial Hypertension Clinical Trial
Official title:
Influencing Factors of Intracranial Hypertension in Patients With Bilateral Transverse Sinus Stenosis
Bilateral transverse sinus stenosis (BTSS) is associated with intracranial hypertension (IH). However, not every BTSS patients presented with IH. The risk factors of IH in BTSS patients remained obscure. Vertebral venous collaterals (VVC) were often found in patients with bilateral transverse sinus stenosis (BTSS). The purpose of this study was to investigate the physiological role of VVC in BTSS patients.
Bilateral transverse sinus stenosis (BTSS) is characterized by narrowing of bilateral
transverse sinus which resulted in obstruction of venous reflux. The majority of BTSS
patients exhibited with intracranial hypertension (IH) which manifested as a triad of
headaches, tinnitus and papilledema. Stenting improved the symptoms in patients with
transverse sinus stenosis (TSS) and reduced the elevated intracranial pressure (ICP). It is
suggested that BTSS is one of the etiologies of IH. Since an alternative pattern of venous
reflux was observed in patients with occluded superior sagittal sinus, it is postulated that
altered pattern of venous reflux also exists in the presence of BTSS. The drainage of
cerebral veins consists of two major pathways: transverse sinus-sigmoid sinus-internal
jugular vein and vertebral venous plexus. Vertebral venous plexus is an extensive
paravertebral system that provides direct venous communication between peritoneum and cranial
cavity. The presence of vertebral venous collaterals (VVC) was reported in 108 consecutive
patients. However, whether VVC is of physiological significance in BTSS patients remained
unknown. This study was aimed to investigate the physiological role of VVC and whether it is
involved in the regulation of IH and related clinical symptoms in BTSS patients.
Besides, it is presumed that serum uric acid (UA) may affect the formation of vertebral
venous collaterals (VVC) and intracranial pressure (ICP). It is reported that UA inhibits the
endothelial NO biological activity. High concentrations of uric acid (UA) suppresses
circulating VEGF in Wistar rats and VEGF secretion in human endothelial cells. It is presumed
that serum UA may affect the formation of VVC and ICP. The aim of this study is to
investigate whether serum UA serves as an influencing factor of VVC and an indicator of IH in
BTSS patients.
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