Influencing Factors of Intracranial Hypertension in Patients With Bilateral Transverse Sinus Stenosis

Bilateral Transverse Sinus Stenosis, Intracranial Hypertension, Serum Uric Acid, Vertebral Venous Collaterals

vertebral venous collaterals, serum uric acid, Bilateral transverse sinus stenosis, intracranial hypertension

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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