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Completed

NCT Number: NCT04492332

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.

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Key information

Sex eligibility

All sexes

Study type

Interventional

Phase

Not applicable

Primary location

Xuanwu Hospital

Beijing, China

About this study

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.

Who can participate

Healthy volunteers accepted: No

Only the study team can determine whether someone qualifies for participation.

Inclusion criteria

  • BTSS confirmed by two of magnetic resonance venography (MRV), computed tomography venography (CTV) or digital subtraction angiography (DSA).

Exclusion criteria

  • medicine related intracranial hypertension;
  • systemic inflammation;
  • moderate to severe stenosis in intracranial, carotid or vertebral arteries;
  • moderate to severe stenosis in intracranial or jugular veins other than transverse sinus;
  • intracranial lesions.

Treatment and study plan

standard lumbar puncture

Diagnostic Test

Subjects underwent a standard lumbar puncture to measure the intracranial pressure (ICP). ICP was measured invasively through lumbar space in the morning.

Primary outcomes

  1. intracranial pressure (ICP)

    Time frame: at admission

    ICP was detected by standard lumbar puncture

Secondary outcomes

  1. serum uric acid (UA)

    Time frame: at admission

    Fasting venous blood was withdrawn simultaneously to assess serum UA.

Other outcomes

  1. Triad of IH: papilledema

    Time frame: at admission

    Fundus photography was graded by using modified Frisén's grade

  2. Triad of IH: headache

    Time frame: at admission

    10-point Numeric Pain Rating Scale (NPRS)

  3. Triad of IH: tinnitus

    Time frame: at admission

    questionnaires for tinnitus handicap inventory (THI)

Sponsors and collaborators

Lead sponsor

Capital Medical University

Other

Registry information

Important dates

Study start
2014
Primary completion
2019
Study completion
2019
First posted
Jul 30, 2020
Registry last updated
Jul 30, 2020

OpenTrials presents study information sourced from ClinicalTrials.gov. The official registry record should be consulted for the latest information.

View the official ClinicalTrials.gov record (opens in a new tab)

This listing is for discovery and informational purposes only. It is not medical advice, does not guarantee that a study is recruiting, and does not determine eligibility. Contact the study team and a qualified healthcare professional when considering participation.

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