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The Factors Cause Vasospasm After Aneurysmal Subarachnoid Hemorrhage

NCT ID: NCT00745758

Last Updated: 2008-09-03

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

UNKNOWN

Total Enrollment

20 participants

Study Classification

OBSERVATIONAL

Study Start Date

2008-05-31

Study Completion Date

2008-09-30

Brief Summary

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Extensive research has shown that the big event that leads to the initiation of vasospasm is the release of oxyhemoglobin (blood breakdown product).Depletion of NO synthase (19,20,21) was also noted after SAH.CSF is produced from choroid plexus in the ventricle. If the SAH is too dense, the blood in the subarachnoid space will not easy to be washed out.

Detailed Description

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Cerebral vasospasm remains a significant source of morbidity and mortality in patients with subarachnoid hemorrhage (SAH) after an aneurysmal rupture. Despite being a significant source of morbidity and mortality, death and disability from vasospasm have declined from approximately 35% in the early 1970's, to between 15% and 20% in the 1980's to \<10% in the 1990's(1,2,3,4).Extensive research has shown that the big event that leads to the initiation of vasospasm is the release of oxyhemoglobin (blood breakdown product)(1,12,13). This mechanism appears to be a multifactorial process that involves the generation of free radicals, lipid peroxidation and activation of protein kinase C as well as phospholipase C and A2 with resultant accumulation of diacylglycerol and the release of endothelin-1(14,15,16,17,18). On the other hand, depletion of NO synthase (19,20,21) was also noted after SAH. Previous reports showed that shunting of CSF through a lumbar drain after an SAH markedly reduces the risk of clinically evident vasospasm and its sequelae, shortens hospital stay, and improves outcome. Its beneficial effects are probably mediated through the removal of spasmogens that exist in the CSF(22). In our preliminary data, we have demonstrated a case with severe vasospasm, CSF was collected both from EVD and lumbar drain. The ADMA level and amount of Nitrate was well correlate with vasospasm and the level was much higher in lumbar drain then EVD. So, we will compared the CSF from EVD and lumbar puncture to see which factor is correlate with vasospasm.

Conditions

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Subarachnoid Hemorrhage Vasospasm, Intracranial

Keywords

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SAH, vasospasm, ADMA

Study Design

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Observational Model Type

COHORT

Study Time Perspective

PROSPECTIVE

Eligibility Criteria

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Inclusion Criteria

* Aneurysmal rupture with SAH

Exclusion Criteria

* Bleeding tendency,
* Large ICH with impending herniation
Minimum Eligible Age

18 Years

Maximum Eligible Age

80 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

No

Sponsors

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National Taiwan University Hospital

OTHER

Sponsor Role lead

Responsible Party

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Devision of neurosurgery

Principal Investigators

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Kuo-Chuan Wang, MD

Role: PRINCIPAL_INVESTIGATOR

NTUH

Locations

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devision of neurosurgery, National taiwan university hospital

Taipei, , Taiwan

Site Status RECRUITING

Countries

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Taiwan

Central Contacts

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Kuo-Chuan Wang, MD

Role: CONTACT

Phone: 886-223123456

Email: [email protected]

Facility Contacts

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Kuo-Chuan Wang, MD

Role: primary

Other Identifiers

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200803080R

Identifier Type: -

Identifier Source: org_study_id