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The Factors Cause Vasospasm After Aneurysmal Subarachnoid Hemorrhage

The Factors Cause Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Status
UNKNOWN
Phases
Unknown
Study type
Observational
Source
ClinicalTrials.gov
Registry ID
NCT00745758
Enrollment
20
Registered
2008-09-03
Start date
2008-05-31
Completion date
2008-09-30
Last updated
2008-09-03

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Subarachnoid Hemorrhage, Vasospasm, Intracranial

Keywords

SAH, vasospasm, ADMA

Brief summary

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

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.

Interventions

None listed

Sponsors

National Taiwan University Hospital
Lead SponsorOTHER

Study design

Observational model
COHORT
Time perspective
PROSPECTIVE

Eligibility

Sex/Gender
ALL
Age
18 Years to 80 Years
Healthy volunteers
No

Inclusion criteria

* Aneurysmal rupture with SAH

Exclusion criteria

* Bleeding tendency, * Large ICH with impending herniation

Countries

Taiwan

Contacts

Primary ContactKuo-Chuan Wang, MD
wang081466@yahoo.com.tw886-223123456

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026