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The Pathogenesis of Terson Syndrome and the Role of CSF Tau / Amyloid-ß 40 and 42 in Patients With Aneurysmatic Subarachnoid Hemorrhage

NCT02129010 · Status: COMPLETED · Type: OBSERVATIONAL · Enrollment: 120

Last updated 2016-03-08

No results posted yet for this study

Summary

Prospective clinical study to investigate the pathogenesis of Terson syndrome and the prognostic value of the CSF-biomarkers tau-protein and amyloid-β 40 and 42 in patients with aneurysmatic subarachnoid hemorrhage. Our two hypotheses are as follows:

1. The incidence of Terson syndrome correlates with the initial intracranial opening pressure (measured with extra ventricular drain)
2. The CSF-biomarkers correlate with the outcome assessed at discharge, 3-, 6- and 12-months postictally using Glasgow-Outcome-Scale-Extended (GOSE) and Euro-Qol-5 as well as with complications related to aneurysmatic subarachnoid hemorrhage such as cerebral vasospasm, delayed cerebral ischemia and re-bleed.

Conditions

  • Subarachnoid Hemorrhage
  • Terson Syndrome
  • CSF-proteines

Sponsors & Collaborators

  • Innogenetics N.V., Belgium

    collaborator UNKNOWN

  • Holger Joswig

    lead OTHER

Principal Investigators

  • Holger Joswig, M.D. · Cantonal Hospital St. Gallen, Dept. of Neurosurgery

Eligibility

Min Age
18 Years
Sex
ALL
Healthy Volunteers
Yes

Timeline & Regulatory

Start
2013-04-30
Primary Completion
2016-02-29
Completion
2016-02-29

Countries

  • Switzerland

Study Locations

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Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT02129010 on ClinicalTrials.gov