1. Dennis A. Velez, MD Cerebrovascular/Endovascular Neurosurgery Dept. of Neurological Surgery Vanderbilt University

2. Objectives To recognize cerebral vasospasm (CVS) as a treatable complication of aSAH To safely and effectively institute optimal medical management of CVS To recognize the different modalities used to diagnose CVS To learn to identify which patients may benefit from endovascular therapy for CVS

3. Definition CVS has been defined in various ways: Clinical vasospasm (delayed cerebral ischemia, DCI) Angiographic vasospasm TCD vasospasm Which one is more clinically relevant?

4. Pathophysiology Prolonged arterial contraction: oxyhemoglobin Structural changes in the arterial wall: arterial hyperplasia, platelet aggregation and edema-luminal narrowing, increased resistance, decreased blood flow Breakdown of blood products: oxyhemoglobin, serotonin, prostaglandins, catecholamines, histamine, angiotensin Inflammatory response: neurogenic and classic inflammation

5. Histological changes

6. Role of Hgb oxidation products

7. Intracellular signaling

8. Inflammatory Response

9. CVS Prediction: Patient-specific factors Clinical grade Blood volume and frequency of SAH Size and location of aneurysm(s) Cocaine use Sex Age Smoking Hypertension

10. Glasgow Coma Scale

11. Hunt and Hess Grading Scale

12. WFNS Grading Scale

13. Fisher Scale

15. Pathological Markers Endothelin 1 Leukocytosis Soluble adhesion molecules Lipid peroxides Cellular proliferation and Growth Factors Hypomagnesemia Genetic markers

16. Diagnostic Neurological Imaging DSA/Conventional angiography CT angiography/CT perfusion TCD SPECT DWI/PWI

19. TCD

22. CVS Treatment Options Triple “H” therapy Albumin 5%/Normal Saline Pressors Hemodilution Nimodipine Statins Lumbar drainage/ Head shaking Endovascular treatment: IA/TBA Intra-aortic balloon counterpulsation (IABC)

27. Lumbar Drainage

28. Head Shaking for CVS

33. Intra-aortic balloon counterpulsation