vasospasme post-hsa

R Manet(1), S Chatard-Baptiste(2) , S Saleme(2) , L Gergelé(3),

P Gromolard(3), C Nuti(1), FG Barral(2)

(1) Service de neurochirurgie – CHU Saint Etienne

(2) Service de radiologie – CHU Saint Etienne

(3) Département anesthésie-réanimation – CHU Saint Etienne

Cours DES neurochirurgie – 22 avril 2011

• Epidémiologie – pronostic

• Physiopathologie

• Diagnostic

– Clinique

– Monitoring

– Imagerie (S. Chatard-Baptiste)

• Prise en charge

– Traitements médicaux

– Traitements interventionnels (S. Saleme)

• Chronologie

– Précoce (<48h ) : 10% des HSA. Physiopathologie différente

mais morbidité similaire ? (Baldwin, Stroke, 2004);

– Incidence max: J5 – J14;

– Jusqu’à 4 semaines.

• Incidence (Charpentier, Stroke, 1999)

– Vasospasme angiographique : 30 -70% des HSA;

– Vasospasme symptomatique : 17 - 40% des HSA.

(Ischémie Cérébrale Différée: ICD)

• Facteurs de risque:

– Age jeune (Rabb Acta Neurochir 1994; Charpentier, Stroke, 1999 );

– HTA pré-existante (Ohman, J Neurosurg, 1991);

– Tabagisme actif (Lasner, J Neurosurg, 1997);

– Sévérité du tableau clinique initial (Lasner, J Neurosurg, 1997;

Charpentier, Stroke, 1999);

– Insuffisance cardiaque initiale (Friedman, Neurosurgery, 2003);

– Sévérité tomodensitométrique initiale (Claassen, Stroke, 2002);

– Hyperglycémie (Charpentier, Stroke, 1999);

– Nécessité d’une dérivation du LCR (Charpentier, Stroke, 1999).

…QUANTITE DE SANG SOUS-ARACHNOIDIEN

• Facteurs de risque

Clinique initiale & TDM initiale

Claassen, Stroke, 2002

Fisher Infarctus

0 0 %

1 6 %

2 14 %

3 12 %

4 28 %

Hunt&Hess ICD

1 22 %

2 33 %

3 52 %

4 53 %

5 74 %

Greenberg, Handbook Neurosurg, 2010

Complication la plus grave chez les survivants d’une HSA:

• L’ICD est un facteur de risque indépendant de séquellesneurologiques à 6 mois (Charpentier, Stroke, 1999);

• Meilleur pnc neurologique chez patients ne développant pas d’ICD(Dorsch, J Clin Neurosci, 1994);

• 30% de mortalité chez patients avec vasospasme (Dorsch, J Clin

Neurosci, 1994).

Décrit en 1951 Ecker, J Neurosurg, 1951;

Compréhension relativement incomplète;

HSA => hypoperfusion cérébrale:

Dépression hémodynamique immédiate

+/- aggravée secondairement par vasospasme

Tb hémodynamiques & microcirculatoires

* = p < 0,05


Tb autorégulation / couplage métabolique

PPC AutorégulationCouplage

métabolique


Tb autorégulation / couplage métabolique

Yundt, J Cereb Blood Flow Metab, 1998

Jaeger, Stroke, 2007

PPC AutorégulationCouplage

métabolique

Ischémie


Phénomènes microthrombotiques

Aggrégation plaquettaire => micro-infarctus;

Akopov, Cerebrovasc Brain Metab, 1996

Consommation plaquettaire à la phase aigüe d’HAS = facteur prédictif;

indépendant d’ICD Hirashima, J Neurosurg, 2005

Ttt antiplaquettaire => amélioration non significative du pnc neuro.

Dorhout, Stroke, 2008


Phénomènes microthrombotiques

SAH => Inflammation => Hypercoagulabilité;

Marqueurs plasmatiques de l’ activité thrombine & fibrinolyse corrélés

avec grade HSA et pnc mais pas de corrélation retrouvée entre ces

marqueurs et ICD/infarctus;

Ilveskero, Neurosurgery, 2005

Activité thrombine dans LCR corrélée à infarctus par ICD.

Kasuya, Acta Neurochir, 1998

Inflammation / Stress oxydatif

Inflammatory mediators ( stroke) Potential therapeutic interventions

Stress oxydatif

i NOS neurotoxicité Relargage NO

Chow M, Neurosurgery, 2002

Ng, Neurosurgery,2001

↑Endothéline-I

Vasoconstriction

Prolif endothéliale & m lisse

Inflammation

DIS ?

Pdts dégradation HB COX-2 => PG

Inflammation

Vasoconstriction

Lésion BHE

Bilirubine

Biliverdine

Hème

BOXesVasospasme angiographique

DIS ?

Woszczyk, Acta Neurochir, 2003

NO

ET-I

Péroxydation

lipidique

BOXes

Pilitsis, J Neurosurg, 2002

Clark, J Cereb Blood Flow Metab, 2006

ICD ?

ICD ?

Stress oxydatif: péroxydation lipidique

Levels of CSF F2-IsoPs (specific

marker of lipid peroxidation) levels

during the first 8 days after

surgery (15SAH/10controls).

(A)Non-SAH controls (n=10).

(B)DIND patients (n=3)

Stress oxydatif

Inflammation

↓CBF Stase leucocytaire ↑ infiltration leucocytaire

Lucas, Br J Pharmaco, 2006

Lindsberg, Ann Neurol, 1996

Rothoerl, Cerebrovasc Dis, 2006

Hallenbeck, Stroke, 1986

Dommages locaux Activation microglialeMacrophages

Cytokines

Complément

C3a C5a MAC

Hémolyse

Lésions neuronales

Médiateurs

proinflammatoires

?

Molécules d’adhésion cellulaireI-CAM (ICAM1) V-CAM

Sélectines (P-selectin E-selectin)

Intégrines

Adhésion & infiltration leucocytaire

Mellergård, Neurosurgery, 2011

Inflammation

IL1β

IL6

IL10

Apoptose

P53 / activité caspase

Inhibition P53 chez rat => ↓mortalité ↓rupture BHE ↑pnc neuro

Apoptose

endothéliale

Apoptose

neuronale

Rupture BHE

Cahill, Stroke, 2006

Influx cationique/hydrique passif massif dépassant les capacités de

transport mbr => dépolarisation « galopante » lente (2-5mm/min)

Situation physiologique

Suractivation des transporteurs ATP-dépendants=> conso énergie ++

=> réponse hémodynamique hyperhémique

Normalisation en qlq min (5-15min)

Agression aiguë (HSA)

=> absence de réponse hémodynamique adaptée = ischémie

=> Spreading ischaemia Dreier, Brain, 2009

Durable / auto-entretenue

Cortical spreading depolarization


Dreier, Brain, 2009

Dreier, Brain, 2009


Dreier, Brain, 2009

Apoptose

Tb

hémodynamiques

Stress

oxydatifInflammation

Réduction DSCDécouplage

métaboliqueTb autorégulation

Spreading

depolarization

Souffrance cérébrale

Vasospasme post-HSA = Ʃ phénomènes pathologiques complexes

dont l’une des expressions est la réduction de diamètre des

vaisseaux.

Déficit Neurologique

Ischémique Différé

Infarctus

cérébral

Clinique

Dégradation neurologique différée survenant entre J5 et J21:

Tb des fonctions supérieures / Désorientation temporo-spatiale;

Tb de la vigilance;

Ʃd méningé;

Apparition ou aggravation d’un déficit neurologique focal:

- ACA => Ʃd frontal (+/- bilatéral si ACoA);

- ACM => mono/hémiparésie, aphasie, apraxie…

Signes systémiques: hyperthermie, hyponatrémie…

Diagnostique différentiel

• Resaignement;

• Hydrocéphalie;

• Œdème cérébral;

• Epilepsie;

• Tb métaboliques;

• Sepsis;

• …

Monitoring non-invasif

Doppler transcrânien Seiler, J Neurosurg, 1986

VELOCITES MOYENNES VASOSPASME

80 - 120 cm/s Discret

120 - 200 cm/s Modéré

> 200 cm/s Sévère

Augmentation > 50 cm/s/j ATTENTION

Lindegaard (Vm ACM / Vm ACI)

> 3 Vasospasme

> 6 Vasospasme sévère

Lindegaard, Acta Neurochir, 1988


Doppler transcrânien

Problèmes: intermittent (=> monitoring continu)

interprétation difficile / opérateur dépendant ++

faible sensibilité (50-67%)

exploration des gros vaisseaux


cEEG / qEEG:

Diminution de l’amplitude du signal EEG;

Labar, EEG clin Neurophys, 1991

Diminution relative de l’activité α (6-14 Hz).

Vespa, EEG clin Neurophys, 1997

Diminution du ratio Alpha/Delta (ADR).

Claassen, Clinical Neurophysiology, 2005


cEEG / qEEG:


cEEG / qEEG:

♀ 57years. SAH/PCoA. Hunt–Hess grade 4

Post-op (SAH day 2) GCS14, no infarct on CT[…]

SAH day 6: ADR progressively decreased […]

Flow velocities in the right MCA were marginally

elevated (144 cm/s).

SAH day 7: GCS dropped from 14 to 12

=> CTscan + Angiography: vasospasm ++

=> intra-arterial Papaverine/Nicardipine


NIRS:

(A) 6 patients (5 WFNS V and 1 WFNS II): only

small changes in CoSO2 (5%) / No vasospasm

on DSA;

(B) 8 patients (5 WFNS V and 3 WFNS II)

showed decreases in CoSO2 by more than 5%

reduction between 5 and 9 days after SAH. 6

exhibited severe vasospasms extending to the

peripheral MCA on DSA. TCD failed to detect in

4 cases.

(A)

(B)

Monitoring invasif

Microdialyse:

15 patients

J Neuroradiol. 2005 Dec;32(5):348-51.

Monitoring invasif

Multimodal

Hourly means ± SD of microdialysis and

PbtO2 measurements 24-hours preceding

CT-scans

- without new infarction (N = 55),

- with new ipsilateral frontal infarction (N = 8)

- with new infarction distant to the monitoring

devices (N = 4)

Biologie

Protéine S100b

LCR Wiesmann, Acta Neurochir, 1997

Plasmatique Takayasu, J Neurosurg, 1985

Autres:

F2-IsoPs LCR Lin, Free Rad Biol Med, 2006

Axe hypothalamo-hypophysaire ? Weant, Neurosurgery, 2008

…

Imagerie

Polygone Angio-imagerie

Micro-circulation (?) Imagerie de perfusion

• Imagerie de premier passage d’un bolus intraveineux d’un agent

exogène non diffusible ( pdc iodé ) dans le réseau capillaire

encéphalique

• Paramètres hémodynamiques cérébraux

• Données qualitatives : cartographies

• Données quantitatives.

TDM perf

TDM perf

TDM perf: cartographie

TDM perf = données quantitatives

Ca bloqueurs: Nimodipine NIMOTOP®

Kazda, Acta Neurochir, 1982 (7 essais randomisés depuis)

→ IVSE / relais Per Os dès que possible

Optimisation rhéologique…

…3H thérapie ? (Hypertension-Hypervolémie-Hémodilution)

Traitements médicaux

3H thérapie (préventive / curative)

• Aucun essai contrôlé randomisé montrant bénéfice.

• Tendance actuelle =

– Normovolémie

– Hypertension contrôlée PAM ≈ 100mmHg - 120mmHg

– Hémodilution est très discutable

– +/- monitoring hémodynamique


• Ca bloqueurs: Nicardipine Haley J Neurosurg 1993

• Antagonistes des rNMDA: SELFOTEL ® Grotta, Stroke, 1995

• Antagonistes des rETA: CLOZANTAN ® Barth, Acta Neurochir, 2007

• Free radical scavengers: FREEDOX® Kassell J Neurosurg 1996

• Nitroprussiate intratéchal Thomas, Stroke, 1999

• Magnésium Veyna, J Neurosurg, 2002

• HBPM Wurm, Clin Neurol Neurosurg, 2004;

• Statines Vergouwen, Stroke, 2010

…

? ? ?


Traitements chirurgicaux

• Epuration des espaces sous-arachnoïdiens (mécanique,

fibrinolytiques, drainage LCR).

• Sympathectomie cervicale Hori, Acta Neurochir, 1979

• Pontages intra-extracrâniens Batjer, Neurosurgery, 1986

• Stimulation du ggl sphénopalatin Yarnitsky, Surg Neurol, 2005

Takahashi, J Neurosurg, 2010

Traitements interventionnels

Traitements endovasculaires

• Angioplastie mécanique;

• Vasodilatation pharmacologique in-situ

• …


Angioplastie transluminale mécanique

• Zubkov, Acta Neurochir, 1984.

• Muizelaar, J Neurosurg, 1999.

• Rationnel: endommagement vasculaire / destruction des fibres de

collagène et des myocytes Smith, J Vasc Interv Radiol, 2000.

• Pb: complications rares mais généralement dramatiques…


Papaverine intra-artérielle:

Un des premier produit utilisé.

Nombreuses publications concernant des effets délétères

Mathis, Neuroradiology, 1997

Polin, Neurosurgery, 1998

Smith, Stroke, 2004

…


Smith, Stroke, 2004


Papaverine intra-artérielle:


Ca bloqueurs intra-artériels:

Nimodipine NIMOTOP Biondi, AJNR, 2004

Nicardipine LOXEN Badjatia, AJNR, 2004

Inhibiteur PDE-3 intra-artériels:

Milrinone COROTROPE ® Khajavi, Neurosurgery, 1997

Amrinone INOCOR ® Yoshida, AJNR, 1997

Autres molécules de mecanisme d’action similaire non rapportée dans

le ttt du vasospasme post-HSA:

Enoximone

Imazodan

Piroximone


Contrôle HSA CORO cisternal CORO ia

Histologie tronc basilaire

HES

Immuno

Histo

AMPc

Animaux tués à J7 (après ttt le cas échéant)


Déficit Neurologique

Ischémique Différé

Infarctus

cérébral

TDMDTCClinique

Pas d’argument

Surveillance

≥ 1 argument

Artériographie

conventionnelle

Echo cœur

Optimisation volémie

Pas de

vasospasmeVasospasme

REFERENCES (1)

• Adams Jr. HP, Kassell NF, Torner JC, Haley Jr. EC. Predicting cerebral ischemia after aneurysmal subarachnoidhemorrhage: influences of clinical condition, CT results, and antifibrinolytic therapy.A report of the CooperativeAneurysm Study. Neurology 1987;37:1586– 91.

• Akopov S, Sercombe R, Seylaz J: Cerebrovascular reactivity: role of endothelium/platelet/leukocyte interactions.Cerebrovasc Brain Metab Rev 8:11-94, 1996.

• Badjatia N, Topcuoglu MA, Pryor JC, Rabinov JD, Ogilvy CS, Carter BS, Rordorf GA. Preliminary experience with intra-arterial nicardipine as a treatment for cerebral vasospasm.AJNR Am J Neuroradiol. 2004 May;25(5):819-26.

• Baldwin ME, Macdonald RL, Huo D et al. (2004) Early vasospasm on admission angiography in patients withaneurysmal subarachnoid hemorrhage is a predictor for in-hospital complications and poor outcome. Stroke 35:2506-11

• Batjer H, Samson D. Use of extracranial-intracranial bypass in the management of symptomatic vasospasm.Neurosurgery. 1986 Aug;19(2):235-46.

• Biondi A, Ricciardi GK, Puybasset L, Abdennour L, Longo M, Chiras J, Van Effenterre R. Intra-arterial nimodipine for the treatment of symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage: preliminary results. AJNR Am J Neuroradiol. 2004 Jun-Jul;25(6):1067-76.

• Block M, Zecca L, Hong JS. Microglia-mediated neurotoxicity: uncovering the molecular mechanisms. NatureReviews Neuroscience 8, 57-69 (January 2007).

• Cahill J, Calvert JW, Solaroglu I, Zhang JH: Vasospasm and p53-induced apoptosis in an experimental model ofsubarachnoid hemorrhage. Stroke 37:1868-1874, 2006.

• Charpentier C, Audibert G, Guillemin F, Civit T, Ducrocq X, Bracard S, et al. Multivariate analysis of predictors ofcerebral vasospasm occurrence after aneurysmal subarachnoid hemorrhage. Stroke 1999; 30:1402–8 N5.

• Claassen J, Carhuapoma JR, Kreiter KT et al. (2002) Global cerebral edema after subarachnoid hemorrhage:frequency, predictors, and impact on outcome. Stroke 33: 1225 32.

• Claassen J, Hirsch LJ, Kreiter KT, Du EY, Connolly ES, Emerson RG, Mayer SA. Quantitative continuous EEG fordetecting delayed cerebral ischemia in patients with poor-grade subarachnoid hemorrhage. Clin Neurophysiol.2004 Dec;115(12):2699-710.

REFERENCES (2)

• Clark JF, Sharp FR: Bilirubin oxidation products (BOXes) and their role in cerebral vasospasm after subarachnoidhemorrhage. J Cereb Blood Flow Metab 26:1223-1233, 2006.

• Chow M, Dumont AS, Kassell NF: Endothelin receptor antagonists and cerebral vasospasm: an update.Neurosurgery 51:1333-1341; discussion 42, 2002.

• Dorhout Mees SM, van den Bergh WM, Algra A, Rinkel GJ: Antiplatelet therapy in aneurysmal subarachnoidhemorrhage. Stroke 2008.

• DorschNW, King MT.A review of cerebral vasospasm in aneurismal hemorrhage. Part I: incidence and effects. JClin Neurosci 1994;1:19– 26.

• Dreier JP, Major S, Manning A, Woitzik J, Drenckhahn C, Steinbrink J, Tolias C, Oliveira-Ferreira AI, Fabricius M,Hartings JA, Vajkoczy P, Lauritzen M, Dirnagl U, Bohner G, Strong AJ; COSBID study group. Cortical spreadingischaemia is a novel process involved in ischaemic damage in patients with aneurysmal subarachnoidhaemorrhage. Brain. 2009 Jul;132(Pt 7):1866-81.

• Eddleman CS, Hurley MC, Naidech AM, Batjer HH, Bendok BR. Endovascular options in the treatment of delayedischemic neurological deficits due to cerebral vasospasm. Neurosurg Focus. 2009;26(3):E6.

• Ecker A, Riemenschneider PA: Arteriographic demonstration of spasm of the intracranial arteries, with specialreference to saccular arterial aneurysms. J Neurosurg 8:660–667, 1951.

• Friedman JA, Pichelmann MA, Piepgras DG, McIver JI, Toussaint 3rd LG, McClelland RL, et al. Pulmonarycomplications of aneurysmal subarachnoid hemorrhage. Neurosurgery 2003;52:1025– 31 N5.

• Greenberg M.S. Handbook of neurosurgery. Ed Thieme. 7 edition (November 1, 2010) ISBN-10: 1604063661.ISBN-13: 978-1604063660.

• Grotta J, Clark W, Coull B, Pettigrew LC, Mackay B, Goldstein LB, Meissner I, Murphy D, LaRue L. Safety andtolerability of the glutamate antagonist CGS 19755 (Selfotel) in patients with acute ischemic stroke. Results of aphase IIa randomized trial. Stroke. 1995 Apr;26(4):602-5.

• Haley Jr. EC, Kassell NF, Torner JC, Truskowski LL, Germanson TP. A randomized trial of two doses ofnicardipine in aneurysmal subarachnoid hemorrhage. A report of the Cooperative Aneurysm Study. J Neurosurg1994;80:788–96.

REFERENCES (3)

• Haley Jr. EC, Kassell NF, Torner JC.A randomized controlled trial of high-dose intravenous nicardipine inaneurysmal subarachnoid hemorrhage. J Neurosurg 1993;78:537–47

• Haley Jr. EC, Kassell NF, Torner JC, Truskowski LL, Germanson TP. A randomized trial of two doses ofnicardipine in aneurysmal subarachnoid hemorrhageA report of the Cooperative Aneurysm Study. J Neurosurg1994;80:788–96 N1.

• Haley Jr. EC, Kassell NF, Apperson-Hansen C, Maile MH, Alves WM. A randomized double-blind vehicle-controlled trial of tirilazad mesylate in patients with aneurysmal subarachnoid hemorrhage: a cooperative study inNorth America. J Neurosurg 1997;86:467–74 N1.

• Hallenbeck JM, Dutka AJ, Tanishima T, Kochanek PM, Kumaroo KK, Thompson CB, Obrenovitch TP, ContrerasTJ: Polymorphonuclear leukocyte accumulation in brain regions with low blood flow during the early postischemicperiod. Stroke 17:246-253, 1986.

• Hijdra A, Van Gijn J, Stefanko S, Van Dongen KJ, Vermeulen M, Van Crevel H. Delayed cerebral ischemia afteraneurysmal subarachnoid hemorrhage: clinicoanatomic correlations. Neurology. 1986;36:329 –333.

• Hirashima Y, Hamada H, Kurimoto M, Origasa H, Endo S: Decrease in platelet count as an independent risk factorfor symptomatic vasospasm following aneurysmal subarachnoid hemorrhage. J Neurosurg 102:882-887, 2005.

• Hop JW, Rinkel GJ,Algra A, Van Gijn J. Initial loss of consciousness and risk of delayed cerebral ischemia afteraneurysmal subarachnoid hemorrhage. Stroke 1999;30:2268–71 N5.)

• Hori S, Suzuki J. Early intracranial operations for ruptured aneurysms. Acta Neurochir (Wien). 1979;46(1-2):93-104.

• Inagawa T. Cerebral vasospasm in elderly patients treated by early operation for ruptured intracranial aneurysms.Acta Neurochir (Wien) 1992;115:79–85.

• Ilveskero S, Juvela S, Siironen J, Lassila R: D-dimer predicts outcome after aneurysmal subarachnoidhemorrhage: no effect of thromboprophylaxis on coagulation activity. Neurosurgery 57:16-24; discussion 16-24,2005.

• Jaeger M, Schuhmann MU, Soehle M, Nagel C, Meixensberger J: Continuous monitoring of cerebrovascularautoregulation after subarachnoid hemorrhage by brain tissue oxygen pressure reactivity and its relation todelayed cerebral infarction. Stroke 38:981-986, 2007.

REFERENCES (4)

• Kassell NF, Torner JC, Haley Jr. EC, Jane JA, Adams HP, Kongable GL. The International Cooperative Study onthe Timing of Aneurysm Surgery. Part 1: Overall management results. J Neurosurg 1990;73:18–36.

• Kassell NF, Haley Jr. EC, Apperson-Hansen C, Alves WM. Randomized double-blind vehicle-controlled trial oftirilazad mesylate in patients with aneurysmal subarachnoid hemorrhage: a cooperative study in Europe Australiaand New Zealand. J Neurosurg 1996;84: 221–8 N1.

• Kasuya H, Shimizu T, Takakura K: Thrombin activity in CSF after SAH is correlated with the degree of SAH thepersistence of subarachnoid clot and the development of vasospasm. Acta Neurochir (Wien) 140:579-584, 1998.

• Khajavi K, Ayzman I, Shearer D, Jones SC, Levy JH, Prayson RA, Skibinski CI, Hahn JF, Chyatte D.Prevention ofchronic cerebral vasospasm in dogs with milrinone. Neurosurgery. 1997 Feb;40(2):354-62.

• Kazda S, Towart R.Nimodipine: a new calcium antagonistic drug with a preferential cerebrovascular action. ActaNeurochir (Wien). 1982;63(1-4):259-65.

• Labar DR, Fisch BJ, Pedley TA, Fink ME, Solomon RA. Quantitative EEG monitoring for patients withsubarachnoid hemorrhage. Electroencephalogr Clin Neurophysiol. 1991 May;78(5):325-32.

• Lanzino G, Kassell NF. Double-blind randomized vehicle-controlled study of high-dose tirilazad mesylate in womenwith aneurysmal subarachnoid hemorrhage. Part II. A cooperative study in North America. J Neurosurg1999;90:1018–24 N1.

• Lanzino G, Kassell NF, Dorsch NW, Pasqualin A, Brandt L, Schmiedek P, et al. Double-blind randomized vehicle-controlled study of high-dose tirilazad mesylate in women with aneurysmal subarachnoid hemorrhage. Part I. Acooperative study in Europe Australia New Zealand and South Africa. J Neurosurg 1999;90:1011–7 N1.

• Lasner TM,Weil RJ, Riina HA, King Jr. JT, Zager EL, Raps EC, et al. Cigarette smoking-induced increase in therisk of symptomatic vasospasm after aneurysmal subarachnoid hemorrhage. J Neurosurg 1997; 87:381–4 N5.

• Lauritzen M, Dreier JP, Fabricius M, Hartings JA, Graf R, Strong AJ. Clinical relevance of cortical spreadingdepression in neurological disorders: migraine, malignant stroke, subarachnoid and intracranial hemorrhage, andtraumatic brain injury. J Cereb Blood Flow Metab. 2011 Jan;31(1):17-35. Epub 2010 Nov 3.

REFERENCES (5)

• Lin CL, Hsu YT, Lin TK, Morrow JD, Hsu JC, Hsu YH, Hsieh TC, Tsay PK, Yen HC. Increased levels of F2-isoprostanes following aneurysmal subarachnoid hemorrhage in humans. Free Radic Biol Med. 2006 Apr15;40(8):1466-73. Epub 2006 Jan 13.

• Lindegaard KF, Nornes H, Bakke SJ, Sorteberg W, Nakstad P. Cerebral vasospasm after subarachnoidhaemorrhage investigated by means of transcranial Doppler ultrasound. Acta Neurochir Suppl (Wien). 1988;42:81-4.

• Lindsberg PJ, Ohman J, Lehto T, Karjalainen-Lindsberg ML, Paetau A, Wuorimaa T, Carpen O, Kaste M, Meri S:Complement activation in the central nervous system following blood-brain barrier damage in man. Ann Neurol40:587-596, 1996.

• Lucas SM, Rothwell NJ, Gibson RM: The role of inflammation in CNS injury and disease. Br J Pharmacol147:S232-S240, 2006.

• Mathis JM, Jensen ME, Dion JE. Technical considerations on intra-arterial papaverine hydrochloride for cerebralvasospasm. Neuroradiology. 1997 Feb;39(2):90-8.

• Mellergård P, Åneman O, Sjögren F, Säberg C, Hillman J. Differences in cerebral extracellular response ofinterleukin-1β, interleukin-6, and interleukin-10 after subarachnoid hemorrhage or severe head trauma in humans.Neurosurgery. 2011 Jan;68(1):12-9; discussion 19.

• Muizelaar JP, Zwienenberg M, Rudisill NA, Hecht ST: The prophylactic use of transluminal balloon angioplasty inpatients with Fisher Grade 3 subarachnoid hemorrhage: A pilot study. J Neurosurg 91:51–58, 1999.

• Ng WH, Moochhala S, Yeo TT, Ong PL, Ng PY: Nitric oxide and subarachnoid hemorrhage: elevated level incerebrospinal fluid and their implications. Neurosurgery 49:622-626; 2001.

• Nishiguchi M, Ono S, Iseda K, Manabe H, Hishikawa T, Date I. Effect of vasodilation by milrinone, aphosphodiesterase III inhibitor, on vasospastic arteries after a subarachnoid hemorrhage in vitro and in vivo:effectiveness of cisternal injection of milrinone. Neurosurgery. 2010 Jan;66(1):158-64; discussion 164.

• Ohman J, ServoA, Heiskanen O. Risks factors for cerebral infarction in good-grade patients after aneurysmalsubarachnoid hemorrhage and surgery: a prospective study. J Neurosurg 1991;74:14–20 N5.

REFERENCES (6)

• Pilitsis JG, Coplin WM, O’Regan MH, Wellwood JM, Diaz FG, Fairfax MR, Michael DB, Phillis JW:Free fatty acidsin human cerebrospinal fluid following subarachnoid hemorrhage and their potential role in vasospasm: apreliminary observation. J Neurosurg 97:272-279, 2002.

• Polin RS, Hansen CA, German P, Chadduck JB, Kassell NF. Intra-arterially administered papaverine for thetreatment of symptomatic cerebral vasospasm. Neurosurgery. 1998 Jun;42(6):1256-64; discussion 1264-7.

• Qureshi AI, Sung GY, Razumovsky AY, Lane K, Straw RN, Ulatowski JA. Early identification of patients at risk forsymptomatic vasospasm after aneurysmal subarachnoid hemorrhage. Crit Care Med 2000;28:984–90 N5.

• Roos YB, de Haan RJ, Beenen LF, Groen RJ, Albrecht KW, Vermeulen M. Complications and outcome in patientswith aneurysmal subarachnoid haemorrhage: a prospective hospital based cohort study in The Netherlands. JNeurol Neurosurg Psychiatry. 2000;68:337–341.

• Rothoerl RD, Schebesch KM, Kubitza M, Woertgen C, Brawanski A, Pina AL. ICAM-1 and VCAM-1 expressionfollowing aneurysmal subarachnoid hemorrhage and their possible role in the pathophysiology of subsequentischemic deficits. Cerebrovasc Dis. 2006;22(2-3):143-9. Epub 2006 May 10.

• Sarrafzadeh A, Haux D, Plotkin M, Lüdemann L, Amthauer H, Unterberg A. Bedside microdialysis reflectsdysfunction of cerebral energy metabolism in patients with aneurysmal subarachnoid hemorrhage as confirmed by15 O-H2 O-PET and 18 F-FDG-PET. J Neuroradiol. 2005 Dec;32(5):348-51.

• Seiler RW, Grolimund P, Aaslid R, Huber P, Nornes H. Cerebral vasospasm evaluated by transcranial ultrasoundcorrelated with clinical grade and CT-visualized subarachnoid hemorrhage. J Neurosurg. 1986 Apr;64(4):594-600.

• Solenski NJ, Haley Jr. EC, Kassell NF, Kongable G, Germanson T, Truskowski L, et al. Medical complications ofaneurysmal subarachnoid hemorrhage: a report of the multicenter, cooperative aneurysm study. Participants ofthe Multicenter Cooperative Aneurysm Study. Crit Care Med 1995;23:1007–17.

• Smith WS, Dowd CF, Johnston SC, Ko NU, DeArmond SJ, Dillon WP, Setty D, Lawton MT, Young WL, HigashidaRT, Halbach VV. Neurotoxicity of intra-arterial papaverine preserved with chlorobutanol used for the treatment ofcerebral vasospasm after aneurysmal subarachnoid hemorrhage. Stroke. 2004 Nov;35(11):2518-22.

REFERENCES (7)

• Solomon RA, Onesti ST, Klebanoff L. Relationship between the timing of aneurysm surgery and the developmentof delayed cerebral ischemia. J Neurosurg 1991;75:56–61.

• Takayasu M, Shibuya M, Kanamori M et al. (1985) S-100 protein and calmodulin levels in cerebrospinal fluid aftersubarachnoid hemorrhage. J Neurosurg 63: 417-20

• Tanaka Y, Masuzawa T, Saito M, Yamada T, Ebihara A, Iwasa H, Mori S.Combined administration of Fasudilhydrochloride and nitroglycerin for treatment of cerebral vasospasm. Acta Neurochir Suppl. 2001;77:205-7.

• Tanaka K, Minami H, Kota M, Kuwamura K, Kohmura E. Treatment of cerebral vasospasm with intra-arterialfasudil hydrochloride. Neurosurgery. 2005 Feb;56(2):214-23.

• Takahashi M, Zhang ZD, Macdonald RL. Sphenopalatine ganglion stimulation for vasospasm after experimentalsubarachnoid hemorrhage. J Neurosurg. 2010 Jul 2. [Epub ahead of print]

• Thomas JE, Rosenwasser RH, Armonda RA, Harrop J, Mitchell W, Galaria I. Safety of intrathecal sodiumnitroprusside for the treatment and prevention of refractory cerebral vasospasm and ischemia in humans. Stroke1999;30:1409–16 N3.

• Vespa PM, Nuwer MR, Juhász C, Alexander M, Nenov V, Martin N, Becker DP. Early detection of vasospasmafter acute subarachnoid hemorrhage using continuous EEG ICU monitoring. Electroencephalogr ClinNeurophysiol. 1997 Dec;103(6):607-15.

• Veyna RS, Seyfried D, Burke DG, Zimmerman C, Mlynarek M, Nichols V, et al. Magnesium sulfate therapy afteraneurysmal subarachnoid hemorrhage. J Neurosurg 2002;96:510–4 N2.

• Weant KA, Sasaki-Adams D, Dziedzic K, Ewend M. Acute relative adrenal insufficiency after aneurysmalsubarachnoid hemorrhage. Neurosurgery. 2008 Oct;63(4):645-9; discussion 649-50.

• Westermaier T, Jauss A, Eriskat J, Kunze E, Roosen K.The temporal profile of cerebral blood flow and tissuemetabolites indicates sustained metabolic depression after experimental subarachnoid hemorrhage in rats.Neurosurgery. 2011 Jan;68(1):223-9; discussion 229-30.

REFERENCES (8)

• Wiesmann M, Missler U, Hagenstrom H, Gottmann D (1997) S-100 protein plasma levels after aneurysmalsubarachnoid haemorrhage. Acta Neurochir (Wien) 139: 1155-60

• Woszczyk A, Deinsberger W, Boker DK: Nitric oxide metabolites in cisternal CSF correlate with cerebralvasospasm in patients with a subarachnoid haemorrhage. Acta Neurochir (Wien) 145:257- 263; 2003.

• Wurm G, Tomancok B, Nussbaumer K, Adelwohrer C, Holl K. Reduction of ischemic sequelae followingspontaneous subarachnoid hemorrhage: a double-blind randomized comparison of enoxaparin vs. placebo. ClinNeurol Neurosurg 2004;106:97–103 N1.

• Yanagisawa M, Kurihara H, Kimura S, Tomobe Y, Kobayashi M, Mitsui Y, Yazaki Y, Goto K, Masaki T. A novelpotent vasoconstrictor peptide produced by vascular endothelial cells. Nature. 1988 Mar 31;332(6163):411-5.

• Yarnitsky D, Lorian A, Shalev A, Zhang ZD, Takahashi M, Agbaje-Williams M, Macdonald RL.Reversal of cerebralvasospasm by sphenopalatine ganglion stimulation in a dog model of subarachnoid hemorrhage. Surg Neurol.2005 Jul;64(1):5-11

• Yoshida K, Watanabe H, Nakamura S.Intraarterial injection of amrinone for vasospasm induced by subarachnoidhemorrhage. AJNR Am J Neuroradiol. 1997 Mar;18(3):492-6.

• Yundt KD, Grubb RL Jr, Diringer MN, Powers WJ. Autoregulatory vasodilation of parenchymal vessels is impairedduring cerebral vasospasm. J Cereb Blood Flow Metab. 1998 Apr;18(4):419-24.

• Zubkov YN, Nikiforov BM, Shustin VA: Balloon catheter technique for dilatation of constricted cerebral arteriesafter aneurysmal SAH. ActaNeurochir (Wien) 70:65–79, 1984.

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